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Heart Failure II: Pathophysiology01:29

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Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Updated: Aug 20, 2025

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Adaptive versus maladaptive right ventricular remodelling.

Zvonimir A Rako1, Nils Kremer1, Athiththan Yogeswaran1

  • 1Department of Internal Medicine, Justus Liebig University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Klinikstrasse 33, 35392, Giessen, Germany.

ESC Heart Failure
|November 24, 2022
PubMed
Summary
This summary is machine-generated.

Assessing right ventricular-pulmonary arterial (RV-PA) coupling is vital in pulmonary hypertension. Non-invasive echocardiographic methods offer alternatives to invasive measurements for evaluating RV-PA coupling and predicting outcomes.

Keywords:
Cardiac magnetic resonance imagingConductance catheterizationEchocardiographyPulmonary hypertensionRight ventricleVentriculoarterial coupling

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Area of Science:

  • Cardiology
  • Pulmonary Medicine
  • Biomedical Engineering

Background:

  • Right ventricular (RV) function and its adaptation to increased afterload (RV-pulmonary arterial [PA] coupling) are critical in pulmonary hypertension, influencing symptoms and prognosis.
  • Progressive afterload leads to RV remodeling for maintaining cardiac output, but eventual decompensation (RV-PA uncoupling) results in heart failure.

Purpose of the Study:

  • To review the mechanisms of RV adaptation and maladaptation to load in pulmonary hypertension.
  • To describe invasive and non-invasive methods for assessing RV-PA coupling.
  • To highlight recent advancements and limitations in non-invasive surrogate parameters for RV-PA coupling.

Main Methods:

  • Review of existing literature on RV-PA coupling in pulmonary hypertension.
  • Explanation of invasive assessment using RV pressure-volume loops (end-systolic elastance [Ees] / arterial elastance [Ea]).
  • Overview of non-invasive echocardiographic surrogates (e.g., TAPSE/PASP, S'/RV end-systolic area index) and their validation.

Main Results:

  • The gold standard for RV-PA coupling is the invasive Ees/Ea ratio, with optimal values between 1.5-2.0 and uncoupling below ~0.7.
  • Non-invasive echocardiographic surrogates like TAPSE/PASP have shown prognostic relevance.
  • Various other echocardiographic measures and PASP-independent surrogates exist, but limitations like tricuspid regurgitation and angle dependence persist.

Conclusions:

  • Non-invasive echocardiographic methods provide valuable, albeit imperfect, alternatives for assessing RV-PA coupling in pulmonary hypertension.
  • Accurate assessment may require combining multiple non-invasive techniques to capture different aspects of RV function.
  • Further large-scale prospective studies with gold-standard validation are necessary to refine and confirm the utility of these non-invasive surrogates.