Background: Significant symptomatic chronic aortic regurgitation (AR) leads to considerable left ventricular remodeling at the expense of myocyte hypertrophy and extracellular matrix remodeling. The relevance of interstitial fibrosis concentration in these patients is unknown. We analyzed the degree of fibrosis in the left ventricle (LV) in symptomatic patients with AR submitted to surgical treatment, and its relationship with functional and anatomical characteristics.
Objective: To evaluate myocardial fibrosis in chronic severe aortic regurgitation.
Methods: Twenty-eight patients with chronic symptomatic AR (16 with normal LV function and 12 with LV dysfunction) were selected and assessed pre- and postoperatively by echocardiography. Functional capacity was measured using maximal oxygen consumption (VO2max) through the cardiopulmonary test. Myocardial fibrosis volume fraction (MFV) was quantified through endomyocardial biopsy performed in all patients during surgery. We compared the histopathologic results with a nine-patient control group.
Results: The mean age was 39 +/- 12 years, 75% of the patients were male, and the rheumatic etiology accounted for 84% of the cases. Twenty-five patients remained in FC l and ll at the end of the study, and there was a significant reduction of the LV diameters between the preoperative and late postoperative timepoints. Three deaths occurred but they were not related to postoperative ventricular dysfunction. The parameters of the cardiopulmonary test were similar between pre- and postoperative timepoints. MFV in patients with AR was significantly higher than in the control group (3.47 +/- 1.9% vs 0.82 +/- 0.96%, respectively, p=0.001). There was no statistical correlation among LV fibrosis and LV diameters, LVEF and MVO2.
Conclusion: In patients with significant symptomatic AR, the presence of limited myocardial fibrosis was not associated with clinical, echocardiographic or functional complications.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1590/s0066-782x2009000100010 | DOI Listing |
Sci Rep
January 2025
Division of Cardiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Myocyte disarray and fibrosis are underlying pathologies of hypertrophic cardiomyopathy (HCM) caused by genetic mutations. However, the extent of their contributions has not been extensively evaluated. In this study, we investigated the effects of genetic mutations on myofiber function and fibrosis patterns in HCM.
View Article and Find Full Text PDFCurr Cardiol Rep
January 2025
Johns Hopkins University Division of Cardiology, Baltimore, MD, USA.
Purpose Of Review: The present review aims to address systemic sclerosis (SSc)-associated myocardial disease, a significant cause of morbidity and mortality, by examining the mechanisms of inflammation, microvascular dysfunction, and fibrosis that drive cardiac involvement. The objective is to elucidate critical risk factors and explore advanced diagnostic tools for early detection, enhancing patient outcomes by identifying those at highest risk.
Recent Findings: Recent studies underscore the importance of specific autoantibody profiles, disease duration, and cardiovascular comorbidities as key risk factors for severe cardiac manifestations in SSc.
Acta Pharmacol Sin
January 2025
Department of Pharmacology, School of Pharmacy, Nantong University, Nantong, 226001, China.
Regulated cell death like pyroptosis is one vital cause of diabetic cardiomyopathy (DCM), which eventually leads to heart failure. Tumor necrosis factor (TNF) receptor-associated death domain protein (TRADD) is an adapter protein with multiple functions that participates in the pathophysiological progress of different cardiovascular disorders via regulating regulated cell death. Studies have shown that TRADD combines with receptor-interacting protein kinase 3 (RIPK3) and facilitates its activation, thereby mediating TNF-induced necroptosis.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Academy of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address:
Dihydrotanshinone I (DHT) is an active ingredient derived from Salvia miltiorrhiza. Previous studies have demonstrated that DHT can improve cardiac function in rats with myocardial ischemia-reperfusion injury (IR). However, the mechanism by which DHT improves myocardial injury in rats still requires further research.
View Article and Find Full Text PDFJ Comp Pathol
January 2025
Department of Comparative Biomedical Sciences, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, UK. Electronic address:
Hypertension is a common condition in older cats, often secondary to chronic kidney disease (CKD). Although the heart is one of the organs damaged by hypertension, the pathology of the feline hypertensive (HT) heart has been poorly studied. The aim of this retrospective study was to describe the gross and microscopic pathology of hearts obtained from cats at post-mortem examination and to compare cats diagnosed with hypertension with cats of similar age and kidney function for which antihypertensive treatment was not deemed clinically necessary.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!