TOPIC: UNSTABLE ANGINA

PRESENTER: DR. APURBA CHAKMA

D-CARD STUDENT
SESSION: JULY 2016

Some Definitions
Acute Coronary Syndrome (ACS): Acute coronary syndrome (ACS) is
a term used to describe a pattern of clinical symptoms that is consistent
with acute myocardial ischemia. It is a collective term used to describe
STEMI, NSTEMI and UA .
Angina: It is the chest pain or discomfort caused when our heart
muscles don't get enough oxygen-rich blood. Angina is not a disease. It
is a symptom of an underlying heart problem, usually coronary heart
disease (CHD).
Unstable Angina (UA): A clinical condition featuring severe chest pain
as a result of myocardial ischaemia caused by dynamic obstruction of a
coronary artery due to plaque rupture or erosion with superimposed
thrombosisis. It is usually secondary to reduced myocardial perfusion
resulting from coronary artery atherothrombosis.

Pathophyisology
of Unstable
angina:
The hallmark of UA is the
imbalance between
myocardial oxygen supply
and demand. The oxygen
supply is hampered mainly
by the atherosclerotic
changes in the cardiac
vasculature that may
ultimately lead to
obstruction of the affected
vessel.

 Continued

CONSEQUENCE OF ACUTE CORONARY

OCCLUSION

Secondary UA/NSTEMI may also be seen in the following

situations where obstruction is not necessary ---

Acute increases in myocardial oxygen demand (eg, fever, tachycardia,

hypertensive emergency),

Reductions in coronary blood flow, (eg, hypotension),

Diminution in myocardial oxygen delivery (eg, severe anemia),

Among individuals with severe left ventricular (LV) hypertrophy.

Coronary dissection or vasculitis.

RISK FACTORS
Non-modifiable:

> Increasing age.

> Male sex.

> Heredity.

Modifiable: > Smoking.

> Dyslipidaemia.
> Hypertension.
> Physical inactivity.
> Obesity & Overweight.
> Diabetes mellitus.

Others factors: > Stress.

> Alcohol.
> Diet and Nutrition.

(ref-AHAwebS)

Clinical presentations of Unstable Angina:

The characteristics of angina include

Most commonly presents as a deep, poorly localized,

pressure-type chest pain lasting >10 minutes

It typically occurs at rest or with minimal exertion.

It frequently starts in the retrosternal area and can

radiate

to either or both arms, the neck, or the jaw.

Pain may also occur in these areas independent of chest

pain.

Patients with ACS may also present with atypical

symptoms, which include no chest pain but present
solely with.

Increasing dyspnea
Stabbing or pleuritic pain,
Epigastric pain, indigestion
Agitation, altered mental status,
Profound weakness, and syncope.
Such presentations are more common in women, advanced
elderly individuals, and patients with long-standing diabetes
mellitus.

Physical findings that may lead to suspicion of Unstable Angina

Can be normal.
Sweating, tachycardia or bradycardia.
May have signs of Heart failure (eg, dyspnea, lung crepitation etc.).
Rare but there maybe signs of myocardial malfunction- eg, overt hypotension
(SBP<100 mm Hg), raised JVP, reverse splitting of S2, presence of S3 or, S4, a
paradoxical splitting of S2, or a new murmur of mitral regurgitation due to papillary
muscle dysfunction.

The coupling of pain on palpation suggesting musculoskeletal disease or

inflammation with a pulsatile abdominal mass suggesting abdominal aortic
aneurysm raises concern for non-ischemic causes of NSTE ACS.

Grading of Angina Pectoris According to Canadian Cardiovascular

Society Classification
Class

Description of Stage

Ordinary physical activity does not causeangina, such as walking or

climbing stairs. Angina occurs with strenuous, rapid, or prolonged
exertion at
work or recreation.

II

Slight limitation of ordinary activity. Angina occurs on walking or climbing

stairs rapidly; walking uphill; walking or stair climbing after meals; in cold,
in
wind, or under emotional stress; or only during the few hours after
awakening.
Angina occurs on walking >2 level blocks and climbing >1
flight of ordinary stairs
at normal pace and under normal conditions.

III

Marked limitation of ordinary physical activity. Angina occurs on walking

1 to 2 level blocks and climbing 1 flight of ordinary stairs under normal
conditions and at normal pace.

IV

Inability to carry on any physical activity without discomfort

symptoms may be present at rest.

anginal

Investigations

ECG: A 12-lead ECG should be performed and interpreted within 10 minutes of the patients
arrival at an emergency.
Findings may include--- > ST depression (especially horizontal or down slopping)
> Transient ST-elevation of at least 0.5 mm or new T-wave inversion.
> Persistent negative T waves over the involved area.
> Deeply negative T waves across all the precordial (anterior) leads that

suggest a proximal, severe, left anterior descending coronary artery stenosis and
bears a high risk.
The ECG can be relatively normal or initially non diagnostic; if this is the case, the ECG should
be repeated (e.g., at 15- to 30 minute intervals during the first hour), especially when symptoms
recur.

Biochemical Cardiac Markers: Important biomarkers include CK-MB, Troponin I &

T. The values of these markers maybe normal or slightly elevated in UA.

A negative cardiac troponin obtained on admission confers a >95% negative

predictive value for MI which makes the suspicion of UA more likely. But serial
cardiac troponin I or T levels should be obtained 3 to 6 hours after symptom onset to
support the diagnosis. (ref-AHA2014)

Troponin I, T

Very specific and more

sensitive than CK

Rises 4-8 hours after injury

CK-MB

Rises 4-6 hours after injury

and peaks at 24 hours

Remains elevated 36-48

hours

May remain elevated for up to

two weeks

Positive if CK/MB > 5% of

total CK and 2 times
normal

Can provide prognostic

information

Elevation can be predictive

of mortality

Causes of Troponin Elevation Other Than Acute

Coronary Syndromes

Pulmonary embolus

Myocarditis

Cardiac contusion

Congestive heart failure

Chemotherapy (Adriamycin, 5-fluorouracil)

Cardioversion or radiofrequency ablation

Septic shock

Extreme endurance athletics

Renal failure

Echocardiography:
Bedside echo should be performed initially when a strong clinical suspicion of acute
coronary syndrome is present and ECG is normal or inconclusive.

It may show transient wall motion abnormalities.

It may also identify an underlying cause of UA, such as aortic stenosis or obstructive
cardiomyopathy.

Alternatively, it can help to exclude other causes of similar presentations, eg, myopericarditis, pericardial effusion, aortic dissection, congestive heart failure (CHF), or
advanced valve disease.

Stress echo. is used for further risk stratification and triaging patients after MI is
excluded by serial ECG and cardiac enzymes measurements.

Myocardial perfusion imaging:

Acute rest myocardial perfusion imaging with technetium-labeled sestamibi is a

relatively sensitive and specific diagnostic test for ACS.

Myocardial perfusion studies using exercise or pharmacological stress are performed

after stabilization, to identify the extent of myocardial ischaemia and direct patients for
possible invasive management.

(ref- Hursts13e + BMJ)

Coronary angiography (joint approach for diagnosis and management)

General recommendation for invasive coronary angiogram and re-vascularization in non-ST-elevation acute
coronary syndromes include:

An immediate invasive strategy (<2 hours) in patients with at least one of the following very-high-risk criteria:

Haemodynamic instability or cardiogenic shock

Recurrent or ongoing chest pain refractory to medical treatment
Life-threatening arrhythmias or cardiac arrest
Mechanical complications of MI
Acute heart failure with refractory angina or ST deviation
Recurrent dynamic ST- or T-wave changes, particularly with intermittent ST-elevation.

An early invasive strategy (<24 hours) in patients with at least one of the following high-risk criteria:
Rise or fall in cardiac troponin compatible with MI
Dynamic ST- or T-wave changes (symptomatic or silent)
GRACE (Global Registry of Acute Coronary Events) score >140.

An invasive strategy (<72 hours) in patients with at least one of the following intermediate-risk criteria:

Diabetes mellitus
Renal insufficiency (estimated GFR <60 mL/minute/1.73 m^2)
Left ventricular ejection fraction 40% or congestive heart failure
Early post-infarction angina
Recent percutaneous coronary intervention
Prior CABG
GRACE risk score >109 and <140
Recurrent symptoms or known ischaemia on non-invasive testing.
Ref- http://bestpractice.bmj.com/best-practice/monograph/149/diagnosis/step-by-step.html

The shortest pathway to detect Unstable Angina

MANAGEMENT OF UNSTABLE ANGINA

Early Hospital Care: MONAC

Morphine: IV morphine sulfate may be reasonable for continued ischemic

chest pain. It should be administered in IV boluses of 1 to 5 mg, which are
repeated as needed to relieve symptoms. Alternatively IV Pethidine is also used in
routine practice.

Oxygen inhalation: Administer supplemental oxygen only with oxygen saturation

<90%, respiratory distress, or other high-risk features for hypoxemia.

Nitrates: Administer sublingual NTG every 5 min x3 for continuing

Aspirin: Nonenteric-coated, chewable aspirin (162 mg to 325 mg)should be given
to all patients with NSTE-ACS without contraindications as soon as possible after
presentation.

Clopidogrel: A P2Y12 inhibitor (eg, clopidogrel or ticagrelor) in addition to aspirin

should be administered to all patients with NSTE-ACS without contraindications.
Clopidogrel: 300-mg or 600-mg loading dose or, Ticagrelor: 180-mg loading dose.

ANTI-PLATELET
THERAPY

ischemic pain. Administer IV NTG for persistent ischemia, HF, or

hypertension.

Continued management

Anticoagulation: In patients with NSTE-ACS, in addition to antiplatelet

therapy, anticoagulation is recommended for all patients irrespective of initial
treatment strategy.
Treatment options include:

Enoxaparin: 1 mg/kg subcutaneous (SC) every 12 hours (reduce dose to 1

mg/kg SC once daily in patients with creatinine clearance <30 mL/min).

Fondaparinux: 2.5 mg SC daily, continued for the duration of hospitalization

or until PCI is performed.

UFH IV: initial loading dose of 60 IU/kg (maximum 4,000 IU) with initial infusion
of 12 IU/kg per hour (maximum 1,000 IU/h) adjusted per APTT to maintain
therapeutic anticoagulation, continued for 48 hours or until PCI is performed.

Intravenous GP IIb/IIIa Receptor Inhibitors: Tirofiban, Eptifibatide.

Continued

Blockers: Reduce heart rate, contractility, and blood pressure, thereby reducing
myocardial oxygen demand (MVO2). It is now recommended that oral beta-blockers
should be initiated within the first 24 hours in patients who do not have any of the
following: 1) signs of HF.
2) evidence of low-output state.
3) increased risk for cardiogenic shock.
4) other contraindications to beta blockade (e.g., PR interval >0.24
second, second or third-degree heart block, active asthma, or
reactive
airway disease).
Recommended blockers include sustained-release Metoprolol succinate, Esmolol,
or Bisoprolol which have selective 1 adrenergic blockade capability.
(ref-AHA2014+Hursts13e)

Continued

Calcium Channel Blockers (CCB): These agents are coronary and

peripheral vasodilators. In continuing or frequently recurring ischemia, and a
contraindication to beta blockers, a nondihydropyridine calcium channel blocker
(CCB) (e.g., verapamil or diltiazem) should be given as initial therapy in the
absence of . . .

> Clinically significant LV dysfunction,

> Increased risk for cardiogenic shock,
> PR interval greater than 0.24 second,
> Second- or third-degree atrioventricular block.
(ref-AHA2014)

Dihydropyridine CCBs do not play a primary role in the management of ACS but
may be useful agents for blood pressure control when persistent hypertension is
present after initiation of -blockers and ACE inhibitors or angiotensin receptor
blockers (ARBs). Only long acting dihydropyridines such as Amlodipine should be
used for this purpose.
(ref-Hursts13e)

Continued

ACE inhibitors (ACEI): These should be started and continued

indefinitely in all patients with LVEF less than 40% and in those with
hypertension, diabetes mellitus, or stable CKD unless contraindicated (egrenal insufficiency, hypotension, cough, hyperkalaemia etc.). They also
prohibit post MI cardiac remodeling. Common agents include Ramipril,
Enalapril, Captopril etc.

Angiotensin II Receptor Blockers (ARB): ARBs should predominantly

be used in place of ACE inhibitors in patients with ACE inhibitor
intolerance. Common agents include Losartan Potassium, Valsartan,
Olmesartan etc.

Continued

Cholesterol

management: High-intensity statin therapy

should be initiated or continued in all patients with NSTE-ACS.

Therapy with statins in patients with UA reduces the rate of
recurrent MI, coronary heart disease mortality, need for
myocardial revascularization, and stroke. Usual agents that
are in clinical practice include atorvastatin, rosuvastatin,
simvastatin, pravastatin etc.

Other Anti-Ischemic medications

Ranolazine: It is an anti-anginal agent which inhibits the

late inward sodium current and reduces the deleterious
effects of intracellular sodium and calcium overload that
accompany myocardial ischemia. Ranolazine is currently
indicated for treatment of chronic angina..
Its Major adverse effects are constipation, nausea, dizziness,
and headache.

Continued

Trimetazidine: is usually prescribed as a long-term

treatment of angina pectoris. It increases coronary flow
reserve, thereby delaying the onset of ischemia associated
with exercise, limits rapid swings in blood pressure without
any significant variations in heart rate, significantly
decreases the frequency of angina attacks, and leads to a
significant decrease in the use of nitrates.
Aderse effects include tremor, rigidity, akinesia, hypertonia
etc.

Continued.

Potassium channel activators: These have arterial and

venous dilating properties but do not exhibit the tolerance
seen with nitrates. Nicorandil (1030 mg twice daily orally)
is the only drug in this class currently available for clinical
use.
Serious side effects of this drug are palpitations, flushing,
perianal

and ileal ulceration etc.

Invasive strategies in management of NSTE ACS

The initial ischemia-guided strategy calls for an invasive

evaluation for those patients who

1) fail medical therapy (refractory angina or angina at rest or

with minimal activity despite vigorous medical therapy),

2) have objective evidence of ischemia (dynamic

electrocardiographic changes, myocardial perfusion defect)
as identified on a noninvasive stress test, or

3) have clinical indicators of very high prognostic risk (eg,

high TIMI or GRACE scores).

Invasive treatment of NSTEMI/UA

Percutaneous coronary
intervention (PCI)

Coronary artery bypass

grafting (CABG)

Secondary prevention and long term management of UA

Drug therapy: Include long term continuation of.
> Antiplatelets
> Nitrates
> Beta Blockers
> CCB
> ACEI/ARB

Cessation of smoking.

Effective blood pressure control.

Doing daily regular physical exercise.
Lipid management: STATINS
Wight management.
Control of DM.

THANK YOU. . . .