Long case presentation

Internal medicine department

Personal history.
Mohammed Ismail Abdelnasser , a 40 years old taxi driver , lives in Fanara, urban area. He is
married for 18 years with 6 children, youngest is 3 years old. He is right handed; and a heavy smoker
with smoking index 1,000. No other special habits of medical importance.
C/O
He complains of chest pain of 5 hours duration.
HPI
The patient is known to be diabetic for 7 years on OHDs. He presented to the ED 2 days ago, 4th of
November, at 3 am, complaining of severe retrosternal chest pain of acute onset, stationary course,
and 5 hours duration. It is described as chest tightness. There is no radiation to other sites; no
relieving factors, including rest and nitrates; and no aggravating factors, including exercise. No
relation to meals, respiration, exertion, nor posture. It was associated with cold sweats and vomiting.
Vomiting was 3-6 times/day, of copious amount. Vomitus was food with no blood. It was not related
to meals. No relieving or aggravating factors. He was admitted to the Internal medicine department
yesterday, 5th of November, at 2 am.
No Dyspnea, no palpitation, no fever
Symptoms of systemic congestion: No LL edema, no ascites, no right hypochondrium pain, no
dyspepsia, no NV, no flatulence.
Symptoms of LCOP: No dizziness, no syncope, no fainting, no headache, no oliguria, no easy
fatigability and claudication, no pallor or cold peripheries, no blurring of vision.
Symptoms of pulmonary congestion: There is chronic productive cough of, gradual onset,
progressive course, and 10 years duration. Sputum is whitish, mucoid, odourless, and of moderate
amount. No relation to posture nor diurnal variation. No dyspnea, no hemoptysis, no wheezes, no
expectoration.
Pressure Symptoms: no dysphonia, no dysphagia, no dyspnea
Symptoms of systemic embolization: no weakness, no bleeding in urine, no left hypochondrium
pain
Symptoms with regard to the body systems:
*Respiratory : There is chronic purulent cough of 10 years duration. No dyspnea, no hemoptysis,
no recurrent chest infections, no expectoration, no wheezes.
* Gastrointestinal : No anorexia , no nausea , no vomiting , no regurgitation of food or sour liquid,
no heart burn , no difficulty in swallowing ,no hoarseness of voice or sore throat , no abdominal
pain , no abnormal bowel habits.
* Genito - Urinary System: no dysuria , no urgency , no polyuria , no polydipsia , no loin pain.
* Musculoskeletal : no arthralgia, no bodyache, malaise, no joint swelling with significant limitation
of movement.
*Hematological:
No history of bleeding , no bruising or echhymosis.

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Internal medicine department

Past history
- No previous similar attacks
- No history of HTN, chronic liver or kidney disease, nor DVT
- No previous operations or blood transfusion
- He was not admitted to the hospital before
- No drug allergy
- No history of recurrent tonsillitis, pharyngitis, fever, nor arthritis

Family history
- There is no similar condition, common or chronic diseases, nor history of cardiac sudden
-

death in his family.

Negative consanguinity.

Socio-economic history
Patient lives in an apartment with 3 rooms, good ventilation, clean water supply and well sewage
disposal. He recieves average income.

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Internal medicine department

Examination :
General exam
- The patient is fully conscious, alert, well oriented to time, place and person. He has an average

body built, calm facial expressions, and no special decubitus. Average mood and memory. The
patient is co-operative and of average intelligence.
Vital Signs:

Pulse: Regular, 84 beat/minute, average volume, no vessel wall abnormality detected,

equal on both sides, no special characte
Bl. Pressure: normal, 110/80 mmHg (Bilateral)
Resp. Rate: 19 breath/minute, regular, average depth, thoraco-abdominal, no use of
accessory muscles, no retractions.
Temperature: 37.5o c (axillary), normal
The patient looks well, no cyanosis, pallor or jaundice.

Head & Neck:

- Normal facial hair distribution with normal eyebrows

- Eyes show no jaundice of the sclera, normal eyelids and eyeballs, with pupils showing normal
dilation and constriction.
- Lips show no pallor nor cyanosis of underside of the tongue.
- Ear showed no abnormalities.
- No presence of swellings including parotid, thyroid, and cervical LNs enlargement.
- Carotid pulsations are normal and palpable bilaterally, no congested neck veins including IJV.
- JVP: 4 cm
Upper limb and lower limbs:
- Hands, feet, and nails show no abnormalities; including clubbing, palmar erythema, pallor,
discoloration, excessive sweating, muscle wasting, nor tremors.
- No UL/LL edema
- Axillary and inguinal LNs are not palpable.
- Peripheral pulsations are intact and show no significant abnormality
- Skin is healthy, showed normal elasticity, no pigmentation, no ulceration, no straie, no
sinuses, no fistulae.

Cardiac Examination:
- Hyperinflated chest.
- No dilated veins.
- No scars of cardiac surgery.
- No pericardial bulge.
- Regarding pulsations :
Apex: Regular apex, 84 beat/min, lies in left 6th space MCL, localized, with no thrill and no
special characters. Apart from weak epigastric pulsations originating from heart, there is no other
visible or palpable pulsations.
By palpation only :
- Pulsations the same as above.

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Internal medicine department

- No Palpable sound in other areas and no palpable thrill .

Percussion :
Hepatic dullness in the Rt. 5th space MCL with positive tidal percussion, no dullness in the Rt.
parasternal area, both aortic and pulmonary areas are resonant, dull bare area.
Auscultation
- Heart sounds: Normal S1 and S2
- Additional sounds: S3 gallop over the apex, no other additional sounds
- No murmurs
- No metallic click
Chest Examination:
Inspection__
Chest Wall: No scars, no dilated veins, no pigmentation.
Resp. Movement:
Rate: 19 breath/minute, regular, average depth, thoraco-abdominal, no use of
accessory muscles, no retractions.
Expansion: normal chest expansion .
Signs of action of accessory Muscles of respiration: No suction of supraclavicular fossa, no
inspiratory indrawing of lower intercostal spaces with no visible contraction of sternomastoid
or elevation of thoracic cage (No working accessory muscles of inspiration). The patient is
not pursing his lips or grasping a chair (Signs of action of accessory muscles of expiration).
Shape of the chest: hyperinflated, symmetrical, obtuse subcostal angle.
Mediastinum: central trachea ,the Apex is in Lt. 6th space MCL.
Pulsations: There is visible epigastric pulsations.
Palpation__

Normal chest expansion on both Sides

Central Trachea.
Obtuse subcostal angle .(120)
Apex is in the left 6th space MCL & epigastric pulsations (Probably cardiac in origin).
TVF: Normal tactile vocal fermitus
No chest wall tenderness.
Percussion__
Lung: Hyper resonance over anterior , lateral and back of patient with :
Resonant Kronig's isthmus.
Tympanitic resonance of Traubs area
Hepatic dullness at Rt. 5th Space MCL.
Dull bare area ( 4th , 5th )
Auscultation__
Normal vesicular breathing, equal on both sides, no adventious sounds, and normal vocal resonance.
Abdominal Examination:

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Internal medicine department

Inspection__
The abdomen is flat and symmetrical . There is wide subcostal angle confirmed by thumb test, mild
epigastric pulsation, and no visible peristalsis. No divarication of recti. There is normal skin elasticity
of the skin with no dilated veins, no scars, no scratch marks, no SC haemorrhage, no pigmentation,
no edema in anterior abdominal wall and no abdominal or inguinal hernias. Regarding the umbilicus,
it is midway between xiphisternum and symphysis pubis, inverted, no hernia and no discharge. The
skin overlying it shows no dilated veins, no nodules, no scars, pigmentation or ulcers. There is normal
female distribution of suprapubic hair with normal genitalia. Regarding the back no deformity, no
swelling, no scars.
Palpation__
By superficial palpation: no swellings, no rigidity, no superficial tenderness, no hyperesthesia.
By deep palpation :there is no palpable abdominal organs, negative Murphys sign, typmanatic
Traubs area, with no evidence of ascites.

Percussion__
Upper border of liver is in the 5th intercostal space in the right midclavicular line detected by heavy

percussion
Normal resonance all over the abdomen with no areas of hepatic or splenic dullness

No ascites detected by percussion .

Auscultation__
There is audible normal intestinal sounds, no vascular sounds (arterial bruit or venous hum)
DD of chest pain
Chest pain has many possible causes, all of which deserve medical attention.

Heart-related causes

Heart attack. A heart attack is a result of a blood clot that's blocking blood flow to your
heart muscle.

Angina. Thick plaques can gradually build up on the inner walls of the arteries that carry
blood to your heart. These plaques narrow the arteries and restrict the heart's blood supply,
particularly during exertion.

Aortic dissection. This life-threatening condition involves the main artery leading from your
heart your aorta. If the inner layers of this blood vessel separate, blood will be forced between
the layers and can cause the aorta to rupture.

Pericarditis. This condition, an inflammation of the sac surrounding your heart, usually
causes sharp pain that gets worse when you breathe in or when you lay down.

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Internal medicine department

Digestive causes

Heartburn. This painful, burning sensation behind your breastbone occurs when stomach
acid washes up from your stomach into the esophagus the tube that connects your throat to
your stomach.

Swallowing disorders. Disorders of the esophagus can make swallowing difficult and even
painful.

Gallbladder or pancreas problems. Gallstones or inflammation of your gallbladder or

pancreas can cause abdominal pain that radiates to your chest.

Muscle and bone causes

Some types of chest pain are associated with injuries and other problems affecting the structures that
make up the chest wall. Examples include:

Costochondritis. In this condition, the cartilage of your rib cage, particularly the cartilage
that joins your ribs to your breastbone, becomes inflamed and painful.

Sore muscles. Chronic pain syndromes, such as fibromyalgia, can produce persistent musclerelated chest pain.
Injured ribs. A bruised or broken rib can cause chest pain.

Lung-related causes
Many lung disorders can cause chest pain, including:

Pulmonary embolism. This cause of chest pain occurs when a blood clot becomes lodged in
a lung (pulmonary) artery, blocking blood flow to lung tissue.

Pleurisy. If the membrane that covers your lungs becomes inflamed, it can cause chest pain
that's made worse when you inhale or cough.

Collapsed lung. The chest pain associated with a collapsed lung typically begins suddenly
and can last for hours. A collapsed lung occurs when air leaks into the space between the lung
and the ribs.

Pulmonary hypertension. High blood pressure in the arteries carrying blood to the lungs
(pulmonary hypertension) also can produce chest pain.

Other causes
Chest pain can also be caused by:

Panic attack. If you have periods of intense fear accompanied by chest pain, rapid heartbeat,
rapid breathing, profuse sweating, shortness of breath, nausea, dizziness and a fear of dying, you
may be experiencing a panic attack.

Shingles. Caused by a reactivation of the chickenpox virus, shingles can produce pain and a
band of blisters from your back around to your chest wall.

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Internal medicine department

Provisional diagnosis
Ischemic anterior myocardial infarction, not complicated.

Clear final diagnosis :

Patient presented to the ED with severe typical chest pain of acute onset, stationary course, 5 hours
duration, described as chest tightness, and associated with cold profuse sweating and vomiting. Upon
cardiac examination, ECG and cardiac enzymes, he is proved to have anterior myocardial infarction.
By looking to Patient File:
On emergency admission: 40 years old male patient, smoker, diabetic on OHD from 7 years,
presented with typical chest pain from 5 hours duration, associated with swerting, maximum from
the start. On examination: the patient looks fair, lying flat, BP: 150/10 mmHg, HR: 110 Bp and
regular, chest is clear, heart: S3 Gallop.
ECG: Q,ST elevation in the anterior leads
Admission date to IMD: 4th of December 2016
Investigations:
Hb conc.: 14.1

ALT: 20 UI

Hct (PCV): 38.0

AST: 151 UI

Red cell count: 4.59

Bilirubin total: 1.28

MCV: 82.8

Bilirubin direct: 0.23

MCH: 30.7

Albumin: 3.90

MCHC: 37.1

Serum sodium: 131 mmol/l

RDW: 12.6
Platelet count: 182.000

Serum potassium: 4.30 mmol/l

TLC: 12.600

Serum calcium: 9.10 mg/dl

PTT: 53.4
Control time: 30.0
PT: 21.7
INR: 1.65
Treatment given:
Thrombolytic therapy
Ator

Creatin kinase 1887 UI

CK-MB: 229 UI
LDH: 2054 UI
Nitrates
Unasyn
Cefotaxime
Paracetamol
Spironolactone

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Internal medicine department

Clopidogrel
Captopril
Biopalol
Final outcome:
Mortality rate of AMI was 34% to 42%. The mortality rate of AMI remains high, and most deaths
occur outside of the hospital. Prehospital care may lower the mortality rate of AMI. Patient has
improved and went back home. Medication must be continued. Approximately half of all patients
with an MI are rehospitalized within 1 year of their index event.
Scientific background:
Myocardial infarction (MI) (ie, heart attack) is the irreversible death (necrosis) of heart muscle
secondary to prolonged lack of oxygen supply (ischemia). Myocardial infarction (MI) usually results
from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with
thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply
to a portion of the myocardium. Although the clinical presentation of a patient is a key component in
the overall evaluation of the patient with MI, many events are either "silent" or are not clinically
recognized. The appearance of cardiac biomarkers in the circulation generally indicates myocardial
necrosis and is a useful adjunct to diagnosis.
MI is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS
continuum representing ongoing myocardial ischemia or injury consists of unstable angina, nonSTsegment elevation MI (NSTEMI)collectively referred to as nonST-segment acute coronary
syndrome (NSTE ACS)and ST-segment elevation MI (STEMI). Patients with ischemic discomfort
may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST
elevations seen on the ECG reflect active and ongoing transmural myocardial injury. Without
immediate reperfusion therapy, most patients with STEMI develop Q waves, reflecting a dead zone
of myocardium that has undergone irreversible damage and death. MI may lead to impairment of
systolic or diastolic function and to increased predisposition to arrhythmias and other long-term
complications.

Pathophysiology:
Cellular effects of myocardial infarction (MI)
Myocardial injury and myocardial cell death
For the normal heart to continue to function and to steadily pump blood efficiently to meet the
demands of the body, it needs to have a constant supply of oxygen and nutrients provided mainly by
the coronary circulation. A condition called myocardial ischemia happens if blood supply to the
myocardium does not meet the demand. If this imbalance persists, it triggers a cascade of cellular,
inflammatory and biochemical events, leading eventually to the irreversible death of heart muscle
cells, resulting in MI.
Evolution of MI and ventricular remodeling
The spectrum of myocardial injury depends not only on the intensity of impaired myocardial
perfusion but also on the duration and the level of metabolic demand at the time of the event. Severe
loss of the ability of the heart muscle cell to contract can be observed as early as within 60 seconds.
Persistence of oxygen deprivation to the myocardium through the cessation of blood supply will lead

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to irreversible myocardial injury within 20 to 40 minutes and up to several hours, depending on

several factors including the existing metabolic state of the body and presence of coronary collateral
.blood flow

Reperfusion injury
In some occasions, restoration of blood flow to the damaged myocardium triggers further ischemic
cellular damage, this paradoxical effect is known as reperfusion injury. This process involves a
complex interaction between oxygen free radicals and intracellular calcium, leading to acceleration
of myocardial damage and death, microvascular dysfunction and fatal arrhythmias. The role of nitric
oxide (an endothelium-derived relaxing factor) as a cardioprotective agent against reperfusion injury,
has been demonstrated, as nitric oxide works to inactivate oxygen free radicals, therefore,
ameliorating the process of reperfusion injury. [12] Despite the improved understanding of the
.process of reperfusion injury, there are no specific therapies to prevent it

Plaque
The atheromatous plaque responsible for acute MI develops in a dynamic process in multiple stages.
Starting with arterial intimal thickening, which consists of vascular smooth muscles with very
minimal or no inflammatory cells, this process can be observed soon after birth. Subsequently, the
formation of fibrous cap atheroma occurs, which has a lipid-rich necrotic core that is surrounded by
fibrous tissue. Eventually, a thin-cap fibroatheroma develops, this is also known as a vulnerable
plaque which is composed mainly of a large necrotic core separated from the vascular lumen by a
thin fibrous cap that is infiltrated by inflammatory cells and is deficient of smooth muscle cells,
.making it vulnerable to rupture
The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of
plaque rupture, and less frequently plaque erosion

Etiology
Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases.
Approximately 90% of myocardial infarctions (MIs) result from an acute thrombus that obstructs an
atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for
coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation,
coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary
.thrombosis and occlusion
Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the
pathogenesis of vulnerable plaque formation. A large body of evidence indicates that in numerous
cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary
tree. Coronary atherosclerosis is especially prominent near branching points of vessels. Culprit

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lesions that are particularly prone to rupture are atheromas containing abundant macrophages, a large
.lipid-rich core surrounded by a thinned fibrous cap

:Nonmodifiable risk factors for atherosclerosis include the following

Age
Sex
Family history of premature coronary heart disease
Male-pattern baldness

: Modifiable risk factors for atherosclerosis include the following

Smoking or other tobacco use

Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders
Dyslipidemia
Diabetes mellitus
Hypertension
Obesity (abdominal obesity)
Psychosocial stress
Sedentary lifestyle and/or lack of exercise
Reduced consumption of fruits and vegetables
Poor oral hygiene
Type A personality
Presence of peripheral vascular disease

MI can also occur for causes other than atherosclerosis. Nonatherosclerotic causes of MI include the
:following

Coronary occlusion secondary to vasculitis

Ventricular hypertrophy (eg, left ventricular hypertrophy, hypertrophic cardiomyopathy)
Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
Coronary trauma
Primary coronary vasospasm (variant angina)
Drug use (eg, cocaine, amphetamines, ephedrine)
Arteritis
Coronary anomalies, including aneurysms of coronary arteries
Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
Factors that decrease oxygen delivery, such as hypoxemia of severe anemia
Aortic dissection, with retrograde involvement of the coronary arteries

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In addition, MI can result from hypoxia due to carbon monoxide poisoning or acute pulmonary
disorders. Although rare, pediatric coronary artery disease may be seen with Marfan
.syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis

Prognosis
Acute myocardial infarction (MI) is associated with a 30% mortality rate; about 50% of the deaths
occur prior to arrival at the hospital. An additional 5-10% of survivors die within the first year after
their myocardial infarction. Approximately half of all patients with an MI are rehospitalized within 1
.year of their index event
Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual left
.ventricular function, and whether the patient underwent revascularization

:Better prognosis is associated with the following factors

Successful early reperfusion (ST-elevation MI [STEMI] goals: patient arrival to fibrinolysis

infusion within 30 minutes OR patient arrival to percutaneous coronary intervention [PCI]
within 90 minutes)
Preserved left ventricular function
Short-term and long-term treatment with beta-blockers, aspirin, and angiotensin-converting
enzyme (ACE) inhibitors

:Poorer prognosis is associated with the following factors

Advanced age
Diabetes mellitus
Previous vascular disease (eg, cerebrovascular disease or peripheral vascular disease)
Elevated thrombolysis in MI and delayed or unsuccessful reperfusion
Poorly preserved left ventricular function (the strongest predictor of outcome)
Evidence of congestive heart failure (Killip classification II) or frank pulmonary edema
(Killip classification III)
Elevated B-type natriuretic peptide (BNP) levels
Elevated high sensitive C-reactive protein (hs-CRP), a nonspecific inflammatory marker
Involvement of electrocardiograph (ECG) lead aVR
Depression

It has been shown that five baseline parameters at presentation of patients with acute MI account for
over 90% of the prognostic predictors of 30-day mortality from acute MI. These parameters include
age, systolic blood pressure on presentation, Killip classification, heart rate, and anatomic location of
.the MI

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Internal medicine department

Diagnosis

A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation
.or depression, or coronary intervention is diagnostic of MI
WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed
:with MI if two (probable) or three (definite) of the following criteria are satisfied
1. Clinical history of ischemic-type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers

Electrocardiogram
For a person to qualify as having a STEMI, in addition to reported angina, the ECG must show
new ST elevation in two or more adjacent ECG leads. This must be greater than 2 mm (0.2 mV) for
males and greater than 1.5 mm (0.15 mV) in females if in leads V2 and V3 or greater than 1 mm
(0.1 mV) if it is in other ECG leads. Previously, a recent left bundle branch block was considered the
same as ST elevation, however, this is no longer the case. In early STEMIs there may just be peaked
.T waves with ST elevation developing later

Cardiac biomarkers
While there are a number of different biomarkers, troponins are considered to be the best and
reliance on older tests (such as CK-MB) or myoglobin is discouraged. This is not the case in the
setting of peri-procedural MI where use of troponin and CK-MB assays are considered
.useful. Copeptin may be useful to rule out MI rapidly when used along with troponin

Imaging
A chest radiograph and routine blood tests may indicate complications or precipitating causes and are
.often performed upon arrival to an emergency department
In stable patients whose symptoms have resolved by the time of evaluation, technetium (99mTc)
sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize
areas of reduced blood flow in conjunction with physiological or pharmacological stress. Thallium
may also be used to determine viability of tissue, distinguishing whether nonfunctional myocardium
is actually dead or merely in a state of hibernation or of being stunned. Medical societies and
professional guidelines recommend that the physician confirm a person is at high risk for myocardial
infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and
who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress

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radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when
.a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem

Differential diagnosis
The differential diagnosis for MI includes other catastrophic causes of chest pain, such as pulmonary
embolism, aortic dissection, esophageal rupture, tension pneumothorax, or pericardial
effusion causing cardiac tamponade. Other noncatastrophic differentials include gastroesophageal
.reflux and Tietze's syndrome

Prevention
Myocardial infarction and other related cardiovascular diseases can be prevented to a large extent by
.a number of lifestyle changes and medical treatments

Lifestyle
Recommendations include increasing the intake of wholegrain starch, reducing sugar intake
(particularly of refined sugar), consuming five portions of fruit and vegetables daily, consuming two
or more portions of fish per week, and consuming 45 portions of unsalted nuts, seeds, or legumes
per week. The dietary pattern with the greatest support is the Mediterranean diet. Vitamins and
.mineral supplements are of no proven benefit, and neither are plant stanols or sterols
There is some controversy surrounding the effect of dietary fat on the development of cardiovascular
disease. People are often advised to keep a diet where less than 30% of the energy intake derives
from fat, a diet that contains less than 7% of the energy intake in the form of saturated fat, and a diet
that contains less than 300 mg/day of cholesterol. Replacing saturated with mono- polyunsaturated
fat is also recommended, as the consumption of polyunsaturated fat instead of saturated fat may
decrease coronary heart disease. Olive oil, rapeseed oil and related products are to be used instead of
.saturated fat
Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to
engage in 150 minutes of moderate or 75 minutes of vigorous intensity aerobic exercise a week.
Keeping a healthy weight, drinking alcohol within the recommended limits, and quitting smoking are
.measures that also appear to reduce the risk of cardiovascular disease

Medication

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Internal medicine department

Aspirin has been studied extensively in people considered at increased risk of myocardial infarction.
Based on numerous studies in different groups (e.g. people with or without diabetes), there does not
appear to be a benefit strong enough to outweigh the risk of excessive bleeding. Nevertheless,
many clinical practice guidelines continue to recommend aspirin for primary prevention, and some
researchers feel that those with very high cardiovascular risk but low risk of bleeding should
.continue to receive aspirin
Cholesterol-lowering drugs from the statin class may be used in those at an elevated risk of
cardiovascular disease. Long term hormone replacement therapy when started around the time of
menopause may decrease heart disease. Following a heart attack, nitrates, when taken for two days,
.and ACE-inhibitors decrease the risk of death

Prognosis
The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage,
.and the treatment given
Using variables available in the emergency room, people with a higher risk of adverse outcome can
be identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in
.high-risk people it was 21.1%
Some risk factors for death include age, hemodynamic parameters (such as heart failure, cardiac
arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation,
diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers. Assessment
of left ventricular ejection fraction may increase the predictive power. Prognosis is worse if a
mechanical complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity
.and mortality from myocardial infarction has improved over the years due to better treatment
Throughout hospital departments, practitioners use TIMI scores to assess mortality risk. There are
TIMI (Thrombolysis in Myocardial Infarction) scores for unstable angina or NSTEMI and STEMI,
both using routine patient data from history taking, medication use and lab results. Both scores have
.been found effective and reliable in multiple settings, including the emergency room

Complications
Complications may occur immediately following the heart attack (in the acute phase) or may need
time to develop (a chronic problem). Acute complications may include heart failure if the damaged
heart is no longer able to pump blood adequately around the body; aneurysm of the left ventricle
myocardium; ventricular septal rupture or free wall rupture; mitral regurgitation, in particular if the
infarction causes dysfunction of the papillary muscle; Dressler's syndrome; and abnormal heart
.rhythms, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and heart block

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Internal medicine department

Plan of management
Pre-hospital management

Arrange an emergency ambulance if an AMI is suspected. Take an ECG as soon as possible

but do not delay transfer to hospital, as an ECG is only of value in pre-hospital management if
pre-hospital thrombolysis is being considered.
Advise any patient known to have coronary heart disease to call for an emergency ambulance

if the chest pain is unresponsive to glyceryl trinitrate (GTN) and has been present for longer
than 15 minutes or on the basis of general clinical state - eg, severe dyspnoea or pain.

Cardiopulmonary resuscitation and defibrillation in the event of a cardiac arrest.

Oxygen: do not routinely administer oxygen but monitor oxygen saturation using pulse
oximetry as soon as possible, ideally before hospital admission. Only offer supplemental
oxygen to:
People with oxygen saturation less than 94% who are not at risk of hypercapnic

respiratory failure, aiming for saturation of 94-98%.

People with chronic obstructive pulmonary disease who are at risk of hypercapnic

respiratory failure, to achieve a target saturation of 88-92% until blood gas analysis is
available.

Pain relief with GTN sublingual/spray and/or an intravenous opioid 2.5-5 mg diamorphine or
5-10 mg morphine intravenously with an anti-emetic. Avoid intramuscular injections, as
absorption is unreliable and the injection site may bleed if the patient later receives thrombolytic
therapy.

Aspirin 300 mg orally (dispersible or chewed).

Take blood tests for FBC, renal function and electrolytes, glucose, lipids, clotting screen, Creactive protein (CRP) and cardiac enzymes (troponin I or T).

Pre-hospital thrombolysis is indicated if the time from the initial call to arrival at hospital is
likely to be over 30 minutes. When primary percutaneous coronary intervention cannot be
provided within 120 minutes of ECG diagnosis, patients with an ST-segment-elevation acute
coronary syndrome (ACS) should receive immediate (pre-hospital or admission) thrombolytic
therapy.

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Internal medicine department

Management initiated in hospital

If not already done, take blood tests for cardiac enzymes (troponin I or T), FBC, renal
function and electrolytes, glucose, lipids, CRP, and clotting screen.

Continue close clinical monitoring (including symptoms, pulse, blood pressure, heart rhythm
and oxygen saturation by pulse oximetry), oxygen therapy and pain relief.

ECG monitoring: features that increase the likelihood of infarction are: new ST-segment
elevation; new Q waves; any ST-segment elevation; new conduction defect. Other features of
ischaemia are ST-segment depression and T-wave inversion.

Reperfusion
Patency of the occluded artery can be restored by percutaneous coronary intervention (PCI) or by
giving a thrombolytic drug. PCI is the preferred method. Compared with fibrinolysis, PCI results in
.less re-occlusion, improved left ventricular function and improved overall outcome

Primary PCI

PCI (or percutaneous transluminal coronary angioplasty - PTCA) is regarded as superior to

fibrinolysis in the management of AMI and is becoming increasingly available for initial patient
care.

Any delay in primary PCI after a patient arrives at hospital is associated with higher mortality
in hospital. Time to treatment should therefore be as short as possible. Door (or diagnosis) to
treatment time should be less than 90 minutes, or less than 60 minutes if the hospital is PCI
ready and symptoms started within 120 minutes.

Fibrinolytic drugs
For patients who cannot be offered PCI within 90 minutes of diagnosis, a thrombolytic drug should
be administered along with either unfractionated heparin (for maximum two days), a low molecular
weight heparin. Thrombolytic drugs break down the thrombus so that the blood flow to the heart
muscle can be restored to prevent further damage and assist healing. Reperfusion by thrombolysis is
often gradual and incomplete and may be inadequate. There is a risk of early or late reocclusion and
a 1-2% risk of intracranial haemorrhage.

Fibrinolytic drugs act as thrombolytics by activating plasminogen to form plasmin, which

degrades fibrin and so breaks up the thrombi.

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Internal medicine department

Streptokinase and alteplase have been shown to reduce mortality. Reteplase and tenecteplase

are also licensed for AMI.

Streptokinase and alteplase are given by intravenous infusion. Reteplase and tenecteplase can

be given by rapid bolus injection.

The benefit is greatest in those with ECG changes that include ST-segment elevation

(especially in those with anterior infarction) and in patients with bundle branch block.
The earlier the treatment is given, the greater the absolute benefit. Alteplase, reteplase and

streptokinase need to be given within 12 hours of symptom onset, ideally within one hour.
Tenecteplase should be given as early as possible and usually within six hours of symptom
onset.
Bleeding complications are the main risks associated with thrombolysis. Contra-indications

for thrombolysis include patients with bleeding disorders, or a history of recent haemorrhage,
trauma, surgery or acute cerebrovascular event.
Persistence of antibodies to streptokinase can reduce the effectiveness of subsequent

treatment and so streptokinase should not be used again after the first administration.

Antithrombotic therapy without reperfusion therapy

In patients presenting within 12 hours after the onset of symptoms but reperfusion therapy is

not given, or in patients presenting after 12 hours, aspirin, clopidogrel and an antithrombin
agent (heparin, enoxaparin or fondaparinux) should be given as soon as possible.
For patients who do not receive reperfusion therapy, angiography before hospital discharge is

recommended (as for patients after successful fibrinolysis) if no contra-indications are present.

Coronary bypass surgery

Only a few patients need a coronary artery bypass graft (CABG) in the acute phase but

CABG may be indicated:

After failed PCI, coronary occlusion not amenable for PCI, or the presence of
refractory symptoms after PCI.

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Internal medicine department

Cardiogenic shock, or mechanical complications - eg, ventricular rupture, acute mitral

regurgitation, or ventricular septal defect.

Multivessel disease.
In patients with a non-emergency indication for CABG (eg, multisystem disease), it is

recommended to treat the infarct-related lesion by PCI and to perform CABG later in more
stable conditions if possible.

Other initial management

Antiplatelet agent:

Long-term low-dose aspirin reduces overall mortality, non-fatal re-infarction, nonfatal stroke and vascular death.

Clopidogrel, in combination with low-dose aspirin, is recommended for AMI with STsegment elevation; the combination is licensed for at least four weeks but the optimum
treatment duration has not been established. Treatment with clopidogrel and aspirin for up
to one year following PCI has also been shown to be cost-effective

Clopidogrel monotherapy is an alternative when aspirin is contra-indicated.

Ticagrelor in combination with low-dose aspirin is recommended by NICE for up to

12 months as a treatment option in adults with STEMI that cardiologists intend to treat
with primary PCI.

Warfarin (INR 2-3) or dabigatran can be considered for patients unable to take aspirin
or clopidogrel.
Beta-blockers:

When started within hours of infarction, beta-blockers reduce mortality, non-fatal

cardiac arrest and non-fatal re-infarction.

Unless contra-indicated, the usual regime is to give intravenously on admission and

then continue orally - titrate upwards to the maximum tolerated dose.

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Internal medicine department

The calcium-channel blockers diltiazem or verapamil can be used if a beta-blocker

cannot be used but diltiazem and verapamil are contra-indicated in patients with left
ventricular dysfunction.

Angiotensin-converting enzyme (ACE) inhibitors:

These reduce mortality whether or not patients have clinical heart failure or left
ventricular dysfunction. They also reduce the risk of non-fatal heart failure.

Titrate the dose upwards to the maximum tolerated or target dose. Measure renal
function, electrolytes and blood pressure before starting an ACE inhibitor (or angiotensinII receptor antagonist) and again within 1-2 weeks.
Cholesterol-lowering agents:

Ideally, initiate therapy with a statin as soon as possible for all patients with evidence
of cardiovascular disease (CVD) unless contra-indicated.

Other treatment:

Heparin infusion is used as an adjunctive agent in patients receiving alteplase but not
with streptokinase. Heparin is also indicated in patients undergoing primary angioplasty.

Prophylaxis against thromboembolism: if not already receiving heparin by infusion,

then patients should be given regular subcutaneous heparin until fully mobile.

Insulin-glucose infusion followed by intensive glucose control with subcutaneous

insulin for all people with type 1 and type 2 diabetes.

The routine use of nitrates, calcium antagonists, magnesium, and high-dose glucoseinsulin-potassium infusion is not currently recommended during the acute phase of
treatment of AMI.