ESC working group position paper on myocardial infarction with non-obstructive coronary arteries

Abstract

The management of acute myocardial infarction (AMI)1 has evolved over the past century and particularly in the past 50 years. Important milestones include the development of the electrocardiogram, coronary care units, coronary angiography, reperfusion therapies, and troponin assays. These innovations are the foundation of contemporary AMI management strategies that include a diagnosis centred on elevated troponin values associated with corroborative clinical evidence,1 early use of coronary angiography, and reperfusion therapies.2–4 Pivotal in the evolution of these contemporary strategies were the early AMI coronary angiography studies undertaken by DeWood et al. These pioneering studies demonstrated that, in patients presenting with ST elevation myocardial infarction (STEMI), almost 90% had an occluded coronary artery provided that angiography was undertaken within 4 h of chest pain onset.5 In contrast, in AMI patients who did not present with ST elevation (non-ST elevation myocardial infarction or NSTEMI), only 26% had an occluded coronary artery when angiography was performed within 24 h of symptom onset.6 In both of these landmark studies,5,6 >90% of the acute MI patients had angiographic evidence of obstructive coronary artery disease (CAD), underscoring the importance of the atherosclerotic process in the pathogenesis of AMI. Although DeWood's studies underscore the importance of obstructive CAD in AMI, it is fascinating that ∼10% had no significant CAD on coronary angiography. This is confirmed in several large AMI registries7–9 where 1–13% of AMI's occurred in the absence of obstructive CAD thereby eliciting an important set of questions—what is the mechanism of the myocardial damage in these patients? Do these patients differ from those with obstructive CAD? Should they be managed with the same clinical strategies? Do patients with non-obstructive atherosclerosis differ in pathophysiology and outcomes from those with angiographically normal coronary arteries? These and other issues have prompted clinical researchers to coin the term myocardial infarction with non-obstructive coronary arteries (MINOCA). This position paper is the first authoritative international expert opinion regarding this intriguing condition. We seek to define MINOCA, describe its associated clinical features and mechanisms, detail an assessment pathway for its evaluation, as well as stimulate research into its mechanisms and treatment.10 As the name implies, the formulation of the MINOCA diagnosis requires both clinical documentation of an AMI and demonstration of non-obstructive coronary arteries (Table 1). Accordingly, the diagnosis is made following coronary angiography in the evaluation of a clinical presentation consistent with AMI. It should be noted that the Universal Definition of Myocardial Infarction specifies that the combination of symptoms and a positive cardiac biomarker in the appropriate clinical scenario is diagnostic of AMI. Therefore, if there is no clinically apparent alternative diagnosis, such as myocarditis or pulmonary embolism, the diagnosis of MINOCA is applicable. The rationale for establishing MINOCA as a clinical diagnosis includes: (i) providing a common nomenclature for this group of patients who are often overlooked in contemporary clinical practice, (ii) encouraging routine evaluation for underlying causes in these patients, and (iii) stimulating further studies into its responsible mechanisms, outcomes, and most appropriate management strategies. Myocardial infarction with non-obstructive coronary arteries should be considered as a ‘working diagnosis’, analogous to heart failure, and thus prompts further evaluation regarding its underlying mechanism(s). Diagnostic criteria for myocardial infarction with non-obstructive coronary arteries AMI criteria.1 (a) Positive cardiac biomarker (preferably cardiac troponin) defined as a rise and/or fall in serial levels, with at least one value above the 99th percentile upper reference limit. (b) Corroborative clinical evidence of infarction evidenced by at least one of the following: Symptoms of ischaemia New or presumed new significant ST-T changes or new LBBB Development of pathological Q waves Imaging evidence of new loss of viable myocardium or new RWMA Intracoronary thrombus evident on angiography or at autopsy Non-obstructive coronary arteries on angiography: Defined as the absence of obstructive CAD on angiography, (i.e. no coronary artery stenosis ≥50%), in any potential infarct-related artery. This includes both patients with: o normal coronary arteries (no stenosis >30%) o mild coronary atheromatosis (stenosis >30% but <50%). No clinically overt specific cause for the acute presentation: At the time of angiography, the cause and thus a specific diagnosis for the clinical presentation is not apparent. Accordingly, there is a necessity to further evaluate the patient for the underlying cause of the MINOCA presentation. AMI criteria.1 (a) Positive