The comparison of ECG, VCG and ECHO data performed in 78 patients with chronic bronchitis allowed us to distinguish 4 grades of right ventricular hypertrophy (RVH): 1) absence of RVH (QRS loop occupies up to 70% of the area in horizontal plane, right ventricular wall thickness (RVWT) up to 5 mm, ECG changes); 2) slightly marked RVH (QRS-loop area 70-89%, RVWT 6-9 mm, electric axis deviation to the right on ECG, and P.100/R + S greater than 20 in lead II); 3) marked RVH (QRS-loop area 90-100%, RVWT 6-10 mm, right ventricular end-diastolic dimension 2-1-3.0 cm, on ECG--the above changes plus R/SV1 greater than 1.0, RV1 greater than or equal to 5 mm, RV1 greater than or equal to 7 mm, and P-pulmonale); 4) marked RVH with significant dilatation and repolarization abnormalities (VCG and ECHO data as above plus right ventricular end-diastolic dimension on ECG more than 3.0 cm, S-T depression, and negative T-wave in leads aVF and V1-3). Apparent ECG signs of RVH in chronic bronchitis develop much later, after the development of secondary pulmonary hypertension.
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Int J Mol Sci
November 2021
Department of Medicine, Mackenzie Evangelical School of Paraná, Curitiba 80730-000, Brazil.
Heart dysfunction and liver disease often coexist. Among the types of cardiohepatic syndrome, Type 2 is characterized by the chronic impairment of cardiac function, leading to chronic liver injury, referred to as congestive hepatopathy (CH). In this study, we aimed to establish a rat model of CH secondary to right ventricular hypertrophy (RVH) related to monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH).
View Article and Find Full Text PDFEur J Pharmacol
January 2021
Laboratory of Cardiovascular Physiology and Reactive Oxygen Species, Physiology Department, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, Brazil. Electronic address:
The time-course of pulmonary arterial hypertension in the monocrotaline (MCT) model was investigated. Male rats were divided into two groups: MCT (received a 60 mg/kg i.p.
View Article and Find Full Text PDFPLoS One
September 2020
Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus-Liebig University Giessen, Giessen, Germany.
The leading cause of death in Pulmonary Arterial Hypertension (PAH) is right ventricular (RV) failure. The tumor suppressor p53 has been associated with left ventricular hypertrophy (LVH) and remodeling but its role in RV hypertrophy (RVH) is unclear. The purpose of this study was to determine whether pharmacological activation of p53 by Quinacrine affects RV remodeling and function in the pulmonary artery banding (PAB) model of compensated RVH in mice.
View Article and Find Full Text PDFPulm Circ
May 2018
4 Cardiovascular Pulmonary Research Laboratories, Departments of Pediatrics and Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Pulmonary arterial (PA) wall modifications are key pathological features of pulmonary hypertension (PH). Although such abnormalities correlate with heightened phosphorylation of c-Jun N-terminal kinases 1/2 (JNK1/2) in a rat model of PH, the contribution of specific JNK isoforms to the pathophysiology of PH is unknown. Hence, we hypothesized that activation of either one, or both JNK isoforms regulates PA remodeling in PH.
View Article and Find Full Text PDFLife Sci
April 2017
Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410078, China; Hunan Provincial Key Laboratory of Cardiovascular Research, Central South University, Changsha, Hunan 410078, China. Electronic address:
Aim: Chronic hypoxia leads to right ventricular hypertrophy (RVH). RVH is believed to result from hypoxia-induced pulmonary hypertension. However, if hypoxia impacts RVH directly awaits clarification.
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