scholarly journals Pulmonary Hypertension Related to Left-Sided Cardiac Pathology

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Todd L. Kiefer ◽  
Thomas M. Bashore
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Therapeutic Strategies ◽  
Left Ventricular ◽  
Right Ventricular Failure ◽  
Valve Disease ◽  
Ventricular Failure ◽  
Cardiac Pathology ◽  
Pathologic Processes

Pulmonary hypertension (PH) is the end result of a variety of diverse pathologic processes. The chronic elevation in pulmonary artery pressure often leads to right ventricular pressure overload and subsequent right ventricular failure. In patients with left-sided cardiac disease, PH is quite common and associated with increased morbidity and mortality. This article will review the literature as it pertains to the epidemiology, pathogenesis, and diagnosis of PH related to aortic valve disease, mitral valve disease, left ventricular systolic and diastolic dysfunction, and pulmonary veno-occlusive disease. Moreover, therapeutic strategies, which focus on treating the underlying cardiac pathology will be discussed.

scholarly journals Right Ventricular Failure Following Chronic Pressure Overload Is Associated With Reduction in Left Ventricular Mass

2011 ◽  
Vol 57 (8) ◽  
pp. 921-928 ◽  
Author(s):  
Maxim Hardziyenka ◽  
Maria E. Campian ◽  
Herre J. Reesink ◽  
Sulaiman Surie ◽  
Berto J. Bouma ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Left Ventricular Mass ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Right Ventricular Failure ◽  
Ventricular Failure ◽  
Ventricular Mass

scholarly journals Pulmonary hypertension with or without right ventricular failure as short-term prognostic predictors in patients with AHF

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
M Quintana Da Silva ◽  
JE Gimenez ◽  
J Martinez ◽  
J Ojeda ◽  
D Gomes
Keyword(s):  
Pulmonary Hypertension ◽  
Logistic Regression ◽  
Multivariate Analysis ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Right Ventricular Failure ◽  
Left Ventricular Ejection ◽  
Ventricular Failure ◽  
Ventricular Ejection Fraction ◽  
Prognostic Predictors

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Different registries have reported Right Ventricular Failure (RVF) as a predictor of IH mortality in patients with AHF. However, the association of different degrees of Pulmonary Hypertension (PH) associated with or without RVF as prognostic predictors of IH mortality and Rehospitalization (RH) at 60 days is not well stablished. Methods We included 394 consecutive patients from January 2012 to August 2020 with the primary diagnosis of AHF and different degrees of PH with or without RVF. IH mortality and RH after 60 days of patients with AHF and the presence of RVF with or without PH were evaluated and stratified by severity into mild, moderate and severe PH and forms of presentation of AHF. Univariate, bivariate and multivariate analysis was performed by logistic regression of the independent variables. The qualitative variables were analyzed by the chi square test and the quantitative variables by T Test. P was considered significant at values <0.05. Results  The mean age was 74 years, 40% female, HBP 49%, dyslipidemia 52%, obesity 52%, type 2 DM 42%, smoking 28% and COPD 26%. 16% were de novo AHF and 84% with exacerbated CHF. Global RVF 6%. PH was present in 60%, being 24% mild, 25% moderate, 10% severe. The Left ventricular Ejection fraction (LVEF) mean was 52% (SD ± 15.1); Preserved 60%, Intermediate Range 18% and Reduced 22%. The IH mortality was 6.6% and the RH rate at 60 days was 21%. In the bivariate analysis for IH mortality, RVF was identified as an independent predictor of mortality (p = 0.001) nor for RH (p = 0.857). The different levels of PH were not identified as predictors of IH Mortality as well as RH. LVEF ranges did not show significant differences, nor in the forms of AHF presentation. The combined analysis of RVF or Left with different degrees of PHT did not show significant differences in IH mortality and RH.In the multivariate analysis by logistic regression for IH mortality, the presence of RVF maintained independence as a predictor variable (p = 0.004). Conclusion  In our population of patients with AHF, the presence of RVF is a predictor of IH mortality regardless of the presence of PH, the PH and LVEF ranges. The presence of RVF was not associated with a higher rate of RH at 60 days.

scholarly journals Delineating the molecular and histological events that govern right ventricular recovery using a novel mouse model of pulmonary artery de-banding

2019 ◽  
Vol 116 (10) ◽  
pp. 1700-1709 ◽  
Author(s):  
Mario Boehm ◽  
Xuefei Tian ◽  
Yuqiang Mao ◽  
Kenzo Ichimura ◽  
Melanie J Dufva ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mouse Model ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Exercise Capacity ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Sequence Of Events ◽  
Reverse Remodelling ◽  
Rv Function

Abstract Aims The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Methods and results Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)—after RV dysfunction and structural remodelling were established—initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. Conclusion We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.

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