Molecular structure pattern

Myocardial Infarction w/ ST-Segment Elevation Disease Background

Last updated: 08 September 2026
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Introduction

Myocardial infarction (MI) is death of cardiac myocytes (irreversible necrosis) caused by prolonged or severe myocardial ischemia from insufficient or absent coronary blood flow and reperfusion injury. It is important to distinguish myocardial injury from MI. Myocardial injury may result from ischemic or non-ischemic causes, whereas MI is myocardial injury caused by prolonged ischemia and resulting in myocardial cell death. The term “acute” usually refers to the time 6 hours to 7 days following the pathologic appearance of the infarct. A recurrent MI is an MI occurring 28 days after an incident MI, while a reinfarction is an acute MI occurring within 28 days of an incident or recurrent MI. 

Acute coronary syndrome (ACS) is any constellation of symptoms compatible with acute myocardial ischemia, usually caused by sudden reduction in coronary blood flow from atherosclerotic plaque rupture or erosion and subsequent thrombosis.

Epidemiology

Cardiovascular disease (CVD) remains the number one cause of mortality in Western countries, with acute coronary disease being the leading cause.  MI with ST-segment elevation constitutes approximately 25% of ACS. 

The incidence rate of MI among Asians was lower than other races. The reason for this may be due to lower prevalence of major risk factors (eg hypertension, smoking, obesity) among Asian people. In Asian countries such as Japan and Korea, the incidence rate is higher in men than in women. 

Pathophysiology

The initial mechanism in acute MI is the rupture of vulnerable, lipid-laden atherosclerotic coronary plaque, resulting in a highly thrombogenic plaque core and matrix material circulation in the blood. Platelets then activate and aggregate at the site of the injury. Thrombin is generated, which accelerates platelet activation, resulting in fibrin trapping of red blood cells and leading to thrombus formation. A totally occluding thrombus leads to ST-elevation MI. Reduced blood flow results in ischemia, leading to myocardial cell injury/death, ventricular dysfunction, and cardiac arrhythmias. Myocardial necrosis begins 20 minutes after coronary occlusion.  

Etiology

The etiologies of MI are:

  • Coronary artery spasm
  • Coronary atherosclerosis and plaque rupture
  • Coronary embolism from atrial fibrillation, rheumatic heart disease, infective endocarditis, or intracavitary thrombus
  • Dissection into coronary arteries (aneurysmal, iatrogenic or spontaneous)
  • Periarteritis and other coronary artery inflammatory diseases
  • Anomalous origin of coronary artery (eg interarterial [aorta and pulmonary artery] course of coronary artery)
  • Increased blood viscosity or hypercoagulable states (eg polycythemia vera, systemic lupus, antiphospholipid syndrome)
  • MI with normal coronaries frequently seen in younger patients and cocaine users
  • Chest pain post-ST-segment elevation MI (STEMI) may be due to reinfarction or recurrent MI, myocardial ischemia (angina), pericarditis or non-cardiac causes

Risk Factors

The risk factors for STEMI are: 

  • Age
  • Sex
  • Family history of heart disease
  • Modifiable risk factors include:
    • Hyperlipidemia
    • Hypertension
    • Diabetes
    • Chronic kidney disease (CKD)
    • Obesity
    • Psychosocial factors (eg stress)
  • Lifestyle risk factors include:
    • Smoking
    • Diet
    • Lack of exercise
    • Alcohol intake

Classification

An acute MI (AMI) is classified clinically as:

  • Primary MI: Spontaneous onset of symptoms or signs of acute myocardial ischemia and injury without an alternative acute condition or cardiac procedure triggering the presentation
    • Diagnosis is confirmed and etiology is defined if atherothrombosis or an alternative acute coronary pathology is identified, including spontaneous coronary artery dissection, coronary embolism, vasospasm, and restenosis, stent thrombosis or bypass graft failure occurring >30 days from procedure
    • When coronary angiography or cardiac imaging is unavailable or unsuitable, primary MI may be diagnosed using the combined assessment of biomarkers, electrocardiographic findings and clinical criteria, without requiring additional confirmatory features
  • Secondary MI: Acute myocardial ischemia and injury secondary to an alternative acute condition resulting in myocardial oxygen supply-demand mismatch (ie increased demand [eg tachycardia or severe hypertension] and/or reduced supply [eg anemia, hypoxia, hypotension])
    • Diagnosis is confirmed if ischemia is a result of obstructive coronary artery disease (CAD) (≥70% stenosis in an epicardial vessel by angiography or ≥50% stenosis that is flow-limiting on physiological assessment) without acute coronary pathology, or myocardial injury results in a new or presumed new regional wall motion abnormality or absence of viable myocardium
  • Procedure-related MI: Acute myocardial ischemia and injury occur due to a coronary complication occurring within 30 days of a percutaneous or surgical cardiac procedure
    • Diagnosis is more likely immediately after a procedure when cardiac biomarker levels exceed preprocedural values and continue to rise at 6 hours (eg >5 times the upper reference limit [URL] following an intervention) and at 24 hours (eg >35 times URL following surgery)
    • Diagnosis is confirmed if there is angiographic evidence of a coronary complication of percutaneous intervention or cardiac surgery, or myocardial injury results in a new or presumed new regional wall motion abnormality or absence of viable myocardium
    • Both a complication and a new or presumed new regional wall motion abnormality or absence of viable myocardium are required when the complication arises during the index procedure, or the procedure is performed in the management of AMI
  • Where MI is the likely cause of death, clinical classification (primary, secondary or procedure-related) should be applied based on setting or post-mortem findings

Myocardial injury with non-obstructive coronary arteries (MINOCA) is a working diagnosis in patients with clinical features of possible MI with no significant coronary artery stenosis (ie <50%) on coronary angiography and includes non-coronary cardiac (eg myocarditis, Takotsubo syndrome, cardiomyopathy) or non-cardiac (eg pulmonary embolism) causes.

A prior or unrecognized/silent MI is a condition that has the following criteria:

 

  • Abnormal Q waves with or without symptoms in the absence of non-ischemic causes
  • Loss of viable myocardium on imaging (preferably with cardiac magnetic resonance [CMR] with late gadolinium enhancement) consistent with an ischemic cause
  • Patho-anatomical findings of a previous MI