The present study investigated whether telmisartan, an angiotensin II type 1 receptor antagonist, has cardioprotective effects on monocrotaline-induced right ventricular (RV) remodeling in rats. Six-week-old male Wistar rats were divided into control group (CONT), monocrotaline (60 mg/kg, i.p.)-treated group (MCT), monocrotaline (60 mg/kg, i.p.) + telmisartan (3 mg/kg per day, p.o.)-treated group (MCT+TEL), and telmisartan (3 mg/kg per day, p.o.) alone-treated group (TEL). Hearts were excised after echocardiography examinations at day 25. Significant increase in RV weight and histologically remarkable fibrosis in RV sections were observed in MCT. Tricuspid annular plane systolic excursion, a parameter for RV systolic function, significantly decreased in MCT. These RV hypertrophy, fibrosis, and dysfunction were inhibited in MCT+TEL. In MCT, the acceleration time/ejection time ratio of pulmonary artery flow velocity, an index of pulmonary hypertension, significantly decreased. This decrease was not affected in MCT+TEL. In MCT, expressions and activities of matrix metalloproteinase (MMP)-2 and MMP-9, which play a critical role in cardiac remodeling, significantly increased in the RV. In MCT+TEL, these increases in expressions and activities were inhibited. MCT showed about 2-fold increase in transforming growth factor-beta1 expression compared with CONT, and such an increase was not decreased in MCT+TEL. There were no significant changes of these parameters in TEL compared with CONT. These results suggest that telmisartan could attenuate the monocrotaline-induced RV remodeling through improvements of RV hypertrophy, fibrosis, dysfunction, and inhibition of MMPs.
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http://dx.doi.org/10.1254/jphs.09112fp | DOI Listing |
J Vis Exp
January 2025
Mechanical, Aerospace, and Biomedical Engineering, University of Tennessee;
Cardiovascular disease (CVD) is the leading cause of death in the United States. Damage in the cardiovascular system can be due to environmental exposure, trauma, drug toxicity, or numerous other factors. As a result, cardiac tissue and vasculature undergo structural changes and display diminished function.
View Article and Find Full Text PDFCirc Cardiovasc Imaging
January 2025
Multimodality Cardiac Imaging Section, IRCCS Policlinico San Donato, Milan, Italy (L.T., G.D., M.L., A.C.).
Echocardiography
February 2025
Department of Cardiology, Loyola University Medical Center, Maywood, Illinois, USA.
The left atrium (LA) is pivotal in cardiac hemodynamics, serving as a dynamic indicator of left ventricular (LV) compliance and diastolic function. The LA undergoes structural and functional adaptations in response to hemodynamic stress, infiltrative processes, myocardial injury, and arrhythmic triggers. Remodeling of the LA in response to these stressors directly impacts pulmonary circulation, eventually leading to pulmonary capillary involvement, pulmonary artery hypertension, and eventually right ventricular failure.
View Article and Find Full Text PDFEchocardiography
February 2025
Department of Obstetrics and Gynecology, Ministry of Health, Ankara City Hospital, Ankara, Turkey.
Purpose: To investigate fetal cardiac functions and remodeling in pregnancies conceived via in vitro fertilization (IVF).
Methods: This prospective case-control study included 40 singleton IVF pregnancies and 46 uncomplicated control pregnancies at 28-36 weeks of gestation. The IVF group consisted of pregnancies applied to the outpatient clinic, excluding those with anatomical or chromosomal abnormalities.
Sci Rep
January 2025
Instituto do Coração (InCor), Faculdade de Medicina, Hospital das Clínicas HCFMUSP, Universidade de São Paulo, São Paulo, Brazil.
Doxorubicin-induced cardiomyopathy (DOX-IC) is a significant and common complication in patients undergoing chemotherapy, leading to cardiac remodeling and reduced heart function. We hypothesized that the intrapericardial injection of hydrogels derived from the cardiac decellularized extracellular matrix (dECM) loaded with adipose tissue-derived stromal cells (ASC) and their secretome dampens or reverses the progression of DOX-IC. DOX-IC was induced in Wistar male rats through ten weekly intra-peritoneal injections of doxorubicin (cumulative dose: 18 mg/kg).
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