Novel CMR techniques in the determining of diagnosis in MINOCA patients

Differential diagnoses of myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) are numerous, including plaque disruption, epicardial coronary vasospasm, coronary embolism/thrombosis, spontaneous coronary artery dissection, supply-demand mismatch (type 2 myocardial infarction) or coronary microvascular dysfunction. CMR is often used in evaluating the possible underlying cause, but is inconclusive in about 25% of cases [1], which is why novel techniques are being developed in order to get closer to a definitive diagnosis and consequently an adequate treatment plan. Objective numerical parameters derived from quantitative stress CMR perfusion mapping, such as myocardial blood flow (MBF) and perfusion reserve (MPR) are already in use for outcome prediction in patients with verified epicardial coronary artery disease and revascularisation [2]. Paper from Johansson et al. explores the possibilities of using multiparametric CMR, including quantitative stress perfusion mapping in the long-term follow-up of MINOCA patients who had initially had a normal CMR scan. The hypothesis was that if MINOCA patients had reduced global stress perfusion in comparison to age- and sex-matched volunteers without comorbidities and without ischaemic heart
disease (IHD) symptoms, that would be suggestive of coronary microvascular disfunction. Despite the presence of myocardial edema and damage revealed by comprehensive CMR examination, including T1 and T2 tissue mapping, LGE and ECV mapping, the underlying pathophysiological mechanism in patients with initially normal CMR exam is still unknown. Coronary microvascular dysfunction is a significant contributor to a variety of cardiac diseases, including acute coronary syndrome, heart failure, different types of cardiomyopathies, or as an isolated entity [3].

Although the CMR exam is mandatory early after the initial event, the estimation of myocardial perfusion is still not a part of everyday clinical practice. It is recently showed that even in patients with the CMR observable evidence of tissue damage, coronary microvascular dysfunction plays a significant role in terms of prognosis [3]. A paperwork by Milzi et al. demonstrated that coronary microvascular dysfunction is a hallmark of all MINOCA subtypes, including coronary cause, Takotsubo cardiomyopathy, infiltrative or inflammatory cardiomyopathy, or in those with unclear cause [4], as it is demonstrated by the following paper by Johansson et al. Although with a small sample size, a study by Johansson provides a unique factor that can be evaluated both invasively and non-invasively and stratify patients with MINOCA independently of their primary cause, even in those without tissue damage. CMD This is important, as the degree of CMD in patients with MINOCA is indicative of their future MACE risk, as demonstrated in the study by Abdu et al [3]. Recently, certain studies also investigated the role of genetic mechanisms associated with the development of mcrocirculatory dysfunction, both in INOCA and MINOCA patients [5]. In conclusion, various pathophysiological mechanisms in patients with MINOCA are leading us toward the usage of highly sophisticated diagnostic modalities to evaluate both tissue and perfusion abnormalities, as these can point out the origin of myocardial damage. A modern cardiac magnetic resonance examination is able to provide significant information even in patients without initially observable tissue damage, underlining that coronary microvascular dysfunction could be a significant contributor in patients with MINOCA. Having in mind recent evidence on the role of CMD in patients with MINOCA, an important question arises: “Should we evaluate myocardial perfusion/the presence of CMD in every MINOCA patient?“ Future larger studies could provide us a sufficient evidence on this important clinical issue.