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This study sought to assess the presence and morphological features of coronary plaques on optical coherence tomography (OCT) as the causes of myocardial infarction with nonobstructive coronary arteries (MINOCA).Although coronary atherosclerosis has been postulated as a potential mechanism of MINOCA, the interaction between disrupted coronary plaques and myocardial injury remains unknown.In a prospective study, consecutive patients with MI but without significant coronary stenosis (≥50%) at angiography underwent OCT and cardiac magnetic resonance (CMR) with late gadolinium-enhancement (LGE). The infarct-related artery (IRA) was identified by localization of ischemic-type LGE.Thirty-eight MINOCA patients (mean age 62 ± 13 years, 55% female, 39% with ST-segment elevation) were enrolled. Maximal diameter stenosis was 35% by angiography, and 5 patients (13%) had normal angiogram results. Plaque disruption and coronary thrombus were observed in 9 patients (24%) and 7 patients (18%), respectively. Sixteen of 31 patients (52%) undergoing CMR showed LGE. Ischemic-type LGE was present in 7 patients (23%) and was more common in patients with than without plaque disruption (50% vs. 13%, respectively; p = 0.053) and coronary thrombus (67% vs. 12%, respectively; p = 0.014). In the per-lesion analysis, the IRA showed significantly more plaque disruption (40% vs. 6%; p = 0.02), thrombus (50% vs. 4%; p = 0.014), and thin-cap fibroatheroma (70% vs. 30%; p = 0.03) than the non-IRA.Plaque disruption and thrombus are not uncommon in MI without obstructive coronary stenoses at angiography and may be associated with the presence and location of ischemic-type myocardial injury on CMR. OCT may be valuable in identifying atherosclerotic etiology in individuals with MINOCA. (Optical Coherence Tomography in Patients With Acute Myocardial Infarction and Nonobstructive Coronary Artery Disease [SOFT-MI]; NCT02783963).

Atheromatous renal artery stenosis (ARAS) often coexists with coronary artery disease (CAD). This study evaluated the prevalence of three polymorphisms: angiotensin-converting enzyme (ACE) insertion/deletion (Ins/Del), endothelial nitric oxide synthase (eNOS) Glu298Asp, and methylenetetrahydrofolate reductase (MTHFR) C677T, in hypertensive patients referred for coronary and renal angiography.The study included 223 hypertensive patients divided into three groups: 72 patients without significant CAD or evidence of ARAS, 111 patients with significant CAD but no ARAS, and 40 patients with coexisting significant CAD and evidence of ARAS. The control group consisted of 195 age- and sex-matched healthy subjects.Patients with coexisting significant CAD and evidence of ARAS were older (p=0.03), less frequently obese (p=0.02), and more likely to have peripheral carotid or femoral artery disease (PAD) (p=0.02) compared with patients with significant CAD but no ARAS. They differed in terms of ACE Del/Del genotype distribution (40% vs. 17.1%, respectively, p=0.007). In a multivariate analysis the independent predictors of ARAS were PAD (OR: 3.7, 95%CI: 1.1-12.3, p=0.005) and ACE Del/Del polymorphism (OR: 3.3, 95%CI: 1.3-8.2, p=0.01). There was a higher prevalence of eNOS Asp/Asp genotype in all patients with significant CAD than in controls (9.3% vs. 3.6%, respectively, p=0.02), but no difference in MTHFR polymorphism between the studied groups was found.In the hypertensive population referred for coronary and renal angiography, the ACE insertion/deletion variant but not eNOS Glu298Asp or MTHFR C677T polymorphism, seems to coexist with atheromatous renal artery stenosis.