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J Am Coll Cardiol, 2001; 37:195-200
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY: HEART TRANSPLANT

Heart failure etiology affects peripheral vascular endothelial function after cardiac transplantation

Ayan R. Patel, MD*, Jeffrey T. Kuvin, MD*, Natesa G. Pandian, MD, FACC*, John J. Smith, MD, PhD, FACC* {dagger}, James E. Udelson, MD, FACC* {dagger}, Michael E. Mendelsohn, MD, FACC{dagger}, Marvin A. Konstam, MD, FACC* {dagger} and Richard H. Karas, MD, PhD, FACC{dagger}

* Cardiovascular Imaging and Hemodynamic Laboratory, New England Medical Center Hospitals Inc., Tufts University School of Medicine, Boston, Massachusetts, USA
{dagger} Molecular Cardiology Research Institute, Division of Cardiology, Department of Medicine, New England Medical Center Hospitals Inc., Tufts University School of Medicine, Boston, Massachusetts, USA

Manuscript received March 17, 2000; revised manuscript received July 21, 2000, accepted September 13, 2000.

Reprint requests and correspondence: Dr. Richard H. Karas, Molecular Cardiology Research Institute, New England Medical Center, 750 Washington Street, Box 80, Boston, Massachusetts 02111
rkaras{at}lifespan.org

OBJECTIVES

The goal of this study was to examine the effect of heart failure etiology on peripheral vascular endothelial function in cardiac transplant recipients.

BACKGROUND

Peripheral vascular endothelial dysfunction occurs in patients with heart failure of either ischemic or nonischemic etiology. The effect of heart failure etiology on peripheral endothelial function after cardiac transplantation is unknown.

METHODS

Using brachial artery ultrasound, endothelium-dependent, flow-mediated dilation (FMD) was assessed in patients with heart failure with either nonischemic cardiomyopathy (n = 10) or ischemic cardiomyopathy (n = 7), cardiac transplant recipients with prior nonischemic cardiomyopathy (n = 10) or prior ischemic cardiomyopathy (n = 10) and normal controls (n = 10).

RESULTS

Patients with heart failure with either ischemic cardiomyopathy or nonischemic cardiomyopathy had impaired FMD (3.6 ± 1.0% and 5.1 ± 1.2%, respectively, p = NS) compared with normal subjects (13.9 ± 1.3%, p < 0.01 compared with either heart failure group). In transplant recipients with antecedent nonischemic cardiomyopathy, FMD was markedly higher than that of heart failure patients with nonischemic cardiomyopathy (13.0 ± 2.4%, p < 0.001) and similar to that of normal subjects (p = NS). However, FMD remained impaired in transplant recipients with prior ischemic cardiomyopathy (5.5 ± 1.5%, p = 0.001 compared with normal, p = 0.002 vs. transplant recipients with previous nonischemic cardiomyopathy).

CONCLUSIONS

Peripheral vascular endothelial function is normal in cardiac transplant recipients with antecedent nonischemic cardiomyopathy, but remains impaired in those with prior ischemic cardiomyopathy. In contrast, endothelial function is uniformly abnormal for patients with heart failure, regardless of etiology. These findings indicate that cardiac transplantation corrects peripheral endothelial function for patients without ischemic heart disease, but not in those with prior atherosclerotic coronary disease.

Abbreviations and Acronyms
  ACE = angiotensin-converting enzyme
  FMD = flow-mediated dilatation
  LVEF = left ventricular ejection fraction
  NYHA = New York Heart Association




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