EXPERIMENTAL STUDY
Reverse remodeling and enhancedadrenergic reserve from passive externalsupport in experimental dilated heart failure
W. Federico Saavedra, MD*,
Richard S. Tunin, MS*,
Nazareno Paolocci, MD, PhD*,
Takayuki Mishima, MD ,
George Suzuki, MD,
Charles W. Emala, MD ,
Pervaiz A. Chaudhry, MD,
Petros Anagnostopoulos, MD,
Ramesh C. Gupta, PhD,
Hani N. Sabbah, PhD, FACC and
David A. Kass, MD, FAHA*,*
* Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
Division of Cardiovascular Medicine, Henry Ford Health System, Detroit, Michigan, USA
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
Manuscript received November 2, 2001;
revised manuscript received March 5, 2002,
accepted March 27, 2002.
* Reprint requests and correspondence: Dr. David A. Kass, Halsted 500, Johns Hopkins Medical Institutions, 600 N. Wolfe Street, Baltimore, Maryland 21287, USA.
dkass{at}bme.jhu.edu
OBJECTIVES: We sought to test the efficacy of a passive elastic containment device to reverse chronic chamber remodeling and adrenergic down-regulation in the failing heart, yet still maintaining preload reserve.
BACKGROUND: Progressive cardiac remodeling due to heart failure is thought to exacerbate underlying myocardial dysfunction. In a pressure–volume analysis, we tested the impact of limiting progressive cardiac dilation by an externally applied passive containment device on both basal and adrenergic-stimulated function in failing canine hearts.
METHODS: Ischemic dilated cardiomyopathy was induced by repeated intracoronary microembolizations in six dogs. The animals were studied before and three to six months after surgical implantation of a thin polyester mesh (cardiac support device [CSD]) that surrounded both cardiac ventricles. Pressure–volume relations were measured by a conductance micromanometer catheter.
RESULTS: Long-term use of the CSD lowered end-diastolic and end-systolic volumes by –19 ± 4% and –22 ± 8%, respectively (both p < 0.0001) and shifted the end-systolic pressure–volume relation to the left (p < 0.01), compatible with reverse remodeling. End-diastolic pressure and chamber diastolic stiffness did not significantly change. The systolic response to dobutamine markedly improved after CSD implantation (55 ± 8% rise in ejection fraction after CSD vs. –10 ± 8% before CSD, p < 0.05), in conjunction with a heightened adenylyl cyclase response to isoproterenol. There was no change in the density or affinity of beta-adrenergic receptors. Diastolic compliance was not adversely affected, and preload-recruitable function was preserved with the CSD, consistent with a lack of constriction.
CONCLUSIONS: Reverse remodeling with reduced systolic wall stress and improved adrenergic signaling can be achieved by passive external support that does not generate diastolic constriction. This approach may prove useful in the treatment of chronic heart failure.
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Abbreviations and Acronyms
| | ATP | | adenosine triphosphate | | cAMP | | cyclic adenosine monophosphate | | CSD | | cardiac support device | | DHA | | 3H-dihydroalprenelol | | ESPVR | | end-systolic pressure–volume relation | | LV | | left ventricle | | LVAD | | left ventricular assist device | | PMSF | | phenylmethylsulfonyl fluoride | | RV | | right ventricle | | SDS | | sodium dodecyl sulfate |
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