Primary Diseases Causing STEMI
The overwhelming majority of STEMI cases result from atherosclerotic coronary artery disease with acute plaque disruption (rupture, erosion, or ulceration) and superimposed thrombotic occlusion of an epicardial coronary artery. 1, 2
Primary Pathophysiological Mechanism
Atherosclerotic plaque disruption with superimposed platelet-rich thrombus formation is the main pathophysiological mechanism causing Type 1 (spontaneous) myocardial infarction. 1 This "plaque + superimposed thrombus complex" creates acute and complete coronary artery occlusion, resulting in STEMI with persistent ST-elevation on ECG. 1
The acute occlusion creates an imbalance between myocardial oxygen demand and supply which, when prolonged and unabated, leads to myocardial cell necrosis and infarction. 1
Underlying Disease States Contributing to STEMI
Coronary Atherosclerosis with Risk Factor Burden
Hypertension, diabetes mellitus, and hyperlipidemia are the classic modifiable risk factors that drive the development of coronary atherosclerosis, creating the substrate for plaque formation that ultimately ruptures to cause STEMI. 3
Diabetes mellitus functions as a particularly aggressive risk factor, independently associated with distal embolization, impaired myocardial perfusion, and significantly higher mortality (12.6% vs 3.9%) in STEMI patients even with optimal treatment. 4 Diabetic patients have more multivessel disease and advanced Killip class at presentation. 4
Hypertension has a clear causal relationship with myocardial infarction through multiple pathophysiological mechanisms, including left ventricular hypertrophy that decreases coronary reserve, increased myocardial oxygen demand, and vascular remodeling that compromises coronary perfusion. 5
Chronic Kidney Disease as Coronary Risk Equivalent
CKD functions as a coronary risk equivalent, independently driving cardiovascular disease development with a dose-dependent relationship, where severe CKD leads to 10 to 30 times higher cardiovascular death rates compared to the general population. 6
CKD patients face additional pathophysiological burdens including intense pro-inflammatory states driving accelerated atherosclerosis, hyperhomocysteinemia creating pro-thrombotic conditions, mineral bone disorders contributing to vascular calcification, and uremia causing direct myocardial and vascular toxicity. 6
Less Common Mechanisms of STEMI
Dynamic Coronary Obstruction
Coronary spasm or vasoconstriction of epicardial and/or microvascular vessels can cause STEMI, representing dynamic obstruction rather than fixed atherosclerotic disease. 1
Cocaine and methamphetamine use cause STEMI through coronary vasospasm and thrombosis, in addition to direct effects on heart rate, arterial pressure, and myocardial toxicity. 1 This should be considered especially in younger patients (age <40 years) with few traditional risk factors. 1
Progressive Mechanical Obstruction
Progressive mechanical obstruction to coronary flow from advancing atherosclerotic disease can lead to STEMI. 1
Coronary arterial inflammation represents another mechanism causing reduced myocardial perfusion. 1
Thromboembolism
Distal microvascular thromboembolism from plaque-associated thrombus or thromboembolism from plaque erosion can cause STEMI. 1
Microembolization of platelet aggregates and components of disrupted plaque are responsible for myocardial marker release in many patients. 1
Critical Clinical Context
In patients presenting with possible acute coronary syndrome, traditional risk factors (hypertension, hypercholesterolemia, smoking) are only weakly predictive of acute ischemia likelihood and are far less important than symptoms, ECG findings, and cardiac biomarkers for determining admission or treatment. 1, 7
However, once ACS is established, these risk factors become major adverse prognostic indicators associated with poor outcomes and should guide aggressive management. 1, 5
Patients without standard modifiable risk factors (SMuRF-less patients) paradoxically have higher mortality rates in the post-STEMI period, with creatinine/albumin ratio serving as a predictor of mortality in these patients. 8