Background: There is controversy regarding the potential effects of statin therapy on mortality in patients with heart failure. The present study analyzed the possible effects of statin therapy on morbidity and mortality in patients with diastolic heart failure over long-term follow-up. Hypothesis: To evaluate potential effect of statin therapy on hospitalization rate and mortality in patients with diastolic heart failure. Methods: Patients with preserved left ventricular ejection fraction (≥50%), hospitalized for clinical symptoms of heart failure were evaluated. Patients on statin therapy started at or prior to their first heart failure admission represented group 1 and patients without statin therapy represented group 2. The effects of statins on hospitalization rates and mortality were assessed during a 5 year follow-up. Results: A total of 270 patients (group 1 n = 81; group 2 n = 189) were followed over 5 years. Patients on statins demonstrated improved survival compared to patients without statin therapy (hazard ratio [HR] = 0.65, 95% confidence interval [CI]: 0.45-0.95, P = .029). The survival benefit was maintained after adjusting for differences in baseline characteristics, comorbidities, and other medications. There was no significant difference in the mean cardiovascular hospitalization rate (3.0 ± 3.2 vs 3.8 ± 4.7, P = .23) and in overall hospitalization rate (7.1 ± 6.3 vs 7.8 ± 7.7, P = .52) between groups 1 and 2, respectively. Conclusion: Statin therapy appears to be associated with improved survival in patients with diastolic heart failure.
We present a rare case of left ventricular to right atrial communication, a Gerbode type defect discovered in an adult female, originally misinterpreted as pulmonary arterial hypertension. The case report will be followed by the review of the literature and a discussion about how to prevent echocardiographic misinterpretation of this defect as pulmonary arterial hypertension using careful echocardiographic examination.
Autophagy plays a critical and seemingly dual-purposed role in cardiomyocytes, being implicated as a mechanism of both cellular survival, for example, during ischemia/reperfusion injury and a mechanism of cell death at stages in which progressive myocyte alterations are beyond repair. This review aims to highlight the current literature as it relates to autophagy in cardiomyocytes. It provides background into the mechanisms of cell death, discusses the details that are known about the ubiquitin proteasome system and autophagy, delves into the pathways that are known to initiate and inhibit autophagy, and comments on the role of autophagy in cardiomyocyte homeostasis and cell death.
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