What is the cause of ST elevation in a myocardial infarction (MI) in an adult patient with risk factors for cardiovascular disease, such as hypertension, diabetes, or hypercholesterolemia?

Pathophysiology of ST Elevation in Myocardial Infarction

ST elevation on ECG occurs due to transmural myocardial ischemia caused by acute and complete occlusion of an epicardial coronary artery, resulting in an electrical injury current between the ischemic subepicardium and the normal myocardium. 1

Mechanism of Coronary Occlusion

The underlying pathophysiology follows a specific sequence:

• Physical disruption of an atherosclerotic plaque with subsequent formation of an occluding thrombus is the primary cause of STEMI in the majority of cases. 1
• Coronary artery plaque rupture, erosion, or ulceration exposes thrombogenic material, triggering platelet adhesion and aggregation followed by fibrin stabilization of the thrombus. 1
• Concomitant coronary vasoconstriction and microembolization contribute to the complete occlusion. 1
• Less commonly, thrombus forms from superficial erosion of the endothelial surface without frank plaque rupture. 1

Electrical Manifestation of Transmural Ischemia

Acute and complete coronary artery occlusion creates an acute imbalance between myocardial oxygen demand and supply, and when prolonged beyond 15-30 minutes without forward or collateral flow, myocardial necrosis begins. 1

• Myocardial necrosis progresses from subendocardium to subepicardium in a time-dependent fashion known as the "wave-front phenomenon." 1
• The ST elevation reflects transmural ischemia extending through the full thickness of the myocardial wall, creating an electrical injury current that manifests as persistent ST-segment elevation on the ECG. 1
• This distinguishes STEMI from NSTEMI, where severely obstructive but incompletely occlusive coronary lesions produce ST depression or T-wave inversion rather than ST elevation. 1

Plaque Characteristics and Vulnerability

Important nuances about the atherosclerotic substrate:

• Three-quarters of all infarct-related thrombi evolve over plaques causing only mild to moderate stenosis, not necessarily severe stenoses. 1
• Plaques with substantial outward remodeling ("compensatory enlargement") can have thin fibrous caps and large lipid pools without luminal encroachment, making them vulnerable despite appearing normal angiographically. 1
• Inflammation plays a critical role in plaque instability, with elevated C-reactive protein and interleukin-6 correlating with clinical outcomes. 1

Dynamic Nature of Thrombosis

A critical pitfall to recognize:

• The thrombotic response to plaque disruption is dynamic, with simultaneous thrombosis and clot lysis often associated with vasospasm, causing intermittent flow obstruction. 1
• There is frequently a delay of up to 2 weeks between plaque rupture and clinical consequences. 1
• In 25-30% of patients undergoing primary percutaneous intervention, initial angiography shows a patent infarct-related artery, indicating spontaneous or intermittent recanalization. 1

Triggering Factors

• The circadian variation of STEMI with higher incidence in early morning hours results from β-adrenergic stimulation (increased vascular tone and blood pressure), hypercoagulability, and platelet hyper-reactivity. 1
• Physical or emotional stress associated with increased sympathetic stimulation and vasoconstriction may trigger plaque disruption and coronary thrombosis. 1