INTERNAL MEDICINE 3B (CARDIOLOGY)

Acute Coronary Syndrome

Department of Medicine

TOPIC OUTLINE Several Features Help to Differentiate ACS from Chronic SA:
I. Acute Coronary Syndromes 1. Sudden onset of symptoms at rest (or with minimal exertion) that last
II. Non-ST Segment Elevation-Acute Coronary Syndromes at least 10 minutes unless treated promptly
a. Pathophysiology 2. Severe pain, pressure, or discomfort in the chest; and
b. Clinical Presentation 3. Accelerating pattern of angina that develops more frequently, with
1. History and Physical Examination greater severity, or that awakens the patient from sleep.
2. Electrocardiogram
3. Cardiac Biomarkers
4. Diagnostic Evaluation
c. Diagnostic Evaluation
d. Risk Stratification
e. Medical Treatment
1. General Measures
2. Anti-Ischemic Therapy
3. Anti-Thrombotic Therapy
4. Anticoagulation Therapy
5. Invasive vs. Conservative Therapy
6. Long-Term Management
III. Prinzmetal’s Variant Angina
a. Clinical and Angiographic Manifestations
b. Medical Treatment
c. Prognosis
IV. ST-Segment Elevation Myocardial Infarction
a. Pathophysiology
b. Clinical Manifestations
c. Laboratory Findings
1. Electrocardiogram
2. Serum Cardiac Biomarkers
3. Cardiac Imaging
d. Initial Management
e. Management in the Emergency Department
f. Control of Discomfort
g. Management Strategies
h. Limitation of Infarct Size
1. Primary Percutaneous Coronary Intervention
2. Fibrinolysis Table 1.1: Comparison within Acute Coronary Syndromes
3. Integrated Reperfusion Strategy Diagnosis Clinical Features ECG Findings Laboratory Findings
i. Hospital Phase Management Ischemic chest pain
j. Pharmacotherapy that occurs at rest
UA or with previously o None
k. Complications and their Management
tolerated levels of o ST-segment Normal troponin
l. Post-Infarction Risk Stratification and Management exertion depression
m. Secondary Prevention o T-wave inversion
V. References NSTEMI
VI. Samplex Questions Prolonged ischemic
LEGEND chest pain in any o ST-segment Elevated troponin
STEMI setting elevation
PPT LECTURE BOOK OTHER TRANS REMEMBER
o New left-bundle
📈 🔊 📖 📃 📌 branch block
ACUTE CORONARY SYNDROMES NON-ST-SEGMENT ELEVATION-ACUTE CORONARY SYNDROME
 Acute Coronary Syndrome (ACS)- describes the condition I. PATHOPHYSIOLOGY
where there is a sudden and decreased blood flow to your
coronaries, leading to unstable angina, NSTEMI, and STEMI. Mechanisms for NSTE-ACS: caused by an imbalance between myocardial
 Ischemic heart disease may manifest clinically as either chronic oxygen supply and demand resulting from any of the 5 processes that lead
stable angina or an acute coronary syndrome (ACS). to thrombus formation:
1. Non-occlusive thrombus – often a platelet plug overlying a fissured
Ischemic Heart Disease
Acute Coronary Syndromes
atherosclerotic plaque
NSTE-ACS ST-Elevation a. Disruption of an unstable coronary plaque due to plaque
NSTE-Myocardial Infarction Myocardial Infarction Stable Angina (SA) rupture, erosion, or
(NSTEMI) (STEMI) b. Calcified protruding nodule that leads to intracoronary thrombus
Unstable Angina (UA) formation and an inflammatory response
 Patients with ACS commonly are classified into two groups 2. Dynamic obstruction – spasm of an epicardial coronary artery
to facilitate evaluation and management: (coronary arterial vasoconstriction)
o Acute MI with ST-segment elevation (STEMI) 3. Severe, organic luminal narrowing – as in restenosis following a PCI
- Pathologic diagnosis of MI requires evidence of (gradual intraluminal narrowing)
myocardial cell death caused by ischemia 4. Arterial inflammation leading to thrombosis
- Relative incidence is declining due to greater use of 5. Increase in myocardial oxygen demands caused by conditions such
aspirin, statins, and less smoking. as tachycardia, fever, and thyrotoxicosis in the presence of fixed,
o Non-ST-segment elevation ACS (NSTE-ACS) severe coronary obstruction
- NSTEMI (have evidence of myocyte necrosis)  Plaque rupture- most common etiology of coronary thrombosis
 Typical symptoms w/o persistent (>20 minutes  Among patients with NSTE-ACS studied at angiography:
continuously) ST-elevation in at 2 contiguous ECG o 10% have stenosis of the left main coronary artery
leads, but w/ elevation of cardiac biomarkers >99th o 35% have three-vessel CAD, 20% have two-vessel disease
percentule of normal o 20% have single-vessel disease
 Relative incidence of NSTEMI is rising due to the o 15% have no apparent critical epicardial coronary artery stenosis
increasing burden of diabetes and chronic kidney  Vulnerable plaques- responsible for ischemia may show an eccentric
disease in an aging population stenosis with scalloped or overhanging edges and a narrow neck on
- Unstable angina (no evidence of myocardial necrosis) coronary angiography.
 Typical symptoms and serial negative markers of o Composed of a lipid-rich core with a thin fibrous cap.
myocardial necrosis  better prognosis o Patients with NSTE-ACS frequently have multiple such plaques that
 Among patients with NSTE-ACS, the proportion with NSTEMI is are at risk of disruption.
rising while that with UA is falling because of the wider use of
troponin assays with higher sensitivity to detect myocyte necrosis,
thereby reclassifying UA as NSTEMI.
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 Chest discomfort- typically located in the substernal region and radiates

to the left arm/shoulder, and/or superiorly to the neck and jaw.
o Anginal equivalents such as dyspnea, epigastric discomfort, nausea,
or weakness may occur instead of chest discomfort.
- They appear to be more frequent in women, the elderly, and
patients with diabetes mellitus.
 PE resembles that in patients with SA and may be unremarkable.
o If the patient has a large area of myocardial ischemia or a large
NSTEMI, the physical findings can include:
- Diaphoresis; pale, cool skin
- Sinus tachycardia
- S3 & S4 sound; basilar rales;
- Hypotension
B. ELECTROCARDIOGRAM

Table 1.2: Most Common Plaques resulting in ACS visualized by

Optical Coherence Tomography:
Plaque OCT Findings
Thrombosis Protruding mass attached to the arterial wall
Identified as lipid plaque with fibrous cap discontinuity
 New ST-segment depression occurs in about 1/3 of patients with NSTE-
Plaque Rupture and cavity formation inside the plaque
Plaque Erosion Confirmed by the presence of attached thrombus
ACS. It may be transient but may persist for several days following NSTEMI.
overlying an intact and visualized plaque.  T-wave changes are more common but are less specific signs of
Appears as a site with fibrous cap disruption (dotted ischemia, unless they are new and deep T-wave inversions (≥0.3 mV).
Calcified Nodule arrow) and underlying plaque characterized by C. CARDIAC BIOMARKERS
protruding calcification, superficial calcium, and
significant calcium adjacent to the lesion (arrows).  Elevated levels of any of these markers distinguish patients with NSTEMI
The asterisks denote guidewire shadow artifact from those with UA
Table 1.3: Main Characteristics of Plaque Rupture and  Proteins released into the circulation from damaged heart muscle.
Superficial Erosion o Cardiac troponin (cTn)- most important cardiac marker, which
Plaque Rupture Plaque Erosion derives only from heart muscle (specific, sensitive, and preferred
Lipid rich Lipid poor markers of myocardial necrosis)
Collagen poor, thin fibrous cap Proteoglycan and GAG rich - Troponin is a complex of three proteins, two of which are suitable
Interstitial collagen breakdown Nonfibrillar collagen breakdown as specific cardiac marker tests: cTnI and cTnT. These two
Abundant inflammation Few inflammatory cells proteins have different properties, but their clinical applications
Smooth muscle cell apoptosis Endothelial cell apoptosis are similar.
Macrophage predominance Secondary neutrophil involvement
- Clinically, MI is now essentially defined as an ACS that causes
Male predominance Female predominance
High level of LDL- cholesterol High level of triglycerides
release of troponin.
- There is a characteristic temporal rise and fall peaking 12–24 h
II. CLINICAL PRESENTATION post onset of symptoms of the plasma concentration of these
markers and a direct relationship between the degree of elevation
and mortality
o MB isoform of creatine kinase (CK-MB)- less sensitive alternative
 In patients with an unclear history, small elevations of cTn, especially if
they are persistent, may not be diagnostic of an ACS. In such cases, both
cardiac and non-cardiac causes of an elevated cTn should be considered
Table 1.4: Causes of Elevated Cardiac Troponin Reflecting Direct
Myocardial Damage Other Than Spontaneous MI (Type 1)
Cardiac Non-Cardiac or Systemic
o Tachyarrhythmias o Pulmonary embolism/pulmonary
o Congestive heart failure hypertension
o Hypertensive emergencies o Trauma (e.g., electrical shock,
o Infection/inflammation (myocarditis or burns, blunt chest wall)
pericarditis) o Hypo or hyperthyroidism
o Stress cardiomyopathy (Tako-Tsubo o Toxicity (e.g., anthracyclines,
cardiomyopathy) snake venom)
o Structural heart disease (aortic o Renal failure
stenosis) o Sepsis, shock
o Aortic dissection o Stroke or other acute neurologic
o Coronary spasm event
o Cardiac procedures (endomyocardial o Exteme endurance efforts (ultra-
A. HISTORY AND PHYSICAL EXAMINATION biopsy, ablation, CABG, PCI) marathon)
o Infiltrative diseases (amyloidosis, o Rhabdomyolysis
 Diagnosis of NSTE-ACS is based largely on the clinical presentation hemochromatosis, malignancy)
 Chest discomfort is severe and has at least 1 of 3 features: D. DIAGNOSTIC EVALUATION
o Occurrence at rest (or with minimal exertion), lasting >10 min
o Relatively recent onset (i.e., within the prior 2 weeks); and/or  Major Non-Invasive Tools Used in the Evaluation of NSTEMI-ACS:
o Crescendo pattern (distinctly more severe, prolonged, or o ECG
frequent than previous episodes) o Cardiac biomarkers
 The diagnosis of NSTEMI is established if a patient with any of o Stress testing
these features (without ST segment elevations) develops evidence
of myocardial necrosis (abnormally elevated levels of biomarkers)

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 In equivocal cases, coronary computed tomographic  Patients should be placed at bed rest with continuous ECG monitoring for
angiography (CCTA) may be useful to improve the accuracy and ST-segment deviation and cardiac arrhythmias
speed of the diagnostic evaluation.  Medical therapy: anti-ischemic, antithrombotic treatments, consideration
 The goals are to: of coronary revascularization
o Recognize or exclude myocardial infarction (MI) using cardiac o IV Heparin should be given for 3-5 days to maintain the partial
biomarkers, preferably cTn; thromboplastin time at 2 to 2.5 times control
o Detect rest ischemia (using serial or continuous ECGs); and - Alternatively, low-molecular-weight heparin (enoxaparin, 1 mg/kg
o Detect significant coronary obstruction at rest with CCTA and/ subcutaneously BID)
or myocardial ischemia using stress testing o Aspirin at a dose of 325 mg/d
III. RISK STRATIFICATION - Initial treatment: at least 162 mg of a rapidly acting preparation
(oral non-enteric coated or intravenous).
 Patients with documented NSTE-ACS exhibit a wide spectrum of: - Lower doses (75–100 mg/d) are recommended thereafter, since
o Early (30 days) risk of death  1 to 10% they maintain efficacy while causing less bleeding
o Recurrent ACS  5–15% during the first year. - Contraindications: severe active bleeding, aspirin allergy
 Assessment of risk can be done by clinical risk scoring o High-risk unstable angina patients – should also receive an
systems: intravenous infusion of a platelet GPIIb/IIIa inhibitor
o Thrombolysis in Myocardial Infarction (TIMI) Trials: includes - With rest pain
seven independent risk factors - ST-segment deviations and/or release of a marker of
1. Age ≥ 65 years myocardial injury (such as Trop I or T)
2. 3 or more of the traditional risk factors for CAD o Beta blocker and Calcium antagonist
3. Known history of CAD or coronary stenosis of at least 50% - Beta blockers – other mainstay of anti-ischemic treatment
4. Daily aspirin use in the prior week
5. More than one anginal episode in the past 24 h
- Heart rate–slowing CCB (verapamil or diltiazem)
6. ST segment deviation of at least 0.5 mm o Nitrates
7. Elevated cardiac specific biomarker above upper limit of normal - Nitroglycerin Sublingual, as needed for angina
 Additional risk factors: DM, left ventricular dysfunction, renal - IV Nitroglycerin – in patients with episodes of ischemia that are
dysfunction, and elevated levels of B-type natriuretic peptides (BNP) particularly severe or prolonged.
 Patients with elevated cTn or new ST-segment abnormalities or
Table 1.5: Risk Criteria in Patients with NSTE-ACS
deemed to be at moderate or high risk based on a validated risk score
Very-High-Risk Criteria
o Hemodynamic instability or cardiogenic shock should be admitted to a specialized cardiovascular ICU.
o Recurrent or ongoing chest discomfort refractory to optimal medical therapy  Ambulation, as tolerated, is permitted if the patient has been stable
o Life-threatening arrhythmias or cardiac arrest without recurrent chest discomfort or ECG changes for at least 12-24 hrs
o Mechanical complications of MI  Patients with atypical symptoms and low risk or those who have
o Acute heart failure symptoms more consistent with another noncardiac cause may be
o Recurrent dynamic ST-T wave changes, particularly with intermittent ST-
observed in the ED or a short-stay unit
elevation
High-Risk Criteria  A second cTn assay should be performed 3 to 6 hours after the first, and
o Rise and fall in cardiac troponin compatible with MI further assessment with noninvasive imaging or stress testing may be
o Dynamic ST-T wave changes without symptoms (silent) considered to permit rapid exclusion of ACS
o Elevated TIMI (>4) or GRACE (>140) risk score B. ANTI-ISCHEMIC TREATMENT
Intermediate-Risk Criteria
o Diabetes mellitus  To provide relief and prevention of recurrence of ischemic discomfort,
o Renal insufficiency (eGFR <60 mL/min/173 m2 ) initial treatment should include:
o LVEF <40% or congestive heart failure o Bed rest
o Early post-MI angina
o Nitrates
o Prior PCI
o Prior CABG o Beta adrenergic blockers
o TIMI (2-3) or GRACE (109-140) risk score o Inhaled oxygen in patients with arterial O2 saturation (<90%) and/or in
Low-Risk Criteria those with heart failure and rales.
o None of the characteristics mentioned above  Guidelines emphasize the early use of anti-ischemic therapies to improve
A. UNSTABLE ANGINA the balance between oxygen supply and demand
 Nitrates- should first be given sublingually or by buccal spray (0.3– 0.6
 Patients with ACS without elevated levels of cTn (infrequently mg) if the patient is experiencing ischemic discomfort.
encountered with the new sensitive troponin assays) o If pain persists after 3 doses given 5 min apart, IV nitroglycerin (5–10
 UA have a more favorable prognosis than NSTEMI μg/min using non-absorbing tubing) is recommended.
 After initial stabilization, either of these can be pursued: - Rate of infusion: increased by 10 μg/min every 3-5 minutes
o Early invasive strategy (coronary angiography & o Endpoints:
revascularization) - Symptoms are relieved
o Early conservative strategy (continued medical therapy) - Systolic arterial pressure falls to < 100 mmHg
- Exercise ECG or perfusion scan - Dose reaches 200 μg/min
- Pharmacologic stress test o Absolute contraindication: hypotension and recent use of PDE-5
 80% improve with rest and medical treatment over a 48- hour period. inhibitor (sildenafil and vardenafil  within 24h; tadalafil  48h)
 TACTICS TIMI 18 Trial:  Beta Blockers- other mainstay of anti-ischemic treatment
o An early invasive strategy conferred a 40% reduction in o Targeted to a heart rate of 50-60bpm is recommended
recurrent cardiac events in patients with an elevated cTn level o Avoided in:
o No benefit was observed in those without detectable troponin - Acute or severe heart failure
- Low cardiac output
IV. MEDICAL TREATMENT
- Hypotension
 Management of patients with NSTE-ACS consists of: - Contraindications to beta-blocker therapy
o Acute phase focused on the clinical symptoms and stabilization  High-degree AV block
of the culprit lesion(s) and  Active bronchospasm
o Longer-term phase that involves therapies directed at the  Calcium Channel Blockers (Verapamil and Diltiazem)
prevention of disease progression and future plaque rupture/ o Recommended for patients who:
erosion. - Have persistent symptoms or ECG signs of ischemia after
A. GENERAL MEASURES treatment with full-dose nitrates and beta blockers
- Have contraindications to either class of these agents
 Patients with new or worsening chest discomfort or an anginal  ACE Inhibitors and ARBs
equivalent symptom suggestive of ACS should be transported rapidly o Benefits are most evident in patients at increased risk.
to the ED by ambulance, if possible, and evaluated immediately. - Diabetes mellitus
o Admit to hospital, placed at bed rest, sedated, and reassured - Left ventricle dysfunction is present
o Acute myocardial infarction should be ruled out (serial ECGs - Those who have not achieved adequate control of blood pressure
and measurements of plasma cardiac enzyme) and LDL cholesterol on beta blockers and statins
 The initial evaluation should include a directed history and physical
examination and ECG performed within 10 minutes of arrival.

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 Statins (Intensive HMG CoA reductase inhibitors)- early  Dual Antiplatelet Therapy (DAPT): clopidogrel is added to aspirin
administration prior to PCI and continued thereafter has been o Confer a 20% relative reduction in cardiovascular death, MI, or stroke,
shown to reduce periprocedural MI and recurrences of ACS. compared to aspirin alone.
o Addition of ezetimibe (10mg daily) for patients who do not o It is however associated with a moderate (absolute 1%) increase in
have an adequate response to maximally tolerated statin has major bleeding.
been shown to reduce future cardiovascular events. o DAPT should continue for at least 1 year in patients with NSTEACS,
o Inadequate response to statins: < 50% decrease in LDL-C especially those with a drug-eluting stent, to prevent stent thrombosis.
from untreated baseline or LDL-C on treatment > 70 mg/dL o Alternate P2Y12 blockers should be considered in patients with
Table 1.6: Drugs Commonly Used in Intensive Medical NSTE-ACS who develop a coronary event while receiving clopidogrel
Management of Patients with Unstable Angina and Non-ST- and aspirin, who are hyporesponsive to clopidogrel, or are at high risk
Segment Elevation MI: for ischemic complications.
Clinical When to Avoid Dosage Table 1.7: Clinical Use of Antithrombotic Therapy
Condition Oral Antiplatelet Therapy
Beta-Blockers Aspirin o Initial dose of 325 mg nonenteric formulation followed by 75–
o PR interval 100 mg/d of an enteric or a nonenteric formulation
(ECG) >0.24 s
Clopidogrel o Loading dose of 300–600 mg followed by 75 mg/d
o 2° or 3° AV block o Metoprolol 25–50 mg by mouth
All patients with o HR <50 bpm every 6 h If needed, and no Prasugrel o Pre-PCI: Loading dose 60 mg followed by 10 mg/d
ACS o SBP <90 mmHg heart failure, 5-mg increments Ticagrelor o Loading dose of 180 mg followed by 90 mg BID
o Shock by slow (over 1–2 min) IV Intravenous Antiplatelet Therapy
o LV failure administration Abciximab o 0.25 mg/kg bolus followed by infusion of 0.125 μg/kg per min
o Severe reactive (maximum 10 μg/min) for 12–24 h
airway disease o 180 μg/kg bolus followed 10 min later by second bolus of 180
Nitrates Eptifibatide μg with infusion of 2.0 μg/kg per min for 72–96 h following first
o Initially administer via sublingual bolus
or buccal route, and, if
Tirofiban o 25 μg/kg/min followed by infusion of 0.15 μg/kg/min for 48–96 h
symptoms persist,
intravenously. Cangrelor o 30 μg/kg bolus followed immediately by 4 μg/kg/min infusion
o Topical or oral nitrates are Anticoagulants
acceptable alternatives for Unfractionated o Bolus 70–100 U/kg (max. 5000 U) IV followed by infusion of
o Hypotension patients without ongoing or heparin (UFH) 12–15 U/kg/hr (initial max:1000 U/h) titrated to ACT 250–300s
Patients with ACS o RV infarction refractory symptoms o 1 mg/kg SC q12 h; the first dose may be preceded by a 30-mg
who have chest o Severe aortic o 5–10 μg/min by continuous Enoxaparin IV bolus; renal adjustment to 1 mg/kg OD if creatine clearance
discomfort or an stenosis infusion titrated up to 75–100 <30 mL/min
anginal equivalent o Patient receiving μg/min until relief of symptoms Fondaparinux o 2.5 mg SC qd
a PDE-5 inhibitor or limiting side effects
(headache or hypotension with a
Bivalirudin o Initial IV bolus of 0.75 mg/kg and an infusion of 1.75 mg/kg/hr
systolic blood pressure <90  TRITON TIMI 38 TRIAL: prasugrel is a thienopyridine which achieves a
mmHg or >30% below starting
mean arterial pressure levels if more rapid onset and higher level of platelet inhibition than clopidogrel
significant hypertension is o It was shown to:
present) - Reduce the risk of cardiovascular death, MI, or stroke significantly
Calcium Channel Blockers - Increase major bleeding
Patients whose - Reduce stent thrombosis by 50% (half)
symptoms are
not relieved by - NOT effective in patients treated by a conservative strategy.
adequate doses o Pulmonary - Contraindications:
of nitrates and edema  With prior stroke
beta blockers, or o Evidence of LV  Transient ischemic attack
in patients unable dysfunction (for  High risk for bleeding
to tolerate diltiazem or o Dependent on specific agent  PLATO TRIAL: ticagrelor (novel potent reversible platelet P2Y12 inhibitor)
adequate doses verapamil)
of one or both of o Reduce the risk of cardiovascular death, MI, or stroke compared with
these agents, or clopidogrel in ACS patients who are treated by either an invasive or
in patients with conservative strategy.
variant angina - Unlike prasugrel, ticagrelor demonstrated benefit whether patients
Morphine Sulfate
were managed conservatively or with an early invasive strategy.
Patients whose
symptoms are o Shown to reduce total mortality
not relieved after o There is increase in the risk of bleeding NOT associated with
three serial o Hypotension o 2–5 mg IV dose coronary artery bypass grafting
sublingual o Respiratory o May be repeated every 5–30 o Some patients may develop dyspnea early after administration
nitroglycerin depression min as needed to relieve
tablets or whose o Confusion symptoms and maintain patient
o Not associated with clinical exacerbations of chronic obstructive
symptoms recur o Obtundation comfort pulmonary disease or congestive heart failure.
with adequate
antiischemic
D. ANTICOAGULATION THERAPY
therapy
 Once the diagnosis of NSTE-ACS has been made, a parenteral
C. ANTI-THROMBOTIC TREATMENT anticoagulant should be initiated in addition to DAPT, unless the patient
has an absolute contraindication (e.g., uncontrolled bleeding)
 Antithrombotic therapy consisting of antiplatelet and anticoagulant  Four options are available for anticoagulant therapy to be added to
drugs represent the second major cornerstone of treatment. antiplatelet agents:
2014 AHA/ACC Practice Guideline: o Unfractionated heparin (UFH): long the mainstay of therapy
o LMWH (enoxaparin) which has been shown to be superior to UFH in
reducing recurrent cardiac events, especially in patients managed by a
conservative strategy. However, it is accompanied by a slight increase in
bleeding compared to UFH
o Bivalirudin (direct thrombin inhibitor) that is similar in efficacy to either UFH or
LMWH but causes less bleeding and is used just prior to and/or during PCI
o Indirect factor Xa inhibitor (fondaparinux) which is equivalent in efficacy to
enoxaparin but has a lower risk of major bleeding
 Excessive bleeding- most important adverse effect of all
antithrombotic agents
o Attention must be directed to the doses of antithrombotic agents,
accounting for:
- Body weight
- Creatinine clearance
- Previous history of excessive bleeding
o Patients who have experienced a stroke are at higher risk of
intracranial bleeding with potent antiplatelet agents and combinations
of antithrombotic drugs.

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E. INVASIVE VS. CONSERVATIVE STRATEGY  Coronary angiography: transient coronary spasm (diagnostic hallmark)
o Atherosclerotic plaques in at least one proximal coronary artery occur
 Invasive strategy: multiple clinical trials have demonstrated the
in about half of patients.
benefit of this strategy in high-risk patients (patients with multiple
o Hyperventilation or intracoronary acetylcholine has been used to
clinical risk factors, ST-segment deviation, and/or positive biomarkers)
provoke focal coronary stenosis on angiography or to provoke rest
o Following initiation of anti-ischemic and antithrombotic agents
angina with ST-segment elevation to establish the diagnosis.
- Initiation of anti-ischemic and antithrombotic agents
- Coronary arteriography (within 48 hours of presentation)  Long-term survival is excellent
- Coronary revascularization (PCI or CABG) II. MEDICAL TREATMENT
o Early invasive strategy is not recommended in patients with
extensive comorbidities in whom the risks of revascularization  Patients with PVA should be strongly urged to discontinue smoking.
outweigh the potential benefits, or in patients with acute chest  Nitrates and CCBs- mainstay of therapy
pain with low clinical likelihood of ACS and a negative  Aspirin- may actually increase the severity of ischemic episodes, possibly as a
troponin assay. result of the sensitivity of coronary tone to modest changes in the synthesis of
o Early invasive strategy is advised in patients with NSTE-ACS prostacyclin.
previously treated with CABG and in patients who have had  Statin therapy- has been shown to reduce the risk of major adverse events
(although the precise mechanism is not established).
NSTE-ACS within 6 months of a previous PCI and in whom
 Beta blockers- variable response.
restenosis may be the cause
 Coronary revascularization- may be helpful in patients who also have
 Conservative strategy: discrete, flow-limiting, proximal fixed obstructive lesions.
o Anti-ischemic and antithrombotic agents  Implantable cardioverter-defibrillator- indicated in patients who have had
o “Selective invasive approach”  the patient is closely observed ischemia-associated ventricular fibrillation despite maximal medical therapy
and coronary arteriography is carried out if:
- Rest pain or ST-segment changes recur III. PROGNOSIS
- Biomarker of necrosis becomes positive, or;
- There is evidence of severe ischemia on stress test
 Many patients with PVA pass through an acute, active phase, with
frequent episodes of angina and cardiac events during the first 6 months
Table 1.8: Factors Associated with Appropriate Selection of after presentation.
Early Invasive Strategy or Ischemia-Guided Strategy in  Survival at 5 years is excellent (~90–95%), but as many as 20% of
Patients with NSTE-ACS patients experience an MI.
Immediate invasive (within 2 h)
 Patients with no or mild fixed coronary obstruction experience a low rate
o Refractory angina
o Signs or symptoms of heart failure or new or worsening mitral regurgitation
of cardiac death or MI compared to patients with associated severe
o Hemodynamic instability obstructive lesions, although about half of the patients without obstructive
o Recurrent angina or ischemia at rest or with low-level activities despite CAD still experience frequent angina at rest.
intensive medical therapy  Patients with PVA who develop serious arrhythmias during spontaneous
o Sustained ventricular tachycardia or ventricular fibrillation episodes of pain are at a higher risk for sudden cardiac death.
Early invasive (within 24 h)  In most patients who survive an infarction or the initial 3- to 6-month
o None of the above, but GRACEa risk score >140 period of frequent episodes, there is a tendency for symptoms and
o Temporal change in troponin
o New or presumably new ST segment depression
cardiac events to diminish over time.
Delayed invasive (within 25–72 h) ST-SEGMENT ELEVATION-ACUTE CORONARY SYNDROME
o None of the above but diabetes mellitus
o Renal insufficiency (eGFR <60 mL/min per 1.73 m2)  Acute myocardial infarction (AMI) is a most common diagnosis in
o Reduced left ventricular systolic function (ejection fraction <0.40) hospitalized patients in industrialized countries.
o Early postinfarction angina  In-hospital mortality rate – declined from 10 to about 5% over the past
o Percutaneous coronary intervention within 6 months prior decade. The 1-year mortality rate after AMI is about 15%.
o Prior coronary artery bypass graft surgery  Mortality is approximately fourfold higher in elderly patients (aged >75) as
o GRACE risk score 109–140 or TIMIb risk score ≥2
compared with younger patients.
Ischemia-guided strategy
o Low-risk score (e.g., TIMI [0 or 1], GRACE [<109]) I. PATHOPHYSIOLOGY: ROLE OF ACUTE PLAQUE RUPTURE
o Low-risk, troponin-negative female patients
o Patient or clinician preference in the absence of highrisk features  STEMI usually occurs when coronary blood flow decreases abruptly after
a thrombotic occlusion (when atherosclerotic plaque fissures, ruptures or
F. LONG-TERM MANAGEMENT ulcerates) of a coronary artery previously affected by atherosclerosis.
 Smoking cessation  STEMI occurs when a coronary artery thrombus develops rapidly at a site
 Achieving optimal weight of vascular injury and when the surface of an atherosclerotic plaque
 Daily exercise becomes disrupted (exposing its contents to the blood) and conditions
 Blood-pressure control (local or systemic) favor thrombogenesis
 Following an appropriate diet  This injury is facilitated by factors:
 Control of hyperglycemia (in diabetic patients) o Cigarette smoking
o Hypertension
 Lipid management as recommended for patients with chronic SA.
o Lipid accumulation
PRINZMETAL’S VARIANT ANGINA
 Syndrome of severe ischemic pain that usually occurs at rest and is
associated with transient ST-segment elevation.
o Caused by focal spasm of an epicardial coronary artery with
resultant transmural ischemia and abnormalities in LV function
that may lead to acute MI, ventricular tachycardia or fibrillation,
and sudden cardiac death.
o The cause of the spasm may be related to hypercontractility of
vascular smooth muscle due to adrenergic vasoconstrictors,
leukotrienes, or serotonin.
 For reasons that are not clear, the prevalence of PVA has
decreased substantially during the past few decades
 They often occur in smokers and younger population
I. CLINICAL AND ANGIOGRAPHIC FINDINGS
 Cardiac examination is usually unremarkable in the absence of
ischemia
 The pain usually occurs at rest, sometimes awakens the patient
from sleep and is characterized by multi-lead ST-segment elevation.
o Clinical diagnosis of PVA is made by the detection of transient ST-
segment elevation with rest pain, although many patients may also
exhibit episodes of silent ischemia.

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 Coronary plaques prone to rupture are those with a rich lipid A. CHEST PAIN
core and a thin fibrous cap.
 Most common presenting complaint in patients with STEMI
 After an initial platelet monolayer forms, various agonists
 Pain is deep and visceral; described as heavy, squeezing, and
(collagen, ADP, epinephrine, serotonin) promote platelet
crushing; although, occasionally, it is described as stabbing or burning
activation.
 Similar in character to the discomfort of angina pectoris but commonly
 After agonist stimulation of platelets, thromboxane A2 (a potent
occurs at rest, is usually more severe, and lasts longer.
local vasoconstrictor) is released, further platelet activation
occurs, and potential resistance to fibrinolysis develops.  Typically, the pain involves the central portion of the chest and/or the
epigastrium, and, on occasion, it radiates to the arms.
 Activation of platelets by agonists promotes a conformational
o Less common sites of radiation: abdomen, back, lower jaw, and neck
change in the glycoprotein IIb/IIIa receptor. Once converted to o Frequent location of the pain beneath the xiphoid and epigastrium (common
its functional state, this receptor develops a high affinity for mistaken impression of indigestion)
soluble adhesive proteins (i.e., integrins) such as fibrinogen. o May radiate as high as the occipital area but not below the umbilicus
 Fibrinogen can bind to two different platelets simultaneously,  It is often accompanied by weakness, sweating, nausea, vomiting,
resulting in platelet cross-linking and aggregation anxiety, and a sense of impending doom.
 The coagulation cascade is activated on exposure of tissue factor  Pain may commence when the patient is at rest, but when it begins
in damaged endothelial cells at the site of the disrupted plaque. during a period of exertion, it does not usually subside with cessation of
o Factors VII and X are activated, ultimately leading to the conversion of activity, in contrast to angina pectoris.
prothrombin to thrombin, which then converts fibrinogen to fibrin -  Differential Diagnosis:
further activation of the coagulation cascade. o Acute pericarditis
 The amount of myocardial damage caused by coronary o Pulmonary embolism
occlusion depends on the: o Acute aortic dissection
o Territory supplied by the affected vessel o Costochondritis
o Whether or not the vessel becomes totally occluded o Gastrointestinal disorders
o Duration of coronary occlusion  Other clinical presentations of chest pain:
o Quantity of blood supplied by collateral vessels to the affected tissue o Painless STEMIs: greater in patients with diabetes mellitus, and it
o Demand for oxygen of the myocardium whose blood supply has been
suddenly limited
increases with age
o Endogenous factors that can produce early spontaneous lysis of the o Sudden-onset breathlessness: seen in the elderly, which may
occlusive thrombus progress to pulmonary edema.
o Adequacy of myocardial perfusion in the infarct zone when flow is o Less common presentations: sudden loss of consciousness, a
restored in the occluded epicardial coronary artery. confusional state, a sensation of profound weakness, the appearance
 Patients at increased risk for developing STEMI: multiple of an arrhythmia, evidence of peripheral embolism, or merely an
coronary risk factors and those with UA unexplained drop in arterial pressure.
 Less common underlying medical conditions:  Increased frequency early in the day: 6:00 A.M. and 12 noon
hypercoagulability, collagen vascular disease, cocaine abuse, and  May be due to a combination of an increase in sympathetic tone and an
intracardiac thrombi or masses that can produce coronary emboli increased tendency to thrombosis
Table 1.9: Physical Examination Findings
General Appearance
o Often appear anxious, restless and in considerable distress.
o Some patients move about in an effort to find a comfortable position
o Substernal chest pain >30 mins + diaphoresis (strongly suggests STEMI)
o Levine’s sign: they often massage or clutch their chests and frequently
describe their pain with a clenched fist held against the sternum
o Patients with LV failure and sympathetic stimulation:
- Cold perspiration and skin pallor may be evident
- They typically sit or are propped up in bed and gasp for breath (may
complain of chest discomfort or a feeling of suffocation)
- Cough producing frothy, pink, or blood-streaked sputum may occur if
pulmonary edema is present.
o Patients in cardiogenic shock:
- Often lie listlessly and make few spontaneous movements
- Skin is cool and clammy, with a bluish or mottled color over the
extremities, and there is marked facial pallor with severe cyanosis of
the lips and nailbeds.
- May converse normally or may be confused.
Heart Rate
o Can vary from marked bradycardia to a rapid regular or irregular
 Following disruption of a vulnerable plaque, patients experience tachycardia, depending on the underlying rhythm and degree of LV failure.
ischemic discomfort resulting from a reduction of flow through the o Typically the pulse is rapid and regular initially (sinus tachycardia at 100-
affected epicardial coronary artery  ischemia  infarction 110 bpm) and slows as the patient’s pain and anxiety are relieved
o Partial occlusion → affects the inner myocardium (subendocardium) → o Premature ventricular contractions
may cause: o Tachycardia is associated with a higher risk for fatal complications of MI
- NSTEMI Blood Pressure
- Unstable angina (if the ischemia does not result in cell death ) o Most patients with uncomplicated STEMI are normotensive
o Complete occlusion → transmural infarction → STEMI o Hypertensive response is occasionally seen during the first few hours,
 Of patients with ST-segment elevation, the majority (wide red presumably because of pain, anxiety, and agitation
arrow) ultimately develop a Q wave on the ECG (Qw MI), while a o Patients with massive infarction: arterial pressure falls acutely because
minority (thin red arrow) do not develop Q wave and, in older of LV dysfunction and may be exacerbated by morphine and/or nitrates
literature, were said to have sustained a non-Q-wave MI (NQMI). o Patients in cardiogenic shock: SBP <90 mm Hg + evidence of end-organ
 Patients who present without ST-segment elevation are suffering hypoperfusion.
from either unstable angina or a non-ST-segment elevation MI o Evidence of autonomic hyperactivity is common and varies in type
(NSTEMI) (wide green arrows), a distinction that is ultimately made with the location of the infarction:
based on the presence or absence of a serum cardiac biomarker. - Anterior infarcton: SNS hypereactivity  tachycardia +/- hypertension
- Inferior infarction: PNS hyperreactivity  bradycardia +/- hypotension
The majority of patients presenting with NSTEMI do not develop a
o The arterial pressure is variable (in most patients with transmural
Q wave on the ECG.
infarction, systolic pressure declines by ~10–15 mmHg from the
II. CLINICAL PRESENTATION preinfarction state)
Carotid Pulse
 Precipitating factor appears to be present before STEMI:
o Often decreased reflecting reduced stroke volume
o Vigorous physical exercise o Palpation of the carotid arterial pulse provides a clue to LV stroke volume
o Emotional stress - Small pulse suggests reduced stroke volume
o Medical or surgical illness. - Sharp, brief upstroke often occurs in patients with mitral regurgitation
 Circadian variations have been reported such that clusters are seen or a ruptured ventricular septum with a left-to-right shunt
in the morning within a few hours of awakening o Pulsus alternans reflects severe LV dysfunction.

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Temperature and Respiration A. ELECTROCARDIOGRAM

o Fever (nonspecific response to tissue necrosis) develops in most
patients with extensive STEMI within 24 to 48 hours of onset of
infarction.
- Body temp: often begins to rise within 4 to 8 hours after onset of
infarction, and rectal temperature may reach 38.3°C to 38.9°C
(101°F to 102°F)
- Fever usually resolves by the fourth or fifth day after MI.
o The respiratory rate may rise slightly soon after the development of
STEMI
- Patients without heart failure (HF): it results from anxiety and
pain and returns to normal with treatment
- RR >20 breaths/  heightened risk
- In patients with LV failure: RR correlates with severity of the
failure (patients with pulmonary edema may have rates >40
breaths/min)
- In patients with cardiogenic shock: RR is not necessarily
elevated
- Cheyne-Stokes (periodic) respiration may occur in elderly
individuals with cardiogenic shock or HF, particularly after
opiate therapy or in the presence of cerebrovascular disease.
Jugular Venous Pressure
o JVP is usually normal in STEMI involving the left ventricle.
o a wave may be prominent in patients with pulmonary hypertension  During the initial stage: total occlusion of an epicardial coronary artery
secondary to LV failure or reduced compliance. produces ST-segment elevation.
o RV infarction often results in marked jugular venous distention in  Most patients initially presenting with ST-segment elevation ultimately
the tall c-v waves of tricuspid regurgitation. evolve Q waves on the ECG.
o Patients with STEMI and cardiogenic shock: generally have o The presence or absence of Q waves on the surface ECG does not reliably
elevated JVP distinguish between transmural and nontransmural (subendocardial) MI,
o In patients without elevated JVP: the depression in LV performance although Q waves are associated with worse outcomes.
probably is related to hypovolemia (2D-echo can help determine the  Some patients initially presenting with ST-segment elevation will not
cause of hypotension) develop Q waves when:
Extremities o Obstructing thrombus is not totally occlusive
o Peripheral edema is a manifestation of RV failure o Obstruction is transient
o Cyanosis of the nailbeds is common in patients with severe LV o If a rich collateral network is present
failure and is particularly striking in patients with cardiogenic shock.
 Contemporary studies using magnetic resonance imaging (MRI) suggest
Neuropsychiatric
that the development of a Q wave on the ECG is more dependent on the
o Altered mental status (depending on the degree of cerebral perfusion)
volume of infarcted tissue rather than the transmurality of infarction.
Table 1.10: Cardiac Examination Findings:
Palpation
o Palpation of the precordium may yield normal results (usually quiet and
apical impulse may be difficult to palpate)
o In patients with anterior wall infarction: abnormal systolic pulsation
caused by dyskinetic bulging of infarcted myocardium may develop in the
periapical area within the first days of the illness
o In patients with transmural STEMI: more often reveals a presystolic
pulsation synchronous with an audible S4 (reflects vigorous left atrial
contraction filling a ventricle with reduced compliance)
o Patients with LV systolic dysfunction: diffuse or dyskinetic LV impulse,
or an outward movement of the LV palpable in early diastole, coincident
with an S3.
Table 2.0: Localization of Myocardial Infarction on 12L ECG
Leads w/ ST- Affected Myocardial Occluded Coronary
Auscultation
Segment Elevation Area Artery
o Heart Sounds: V1-V2 Septal proximal LAD
- S1 is frequently muffled and occasionally inaudible immediately after V3-V4 Anterial LAD
an infarct, and their intensity increases during convalescence. V5-V6 Apical distal LAD, LCx, or RCA
- Soft S1 may also reflect prolongation of the PR interval I, aVL Lateral LCx
- Patients with marked ventricular dysfunction and/or LBBB: may have II, aVF, III Inferior 90% RCA, 10% LCx
paradoxical splitting of the S2. V7, V8, V9 Posterolateral (inferobasal or RCA or LCx
- S4 is almost universally present in patients in sinus rhythm with STEMI posterior)
- S3 in patients with STEMI usually reflects severe LV dysfunction
with elevated ventricular filling pressure (detected best at the apex B. SERUM CARDIAC BIOMARKERS
with the patient in the left lateral recumbent position)
o Murmurs:  Proteins released from necrotic heart muscle after STEMI.
- Patients with STEMI typically have systolic murmurs (transient  Cardiac biomarkers become detectable in the peripheral blood once the
midsystolic or late systolic apical systolic murmur due to dysfunction capacity of the cardiac lymphatics to clear the interstitium of the infarct
of the mitral valve apparatus) zone is exceeded and spillover into the venous circulation occurs.
- A new, prominent, apical holosystolic murmur accompanied by a  The criteria for AMI require a rise and/or fall in cardiac biomarker values
thrill may represent rupture of a head of a papillary muscle
o Pericardial Friction rubs:
with at least one value above the 99th percentile of the upper reference
- Can be heard within 24 hours or as late as 2 weeks after onset of limit for normal individuals
infarction, they occur most frequently on the second or third day. Table 2.1: Serum Cardiac Biomarkers
- Patients with STEMI and a PFR may have a pericardial effusion on Rise Maximum Normalization Characteristics
echocardiographic study Cardiac Troponin T/I (cTnT/cTnI)
- Delayed onset of the rub and the associated discomfort of o Have amino-acid sequences different
pericarditis (as late as 3 months after infarction) characterizes the from those of the skeletal muscle forms
now rare post-MI (Dressler) syndrome. Regular cTnI: 7-10 of these proteins
- Most readily audible along the LSB or just inside the apical impulse. assay: 6-8 days o May increase after STEMI to levels
hrs many times higher than the upper
III. LABORATORY FINDINGS 12-24 hrs cTnT: 10-14 reference limit (preferred biochemical
High- days markers for MI)
STEMI progresses through the following temporal stages:
sensitive o Elevated cardiac-specific troponin level,
1. Acute (first few hours–7 days) assays: 1- even in the presence of normal CK and
2. Healing (7–28 days) 3 hrs CK-MB levels, is indicative of an
3. Healed (≥29 days) adverse prognosis.

When evaluating the results of diagnostic tests for STEMI, the

temporal phase of the infarction must be considered. The laboratory
tests of value in confirming the diagnosis may be divided into four
groups: (1) ECG, (2) serum cardiac biomarkers, (3) cardiac imaging,
and (4) nonspecific indices of tissue necrosis and inflammation.
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CK-MB D. CARDIAC IMAGING

o Lacks specificity for STEMI, as
CK may be elevated with  2D-Echocardiography- abnormalities of wall motion are almost
skeletal muscle disease or universally present
trauma, including intramuscular
injection
o Estimation of left ventricular (LV) function- useful prognostically
o MB isoenzyme of CK has the (detection of reduced function serves as an indication for therapy
advantage over total CK that it is with an inhibitor of the renin-angiotensin-aldosterone system)
not present in significant o May also identify presence of right ventricular (RV) infarction,
4-8 hrs 12-24 hrs 2-3 days concentrations in extracardiac ventricular aneurysm, pericardial effusion, and LV thrombus
tissue (more specific)
o CK-MB elevation is also seen in o Doppler echocardiography– useful in detection and quantitation of a
cardiac surgery, myocarditis and ventricular septal defect and mitral regurgitation
electrical cardioversion  Radionuclide Imaging Techniques- used less often than
o CKMB2:CKMB1 ratio of >1.5 is echocardiography → more cumbersome and lack sensitivity and
highly sensitive
o A ratio (relative index) of CK-MB specificity in many clinical circumstances
mass to CK activity ≥2.5 o Myocardial perfusion imaging with 201TI or 99mTc sestamibi
suggests but is not diagnostic of - Distributed in proportion to myocardial blood flow and concentrated by
a myocardial rather than a viable myocardium
skeletal muscle source for the - Reveals a defect (“cold spot”) in most patients during the first few hours
CK-MB elevation after development of a transmural infarct
Myoglobin - It cannot distinguish acute infarcts from chronic scars and thus is NOT
o Released within only a few SPECIFIC
hours of the onset of AMI
1 hr 4-12 hrs 1 day o Lacks cardiac specificity
 High-Resolutation Cardiac MRI- can detect MI accurately using a
o Rapidly excreted in the urine technique referred to as late enhancement.
and return to the normal range o A standard imaging agent (gadolinium) is administered and images are
within 24 h of the onset of obtained after a 10-min delay (there is a bright signal in areas of infarction
infarction that appears in stark contrast to the dark areas of normal myocardium)
 Many hospitals are using cTnT or cTnI rather than CK-MB as the Table 2.2: Definition of Myocardial Infarction
routine serum cardiac marker for diagnosis of STEMI, although any Criteria for Acute Myocardial Infarction
The term acute myocardial infarction (MI) should be used when there is evidence of
of these analytes remains clinically acceptable.
myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. Under
 It is not cost-effective to measure both a cardiac-specific troponin these conditions, any one of the following criteria meets the diagnosis for MI:
and CK-MB at all time points in every patient. o Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin
 Peak protein concentration correlates only weakly with infarct size. [cTn]) with at least one value above the 99th percentile upper reference limit (URL)
and with at least one of the following:
 Recanalization of a coronary artery occlusion (either spontaneously - Symptoms of ischemia
or by mechanical or pharmacologic means) in the early hours of - New or presumed new significant ST-segment T-wave (ST-T) changes or new
STEMI causes earlier peaking of biomarker measurements because left bundle branch block (LBBB)
of a rapid washout from the interstitium of the infarct zone, quickly - Development of pathologic Q waves in the electrocardiogram (ECG)
- Imaging evidence of new loss of viable myocardium or new regional wall motion
overwhelming lymphatic clearance of the proteins abnormality
- Identification of an intracoronary thrombus by angiography or autopsy
o Cardiac death with symptoms suggestive of myocardial ischemia and presumed new
ischemic ECG changes of new LBBB, but death occurred before cardiac biomarkers
were obtained or before cardiac biomarker values would be increased.
o Percutaneous coronary intervention (PCI)–related MI is arbitrarily defined by elevation
of cTn values (>5 × 99th percentile URL) in patients with normal baseline values
(≤99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated
and are stable or falling. In addition, either:
- Symptoms suggestive of myocardial ischemia, or
- New ischemic ECG changes, or
- Angiographic findings consistent with a procedural complication, or
- Imaging demonstration of new loss of viable myocardium or new regional wall
motion abnormality are required.
o Stent thrombosis associated with MI when detected by coronary angiography or
autopsy in the setting of myocardial ischemia and with a rise and/or fall of cardiac
biomarker values with at least one value >99th percentile URL.
o Coronary artery bypass grafting (CABG)–related MI is arbitrarily defined by elevation of
cardiac biomarker values (>10 × 99th percentile URL) in patients with normal baseline
cTn values (≤99th percentile URL). In addition, either:
- New pathologic Q waves or new LBBB, or
- Angiographic documented new graft or new native coronary artery occlusion, or
- Imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality.
Criteria for Prior Myocardial Infarction
Any one of the following criteria meets the diagnosis for prior MI:
“Markers such as myoglobin and CK isoforms are rapidly o Pathologic Q waves with or without symptoms in the absence of non-ischemic causes.
o Imaging evidence of a region of loss of viable myocardium that is thinned and fails to
released, and blood levels rise quickly above the cutoff limit; this is contract, in the absence of a nonischemic cause.
then followed by a more protracted release of biomarkers from the o Pathologic findings of a prior MI.
disintegrating myofilaments that may continue for several days.
Table 2.3: Classification of Myocardial Infarction
Cardiac troponin levels rise to about 20–50 times the upper reference Type I: Spontaneous Myocardial Infarction
limit (the 99th percentile of values in a reference control group) in o Spontaneous myocardial infarction related to atherosclerotic plaque rupture,
patients who have a “classic” acute myocardial infarction (MI) and ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one
sustain sufficient myocardial necrosis to result in abnormally elevated or more of the coronary arteries leading to decreased myocardial blood flow or distal
levels of the MB fraction of creatine kinase (CK-MB). Clinicians can platelet emboli with ensuing myocyte necrosis. The patient may have underlying
severe coronary artery disease (CAD) but on occasion nonobstructive or no CAD.
now diagnose episodes of microinfarction by sensitive assays that Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance
detect cardiac troponin elevations above the upper reference limit, o In instances of myocardial injury with necrosis where a condition other than CAD
even though CK-MB levels may still be in the normal reference range contributes to an imbalance between myocardial oxygen supply and/ or demand, e.g.,
(not shown). CV, coefficient of variation.” coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-
brady-arrhythmias, anemia, respiratory failure, hypotension, and hypertension with or
C. OTHER LABORATORY FINDINGS without left ventricular hypertrophy
Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are
 The nonspecific reaction to myocardial injury is associated with Unavailable
polymorphonuclear leukocytosis. o Cardiac death with symptoms suggestive of myocardial ischemia and presumed new
o Appears within a few hours after the onset of pain and persists ischemic electrocardiogram (ECG) changes or new left bundle branch block (LBBB),
for 3–7 days but death occurring before blood samples could be obtained or before cardiac
biomarker could rise, or in rare cases, cardiac biomarkers were not collected
o WBC count often reaches levels of 12,000–15,000/μL.
 The ESR rises more slowly than the WBC count, peaking during
the first week and sometimes remain elevated for 1 or 2 weeks.

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Type 4a: Myocardial Infarction Related to Percutaneous Coronary  Intravenous beta blockers- also useful in the control of the pain of STEMI,
Intervention (PCI) presumably by diminishing myocardial O2 demand and hence ischemia.
o Myocardial infarction associated with PCI is arbitrarily defined by elevation of
cardiac troponin (cTn) values >5 × 99th percentile upper reference limit (URL)
o Reduces in-hospital mortality
in patients with normal baseline values (≤99th percentile URL) or a rise of cTn o Reduces the risks of reinfarction and ventricular fibrillation
values >20% if the baseline values are elevated and are stable or falling. o Commonly employed regimen is metoprolol (5 mg q2–5 min x3 doses
o In addition, either (i) symptoms suggestive of myocardial ischemia, or (ii) new provided the patient has:
ischemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a - Heart rate >60 beats/min
major coronary artery or a side branch or persistent slow or no flow or
- Systolic pressure >100 mmHg
embolization, or (iv) imaging demonstration of new loss of viable myocardium
or new regional wall motion abnormality is required
- PR interval <0.24 s
Type 4b: Myocardial Infarction Related to Stent Thrombosis
- Rales that are <10 cm up from the diaphragm.
o Myocardial infarction associated with stent thrombosis is detected by coronary o Oral beta blocker therapy should be initiated in the first 24 h for
angiography or autopsy in the setting of myocardial ischemia and with a rise patients who do not have any of the following:
and/or fall of cardiac biomarker values with at least one value above the 99th - Signs of heart failure
percentile URL. - Evidence of a low-output state
Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting - Increased risk for cardiogenic shock
o Myocardial infarction associated with CABG is arbitrarily defined by elevation of - Other relative contraindications to beta blockade (PR interval >0.24 s,
cardiac biomarker values >10 × 99th percentile URL in patients with normal second- or third-degree HB, active asthma, or reactive airway disease)
baseline cTn values (≤99th percentile URL).
 Glucocorticoids and NSAIDs – should be AVOIDED in patients with
o In addition, either (i) new pathologic Q waves or new LBBB, or (ii) angiographic
documented new graft or new native coronary artery occlusion, or (iii) imaging STEMI (with the exception of Aspirin)
evidence of new loss of viable myocardium or new regional wall motion o Can impair infarct healing o Increase the risk of myocardial rupture
abnormality. o Use may result in a larger infarct scar
IV. INITIAL MANAGEMENT o Can increase coronary vascular resistance, thereby potentially
reducing flow to ischemic myocardium
A. PREHOSPITAL CARE
VII. MANAGEMENT STRATEGIES
 Major elements of prehospital care of patients:
Reperfusion therapy for patients with STEMI:
o Recognition of symptoms by the patient and prompt seeking of
medical attention
o Rapid deployment of an emergency medical team capable of
performing resuscitative maneuvers, including defibrillation
o Expeditious transportation of the patient to a hospital facility that is
continuously staffed by physicians and nurses skilled in managing
arrhythmias and providing advanced cardiac life support
o Expeditious implementation of reperfusion therapy.
V. MANAGEMENT IN THE EMERGENCY DEPARTMENT
 Goals for the management of patients:
o Control of cardiac discomfort
o Rapid identification of patients who are candidates for urgent
reperfusion therapy
- The overarching goal is to minimize the time from first medical
contact to initiation of reperfusion therapy.
- Goal: initiate PCI within 120 min of first medical contact
o Triage of lower-risk patients to appropriate location in the hospital
o Avoidance of inappropriate discharge of patients with STEMI.
 Aspirin- essential in the management of patients with suspected
STEMI and is effective across the entire spectrum of ACS
o Buccal absorption of a chewed 160–325-mg tablet in ER  provides
rapid inhibition of COX-1 in platelets and reduction of TXA2
o This measure should be followed by daily oral administration of aspirin in
a dose of 75–162 mg.  When ST-segment elevation of at least 2 mm in two contiguous precordial
 Supplemental O2- when hypoxemia is present, O2 should be leads and 1 mm in two adjacent limb leads is present, a patient should be
administered by nasal prongs or face mask (2–4 L/min) for the first considered a candidate for reperfusion therapy
6–12 h after infarction  In the absence of ST-segment elevation, fibrinolysis is not helpful, and
o Hypoxemia may develop secondary to ventilation-perfusion evidence exists suggesting that it may be harmful.
abnormalities from LV failure and intrinsic pulmonary disease.
VIII. LIMITATION OF INFARCT SIZE
VI. CONTROL OF DISCOMFORT
 Infarct size is an important determinant of prognosis
 Sublingual nitroglycerin- can be given safely to most patients with  The quantity of myocardium that becomes necrotic as a consequence of a
STEMI. Up to three doses of 0.4 mg should be administered at coronary artery occlusion is determined by factors other than just the site
about 5-min intervals. of occlusion.
o Diminishes or abolishes chest discomfort  Central zone of the infarct (contains necrotic tissue)  irretrievably lost
o Capable of both decreasing myocardial oxygen demand (by o The fate of the surrounding ischemic myocardium (ischemic
lowering preload) and increasing myocardial oxygen supply (by penumbra) may be improved by:
dilating infarct-related coronary vessels or collateral vessels). - Timely restoration of coronary perfusion either pharmacologically (by
o Should be avoided in: thrombolysis) or mechanically (by angioplasty and/or stenting)
- Low systolic arterial pressure (<90 mmHg) - Reduction of myocardial O2 demands
- Clinical suspicion of RV infarction (inferior infarction on ECG, - Prevention of the accumulation of noxious metabolite
elevated jugular venous pressure, clear lungs, and hypotension) - Blunting of the impact of mediators of reperfusion injury (calcium overload
- Patients who have taken a phosphodiesterase-5 inhibitor for erectile and oxygen-derived free radicals).
dysfunction within the preceding 24 h (because it may potentiate the  Up to one-third of patients with STEMI may achieve spontaneous
hypotensive effects of nitrates) reperfusion of the infarct-related coronary artery within 24 h and
o An idiosyncratic reaction to nitrates can usually be reversed experience improved healing of infarcted tissue.
promptly by the rapid administration of intravenous atropine.
 Timely restoration of flow in the epicardial infarct–related artery combined
 Morphine- very effective analgesic for the pain associated with with improved perfusion of the downstream zone of infarcted myocardium
STEMI. results in a limitation of infarct size.
o May reduce sympathetically mediated arteriolar and venous
 Protection of the ischemic myocardium by the maintenance of an
constriction, and the resulting venous pooling may reduce CO
optimal balance between myocardial O2 supply and demand
and arterial pressure.
through:
o It also has a vagotonic effect and may cause bradycardia or
o Pain control
advanced degrees of heart block (particularly in patients with
o Treatment of congestive heart failure (CHF)
inferior infarction).
o Minimization of tachycardia and hypertension
- These side effects usually respond to atropine (0.5 mg IV).
o Routinely administered by repetitive (q5 min) IV injection of
small doses (2–4 mg), rather than by the SC administration of a
larger quantity

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A. PRIMARY PERCUTANEOUS CORONARY INTERVENTION Table 2.6: Contraindications for Fibrinolysis

Absolute Contraindications
 PCI (usually angioplasty and/or stenting without preceding o History of cerebrovascular hemorrhage at any time
fibrinolysis), referred to as primary PCI, is effective in restoring o Non-hemorrhagic stroke or other cerebrovascular event within the past year
perfusion in STEMI when carried out on an emergency basis in the o Marked hypertension (reliably determined systolic arterial pressure >180 mmHg
and/or a diastolic pressure >110 mmHg) at any time during the acute presentation
first few hours of MI. o Suspicion of aortic dissection
 Advantages of PCI: o Active internal bleeding (excluding menses)
o Applicable to patients who have contraindications to fibrinolytic Relative Contraindications
therapy but otherwise are considered appropriate candidates for o Current use of anti-coagulants (INR ≥2)
reperfusion. o Recent (<2 weeks) invasive or surgical procedure
o More effective than fibrinolysis in opening occluded coronary o Prolonged (>10 min) cardiopulmonary resuscitation
arteries and, is associated with better short-term and long-term o Known bleeding diathesis
o Pregnancy
clinical outcomes. o Hemorrhagic ophthalmic condition (e.g., hemorrhagic diabetic retinopathy)
o Generally preferred when the diagnosis is in doubt, cardiogenic o Active peptic ulcer disease
shock is present, bleeding risk is increased, or symptoms have been o History of severe hypertension that is currently adequately controlled
present for at least 2–3 h when the clot is more mature and less o Patients should not receive streptokinase if that agent had been received within the
easily lysed by fibrinolytic drugs. preceding 5 days to 2 years due to risk of allergic reaction
 Disadvantages:  Although patients (younger than 65 years) achieve a greater relative
o PCI is expensive in terms of personnel and facilities reduction in the mortality rate than elderly patients
o Applicability is limited by its availability, around the clock, in only a
 The higher absolute mortality rate (15 to 25%) in elderly patients results in
minority of hospitals
similar absolute reductions in the mortality rates for both age groups.
B. FIBRINOLYSIS
C. INTEGRATED REPERFUSION STRATEGY
 If no contraindications are present, fibrinolytic therapy should
 Cardiac catheterization and coronary angiography- should be carried
ideally be initiated within 30 min of presentation (door-to-needle
out after fibrinolytic therapy if there is evidence of either:
time ≤30 min). o Failure of reperfusion (persistent chest pain and ST-segment elevation >90 min)
 Principal goal of fibrinolysis: prompt restoration of full coronary  rescue PCI should be considered
arterial patency o Coronary artery reocclusion (re-elevation of ST segments and/or recurrent
 FDA-Approved Thrombolytic agents: chest pain) or the development of recurrent ischemia  urgent PCI should be
o Tissue plasminogen activator (tPA) considered.
o Streptokinase  Coronary artery bypass surgery- should be reserved for patients whose
o Tenecteplase (TNK) coronary anatomy is unsuited to PCI but in whom revascularization
o Anisoylated plasminogen streptokinase activator complex (APSAC) appears to be advisable because of extensive jeopardized myocardium or
o Reteplase (rPA) recurrent ischemia.
Table 2.5: Comparison of Approves Fibrinolytic Agents IX. HOSPITAL CARE MANAGEMENT
Fibrinolytic Dose Fibrin Fibrinogen Antigenic Patency
Agent Specificity Depletion Rate  Patients should be admitted to a coronary care unit early in their illness
Fibrin Specific when it is expected that they will derive benefit from the sophisticated and
TNK Single IV weight- ++++ Minimal No 85% expensive care provided.
based bolus
10U + 10U IV ++ Moderate No 84%
 The duration of stay in the coronary care unit is dictated by the ongoing
r-PA boluses given need for intensive care.
30min apart o If symptoms are controlled with oral therapy, patients may be transferred
t-PA 90min weight- ++ Mild No 73-84% out of the coronary care unit.
based infusion o Patients who have a confirmed STEMI but who are considered to be at low
Non-Fibrin Specific risk (no prior infarction and no persistent chest discomfort, CHF,
Streptokinase 1.5M U IV given No Marked Yes 60-68% hypotension, or cardiac arrhythmias) may be safely transferred out of the
over 30-60 mins
coronary care unit within 24 h.
 These drugs all act by promoting the conversion of plasminogen to Table 2.7: Care in Coronary Care Unit
plasmin, which subsequently lyses fibrin thrombi. Activity
 TNK and rPA are referred to as bolus fibrinolytics since their o First 12hrs: should be kept at bed rest
administration does not require a prolonged intravenous infusion o Within the first 24 h: in the absence of complications, patients should be
 Reduce the relative risk of in-hospital death by up to 50% when encouraged, under supervision, to resume an upright posture by dangling
administered within the first hour of the onset of symptoms their feet over the side of the bed and sitting in a chair
o This benefit is maintained for at least 10 years o Second or Third day: in the absence of hypotension and other
o Appears to reduce infarct size complications, patients typically are ambulating in their room with
o Limit LV dysfunction increasing duration and frequency, and they may shower or stand at the
 Reduce the incidence of serious complications such as septal sink to bathe.
rupture, cardiogenic shock, and malignant ventricular arrhythmias o Day 3 or 4 after infarction: patients should be increasing their ambulation
 Some benefit appears to be possible up to 12 h: progressively to a goal of 600 ft at least three times/day
o If chest discomfort is still present Diet
o ST segments remain elevated in ECG leads that do not yet o NPO for the first 4–12 h → due to the risk of emesis and aspiration
demonstrate new Q waves o Typical CCU diet:
 Late Coronary Reperfusion: - ≤30% of total calories as fat (cholesterol content of ≤300 mg/d)
o Appear to result from improvement of tissue healing in the infarct - 50 to 55% complex carbohydrates
zone with prevention of infarct expansion - High in potassium, magnesium, and fiber
o Enhancement of collateral flow - Low in sodium
o Improvement of myocardial contractile performance - DM and hypertriglyceridemia are managed by restriction of
o Reduction in the tendency to electrical instability concentrated sweets in the diet
 Hemorrhage- most frequent and most serious complication Bowel Management
o Hemorrhagic stroke- most serious complication and occurs in o Bed rest and the effect of the narcotics used for the relief of pain often lead
~0.5–0.9% of patients being treated with these agents. to constipation
- This rate increases with advancing age, with patients >70 years o Routine use of a stool softener: dioctyl sodium sulfosuccinate (200 mg/d)
experiencing roughly twice the rate of intracranial hemorrhage as o If the patient remains constipated, a laxative can be prescribed
those <65 years. Sedation
- Large-scale trials have suggested that the rate of intracranial o Diazepam (5mg), Oxazepam (15 to 30mg), or Lorazepam (0.5 to 2mg),
hemorrhage with tPA or rPA is slightly higher than with streptokinase given three or four times daily is usually effective.
Clinical factors that favor thrombolytic therapy include: X. PHARMACOTHERAPY
1. anterior wall injury
2. hemodynamically complicated infarction A. ANTI-THROMBOTIC THERAPY
3. widespread ECG evidence of myocardial jeopardy  Primary goal of treatment is to maintain patency of infarct-related artery
 The secondary goal is to reduce the patient’s tendency to thrombosis and,
thus, the likelihood of mural thrombus formation or deep-venous
thrombosis, either of which could result in pulmonary embolization.

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 These individuals should receive full therapeutic levels of  The mechanism involves a reduction in ventricular remodeling after
anticoagulant therapy (LMWH or UFH) while hospitalized, infarction with a subsequent reduction in the risk of CHF.
followed by at least 3 months of warfarin therapy:  The rate of recurrent infarction may also be lower in patients treated
o Patients with an anterior location of the infarction chronically with ACE inhibitors after infarction.
o Severe LV dysfunction  Angiotensin receptor blockers (ARBs) should be administered to
o Heart failure STEMI patients who are intolerant of ACE inhibitors and who have
o History of embolism either clinical or radiologic signs of heart failure
o 2D-echo evidence of mural thrombus
o Atrial fibrillation at increased risk of systemic or pulmonary Table 2.9: Other Pharmacologic Agents
thromboembolism Agents Clinical Use/Benefits
o Actual impact on the mortality rate is slight
Table 2.8: Anti-Coagulants and Anti-Thrombotic Agents Nitrates o Favorable effects on the ischemic process and ventricular
Agents Clinical Use/Benefits remodeling
o Standard antiplatelet agent for patients with STEMI Calcium o Trials have failed to establish a role for these agents
o Antiplatelet Trialists’ Collaboration: relative reduction of
Antagonists o Routine use cannot be recommended
27% in the mortality rate, from 14.2% in control patients to
Aspirin 10.4% in patients receiving antiplatelets o Lowers the concentration of plasma free fatty acids and
o Prevention of 24 deaths for every 1000 Glucose-insulin- improves ventricular performance
o Similarly, 2 strokes and 12 recurrent infarctions are potassium (GIK) o Strict control of blood glucose in diabetic patients with AMI
prevented for every 1000 patients has been shown to reduce the mortality rate
o Appear useful for preventing thrombotic complications in Infusions of o Deficits should be corrected to minimize risk of arrhythmias
Glycoprotein patients with AMI undergoing PCI Magnesium o Does not appear to be any benefit in the routine use of Mg
IIb/IIIa o Reduce the rate of the composite endpoint of death and
Receptor recurrent AMI in the medical management of patients XI. COMPLICATIONS AND THEIR MANAGEMENT
without ST-segment elevation at presentation
o In addition to a regimen of aspirin and tPA, helps to  The prognosis in STEMI is largely related to the occurrence of two
facilitate thrombolysis and to establish and maintain general classes of complications:
Unfractionated Heparin patency of the infarct-related artery o Electrical complications (arrhythmias)
(UFH) o This effect is achieved at the cost of a small increased risk - Most out-of-hospital deaths from STEMI are due to the sudden
of bleeding. development of ventricular fibrillation (occurs within the first 24 h of the
o aPTT - should be 1.5 to 2 times the control value. onset of symptoms, and over half occur in the first hour)
o High bioavailability permitting administration
o Mechanical complications (pump failure)
subcutaneously, reliable anticoagulation without
monitoring, and greater antiXa:IIa activity
Low-molecular- o Treatment with enoxaparin is associated with higher rates A. VENTRICULAR DYSFUNCTION
weight Heparin of serious bleeding, but net clinical benefit still favors
(LMWHs) enoxaparin over UFH
 Ventricular Remodeling- after STEMI, the LV undergoes a series of
o Fondaparinux should not be used alone at the time of changes in shape, size, and thickness in both the infarcted and
coronary angiography and PCI due to risk of catheter noninfarcted segments.
thrombosis o This precedes the development of clinically evident CHF in the
B. BETA-ADRENORECEPTOR BLOCKERS months to years after infarction.
o Soon after STEMI, the left ventricle begins to dilate.
 Use of beta blockers for the treatment of patients with STEMI can - Acutely: this results from expansion of the infarct
cause both immediate effects (when the drug is given early in the  Slippage of muscle bundles
course of infarction) and long-term effects (secondary prevention).  Disruption of normal myocardial cells
 Acute intravenous beta blockade improves:  Tissue loss within the necrotic zone  disproportionate thinning and
o Myocardial O2 supply-demand relationship elongation of the infarct zone.
o Decreases pain - Later: lengthening of the noninfarcted segments occurs as well.
o Reduces infarct size o The overall chamber enlargement that occurs is related to the size
o Decreases the incidence of serious ventricular arrhythmias and location of the infarct, with greater dilation following infarction of
 15% relative reduction in mortality, non-fatal reinfarction, and non- the anterior wall and apex of the left ventricle and causing:
fatal cardiac arrest and increases the probability of long-term survival - More marked hemodynamic impairment
- More frequent heart failure  poorer prognosis.
Table 2.8: Recommendations for Beta-Blocker Therapy for ST-
o Progressive dilation and its clinical consequences may be ameliorated
Elevation Myocardial Infarction (STEMI):
by therapy with ACE inhibitors and other vasodilators (nitrates).
Recommendations
o Oral beta blockers should be initiated in the first 24 hours in patients with
o In patients with an EF <40%, regardless of whether or not heart
STEMI who do not have any of the following: failure is present, ACE inhibitors or ARBs should be prescribed
- Signs of heart failure or evidence of a low-output state B. HEMODYAMIC ASSESSMENT
- Increased risk for cardiogenic shock:
 Age >70 years  Pump failure- now the primary cause of in-hospital death from STEMI.
 Systolic blood pressure <120 mm Hg o Extent of infarction correlates well with the degree of pump failure and
 Sinus tachycardia >110 beats/min or heart rate <60 beats/min with mortality, both early (within 10 days of infarction) and later.
 Increased time since the onset of symptoms of STEMI
o Most common clinical signs: pulmonary rales and S3 and S4 gallop
- Other relative contraindications to use of oral beta blockers:
 PR interval longer than 0.24 second sounds + pulmonary congestion is also frequently seen on CXR
 Second- or third-degree heart block o Characteristic hemodynamic findings: elevated LV filling pressure and
 Active asthma or reactive airways disease elevated pulmonary artery pressure
o Beta blockers should be continued during and after hospitalization for all - These findings may result from a reduction of ventricular compliance
patients with STEMI and no contraindications to their use. (diastolic failure) and/or a reduction of stroke volume with secondary
o Patients with initial contraindications to the use of beta blockers in the first cardiac dilation (systolic failure)
24 hours after STEMI should be reevaluated to determine their subsequent
eligibility. Table 3.0: Killip’s Classification
o It is reasonable to administer IV beta blockers at initial encounter to Definition Mortality Rate
patients with STEMI and no contraindications to their use who are Class Based on Based on Invasive
hypertensive or have ongoing ischemia. Clinical Examination Monitoring
No signs of pulmonary or venous Normal hemodynamics
C. INHIBITION OF RENIN-ANGIOTENSIN-ALDOSTERONE I congestion 0-5%
SYSTEM (RAAS) PCWP <18, CI >2.2
Moderate heart failure as
 ACE inhibitors reduce the mortality rate after STEMI, and the evidenced by rales at the lung
mortality benefits are additive to those achieved with aspirin and bases; S3 gallop, tachypnea, Pulmonary congestion 10-20%
II or signs of failure of the right
beta blockers. side of the heart including PCWP >18, CI >2.2
 Maximum benefit is seen in high-risk patients: venous and hepatic
o Elderly congestion
o Anterior infarction Peripheral hypoperfusion
o Prior infarction III Severe heart failure + 35-45%
o Globally depressed LV function pulmonary edema PCWP <18, CI <2.2
 Short-term benefit occurs when ACE inhibitors are prescribed Shock with SBP < 90mmHg Pulmonary congestion
Evidence of peripheral and peripheral 85-95%
unselectively to all hemodynamically stable patients with STEMI IV vasoconstriction, peripheral hypoperfusion
(SBP >100 mmHg). cyanosis, mental confusion
and oliguria PCWP >18, CI <2.2
*CI, Cardiac index; PCWP, pulmonary capillary wedge pressure.

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 With advances in management, the mortality rate in each class has

fallen, perhaps by as much as one-third to one-half
 Hemodynamic evidence of abnormal global LV function appears
when contraction is seriously impaired in 20–25% of the LV.
 Infarction of ≥40% of the LV usually results in cardiogenic shock
 Hemodynamic monitoring:
o Positioning of a balloon flotation (Swan-Ganz) catheter in the
pulmonary artery permits monitoring of LV filling pressure
(useful in patients who exhibit hypotension and/or clinical
evidence of CHF)
o CO can also be determined with a pulmonary artery catheter.
o Intraarterial pressure monitoring: systemic vascular resistance
can be calculated as a guide to adjusting vasopressor and
vasodilator therapy.
Table 3.1: Indications for Hemodynamic Monitoring in Patients
with ST-Elevation Myocardial Infarction
Indications for Hemodynamic Monitoring in STEMI Patients
o Management of complicated acute myocardial infarction
- Shock with unclear clinical assessment of hemodynamics (e.g. filling
pressures, vascular tone)
- Ventricular septal rupture versus acute mitral regurgitation
- Severe cardiogenic shock caused by right or left ventricular failure with
a need for escalating vasopressor, inotropic, or mechanical circulatory
support
o Refractory ventricular tachycardia
o Difficulty differentiating severe pulmonary disease from left ventricular
failure with available noninvasive data
o Assessment of cardiac tamponade
 Cardiogenic shock complicating MI most often results from LV dysfunction
C. HYPOVOLEMIA (80%); the remainder have a mechanical defect (VSD, papillary muscle
rupture) or predominant RV infarction
 This is an easily corrected condition that may contribute to the
 It is generally associated with a mortality rate of > 70%
hypotension and vascular collapse associated with STEMI
 Coronary angioplasty or surgical revascularization → can lower
 Causes of hypovolemic in STEMI patients:
o Previous diuretic use
mortality rate by as much as one-half (50%).
o Reduced fluid intake during the early stages of the illness  Pathophysiology of Severe Power Failure:
o Vomiting associated with pain or medications. o Marked reduction in the quantity of contracting myocardium
 This should be identified and corrected in patients with STEMI and o Initial insult reduces arterial pressure, and the reduction in coronary
hypotension before more vigorous forms of therapy are begun. perfusion pressure and myocardial blood flow initiates a vicious cycle
 CVP reflects RV rather than LV filling pressure that impairs myocardial function further and may increase the size of
 LV filling or PA wedge pressure should be monitored. and is an the infarct
inadequate guide for adjustment of blood volume o Arrhythmias and metabolic acidosis also contribute to this
o Each patient’s ideal level (generally ~20 mmHg) is reached by cautious deterioration
fluid administration during careful monitoring of oxygenation and CO.  Risk factors: advanced age, decreased LV ejection fraction on
D. TREATMENT OF CONGESTIVE HEART FAILURE admission, large infarct, previous MI, and history of diabetes mellitus
 Treatment:
 The management of CHF in association with STEMI is similar to o Primary objective: maintain coronary perfusion by raising arterial BP
that of acute heart failure secondary to other forms of heart disease, o Treatment modalities include:
except that the benefits of digitalis to patients with STEMI are - Vasopressors- maintains MAP and augment cardiac output
unimpressive (should be administered at the lowest possible doses)
o avoidance of hypoxemia - Intraaortic balloon counterpulsation
o diuresis  Those with hemodynamic instability who require support of the
o afterload reduction circulation for the performance of cardiac catheterization and
o inotropic support angiography to assess lesions that are potentially correctable
 Diuretic agents- extremely effective, as they diminish pulmonary surgically or by angioplasty
congestion in the presence of systolic and/or diastolic heart failure.  Those with cardiogenic shock that does not respond to medical
o LV filling pressure falls and orthopnea and dyspnea improve after management
the intravenous administration of furosemide or other loop diuretics.  Those with refractory ischemia that is not alleviated by other
treatments, or who await definitive revascularization
 Nitrates- may be used to decrease preload and congestive
- Manipulation of blood volume to a level that ensures an optimum
symptoms.
LV filling pressure (20 mmHg)
o Oral isosorbide dinitrate, topical nitroglycerin ointment, and
 Only 10% of patients with this condition present with it on admission,
intravenous nitroglycerin all have the advantage over a diuretic
while 90% develop it during hospitalization.
of lowering preload through venodilation without decreasing the
total plasma volume.  Aortic Counterpulsation- capable of augmenting both diastolic pressure
o Nitrates may improve ventricular compliance if ischemia is and cardiac output
present, as ischemia causes an elevation of LV filling pressure. o A sausage-shaped balloon at the end of a catheter is introduced
o Vasodilators must be used with caution to prevent serious percutaneously into the aorta via the femoral artery, and the balloon is
hypotension. automatically inflated during early diastole, thereby augmenting
coronary blood flow
 ACE inhibitors- ideal class of drugs for management of ventricular
o The balloon collapses in early systole, thereby reducing the afterload
dysfunction after STEMI, especially for the long term.
against which LV ejection takes place
E. CARDIOGENIC SHOCK o Best be reserved for patients whose condition merits mechanical
 Characterized by: congestion and inadequate tissue or end-organ (surgery or angioplasty) intervention (e.g., patients with continuing
ischemia, ventricular septal rupture, or mitral regurgitation)
perfusion secondary to cardiac insufficiency
o Contraindications: aortic regurgitation and aortic dissection
Table 3.2: Diagnostic Criteria for Cardiogenic Shock  SHOCK trial: Emergency revascularization (PCI or CABG) versus
Generally Accepted Criteria for Cardiogenic Shock: medical stabilization and delayed revascularization
o Frank or relative hypotension: SBP <80 or 90 mmHg or MAP 30 mmHg
o 30-day mortality rates in the two groups did not differ significantly
o Inadequate cardiac index (CI): <1.8 liters/min/m2 without mechanical
or pharmacologic support, or <2.2 liters/min/m2 with support
o 6-month and 1-year mortality rates in the emergency
o Elevated end-diastolic pressures on the right (>10 to 15 mm Hg) revascularization group were significantly lower than corresponding
and/or left (>18 mm Hg) side of the heart rates in the stabilization and delayed revascularization group
o Evidence of end-organ hypoperfusion: altered mental status, o Patients younger than 75 years showed particular
decreased UO, AKI, cool or mottled extremities, acute liver injury, or benefit from emergency revascularization
lactic acidosis.

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Table 3.3: Inotropic and Vasopressor Agents

Drug Clinical Indication/s Dose Range Receptor Binding Major Side Effects
Catecholamines
DA > A1 = B2 > B2

Low doses: o Severe hypertension (especially in

<2 µg/kg/min: renal and splanchnic patients taking nonselective beta
o Shock (vasodilatory, vasodilator blockers)
Dopamine cardiogenic) 2.0 to 20 (max 50) µg/kg/min 2-10 µg/kg/min: positive o Ventricular arrhythmias
o Symptomatic bradycardia chronotropic and inotropic effects o Cardiac ischemia
unresponsive to atropine or due to beta receptor stimulation o Tissue ischemia, gangrene (high doses
pacing or caused by tissue extravasation)
High doses: vasoconstrictor effects
due to alpha receptor stimulation
o Low CO (decompensated o Tachycardia
HF, cardiogenic shock, B1 > B2 > A1 (lesser extent) o Increased ventricular response rate in
sepsis-induced myocardial 2.0 to 20 (max 40) µg/kg/min patients with atrial fibrillation
Dobutamine dysfunction) positive inotropic and minimal o Ventricular arrhythmias
o Symptomatic bradycardia chronotropic action or peripheral o Cardiac ischemia
unresponsive to atropine or vasocontrictive activity o Hypotension
pacing
o Arrhythmias
o Shock (vasodilatory, A1 > B1 > B2 o Bradycardia
Norepinephrine cardiogenic) 0.01 to 3 µg/kg/min o Peripheral (digital) ischemia
powerful vasocontrictor and o Hypertension (especially nonselective
enhances contractility beta-blocker patients)
o Cardiac arrest o Infusion: 0.01 to 0.10
o Anaphylaxis µg/kg/min A1 > B1 > B2 o Ventricular arrhythmias
Epinephrine o Shock (cardiogenic, o Bolus: 1 mg IV every 3 to 5 o Severe hypertension
vasodilatory) min (max 0.2 mg/kg) *B1 and B2 receptor binding is o Cardiac ischemia
o IM: (1:1000):0.1 to 0.5 mg greater than NE
(max 1 mg)
o Bradyarrhythmias (especially B1 = B2
torsade des pointes) o Ventricular arrhythmias
Isoproterenol Brugada syndrome 2 to 10 µg/min Increases s contractility, peripheral o Cardiac ischemia
vasodilation, HR o Hypertension
o Hypotension (vagally o Reflex bradycardia
mediated, medication o Bolus: 0.1 to 0.5 mg IV every o Hypertension (especially with
induced) 10 to 15 min Purely A1 nonselective beta blockers)
Phenylephrine o Increase MAP with aortic o Infusion: 0.4 to 9.1 µg/kg/min o Severe peripheral and visceral
stenosis and hypotension vasoconstriction
o Decrease LV outflow tract o Tissue necrosis with extravasation
gradient in HCM
Phosphodiesterase Inhibitors (PDEIs)
o Bolus: 50 µg/kg bolus over
10 to 30 min o Ventricular arrhythmias
Milrinone o Low CO (decompensated o Infusion: 0.375 to 0.75 o N/A o Hypotension
HF, after cardiotomy) µg/kg/min (dose adjustment o Positive inotropic agent o Cardiac Ischemia
necessary for renal o Torsade des pointes
impairment)
o Arrhythmias; enhanced AV conduction
o Bolus: 0.75 mg/kg over 2 to 3 (increased ventricular response rate in
Amrinone o Low CO (refractory HF) min o N/A atrial fibrillation)
o Infusion: 5 to 10 µg/kg/min o Positive inotropic agent o Hypotension
o Thrombocytopenia
o Hepatotoxicity
Other Agents
o Arrhythmias
o Hypertension
o Shock (vasodilatory, o V1 receptors (vascular smooth o Decreased CO (at doses >0.4 U/min)
Vasopressin cardiogenic) o Infusion: 0.01 to 0.1 U/ min muscles) o Cardiac ischemia
o Cardiac arrest o Bolus: 40-U IV bolus o V2 receptors (renal collecting o Severe peripheral vasoconstriction
duct system) causing ischemia (especially skin)
o Splanchnic vasoconstriction
o Loading dose: 12 to 24 µg/kg o Tachycardia, enhanced
Levosimendan o Decompensated HF over 10 min o N/A o AV conduction
o Infusion: 0.05 to 0.2 o Hypotension
µg/kg/min

F. RIGHT-VENTRICULAR INFARCTION G. MECHANICAL CAUSES OF HEART FAILURE

 Approximately 1/3 of patients with inferior infarction demonstrate at  Free Wall Rupture- occur during the first week after the onset of
least a minor degree of RV necrosis. symptoms
 Hemodyamic characteristics: o The tear is usually preceded by a large infarct with subsequent
o Right-sided heart filling pressures (CVP, RA, RV end-diastolic) expansion, sometimes with a dissecting hematoma, and occurs near
are elevated the junction of the infarct and normal muscle.
o LV filling pressure is normal or only slightly raised o Rupture is more common in the left ventricle
o RV systolic and pulse pressures are decreased o Frequency increases with the age
o Cardiac output is often greatly depressed. o Higher incidence of cardiac rupture
 RV infarction causes signs of severe RV failure: - First infarction
- History of hypertension
o Jugular venous distention, Kussmaul’s sign, hepatomegaly with - No history of angina pectoris
or without hypotension - Large Q-wave infarct
o ECG: ST-segment elevations on V4R o Clinical presentation: apparent electromechanical dissociation or
o 2D echo is helpful in determining the degree of RV dysfunction. pulseless electrical activity, cardiac tamponade
o Catheterization of the right side of the heart resembling o Almost universally fatal
constrictive pericarditis (steep right atrial “y” descent and an  Ventricular Septal Defect- sudden, severe LV failure in association with
early diastolic dip and plateau in RV waveforms) the appearance of a pansystolic murmur, often accompanied by a
 Therapy consists of volume expansion to maintain adequate RV parasternal thrill
preload and efforts to improve LV performance with attendant o To differentiate this condition from rupture of a papillary muscle with
reduction in PACWP and pulmonary arterial pressures. resulting mitral regurgitation (MR): presence of a tall "v" wave in the
pulmonary capillary wedge pressure
o Demonstration of left-to-right shunt (O2 step-up at the level of RV)
o Color flow Doppler echocardiography
o Early intervention, including nitroprusside infusion and intraaortic balloon
counterpulsation
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Table 3.4: Characteristics of Mechanical Causes of HF:

Characteristics Ventricular Septal Rupture Rupture of Ventricular Free Wall Papillary Muscel Rupture
o 1-3% without reperfusion therapy o Approximately 1% o Approximately 1% (posteromedial more
Incidence o 0.2-0.34% with fibrinolytic therapy o Fibrinolytic therapy does not reduce risk frequent than anterolateral papillary
o 3.9% in patients with cardiogenic o Primary PCI seems to reduce risk muscle rupture)
shock
o Bimodal peak; within 24 hr and 3-5 dayso Bimodal peak; within 24 hr and 3-5 days o Bimodal peak; within 24 hr and 3-5 days
Time course o Range: 1-14 days o Range: 1-14 days o Range: 1-14 days
Clinical o Chest pain, shortness of breath, o Anginal, pleuritic, or pericardial chest pain; o Abrupt onset of shortness of breath and
manifestations hypotension syncope; hypotension; restlessness; pulmonary edema; hypotension
sudden death
o Harsh holosystolic murmur, thrill, o Jugular venous distention (29% of o A soft murmur in some cases, no thrill,
Physical findings S3, accentuated S2, pulmonary patients), pulsus paradoxus (47%), variable signs of RV overload, severe
edema, RV and LV failure, electromechanical dissociation, pulmonary edema, cardiogenic shock
cardiogenic shock cardiogenic shock
o Ventricular septal rupture o >5 mm pericardial effusion not visualized o Hypercontractile LV, torn papillary
Echocardiographic o Left-to-right shunt on color flow in all cases; layered, high-acoustic echoes muscle or chordae tendineae, flail
findings o Doppler echo through the within the pericardium (blood clot); direct leaflet, severe mitral regurgitation on
ventricular septum, pattern of RV visualization of tear; signs of tamponade color flow Doppler echo
overload
o Increase in oxygen saturation from o Ventriculography insensitive o No increase in oxygen saturation from
Right-heart the RA to RV o Classic signs of tamponade not always the RA to RV
catheterization o Large v waves present (equalization of diastolic o Large v waves
pressures in the cardiac chambers) o Very high PCWP
 Mitral Regurgitation- dysfunction of the mitral valve o Prophylactic use of lidocaine can
o LV dilatation or alteration in the size or shape of the LV due to impaired o Can occur without reduce occurrence of Vfib but has
contractility or to aneurysm formation causes disordered contraction of warning not been shown to reduce overall
the papillary muscles and failure of coaptation of the mitral valve leaflets arrythmias within mortality from AMI
o Papillary muscle may rupture the first 24 hours o Use of beta-blockers, and the
o Surgical repair or replacement of the mitral valve of STEMI nearly universal success of
o Intraaortic balloon counterpulsation (IABC) and infusion of nitroglycerin electrical cardioversion or
or sodium nitroprusside defibrillation
o Stable-sustained V-tach:
H. ARRHYTHMIAS - IV lidocaine (bolus of 1.0-1.5 mg/kg; infusion of 20-50
Algorithm for assessment of need for implantation of a ug/kg/min)
- Procainamide (bolus of 15 mg/kg over 20-30 min;
cardioverter-defibrillator:
infusion of 1 to 4 mg/min)
- Amiodarone (bolus of 75-150 mg over 10 to 15 min
followed by infusion of 1.0 mg/min for 6 h and then 0.5
Ventricular mg/min)
Tachycardia - Electrocardioversion
and Fibrillation o Vfib/Vtach w/ hemodynamic deterioration:
- Defibrillation at 200 – 300J
- VT or VF refractory to electroshock – more responsive
after patient is treated with:
 Epinephrine (1 mg IV or 10 mL of a 1:10,000
solution via the intracardiac route)
 Bretylium (5 mg/kg bolus)
 Amiodarone (75 to 150 mg bolus)
o Torsades de pointes- due to other concurrent problems
(such as hypoxia, hypokalemia, or other electrolyte
disturbances) or of the toxic effects of an agent being
administered to the patient (such as digoxin or quinidine)
o Primary Vfib- VF that is a primary response to acute
ischemia which occurs during the first 48 hours
- In-hospital mortality rate is increased
- Long-term survival is good
o Secondary Vfib- associated with predisposing factors
such as CHF, shock, bundle branch block, or ventricular
aneurysm
- Poor prognosis
 The incidence of arrhythmias after STEMI is higher in patients seen - VT or VF late in the hospital course (after first 48h)
early after the onset of symptoms. - The mortality rate is increased both in-hospital and
 Mechanisms responsible for infarction-related arrhythmias: during long-term follow-up.
o Autonomic nervous system imbalance o Slow ventricular
tachycardia
o Electrolyte disturbances
o Ventricular
o Ischemia
rhythm with a rate
o Slowed conduction in zones of ischemic myocardium of 60–100 bpm,
Table 3.5: Infarction-Related Arrhythmias Accelerated often occurs o Most episodes of AIVR do not
Arrhythmia Clinical Features Therapeutic Options Idioventricular transiently during require treatment if the patient is
Electrical instability Rhythm fibrinolytic therapy monitored carefully
o Infrequent, sporadic o Do not require treatment at the time of o AIVR can generally be readily
ventricular o Therapy is reserved for reperfusion treated with a drug that increases
premature patients with sustained o Does not presage the sinus rate (atropine)
Ventricular depolarizations ventricular arrhythmias the development
Premature occur in almost all o Prophylactic antiarrhythmic tx of classic Vtach
Beats patients with STEMI (either IV lidocaine early or o Degeneration into
o Hypokalemia and oral agents later) is a more serious
hypomagnesemia contraindicated for VPB in arrhythmia is rare
are risk factors for the absence of clinically Pump failure, excessive sympathetic stimulation (Supraventricular Arrythmias)
ventricular important ventricular o Most common
fibrillation (correct tachyarrhythmias, because o Secondary to
serum K+ and Mg2+) such therapy may actually another cause o Antipyretics; analgesics; consider
increase the mortality rate Sinus (anemia, fever, beta blocker unless heart failure
o Beta blocking agents are Tachycardia heart failure, or a present
effective in abolishing metabolic
ventricular ectopic activity derangement)
o Due to
sympathetic
overstimulation

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o Often secondary to LV o Digoxin – DOC for o Occurs in association with:

failure, pulmonary SVA if HF is present - Large infarcts (especially anterior)
emboli, or atrial o If HF is absent, beta - CHFLV thrombus detected by echo
infarction blockers, verapamil, or o Systemic anticoagulation for 3 to 6 months
o Usually transient in diltiazem are suitable  Left Ventricular Aneurysm- usually used to describe dyskinesis or local
patients with STEMI alternatives for
o Increased VR and loss controlling the VR, as
expansile paradoxical wall motion.
of the atrial they may also help to o Complications do not usually occur for weeks to months after STEMI
Atrial contribution to LV control ischemia - CHF
fibrillation filling can reduce CO o If the abnormal rhythm - Arterial embolism
and/or Atrial considerably persists for > 2h with a - Ventricular arrhythmias
flutter o AF during STEMI is VR in excess of 120 o Apical aneurysms- most common and the most easily detected by
associated with bpm, or if tachycardia clinical examination.
increased mortality induces heart failure, o Pseudoaneurysm- often ruptures spontaneously and should be
and stroke shock, or ischemia, a surgically repaired if recognized
o AF is probably a synchronized
 Dressler Syndrome- usually occurs 1 to 8 weeks after infarction
marker of a poor electroshock (100 to
prognosis 200 J) should be used. o Patients with Dressler syndrome have malaise, fever, pericardial
o May occur in patients o In severely discomfort, leukocytosis, an elevated ESR, and a pericardial effusion.
Accelerated with inferoposterior compromised LV o Localized fibrinous pericarditis containing polymorphonuclear
Junctional infarction function: right atrial or leukocytes and detection of antibodies to cardiac tissue suggests an
Rhythms o Digitalis excess must coronary sinus pacing immunopathologic process.
be ruled out is indicated o Treatment is with aspirin, 650 mg as often as q4 hrs
Bradyarrhythmias, conduction disturbances o Glucocorticosteroids and NSAIDs are best avoided in patients with
o Treatment is indicated Dressler syndrome within 4 weeks of STEMI because of their
o Frequently occurs if hemodynamic
during the early compromise results
potential to impair infarct healing, cause ventricular rupture, and
phases of STEMI, from the slow HR increase coronary vascular resistance
particularly in patients o Atropine- most useful XII. POST-INFARCTION RISK STRATIFICATION AND MANAGEMENT
with inferior and drug for increasing HR
Sinus posterior infarctions and should be given  Many clinical and laboratory factors have been identified that are
Bradycardia o Increased vagal tone IV (0.5 mg initially) associated with an increase in cardiovascular risk after initial recovery
that produces sinus o If the rate remains from STEMI.
bradycardia during the <50–60 beats/min,
early phase of STEMI additional doses of 0.2
 Most important factors include:
o Persistent ischemia (spontaneous or provoked)
may actually be mg, up to a total of 2.0
o Depressed LV ejection fraction (<40%)
beneficial, perhaps mg, may be given.
o Rales above the lung bases on PE or congestion on CXR
because it reduces o Persistent bradycardia
myocardial oxygen (<40 beats/min) o Symptomatic ventricular arrhythmias
demand despite atropine: o Age >75
electrical pacing o Diabetes mellitus
o Isoproterenol should o Prolonged sinus tachycardia
o Hypotension
be avoided.
o ST-segment changes at rest without angina (silent ischemia)
o Mortality rate of
o Abnormal signal-averaged ECG
patients with CHB –
o Non-patency of the infarct-related coronary artery
markedly higher o Temporary electrical
o Persistent advanced heart block
anterior infarction than pacing – has a limited
o New intraventricular conduction abnormality on the ECG.
those of patients with impact on prognosis in
inferior infarction anterior infarction and  In stable patients:
o Heart block is complete heart block o Submaximal exercise stress testing may be carried out before
common in inferior o Permanent pacing - hospital discharge to detect residual ischemia and ventricular ectopy
Atrioventricula infarction – transient may reduce the long- and to provide the patient with a guideline for exercise in the early
r and and result of increased term risk of sudden recovery period.
Intraventricular vagal tone and/or the death due to o Maximal (symptomlimited) exercise stress test may be carried out 4–6
Conduction release of adenosine bradyarrhythmias in
Disturbances o In anterior wall patients who develop
weeks after infarction.
infarction, heart block combined persistent o Evaluation of LV function is usually warranted as well.
is usually related to bifascicular and  Patients high risk for recurrent MI or death from arrythmia: cardiac
ischemic malfunction transient third-degree catheterization with coronary angiography and/or invasive
of the conduction heart block during electrophysiologic evaluation is advised
system, which acute phase of MI o Patients in whom angina is induced at relatively low workloads
commonly is
o Those who have a large reversible defect on perfusion imaging or a
associated with
extensive myocardial depressed ejection fraction
necrosis o Those with demonstrable ischemia
o Those in whom exercise provokes symptomatic ventricular
I. OTHER COMPLICATIONS arrhythmias.
 Recurrent Chest Discomfort- recurrent or persistent  Exercise tests- also aid in formulating an individualized exercise
ischemia/angina (25%) often heralds extension of the original prescription, which can be much more vigorous in patients who tolerate
infarct or reinfarction in a new myocardial zone exercise without any of the previously mentioned adverse signs.
o Associated with a doubling of risk after AMI o May provide an important psychological benefit, building the patient's
o Should be referred for prompt coronary arteriography and confidence by demonstrating a reasonable exercise tolerance
mechanical revascularization o The patient benefits by the physician's reassurance that objective
o Thrombolysis is an alternative to early mechanical evidence suggests no immediate jeopardy
revascularization  Cardiac rehabilitation program with progressive exercise is initiated in
 Pericarditis- pericardial friction rubs and/ or pericardial pain are the hospital and continued after discharge.
frequently encountered in patients with STEMI involving the o Should include an educational component that informs patients about their
epicardium. disease and its risk factors
o Can usually be managed with aspirin (650 mg QID).  Usual duration of hospitalization for uncomplicated STEMI: 3–5 days.
o May lead to the erroneous diagnosis of recurrent ischemic pain  During first 1–2 weeks: the patient should be encouraged to increase
and/ or infarct extension (complaints of pain radiating to either activity by walking about the house and outdoors in good weather.
trapezius muscle is helpful  pattern of discomfort is typical of o Normal sexual activity may be resumed during this period.
pericarditis)  After 2 weeks: the physician must regulate the patient’s activity on the
o Anticoagulants potentially could cause tamponade (should not be basis of exercise tolerance.
used unless there is a compelling indication)
 Most patients will be able to return to work within 2–4 weeks.
 Thromboembolism- complicates STEMI in ~10% of cases
o Considered to be an important contributing cause of death in 25%
of patients with STEMI who die after admission to the hospital.
o Arterial emboli originate from LV mural thrombi, while most
pulmonary emboli arise in the leg veins

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XIII. SECONDARY PREVENTION Classic sign of angina pectoris

a. Lapras sign c. Lotad sign
 Long-term treatment with an antiplatelet agent (usually aspirin) b. Levine sign d. De musset sign
after STEMI is associated with a 25% reduction in the risk of One forth of patients with Anterior wall myocardial injury presents with:
recurrent infarction, stroke, or cardiovascular mortality a. Hypotension and tachycardia c. Hypotension and bradycardia
o Alternative antiplatelet in patients intolerant of aspirin is b. Hypertension and tachycardia d. Hypertension and bradycardia
clopidogrel (75 mg orally daily) Anginal equivalents will most likely present in:
o AMIs tend to be smaller and are more likely to be non-Q wave a. A 43 year old triathlete without comorbids in the middle of a race
 ACE inhibitors or ARBs- should be used indefinitely by patients b. A 65 Year old, diabetic senator
with clinically evident heart failure, moderate decrease in global c. A 22 year old medical student taking online classes
d. A 45 year old, noncompliant smoker
ejection fraction, or a large regional wall motion abnormality to
prevent late ventricular remodeling and recurrent ischemic events. The following are risk factors fort STEMI
a. Hypercoaguable state c. Cocaine abuse
 Chronic routine use of oral beta- blockers for at least 2 years after b. 40 pack yr smoker d. All of the choices
STEMI is supported by well-conducted, placebocontrolled trials.
February 2021:
 Warfarin lowers the risk of late mortality and the incidence of Antiplatelet agent:
reinfarction after STEMI. a. Clopidogrel c. Abxicimab
o Most physicians prescribe aspirin routinely for all patients b. Enoxaparin d. Fondaparinux
without contraindications and add warfarin for patients at Chest discomfort in ACS
increased risk of embolism a. Less frequent than previous episodes c. Occurs even at rest lasting for 2 minutes
o Patients <75 years old: low dose of aspirin (75–81 mg/d) in b. Crescendo-decrescendo pattern d. Relatively recent onset
combination with warfarin administered to achieve an INR
Large-area of myocardial ischemia
>2.0 is more effective than aspirin alone for preventing a. Bradycardia c. Hypertension
recurrent MI and embolic cerebrovascular accident. b. S3 and S4 sound d. Soft S1
However, there is an increased risk of bleeding and a high
rate of discontinuation of warfarin that has limited clinical Most common cause of myocardial ischemia
a. Atherosclerotic cardiovascular c. Coronary spasm
acceptance of combination antithrombotic therapy. disease d. Arterial thrombi
o Patients who have had a stent implanted and have an indication b. Imbalance between myocardial supply
for anticoagulation should receive dual antiplatelet therapies in and demand
combination with warfarin. Troponins can be elevated in:
 Control of Risk Factors for Atherosclerosis: should be discussed a. Myocarditis c. Pulmonary embolism
with the patient and favorably modified b. CHF d. All of the choices
o Cessation of smoking True regarding Prinzmetal's variant angina:
o Control of hypertension a. Usually occcurs in exertion c. Drug of choice is beta blockers
o Control of hyperlipidemia (the target LDL level is < 70 mg/dL) b. Transient coronary spasm d. Non-smokers
SAMPLEX QUESTIONS September 2021
The coronary artery which supplies the anterior LV free wall:
September 2020: a. Left circumflex c. Right coronary artery
A CKMB:Total CK ratio of ____ suggests a myocardial injury b. Left anterior descending d. Obtuse marginals and diagonal
a. 1.0 c. 1.5 branches
b. 0 d. 2.5
Which is TRUE about Beta blocker treatment in patient with Acute Coronary syndrome?
More reliable ECG finding in NSTEMI: a. It can be given even in patients with acute pulmonary congestion.
a. Bifid configuration c. Horizontal ST depression b. It can be safely given in a patient with complete heart block
b. Downsloping d. Upsloping c. It can be given at a dose of 25-50 mg by mouth every 6 hours
d. It is contraindicated in a patient with previous use of Sildenafil
In UA/NSTEMI, you would like to maintain HR at:
a. 45 bpm c. HR does not matter as long as patient is The coronary artery which provides for the infero-posterior wall in majority of humans:
b. 50-60 bpm asymptomatic a. Septal branches c. Right coronary artery
d. 100 bpm b. Left circumflex d. Left anterior descending
Absolute contrainidication for nitrates: Which of the following symptoms is highly suggestive of acute coronary syndrome?
a. Hypertension c. Use of viagra 2 weeks ago a. tearing pain of sudden onset in anterior chest pain radiating to back
b. Hypotension d. Bradycardia with diziness b. chest pain aggravated by change on position
c. sudden chest heaviness about 20minutes in duration accompanied with diaphoresis
Cells that predominate at the site of plaque rupture d. chest pain of 6-8 minutes duration with crescendo pattern relieved by rest
a. Macrophage c. Smooth muscle cells
b. T lymphocyte d. All of the choices Which population will benefit BEST from early invasive strategy for patients treated as
ACS – NSTEMI?
Initial response when you encounter a STEMI patient in the ER: a. patient in cardiogenic shock c. atrial fibrillation
a. Nitrates c. Morphine b. diabetic patient d. patient with EF 60%
b. Oxygen and aspirin d. All of the choices
True about loading dose of anti-platelet therapy
High risk feature in Unstable Angina or NSTEMI
a. clopidogrel- 300mg c. aspirin-200mg
a. Diabetic senior citizen c. Pulmonary congestion 2/3 of the lungs b. clopidogrel- 180mg d. aspirin-100mg
b. Troponin 10,000 above d. All of the choices
normal Which of the following will benefit from thrombolysis with Streptokinase?
The following are possible causes of STEMI except: a. ACS-STEMI c. ACS-Unstable angina
a. Coronary artery fistula c. Anomalous origin of a patent coronary artery b. Chronic stable angina d. Prinzmetal Variant angina
b. Vasospasm d. Acute thrombus formation Marker for myocardial necrosis.
Cardiac imaging that recognizes a “cold spot” in a specific myocardial region affected a. Troponin I c. CRP
by a transmural or nontransmural thrombus: b. Pro-BNP d. SGPT
a. Cardiac CT scan c. Myocardial perfusion scan True about Prinzmetal variant angina.
b. 2D echocardiogram d. Cardiac catheterization a. The diagnostic hallmark is the presence of atherosclerotic plaque at proximal
Most common cause of death in STEMI patients: coronary artery.
a. VSD c. Complete heart block b. It is most common at left coronary artery.
b. Ventricular fibrillation d. Wolf-Parkinson White Anomaly c. It is related to hypocontractility of vascular smooth muscle.
d. It can present as ST elevation on ECG.
An ECG finding of ST Elevation in V1 to V4 has a thrombus most likely in the:
a. Right coronary artery c. Right anterior descending artery A 70 year old male hypertensive patient came in due to acute onset of chest pain
b. Left obtuse marginals d. Left anterior descending artery accompanied with dyspnea and diaphoresis. 12L ECG done showed this tracing: 4-5mm J
point elevation at Leads II, III and AVF. The cardiac enzyme showed elevated result. How
A patient who suffered a STEMI 10 days ago is said to be in the: should you treat the patient? a. Chronic Stable Angina b. Acute Coronary Syndrome STEMI
a. Acute stage c. Healing stage c. Acute Coronary Syndrome- Unstable Angina d. Acute Coronary Syndrome Non STEMI
b. Chronic stage d. Healed stage a. Chronic stable angina c. ACS-Unstable angina
Unstable Angina may be the ff EXCEPT: b. ACS-STEMI d. ACS-NSTEMI
a. Chronic c. At rest REFERENCES
b. Crescendo d. New onset
1. 2022 Lecture
Indication for coronary Angiography in ACS, except: 2. Jameson, J. L., & Loscalzo, J. (2018). Harrison's principles of internal medicine (20th
a. 1 hour after the onset of pain edition.). New York: McGraw Hill Education
b. Patient revived after ACLS of 5minutes 3. Mann, D. L., Zipes, D. P., Libby, P., Bonow, R. O., & Braunwald, E. (2019).
c. A VIP with point tenderness over the nipple area Braunwald's heart disease: A textbook of cardiovascular medicine (11th edition.).
d. Intractable ventricular arrhythmias Philadelphia, PA: Elsevier/Saunders

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