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Background and Objectives: Mitral valve pathology and mitral regurgitation (MR) are very common in patients with hypertrophic cardiomyopathy (HCM), and the evaluation of mitral valve anatomy and degree of MR is important in patients with HCM. The aim of our study was to examine the potential influence of moderate or moderately severe MR on the prognosis, clinical presentation, and structural characteristics of HCM patients. Materials and Methods: A prospective study examined 176 patients diagnosed with primary asymmetric HCM. According to the severity of the MR, the patients were divided into two groups: Group 1 (n = 116) with no/trace or mild MR and Group 2 (n = 60) with moderate or moderately severe MR. All patients had clinical and echocardiographic examinations, as well as a 24 h Holter ECG. Results: Group 2 had significantly more often the presence of the obstructive type of HCM (p < 0.001), syncope (p = 0.030), NYHA II class (p < 0.001), and atrial fibrillation (p = 0.023). Also, Group 2 had an enlarged left atrial dimension (p < 0.001), left atrial volume index (p < 0.001), and indirectly measured systolic pressure in the right ventricle (p < 0.001). Patients with a higher grade of MR had a significantly higher E/e' (p < 0.001) and, as a result, higher values of Nt pro BNP values (p < 0.001) compared to Group 1. Kaplan-Meier analysis demonstrated that the event-free survival rate during a median follow-up of 88 (IQR 40-112) months was significantly higher in Group 1 compared to Group 2 (84% vs. 45% at 8 years; log-rank 20.4, p < 0.001). After adjustment for relevant confounders, the presence of moderate or moderately severe MR remained as an independent predictor of adverse outcomes (HR 2.788; 95% CI 1.221-6.364, p = 0.015). Conclusions: The presence of moderate or moderately severe MR was associated with unfavorable long-term outcomes in HCM patients.

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AIMS: Previous studies indicated that a chronic total occlusion (CTO) in a non-infarct-related artery is linked to higher mortality mainly in the acute setting in patients with ST-elevation myocardial infarction (STEMI). Our aim was to assess the temporal distribution of mortality risk associated with non-culprit CTO over years after STEMI. METHODS AND RESULTS: The study included 8679 STEMI patients treated with primary percutaneous coronary intervention (PCI). Kaplan-Meier cumulative mortality curves for non-culprit CTO vs. no CTO were compared with log-rank test, with landmarks set at 30 days and 1 year. Adjusted Cox regression models were constructed to assess the impact of non-culprit CTO on mortality over different time intervals. Tests for interaction were pre-specified between non-culprit CTO and acute heart failure and left ventricular ejection fraction. The primary outcome variable was all-cause mortality, and the median follow-up was 5 years. Non-culprit CTO was present in 11.6% of patients (n = 1010). Presence of a CTO was associated with increased early [30-day adjusted hazard ratio (HR) 1.91, 95% confidence interval (CI) 1.54-2.36; P < 0.001] and late mortality (5-year adjusted HR 1.66, 95% CI 1.42-1.95; P < 0.001). Landmark analyses revealed an annual two-fold increase in mortality in patients with vs. without a CTO after the first year of follow-up. The observed pattern of mortality increase over time was independent of acute or chronic LV impairment. CONCLUSIONS: Non-culprit CTO is independently associated with mortality over 5 years after primary PCI for STEMI, with a constant annual two-fold increase in the risk of death beyond the first year of follow-up.

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