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Heart Failure II: Pathophysiology01:29

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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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Left ventricular hypertrophy in ADPKD: changing demographics.

Ahsan Alam1, Ronald D Perrone

  • 1McGill University, Royal Victoria Hospital - McGill University Health Centre, 687Pine Avenue West, Montreal, Canada. H3A 1A1.

Current Hypertension Reviews
|August 27, 2013
PubMed
Summary

Left ventricular hypertrophy (LVH) prevalence in autosomal dominant polycystic kidney disease (ADPKD) patients has decreased due to better hypertension management and RAAS antagonist use. This shift impacts cardiovascular risk management in ADPKD.

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Published on: April 30, 2020

Area of Science:

  • Nephrology
  • Cardiology
  • Medical Imaging

Background:

  • Left ventricular hypertrophy (LVH) is a significant complication in autosomal dominant polycystic kidney disease (ADPKD), linked to arrhythmias, heart failure, and cardiac mortality.
  • Systemic hypertension, common in ADPKD, drives myocardial remodeling and LVH.
  • Previous echocardiography studies reported LVH prevalence from 20-40% in ADPKD patients.

Purpose of the Study:

  • To investigate the evolving prevalence and pathophysiology of LVH in ADPKD patients.
  • To understand the impact of modern hypertension management and RAAS antagonism on LVH in ADPKD.

Main Methods:

  • Review of observational studies and the HALT-PKD trial.
  • Comparison of LVH prevalence using echocardiography versus magnetic resonance imaging (MRI).
  • Analysis of factors influencing LVH trends, including hypertension control and RAAS inhibitor use.

Main Results:

  • Recent studies, like HALT-PKD using MRI, show significantly lower LVH prevalence (<4%) compared to older echocardiography data (20-40%).
  • Improved hypertension detection, control, and increased use of RAAS antagonists are key factors in this trend.
  • RAAS inhibitors demonstrate potential for LVH regression in ADPKD.

Conclusions:

  • The pathophysiology and prevalence of LVH in ADPKD appear to be shifting, likely due to advancements in cardiovascular risk management.
  • Earlier and more effective management of hypertension and the use of RAAS antagonists are crucial for reducing LVH and cardiovascular risk in ADPKD patients.
  • Ongoing research is vital to further elucidate these evolving relationships and optimize patient care.