Summary

There are no prospective, randomised, controlled trials to guide the management of myocardial infarction with non-obstructive coronary arteries (MINOCA) and so far it has been managed based on limited evidence. The recent 2019 AHA Scientific Statement, however, provides guidance for the management of this intriguing condition.

The Fourth Universal Definition of MI Expert Consensus Document for clinicians advocates the increased use of high-sensitivity cardiac troponin (hs-cTn) to make a diagnosis of MINOCA. However, clinical observations, ECG patterns, laboratory data, imaging procedure findings, and sometimes pathological findings are all needed to diagnose MI.

MI patients with no angiographic obstructive coronary artery disease (≥50% diameter stenosis in a major epicardial vessel) have myocardial infarction with non-obstructive coronary arteries (MINOCA). 5 to 6 percent of acute myocardial infarction (AMI) cases present as MINOCA but a range of 5 to 15% has been reported as well. MINOCA is seen to occur more often in younger patients, in women, and in patients less likely to have dyslipidaemia.

Causes of MINOCA

• Coronary plaque disease, coronary dissection, coronary artery spasm, coronary microvascular spasm, Takotsubo cardiomyopathy, myocarditis, and coronary thromboembolism are the common causes of MINOCA
• Other forms of type 2 myocardial infarction and MINOCA due to uncertain etiology may also be seen
• Vasoconstriction of an epicardial coronary artery (>90% vasoconstriction) can also result in MINOCA due to coronary vasospasm leading to compromised coronary blood flow
• Spontaneous coronary artery dissection (SCAD) is another cause that should be kept in mind

Diagnosis of MINOCA

When there is no obstructive coronary artery disease (CAD) (no lesion ≥50%), the Fourth Universal Definition of MI should be used to diagnose MIINOCA. The American Heart Association Scientific Statement for clinicians deals with patients with possible acute MI. The key points of this document are as follows:

1. The definition of MI accommodates the increased use of high-sensitivity cardiac troponin (hs-cTn).
2. A myocardial injury is detected when the cTn value is elevated above the 99th percentile upper reference limit (URL). If there is a rise and/or fall in cTn values, acute injury is considered.
3. Type 1 MI detection includes a rise and/or fall of cTn with at least one value above the 99th percentile along with either one of these criteria: Acute MI symptoms, novel ECG changes of ischemia, pathological Q waves, image proof of viable myocardial loss or abnormalities in new wall movement consistent with changes normally seen with ischemia.
4. Type 2 MI detection includes a rise and/or fall of cTn with at least one value above the 99th percentile along with myocardial oxygen supply and demand imbalance not related to coronary thrombosis in which one of these criteria is also present: Acute myocardial ischemia ischemia, novel ECG changes of ischemia, pathological Q waves, image proof of viable myocardial loss or abnormalities in new wall movement consistent with changes normally seen with ischemia.
5. The arbitrarily defined meaning of cardiac procedural myocardial injury is when there are increases in cTn values (>99th percentile URL) in patients with normal baseline values (≤99th percentile URL) or a rise of cTn values >20% of the baseline value when it is above the 99th percentile, but cTn values are stable or falling.
6. Elevation of cTn values >5 times the 99th percentile URL in patients with normal baseline values arbitrarily defines coronary intervention-related MI. The post-procedure cTn must increase by >20% in patients with high pre-procedure cTn in whom the cTn levels are stable (≤20% variation) or falling. The absolute post-procedural value should be at least five times the 99th percentile URL. Additionally, one of the following must occur: Novel ECG changes suggestive of ischemia, pathological Q waves, or on angiography, a procedural flow-limiting complication like coronary dissection, occlusion of a major epicardial artery or a side branch occlusion/thrombus, disruption of collateral flow or distal embolization.
7. An elevation of cTn values >10 times the 99th percentile URL in patients with normal baseline cTn values is used to arbitrarily define coronary artery bypass grafting (CABG)-related MI. The post-procedure cTn must rise by >20% in patients with elevated pre-procedure cTn in whom cTn levels are stable (≤20% variation) or falling. The absolute post-procedural value should be >10 times the 99th percentile URL. Additionally, one of the following must occur: Pathological Q waves, angiographic proof of new graft occlusion or new native coronary artery occlusion, or imaging proof of new loss of viable myocardium or new regional wall motion abnormality consistent with an ischemic cause.
8. Sepsis due to endotoxins may result in elevated cTn values and marked decreases in ejection fraction. After treating the sepsis, complete recovery of myocardial functioning with a normal ejection fraction occurs.
9. Clinical observations, ECG patterns, laboratory data, imaging procedure findings, and sometimes pathological findings need to be integrated in the proper context of the time frame as and when suspected events occur to reach the diagnosis of MI using the criteria of the Fourth Universal Definition of MI.

Treatment of MINOCA

1. There are no prospective, randomised, controlled trials to guide the management of MINOCA and therefore MINOCA is managed based on limited evidence. Aspirin, statins, beta-blockers, clopidogrel, angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers are medications that may be given to patients based on their individual mechanism for MINOCA.
2. Modifiable CAD risk factors should be treated aggressively if proof of atherosclerosis is found.
3. Calcium channel blockers are the best agents to treat coronary vasospasm since the advantages of long-acting nitrates are not that clear.