Acute Myocardial Infarction -Pathophysiology and Precipitating Factors

Coronary Artery Disease (CAD) is a complete succession of events that starts with endothelial dysfunction, lipid accumation and migration of inflammatory cells into the arterial wall. Over the course of many decades they lead to the development of atherosclerosis and plaque formation. Plaque stability is an important determinant of the clinical outcome.

Clinically the presentation of CAD ranges from asymptomatic patients with stable CAD (SCAD) to patients with chest pain at rest experiencing acute coronary syndromes.

Acute coronary syndromes (ACS) comprised of

1. Unstable angina
2. Non – ST – elevation myocardial infraction (NSTEMI)
3. ST elevation myocardial infarction (STEMI).

Acute Myocardial Infarction:

Myocardial infarction occurs during the period when coronary circulation is obstructed and compromised, resulting in the necrosis of the heart tissue. Irreversible cardiac injury occurs if occlusion is complete for at least 15 to 20 minutes.

Pathophysiology:

The major causes of AMI are atherosclerotic myocardial ischemia and subsequent infarction usually begin in the endocardium and spread toward the epicardium.

When the necrosis occurs through the full thickness of the myocardium, the infarct is termed transmural.

Precipitating factors:

AMI occurs more frequently during:

• Physical exertions
• After surgical procedures
• Early in the morning
• In the winter months
• During emotional stress.

During the early morning, adrenergic activity, plasma fibrinogen levels, and platelet adhesiveness all increase naturally.