Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA): Contemporary Insights for Clinicians
Myocardial infarction with nonobstructive coronary arteries (MINOCA) is increasingly recognized as a distinct clinical syndrome within the spectrum of acute coronary syndromes. It describes patients who meet the universal criteria for myocardial infarction (MI), including a rise and/or fall in cardiac biomarkers with clinical evidence of ischemia, but who have no coronary artery stenosis ≥50% on invasive coronary angiography. Importantly, MINOCA should be viewed as a working diagnosis requiring further mechanistic evaluation rather than a final label.
Epidemiology & Clinical Profile
MINOCA accounts for ~5-10% of patients presenting with acute MI. Affected patients are often younger and more frequently female than those with MI due to obstructive coronary artery disease (CAD). Traditional atherosclerotic risk factors may be less prevalent, which can contribute to under-recognition. Despite prior assumptions of a benign course, mortality and major adverse cardiovascular event (MACE) rates in MINOCA are not negligible and may approach those seen in obstructive CAD in some cohorts.
Pathophysiological Mechanisms
MINOCA is heterogeneous, with multiple potential ischemic and nonischemic etiologies. Common mechanisms include:
Atherosclerotic plaque disruption without significant residual stenosis (e.g., plaque rupture or erosion).
Epicardial coronary vasospasm, leading to transient severe constriction and ischemia.
Coronary microvascular dysfunction, impairing perfusion at the microcirculatory level.
Coronary thrombosis or embolism, sometimes related to hypercoagulable states or paradoxical emboli.
Spontaneous coronary artery dissection (SCAD), particularly in younger women.
Other causes (e.g., supply–demand mismatch, nonischemic myocardial injury) must be excluded.
Diagnostic Approach
After confirming MI and nonobstructive coronary anatomy on coronary angiogram, clinicians should systematically:
Exclude nonischemic causes of troponin elevation (e.g., myocarditis, pulmonary embolism).
Identify overlooked obstructive disease or small branch occlusions on coronary angiogram.
Use advanced imaging:
Intravascular imaging (OCT/IVUS) to detect plaque disruption not apparent on angiography. This is done in the cath lab.
Cardiac magnetic resonance (CMR) to distinguish ischemic from nonischemic injury and identify scar or edema patterns. This should ideally be done in the first few days-week after MINOCA, however even CMR months after may help reveal a diagnosis.
Provocative testing for vasospasm where appropriate which is usually not done at the time of MINOCA
Management Principles
The initial management of MINOCA is similar to any other cause of ACS. There are no large randomized clinical trials guiding therapy specifically in MINOCA. Management is typically mechanism-guided:
If atherosclerotic features are present, consider antiplatelet agents, statins, ACE inhibitors/ARBs, and beta-blockers as would be used in conventional MI.
Vasospastic mechanisms may merit calcium channel blockers and avoidance of beta-blocker monotherapy.
Treat modifiable risk factors aggressively.
Tailored therapy based on advanced diagnostic findings is increasingly emphasized.
Prognosis & Research Directions
Although historically thought to confer a better prognosis than obstructive MI, recent data suggest similar long-term risks for adverse outcomes. Improved diagnostic phenotyping, understanding sex-based differences, and dedicated clinical trials are priorities to optimize patient-centered care.
More information:
Myocardial infarction with nonobstructive coronary artery disease in a 56-year-old woman | CMAJ
