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Protective Effect of Aortic Stenosis on the Coronary Arteries. Hypothetic Considerations to an Old Enigma

Paulo Roberto Barbosa Evora1, Livia Arcêncio1, Alfredo José Rodrigues1

  • 1Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, São Paulo, SP, Brazil.

Arquivos Brasileiros De Cardiologia
|May 5, 2016
PubMed

Insights

Aortic stenosis (AS) may protect against coronary artery disease (CAD) through a mechanism involving endothelium-myocardial crosstalk. This interaction, triggered by left ventricular overload, activates the cGMP/NO pathway, potentially explaining the lower CAD incidence observed in AS patients.

Area of Science:

  • Cardiology
  • Vascular Biology
  • Cardiac Physiology

Background:

  • Prevalence of significant coronary artery disease (CAD) in patients with aortic stenosis (AS) ranges from 20-60% based on angiographic studies.
  • Early research suggested AS might have a protective effect against CAD, a concept now being re-evaluated.
  • The traditional view of AS protection against CAD requires a more nuanced explanation beyond simple prevalence data.

Purpose of the Study:

  • To explore the potential protective mechanisms of aortic stenosis (AS) against coronary artery disease (CAD).
  • To investigate the role of endothelium-myocardial interaction in the context of AS and CAD.
  • To elucidate the signaling pathways involved in the observed lower incidence of CAD in AS patients.

Main Methods:

  • Literature review of angiographic studies on CAD prevalence in AS patients.
  • Analysis of historical necropsy data regarding CAD incidence in AS.
  • Review of physiological mechanisms linking cardiac overload to vascular protection.

Main Results:

  • Angiographic studies report a wide prevalence (20-60%) of significant CAD in AS patients.
  • Early studies indicated a lower-than-expected CAD incidence in AS, proposing a protective effect.
  • The protective effect is hypothesized to stem from endothelium-myocardial crosstalk triggered by left ventricular overload.

Conclusions:

  • The 'protective effect' of AS against CAD is better understood as a result of endothelium-myocardial crosstalk.
  • Left ventricular overload in AS activates the cGMP/NO pathway, contributing to reduced CAD incidence.
  • This pathway offers a plausible explanation for the observed low CAD rates and the favorable long-term progression of aortic stenosis.

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