Kounis syndrome: an additional etiologic factor of myocardial infarction with non-obstructive coronary arteries

Nicholas G. Kounis, Ioanna Koniari, George D. Soufras, Grigorios Tsigkas, Emmanouil Chourdakis, Stefanos Despotopoulos, Periklis Davlouros, George Hahalis
2018 Cardiology Journal  
In an interesting report published in the "Cardiology Journal" concerning 95 patients treated for myocardial infarction with non-obstructive coronary arteries (MINOCA), López Pais et al. [1] found that when non-takotsubo MINOCA patients were evaluated the difference regarding psychiatric illnesses was 29.7% vs. 12.9%, p = 0.001 compared to myocardial infarction (MI) with obstructive coronary arteries. Furthermore, in 11 (11.6%) of these patients, pathophysiological mechanisms of MINOCA remained
more » ... of MINOCA remained unknown. In another recent report, involving 998 patients with angiografically proven MI in the real world, 82 (8.2%) had a MINOCA and 40% were women. No evident etiology was detected in over 70% of MINOCA [2]. Therefore, it seems possible that new, yet unknown, pathophysiological mechanisms are involved in the pathogenesis of this conundrum. So far, several other causes and pathogenetic mechanisms have been reported to be associated with this syndrome including coronary artery spasm, coronary artery dissection, coronary embolism, arrhythmias, mild plaque disruption, hypercoagulable status, type 2 MI, amyloid lightchain AL amyloidosis and clinically unrecognized myocarditis or takotsubo cardiomyopathy [2] . The prevalence of MINOCA among the MI patients ranged between 5% and 25% according to the registries [3]. In a recent report involving 199,163 MI admissions, 9092 consecutive unique patients had MINOCA, 2147 of them experienced a new major adverse cardiovascular event (MACE) and 1254 (14%) of the patients died during mean follow-up of 4.5 years [4] . In this report, even after adjustment, low levels of total cholesterol were significantly associated with the composite endpoint of MACE as well as with long-term mortality. The authors had wondered about these results because hypercholesterolemia is considered as a causal factor for coronary artery disease and that the lowering of total cholesterol and low-density lipoprotein reduces cardiovascular risk in both primary and secondary prevention settings. Indeed, it is being considered why, the Kounis hypersensitivity-associated type I variant coronary spasm which represents a manifestation of endothelial dysfunction or microvascular angina has not been included in this MINOCA report [1] as well as in others [5] . This variant includes patients with normal or nearly normal coronary arteries without predisposing factors for coronary artery disease and represents the most common type (72.6%) of Kounis syndrome. In this variant, the acute release of inflammatory mediators may induce either coronary artery spasm without increased cardiac enzymes and troponins or coronary artery spasm progressing to acute MI with raised cardiac enzymes and troponins. The ensuing acute MI could lead to MACE including cardiogenic shock (2.3%), cardiac arrest (6.3%), death 5 (2.9%) due to ventricular fibrillation,
doi:10.5603/cj.2018.0132 fatcat:j3tu7onvk5dqrcqtk5emcu4luq