Unraveling the Multitude of Etiologies in Myocardial Infarction With Nonobstructive Coronary Arteries.

Although recent studies revealed suboptimal outcomes in patients with myocardial infarction with nonobstructive coronary arteries (MINOCAs), the underlying etiology remains unknown in most patients. Therefore, adequate treatment modalities have not yet been established. We aimed to assess demographics, treatment strategies, and long-term clinical outcome in MINOCA subgroups. We retrospectively analyzed data from a large, prospective observational study of patients with acute coronary syndrome admitted to the Isala hospital in Zwolle, The Netherlands between 2006 and 2014. Patients with MINOCA were divided into subgroups based on the underlying cause of the event. From 7,693 patients, 402 patients (5%) concerned MINOCA. After the exclusion of missing cases (n = 47), 5 subgroups were distinguished: "true" acute myocardial infarction (10%), perimyocarditis (13%), cardiomyopathy (including Takotsubo cardiomyopathy) (19%), miscellaneous causes (21%), and an indeterminate group (38%). Patients with cardiomyopathy were predominantly women (78%) and showed the highest incidence of major adverse cardiovascular events at 30 days follow-up (7%; p = 0.012), 1 year (19%; p = 0.004), and mortality at long-term follow-up (27%; p = 0.010) compared with any other MINOCA subgroup. The cardiomyopathy group was followed by the indeterminate group, with major adverse cardiovascular events rates of 1% and 5%, respectively, and 17% long-term all-cause mortality. In conclusion, long-term prognosis in MINOCA depends on the underlying etiology. Prognosis is worst in the cardiomyopathy group followed by the indeterminate group. This underlines the importance of revealing the diagnosis to ultimately optimize treatment.

MINOCA: The caveat of absence of coronary obstruction in myocardial infarction.

AIMS: Whether patients with MINOCA (myocardial infarction with non-obstructive coronary arteries) have better outcomes than patients with obstructive coronary artery disease remains contradictory. The current study focussed on the clinical profile and prognosis of MINOCA patients. METHODS AND RESULTS: We performed a retrospective analysis of patients with acute coronary syndrome (ACS) admitted to the Isala hospital in Zwolle, the Netherlands, between 2006 and 2014. A total of 7693 patients were categorized into three groups: MINOCA, single-vessel obstructive ACS (SV-ACS), and multi-vessel obstructive ACS (MV-ACS). MINOCA patients (5.2% of the total population) were more likely to be female (51.5% vs. 30.3% and 26.0% in SV-ACS and MV-ACS, respectively, p < 0.001 for both). The prevalence of risk factors in the MINOCA group was in between the SV-ACS and MV-ACS groups. Logistic regression revealed a lower odds of dying in SV-ACS (odds ratio (OR) = 0.70 (p = 0.04)) and a similar odds in MV-ACS (OR = 0.88, p = 0.45) compared to MINOCA. CONCLUSIONS: Patients with MINOCA show an 'intermediate' risk profile with mortality rates in between those of both ACS groups. Hence, MINOCA should be recognised as a potential risk factor for mortality, requiring adequate treatment and follow-up.

Angiographic underestimation of disease severity in the left anterior descending artery: a fractional flow reserve analysis.

OBJECTIVES: This study compared the prevalence of angiographic underestimation of left anterior descending artery (LAD) lesions with non-LAD lesions. BACKGROUND: Coronary angiography cannot assess the functional severity of a coronary stenosis. Previous studies suggested that lesions of the LAD are more often angiographically underestimated, but evidence is limited. MATERIALS AND METHODS: Fractional flow reserve (FFR) was performed in 335 coronary lesions (187 LAD lesions and 148 non-LAD lesions). A visually estimated diameter stenosis of at least 70% was considered functionally significant. An FFR value of up to 0.80 was considered significant. Multivariable analyses were carried out. RESULTS: Angiographically, LAD lesions as well as non-LAD lesions were considered functionally significant in 29% (P=0.94). FFR showed significant stenosis of the LAD in 52% compared with 24% in non-LAD lesions (P<0.001). Underestimation was observed in 30% of LAD lesions compared with 11% in non-LAD lesions (P<0.001). The adjusted odds ratio for underestimation in LAD lesions in comparison with non-LAD lesions was 3.48 (95% confidence interval 1.89-6.41; P<0.001). CONCLUSION: Underestimation of the functional severity of a coronary stenosis is more common in LAD lesions. FFR should be performed more often for intermediate stenosis of the LAD.

Independent association between symptom onset time and infarct size in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Recent studies have reported on circadian variation in infarct size in ST-elevation myocardial infarction (STEMI) patients. Controversy remains as to whether this finding indicates circadian dependence of myocardial tolerance to ischemia/reperfusion injury or that it can simply be explained by confounding factors such as baseline profile and ischemic time. We assessed the clinical impact and independent association between symptom onset time and infarct size, accounting for possible subgroup differences. From a multicenter registry, 6799 consecutive STEMI patients undergoing primary percutaneous coronary intervention (PCI) between 2004 and 2010 were included. Infarct size was measured using peak creatine kinase (CK). Infarct size exhibited circadian variation with largest infarct size in patients with symptom onset around 03:00 at night (estimated peak CK 1322 U/l; 95% confidence interval (CI): 1217-1436) and smallest infarct size around 11:00 in the morning (estimated peak CK 1071 U/l; 95% CI: 1001-1146; relative reduction 19%; p = 0.001). Circadian variation in infarct size followed an inverse pattern in patients with prior myocardial infarction (p-interaction <0.001) and prior PCI (p-interaction = 0.006), although the later did not persist in multivariable analysis. Symptom onset time remained associated with infarct size after accounting for these interactions and adjusting for baseline characteristics and ischemic time. Symptom onset time did not predict one-year mortality (p = 0.081). In conclusion, there is substantial circadian variation in infarct size, which cannot be fully explained by variations in baseline profile or ischemic time. Our results lend support to the hypothesis of circadian myocardial ischemic tolerance and suggest a different mechanism in patients with prior myocardial infarction.