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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

View larger version (120K): [in a new window]   Figure 1 The cardiac support device wrap placed around the heart. The polyester mesh material is sutured along an anterior wall seam to achieve containment around both the right and left ventricles. The material is snug to the surface to remove surface wrinkling, but not to constrict diastolic filling.

View larger version (23K): [in a new window]   Figure 2 Hemodynamic effects of the cardiac support device (CSD). (A) Left ventricular pressure–volume relations in one animal before and after long-term CSD use. The darker loops for each condition reflect basal conditions, and the thinner loops were measured during transient load reduction. There was a reduction in both end-diastolic and end-systolic chamber volumes, with preservation of cardiac stroke volume (loop width), and the end-systolic pressure–volume relation shifted leftward, consistent with reversal of chamber remodeling. The diastolic pressure–volume boundary was not altered. (B) Summary of hemodynamic variables before and after long-term CSD use. There was a consistent significant decline in chamber volumes (end-diastolic volume [EDV] and end-systolic volume [ESV]), without a change in cardiac output (CO). End-diastolic pressure (EDP) and end-systolic pressure (ESP) were not significantly changed. EF = ejection fraction.

View larger version (19K): [in a new window]   Figure 3 Effects of an early preload increase in the failing heart after cardiac support device (CSD) implantation. (A) Example of pressure–volume relations before and after infusion of 400 ml of dextran. (B) Summary of hemodyanmic variables in relation to incremental volume expansion. For a near 10 mm Hg rise in end-diastolic pressure (EDP), cardiac output (CO) rose by nearly 100%, and there were significant changes in both the maximal and minimal rates of pressure change. Thus, preload-dependent reserve function was not inhibited by CSD placement. dP/dtmx and dP/dtmn = rate of rise in left ventricular pressure, maximal and minimal, respectively. *p < 0.05 versus baseline, e.g. 0 volume expansion.

View larger version (31K): [in a new window]   Figure 4 Enhancement of the dobutamine (Dob) response with long-term cardiac support device (CSD) treatment. (A) Example of pressure–volume loops and relations during early dobutamine infusion stimulation at baseline and after long-term CSD treatment. The pre-dobutamine end-systolic pressure–volume relation (ESVPR) (control) is shown for baseline and CSD treatment. Before CSD placement, the dobutamine response was very small, with only a slight leftward shift in the ESPVR. However, the magnitude of the response to this same dose was greatly augmented by long-term CSD treatment. (B) Percent changes in systolic function in response to dobutamine, comparing baseline with CSD treatment. Substantial increases were observed in response to multiple ejection variables: CO = cardiac output; EF = ejection fraction; SV = stroke volume; SW = stroke work; power index = maximal power/end-diastolic volume (EDV)2. *p 0.001 and p < 0.02 compared with baseline response, by three-way analysis of variance of raw data.

View larger version (14K): [in a new window]   Figure 5 (A) Isoproterenol-stimulated adenylate cyclase activity in the failing myocardium, with or without cardiac support device (CSD) treatment. The CSD resulted in an enhanced dose response to isoproterenol. The p value is for the CSD effect on the dose response, by two-way analysis of variance. (B) Adenylyl cyclase activity with direct activation by forskolin revealed no difference between the groups, suggesting altered up-stream signaling as the major source for the disparity in part A. CHF = chronic heart failure.