Myocardial infarction, or heart attack, occurs when blood flow to the heart is blocked, depriving heart muscle cells of oxygen and nutrients and causing cell death. It is typically caused by atherosclerosis leading to coronary artery blockage by a blood clot. Diagnosis involves cardiac enzyme tests, electrocardiograms, and imaging. Treatment focuses on restoring blood flow through medications or procedures like angioplasty and aims to prevent further damage through medications, lifestyle changes, and managing complications.

1. MYOCARDIAL INFARCTION

2. Definition
Myocardial infarction (MI), commonly known as a heart attack, is defined pathologically as the
irreversible death of myocardial cells caused by ischemia. Clinically, MI is a syndrome that can be
recognized by a set of symptoms, chest pain being the hallmark of these symptoms in most cases,
supported by biochemical laboratory changes, electrocardiographic (ECG) changes, or findings
on imaging modalities able to detect myocardial injury and necrosis.

3. Acute Coronary syndrome (ACS)
The term "acute coronary syndrome" (ACS) refers to a spectrum of conditions that occur due to
acute myocardial ischemia and/or infarction as a result of an abrupt reduction in blood flow
through the coronary artery circulation.
 non–ST elevation (NSTE) ACS
NSTE ACS is further divided into unstable angina (UA) and non–ST-elevation myocardial infraction
(NSTEMI). These two conditions resemble each other very closely. UA is distinguished from NSTEMI by the
absence of an elevation of cardiac biomarker levels.
 ST-elevation MI (STEMI)
The major discriminating feature of STEMI is the presence of symptoms of myocardial
ischemia/injury along with persistent ECG ST-segment elevation in addition to the presence of cardiac
biomarkers.

4. Pathophysiology
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
events, leading eventually to thecascade of cellular, inflammatory and biochemical
irreversible death of heart muscle cells, resulting in MI.
Evolution of MI and ventricular remodeling
Reperfusion injury

6. 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.

7. MI can also occur for causes other than atherosclerosis. Nonatherosclerotic causes of MI include thefollowing:
 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
 Respiratory infections, particularly influenza
In addition, MI can result from hypoxia due to carbon monoxide poisoning or acute pulmonarydisorders.

8. Clinical presentation
Patients with typical acute MI usually present with chest pain and may have prodromal symptoms of
fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical ST-
elevation MI (STEMI) may occur suddenly without warning.
The typical chest pain of acute MI usually is intense and unremitting for 30-60 minutes. It is
retrosternal and often radiates up to the neck, shoulder, and jaws, and down to the left arm. The
chest pain is usually described as a substernal pressure sensation that is also perceived as squeezing,
aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of
indigestion or of fullness and gas.

9. In some cases, patients do not recognize the chest pain, have an unusually high pain threshold, or have a
disorder that impairs pain perception and results in a defective anginal warningsystem
Other symptoms of myocardial infarction include thefollowing:
 Anxiety, commonly described as a sense of impending doom
 Pain or discomfort in areas of the body, including the arms, left shoulder, back, neck, jaw, or stomach
 Lightheadedness, with or without syncope
 Cough
 Nausea, with or without vomiting
 Profuse sweating
 Shortness of breath
 Wheezing
 Rapid or irregular heart rate
 Fullness, indigestion, or choking feeling

10. Diagnosis
The objectives of laboratory testing and imaging include the following:
 To determine the presence or absence of myocardial infarction (MI) for diagnosis and differential diagnosis
(point–of-care testing and testing in central laboratory of cardiac troponin levels)
 To characterize the locus, nature (ST-elevation MI [STEMI] or non–ST-elevation MI [NSTEMI]), and extent of
MI (ie, to estimate infarct size)
 To detect recurrent ischemia or MI (extension of MI)
 To detect early and late complications of MI
 To estimate the patient's prognosis

11. The electrocardiogram (ECG) is the most important tool in the initial evaluation and
triage of patients in whom an acute coronary syndrome (ACS) is suspected.
Laboratory tests used in the diagnosis of myocardial infarction (MI) include the
following:
 Cardiac biomarkers/enzymes: cardiac troponin is recommended as the only cardiac
biomarker that should be measured at presentation in patients with suspected MI, due to
its superior sensitivity and accuracy. Troponin is a contractile protein that is not normally
found in serum; it is released only when myocardial necrosis occurs.
 Complete blood cell (CBC) count
 Comprehensive metabolic panel
 Lipid profile

12. Management
The first goal for healthcare professionals in management of acute myocardial infarction (MI) is to
diagnose the condition in a very rapid manner.
As a general rule, initial therapy for acute MI is directed toward restoration of perfusion as soon as
possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished
through medical or mechanical means, such as percutaneous coronary intervention (PCI), or coronary
artery bypass graft (CABG) surgery.
The initial management of the overall management plan for patients with acute MI has the following
aims:
 Restoration of the balance between oxygen supply and demand to prevent further ischemia
 Pain relief
 Prevention and treatment of complications

13. Oxyge
n Aspirin (162 to 325 mg)
Reduction of cardiac pain
 Nitrates are usually given as a 0.4 mg dose in a sublingual tablet
 Refractory or severe pain should be treated symptomatically with IV morphine.

14. ST-elevation myocardial infarction
Reperfusion
 Primary percutaneous intervention (PCI)
 Fibrinolysis (streptokinase, alteplase)
 Coronary artery bypass grafting (CABG)
Anticoagulation
 For primary PCI, unfractionated heparin (UFH), bivalirudin, and low molecular weight heparin (LMWH) (eg,
enoxaparin) are the available options. Fondaparinux is not used in this setting because of the increased risk of
catheter thrombosis.
 In patients receiving fibrinolytic therapy, anticoagulation should be given until revascularization is performed;
if reperfusion is not feasible anticoagulants should be given for at least 48 hours or for the duration of hospital
stay up to 8 days. UFH or LMWH may be used, with LMWH (enoxaparin) being preferred.

15. Antiplatelet agents
 All patients with STEMI should receive an empiric loading dose of aspirin (150.5 to 325 mg) as early as
possible and prior to reperfusion, regardless of the reperfusion method. A lifelong maintenance dose of (75 to
81 mg) daily should be prescribed to all patients after STEMI.
 Other antiplatelet agents used for dual antiplatelet therapy are the P2Y12 receptor inhibitors (eg, clopidogrel,
ticagrelor, prasugrel); a loading dose of these agents is given before or at the time of reperfusion and an
extended duration maintenance dose is administered thereafter, depending on the method of reperfusion.

16. Non-ST-elevation (NSTE) ACS
There are two alternative management strategies, either an early invasive strategy with angiography,
with intent for revascularization with percutaneous coronary intervention (PCI) or coronary artery
bypass grafting (CABG), or a conservative strategy with initial medical therapy and noninvasive
cardiovascular imaging. Regardless of the strategy, both entail aggressive utility of medications such as
anticoagulants, antiplatelet agents, beta blockers, statins, and possible use of angiotensin-converting
enzyme (ACE) inhibitors for appropriate patient populations.

17. Beta blockers (metoprolol, carvedilol, or bisoprolol)
Non-dihydropyridine calcium channel blockers (eg, verapamil or diltiazem)
Antiplatelet agents (aspirin, clopidogrel, ticagrelor, prasugrel)
Anticoagulants (unfractionated heparin, low molecular weight heparin, bivalirudin,
fondaparinux)

18. Additional aspects of management
Cardioprotective medications (ACEIs, ARBs, beta blockers, statins)
Lifestyle modifications (dietary changes, aerobic exercise)
Special considerations for elderly (high risk of bleeding)

19. Complications
Arrhythmic complications
Mechanical complications
 Ventricular free wall rupture
 Ventricular septal defect
 Papillary muscle rupture with severe mitral regurgitation
Left ventricular aneurysm formation
Ventricular septal defect
Associated right ventricular infarction
Ventricular pseudoaneurysm

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