Acute Myocardial Infarction With No Obstructive Coronary Atherosclerosis: Mechanisms and Management | Journal Scan
What are the causes, mechanisms, and management of acute myocardial infarction with no obstructive coronary atherosclerosis (MINOCA)?
The presence of MINOCA is reported from large registries as between 5% and 25%. Diagnosis of MINOCA starts with clinical history, electrocardiogram (ECG), cardiac enzymes, echocardiography, coronary angiography, and left ventricular (LV) angiography. Regional wall motion abnormalities limited to a single epicardial coronary artery territory identify an “epicardial pattern,” whereas regional wall motion abnormalities extended beyond a single epicardial coronary artery territory identify a “microvascular pattern.”
Epicardial causes of MINOCA include coronary artery spasm and eccentric plaque. Coronary artery spasm represents an important epicardial cause of MINOCA. The prevalence ranges between 3% and 95% of MINOCA patients; this wide difference in rates depends on the stimuli used to trigger spasm, definitions of spasm, and ethnic reasons. Coronary artery spasm results from the interaction of two components: a usually localized, but sometimes diffuse, hyper-reactivity of vascular smooth muscle cells and a transient vasoconstrictor stimulus acting on the hyper-reactive vascular smooth muscle cells. Patients often report angina at rest and have ST-segment elevation with symptoms. Diagnostic testing includes intracoronary provocative testing with ergonovine or acetylcholine. Nonspecific vasodilators such as nitrates and calcium channel blockers are standard treatments.
Eccentric plaque with positive remodeling is another cause of MINOCA. Plaques may rupture, leading to transient or partial thrombosis, after which spontaneous fibrosis occurs. This scenario is thought to occur more often in women with cardiovascular risk factors. Intracoronary ultrasound can be helpful in examining plaque characteristics. Management is similar to that of traditional acute coronary artery patients with aggressive risk factor management and antiplatelet therapy.
Microvascular causes of MINOCA include Takotsubo syndrome, coronary microvascular spasm, myocarditis, and coronary embolism. Takotsubo is more common in women than men and often after severe physical or emotional stress. Patients often have severe LV dysfunction, which improves over subsequent days to weeks. Wall motion abnormalities are often seen in the mid to apical segments, but can be seen in other segments. Cardiac magnetic resonance demonstrates LV dysfunction without evidence of necrosis and is compatible with the lack of obstructive coronary artery disease observed with coronary angiography. Treatment with beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and diuretics for LV dysfunction is standard treatment.
Coronary microvascular spasm is associated with transient ischemia and ST-segment changes. Provocative testing can assist with the diagnosis. Prognosis is generally good; however, approximately one third of patients continue to have symptoms despite treatment with calcium channel blockers.
Myocarditis can mimic MI, and thus, is one of the potential causes of MINOCA. Patients are often young, with a recent history of infection. Gadolinium enhancement with magnetic resonance imaging often reveals a pattern of intramural, rim-like patter in the septal wall of a subepicardial patchy distribution in the free wall of the LV. Prognosis may depend on clinical signs and symptoms at presentation, with more severe heart failure associated with poorer prognosis. Management includes beta-blocker therapy and ACE inhibitors.
Coronary embolism is also a possible etiology of MINOCA, usually leading to dysfunction in the microcirculation (although epicardial embolus can occur). Patients at higher risk of systemic emboli are at risk. Anticoagulation should be considered for such patients.
The authors concluded that patients with MINOCA, in particular those with angiographically normal coronary arteries, are frequently labeled as “noncardiac patients,” thus missing the opportunity to appropriately treat patients with an outcome worse than previously believed. An accurate and systematic diagnostic workup is crucial for the identification of the cause of MINOCA in each individual patient, and then for risk stratification and for the implementation of the most appropriate forms of treatment.
This is a well written clinical update of an important aspect of acute coronary syndromes, which is often overlooked and thus often not well managed. Patients with MINOCA do not have an event-free survival; improvement in care will likely lead to reduced adverse outcomes after a MINOCA event.
Clinical Topics: Acute Coronary Syndromes, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Atherosclerotic Disease (CAD/PAD), Interventions and ACS, Interventions and Coronary Artery Disease, Interventions and Imaging, Angiography, Magnetic Resonance Imaging, Nuclear Imaging
Keywords: Acute Coronary Syndrome, Angiotensin-Converting Enzyme Inhibitors, Calcium Channel Blockers, Coronary Artery Disease, Coronary Angiography, Muscle, Smooth, Vascular, Magnetic Resonance Imaging, Myocardial Infarction, Myocarditis, Nitrites, Takotsubo Cardiomyopathy
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