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Cardiomyopathy is commonly observed in patients with autosomal dominant polycystic kidney disease (ADPKD), even when they have normal renal function and arterial pressure. The role of cardiomyocyte polycystin-1 (PC1) in cardiovascular pathophysiology remains unknown. PC1 is a potential regulator of BIN1 that maintains T-tubule structure, and alterations in BIN1 expression induce cardiac pathologies. We used a cardiomyocyte-specific PC1-silenced (PC1-KO) mouse model to explore the relevance of cardiomyocyte PC1 in the development of heart failure (HF), considering reduced BIN1 expression induced T-tubule remodeling as a potential mechanism. PC1-KO mice exhibited an impairment of cardiac function, as measured by echocardiography, but no signs of HF until 7-9 months of age. Of the PC1-KO mice, 43% died suddenly at 7 months of age, and 100% died after 9 months with dilated cardiomyopathy. Total BIN1 mRNA, protein levels, and its localization in plasma membrane-enriched fractions decreased in PC1-KO mice. Moreover, the BIN1 + 13 isoform decreased while the BIN1 + 13 + 17 isoform was overexpressed in mice without signs of HF. However, BIN1 + 13 + 17 overexpression was not observed in mice with HF. T-tubule remodeling and BIN1 score measured in plasma samples were associated with decreased PC1-BIN1 expression and HF development. Our results show that decreased PC1 expression in cardiomyocytes induces dilated cardiomyopathy associated with diminished BIN1 expression and T-tubule remodeling. In conclusion, positive modulation of BIN1 expression by PC1 suggests a novel pathway that may be relevant to understanding the pathophysiological mechanisms leading to cardiomyopathy in ADPKD patients.

Background: Patients with a cardiovascular (CV) history may be at greater risk of becoming ill and die due to SARS-CoV-2., Aim: To assess the incidence of CV complications in COVID-19 patients, the type of complication, and their association with CV history., Material and Methods: The clinical course of 1,314 patients with COVID-19 admitted consecutively to critical care units of 10 Chilean hospitals was registered between April and August of 2020., Results: The median age of patients was 59 years and 66% were men. One hundred-four (8%) had a CV history, namely heart failure (HF) in 53 (4.1%), coronary heart disease in 50 (3.8 %), and atrial fibrillation in 36 (2.7 %). There were CV complications in 359 patients (27.3%). The most common were venous thrombosis in 10.7% and arrhythmias in 10.5%, HF in 7.2%, type 2 acute myocardial infarction in 4.2%, arterial thrombosis in 2.0% and acute coronary syndrome (ACS) in 1.6%. When adjusted by age, sex and risk factors, only HF (Odds ratio (OR) = 7.16; 95% confidence intervals (CI), 3.96-12.92) and ACS (OR = 5.44; 95% CI, 1.50-19.82) were significantly associated with CV history. There was no association with arrhythmias, type 2 acute myocardial infarction, arterial or venous thrombosis., Conclusions: Patients with a history of CV disease are at greater risk of suffering HF and ACS when hospitalized due to COVID-19. Arrhythmias, type 2 AMI, and arterial or venous thrombosis occur with the same frequency in patients with or without CV history, suggesting that these complications depend on inflammatory phenomena related to the infection.

Introduction and Objective: In patients with congestive heart failure, neurohormonal activation plays an important role in disease progression and prognosis. The aim of this study was to document the evolution of neurohormonal activation after heart transplantation., Patients and Method: Thirty-seven patients on the waiting list for heart transplantation were included in the study. Plasma levels of angiotensin II, aldosterone, endothelin, atrial natriuretic peptide and adrenomedullin were measured before heart transplantation and again 1, 4, 9 and 12 months afterwards. Plasma levels of norepinephrine and renin were measured before and 1 month after heart transplantation., Results: The levels of angiotensin II, norepinephrine and renin showed a nonsignificant trend towards reduction. The levels of aldosterone were unchanged, and an increase in endothelin levels was seen 9 and 12 months after transplantation. Plasma levels of atrial natriuretic peptide and adrenomedullin were significantly lower 1, 4, 9 and 12 months after heart transplantation compared to pretransplant levels., Conclusions: During the first several months after heart transplantation there were no significant reductions in plasma levels of angiotensin II, aldosterone and endothelin, and there were significant reductions soon after surgery in peptides with a predominantly vasodilator effect (atrial natriuretic peptide and adrenomedullin). This unfavorable neurohormonal profile may contribute to the development of posttransplant complications such as edema, arterial hypertension and endothelial dysfunction.