(Circulation. 2001;103:1844.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Decreased Expression of Tumor Necrosis Factor-
and Regression of Hypertrophy After Nonsurgical Septal Reduction Therapy for Patients With Hypertrophic Obstructive Cardiomyopathy
From the Sections of Cardiology and Cardiovascular Sciences, the Winters Center for Heart Failure Research, the Gene and Judy Campbell Laboratories for Cardiac Transplant Research and the DeBakey Heart Center from the Methodist Hospital, and Baylor College of Medicine, Houston, Tex.
Correspondence to Guillermo Torre-Amione, MD, PhD, Baylor College of Medicine, 6550 Fannin, Suite 1901, Houston, TX 77030. E-mail gtorre{at}bcm.tmc.edu
Background—Nonsurgical
septal reduction therapy (NSRT) is a novel therapeutic strategy for
patients with hypertrophic obstructive
cardiomyopathy (HOCM). Although the clinical
benefits of this technique appear to be clear, the structural and
functional changes that lead to improvements in cardiac function are
not completely defined. In these studies, we sought to define the
effect of NSRT on myocardial function as well as various markers of
hypertrophy including the expression of tumor necrosis
factor (TNF)-
, a cytokine capable of producing fibrosis,
left ventricular hypertrophy (LVH), and
cardiomyopathy.
Methods and Results—We
performed endomyocardial biopsies of the RV side of
the septum and echocardiograms on 15 HOCM patients at baseline and
after successful NSRT. Comparative analysis on paired
myocardial samples were performed to determine the effects of NSRT on
LVH, end-diastolic volume and chamber stiffness, myocyte
size, collagen content, and TNF- levels. At baseline, myocardial
TNF- levels were increased in all patients. After NSRT, myocyte
size, collagen content, and TNF- were significantly decreased. These
changes were accompanied by an increase in left ventricular
volumes and a reduction in LVH and chamber
stiffness.
Conclusions—We suggest
that pressure overload in HOCM patients contributes to the development
of hypertrophy. These data provide the initial experimental
evidence to suggest that TNF- may play a pathogenetic role in the
hypertrophy of pressure
overload.
Key Words: surgery • hypertrophy • cardiomyopathy
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