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Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption

U E Heidland1, B E Strauer

  • 1Department of Cardiology, Pneumology, and Angiology, School of Internal Medicine, Heinrich-Heine-University, Düsseldorf, Germany. heidland@med.uni-duesseldorf.de

Circulation
|September 26, 2001
PubMed

Insights

Hemodynamic forces, increased left ventricular muscle mass, and higher heart rates are linked to plaque disruption in coronary atherosclerosis. Beta-blocker use was associated with a lower risk of plaque disruption.

Area of Science:

  • Cardiology
  • Cardiovascular Pathophysiology
  • Atherosclerosis Research

Background:

  • Plaque disruption is a key factor in acute coronary syndromes and atherosclerosis progression.
  • Limited information exists regarding factors contributing to plaque disruption.
  • This study investigates the role of hemodynamic forces in plaque disruption pathogenesis.

Purpose of the Study:

  • To analyze the contribution of hemodynamic forces to the pathogenesis of plaque disruption.
  • To identify factors associated with plaque disruption in patients with coronary stenosis.

Main Methods:

  • Retrospective analysis of 106 patients undergoing two coronary angiograms within six months.
  • Comparison of 53 patients with plaque disruption versus 53 controls with stable stenoses.
  • Analysis of central hemodynamics, echocardiographic measurements, and medication use.

Main Results:

  • Logistic regression identified increased left ventricular muscle mass (>270 g) and mean heart rate (>80 bpm) as positively associated with plaque disruption.
  • Use of beta-blockers showed a negative association with plaque disruption.
  • Plaque disruption was diagnosed via coronary angiography in stenosed arteries.

Conclusions:

  • Hemodynamic forces appear to play a significant role in the pathogenesis of plaque disruption.
  • Findings may aid in identifying high-risk patients for plaque disruption.
  • Pharmacological interventions targeting heart rate reduction (e.g., beta-blockers) and left ventricular hypertrophy may be beneficial.
Abstract

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