Myocardial infarction

Introduction

Myocardial infarction, commonly known as a heart attack, is a leading cause of morbidity and mortality worldwide. It occurs when blood flow to a portion of the heart muscle is abruptly blocked, leading to tissue necrosis. Prompt recognition and management are critical to improving survival and reducing complications.

Definition and Classification

Definition

Myocardial infarction is defined as irreversible myocardial cell death resulting from prolonged ischemia. The diagnosis is typically confirmed by a combination of clinical symptoms, electrocardiographic changes, and elevated cardiac biomarkers.

Classification

• ST-elevation myocardial infarction (STEMI): Characterized by persistent ST-segment elevation on ECG and usually caused by complete coronary artery occlusion.
• Non-ST-elevation myocardial infarction (NSTEMI): ECG may show ST-segment depression or T-wave inversion; typically caused by partial coronary artery blockage.
• Type 1 to Type 5 MI: Based on the Fourth Universal Definition, including spontaneous MI, MI related to ischemia due to increased demand or decreased supply, peri-procedural MI, and MI related to stent thrombosis or bypass surgery.

Epidemiology

Prevalence and Incidence

Myocardial infarction is a major public health problem, with millions of cases occurring worldwide each year. Incidence varies depending on region, socioeconomic status, and access to healthcare. Improved awareness and preventive measures have led to a gradual decline in mortality in developed countries, though the absolute burden remains high.

Demographic Patterns

• Age and Gender Distribution: MI is more common in older adults, with men typically affected earlier than women. Risk increases significantly after age 45 in men and 55 in women.
• Ethnic and Geographic Variations: Higher prevalence is observed in populations with elevated rates of cardiovascular risk factors such as hypertension, diabetes, and smoking. Geographic differences reflect lifestyle, dietary habits, and healthcare access.

Etiology and Risk Factors

Atherosclerosis

Atherosclerotic plaque formation in coronary arteries is the most common cause of myocardial infarction. Plaque rupture or erosion triggers thrombosis, leading to obstruction of blood flow and myocardial ischemia.

Coronary Artery Thrombosis

Acute formation of a thrombus at the site of plaque rupture or erosion can completely block coronary blood flow, resulting in infarction. Platelet aggregation and coagulation cascade activation play key roles in thrombus formation.

Other Causes

• Coronary artery spasm: Transient constriction of coronary vessels can cause ischemia without significant atherosclerosis.
• Embolism: Coronary emboli from cardiac or systemic sources can occlude coronary arteries.
• Vasculitis or trauma: Inflammation or injury to coronary vessels may precipitate MI.

Modifiable and Non-modifiable Risk Factors

• Modifiable: Hypertension, diabetes mellitus, dyslipidemia, smoking, obesity, sedentary lifestyle.
• Non-modifiable: Advanced age, male gender, family history of premature coronary artery disease.

Pathophysiology

Ischemic Cascade

Myocardial infarction occurs when oxygen supply to the heart muscle is insufficient to meet metabolic demands. The ischemic cascade begins with impaired myocardial perfusion, leading to metabolic disturbances, loss of contractility, and eventual cell death if perfusion is not restored.

Myocyte Injury and Necrosis

Prolonged ischemia results in irreversible injury to cardiac myocytes. Cellular membranes break down, intracellular enzymes are released into the bloodstream, and necrosis progresses from the subendocardium to the full thickness of the myocardium depending on the duration and severity of the occlusion.

Inflammatory Response

Necrotic myocardial tissue triggers an inflammatory response. Neutrophils and macrophages infiltrate the infarcted area, clearing debris and releasing cytokines that influence tissue repair and scar formation.

Remodeling and Scar Formation

Over weeks to months, the infarcted myocardium is replaced by fibrous scar tissue. Ventricular remodeling may alter chamber size and shape, potentially leading to systolic dysfunction, heart failure, or aneurysm formation.

Clinical Features

Symptoms

• Chest Pain: Typically described as pressure, heaviness, or squeezing in the retrosternal area, often lasting more than 20 minutes.
• Radiation: Pain may radiate to the left arm, neck, jaw, or back.
• Associated Symptoms: Dyspnea, diaphoresis, nausea, vomiting, palpitations, or syncope.

Signs

• Vital Signs Changes: Tachycardia, hypotension, or hypertension may be observed.
• Physical Examination Findings: S3 heart sound, new systolic murmur (suggestive of papillary muscle dysfunction), signs of heart failure, or pulmonary congestion.

Diagnosis

Electrocardiography (ECG)

ECG is the primary diagnostic tool for myocardial infarction. ST-segment elevation indicates STEMI, while ST-segment depression, T-wave inversion, or nonspecific changes may suggest NSTEMI. Serial ECGs are important to monitor dynamic changes in ischemia.

Cardiac Biomarkers

• Troponins: Highly sensitive and specific markers of myocardial injury; levels rise within hours of infarction and remain elevated for days.
• Creatine Kinase-MB (CK-MB): Less specific than troponins, useful for detecting reinfarction.

Imaging Studies

• Echocardiography: Evaluates wall motion abnormalities, left ventricular function, and complications such as aneurysm or thrombus.
• Coronary Angiography: Identifies occluded or stenotic coronary arteries and guides revascularization therapy.
• Cardiac MRI: Assesses infarct size, myocardial viability, and tissue characterization.

Differential Diagnosis

• Angina pectoris
• Pulmonary embolism
• Aortic dissection
• Pericarditis and myocarditis

Complications

Early Complications

• Arrhythmias, including ventricular tachycardia and fibrillation
• Cardiogenic shock due to extensive myocardial damage
• Acute heart failure
• Mechanical complications such as ventricular septal rupture, papillary muscle rupture, and cardiac tamponade

Late Complications

• Chronic heart failure resulting from reduced ejection fraction
• Ventricular aneurysm formation
• Dressler syndrome, a post-MI autoimmune pericarditis

Treatment and Management

Acute Management

• MONA Protocol: Administration of morphine for pain relief, oxygen if hypoxic, nitrates to reduce myocardial oxygen demand, and aspirin to inhibit platelet aggregation.
• Reperfusion Therapy: Immediate restoration of coronary blood flow through thrombolytic therapy or percutaneous coronary intervention (PCI) to minimize myocardial damage.

Secondary Prevention

• Antiplatelet Therapy: Aspirin and P2Y12 inhibitors to prevent recurrent thrombotic events.
• Beta-blockers: Reduce myocardial oxygen demand and prevent arrhythmias.
• ACE Inhibitors or ARBs: Improve ventricular remodeling and reduce risk of heart failure.
• Statins: Lower LDL cholesterol and stabilize atherosclerotic plaques.
• Lifestyle modifications including smoking cessation, weight management, and regular physical activity.

Rehabilitation

• Participation in structured cardiac rehabilitation programs to improve functional capacity and cardiovascular health.
• Psychosocial support and counseling to address anxiety, depression, or post-MI stress.

Prognosis

Factors Influencing Outcome

• Extent and location of myocardial damage
• Time to reperfusion and quality of acute care
• Presence of comorbidities such as diabetes, renal disease, or prior cardiovascular events

Long-term Survival and Quality of Life

Survival rates have improved due to early diagnosis, reperfusion strategies, and secondary prevention. Long-term prognosis depends on left ventricular function, adherence to medical therapy, and ongoing lifestyle modifications. Patients may experience reduced exercise tolerance or psychological impact, which can be mitigated through cardiac rehabilitation and follow-up care.

Prevention

Primary Prevention

• Modification of risk factors including blood pressure control, blood sugar management, and lipid lowering.
• Adoption of a healthy diet rich in fruits, vegetables, and whole grains, and low in saturated fats.
• Regular physical activity to improve cardiovascular fitness and reduce obesity.
• Smoking cessation and limitation of alcohol consumption.

Secondary Prevention

• Adherence to prescribed medications such as antiplatelets, beta-blockers, ACE inhibitors, and statins.
• Regular follow-up with healthcare providers to monitor cardiac function and prevent recurrence.
• Participation in cardiac rehabilitation programs to enhance functional recovery and lifestyle modification.

References

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