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Left ventricular function in chronic aortic regurgitation with reference to end-systolic pressure, volume and stress relations

  • Mary Osbakken
    Footnotes
    Affiliations
    From the Section of Cardiology, Department of Medicine, Temple University Medical School, Philadelphia, Pennsylvania USA
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  • Alfred A. Bove
    Correspondence
    Address for reprints: Alfred A. Bove, MD, PhD, Cardiology Section, Temple University Medical School, 3400 North Broad Street, Philadelphia, Pennsylvania 19140.
    Footnotes
    Affiliations
    From the Section of Cardiology, Department of Medicine, Temple University Medical School, Philadelphia, Pennsylvania USA
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  • James F. Spann
    Affiliations
    From the Section of Cardiology, Department of Medicine, Temple University Medical School, Philadelphia, Pennsylvania USA
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  • Author Footnotes
    ∗ Current address: Cardiology Section, Milton S. Hershey Medical Center, Hershey, Pennsylvania.
    † Work done during tenure as an Established investigator of the American Heart Association, Dallas, Texas.
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      Abstract

      Left ventricular muscle and pump performance were evaluated in 12 normal subjects and 21 patients with aortic regurgitation (10 with minimal symptoms and 11 with congestive heart failure). A computer-based quantitative analysis of biplane left ventriculograms was used. Both patient groups had significant aortic regurgitation documented by ventriculography. Contractile function measured by peak systolic stress/end-diastolic volume and end-systolic pressure/volume curves was poorer than that in normal subjects in patients with heart failure but not in asymptomatic patients. When normalized for muscle mass, stroke work was not depressed in either asymptomatic patients (mean ± standard error of the mean 0.008 ± 0.001 joules/g) or patients with heart failure (0.009 ± 0.004) by comparison with the value in normal subjects (0.010 ± 0.001).
      Angiographically determined cardiac index (CI) increased with increasing volume overload even though forward cardiac index measured by the Fick method remained essentially unchanged: normal subjects (total CI 3.7 ± 0.4 liters/min per m2, Fick CI 2.4 ± 0.1); asymptomatic patients (total CI 7.6 ± 0.7, Pick CI 2.3 ± 0.2); patients with heart failure (total CI 9.1 ± 0.82, Fick CI 2.1 ± 0.18). Left ventricular peak stress increased significantly in patients with heart failure (511 ± 55 dynes/cm2 × 10−3) compared with values in normal subjects (360 ± 33) and asymptomatic patients (428 ± 50).
      The combination of decreased muscle function and increased demands on pump function causes a significant increase in end-diastolic pressure only in patients with heart failure (23 ± 2 mm Hg), which results in pulmonary congestive symptoms.
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