Geometric and functional correlates of electrocardiographic repolarization and voltage abnormalities in aortic regurgitation Academic Article uri icon

Overview

MeSH Major

  • Aortic Valve Insufficiency
  • Electrocardiography

abstract

  • Although electrocardiographic left ventricular hypertrophy is a recognized marker of disease severity in patients with chronic aortic regurgitation, the quantitative relations of repolarization abnormalities and QRS voltage to measurements of cardiac structure and function have not been established. The presence or absence of the "strain" pattern of repolarization and QRS voltage was compared with echocardiographic and radionuclide cineangiographic findings in 95 adults with sever, pure, chronic aortic regurgitation and no evidence of coronary artery disease. In contrast to 54 patients with normal repolarization, 41 patients with an abnormal repolarization pattern had greater left ventricular end-diastolic and end-systolic dimensions (7.2 +/- 1.1 versus 6.6 +/- 0.8 cm, p less than 0.002 and 5.2 +/- 1.2 versus 4.4 +/- 0.7, p less than 0.001, respectively), greater left ventricular mass (431 +/- 138 versus 303 +/- 89 g, p less than 0.001), higher end-systolic stress (128 +/- 46 versus 95 +/- 27 dynes-cm2 X 10(3), p less than 0.001), lower fractional shortening (28 +/- 8 versus 34 +/- 5%, p less than 0.001) and lower exercise ejection fraction (39 +/- 11 versus 51 +/- 8%, p less than 0.001). Multiple logistic regression analysis revealed that left ventricular mass and end-systolic stress were independently related to the presence of repolarization abnormalities (p less than 0.005). Among the 73 asymptomatic patients, those with normal repolarization had significantly lower prevalences of fractional shortening less than 25% (1 of 45 versus 5 of 27, p less than 0.05), left ventricular systolic dimension greater than 5.5 cm (1 of 45 versus 8 of 27, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

publication date

  • April 24, 1987

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 3819197

Additional Document Info

start page

  • 500

end page

  • 8

volume

  • 9

number

  • 3