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Department of Medicine, University of California, San Francisco, and the San Francisco Veterans Affairs Medical Center, San Francisco, CA 94121
Department of Surgery, VAMC Surgery 112D, San Francisco Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121
(Email: mratcliffe{at}hotmail.com).
Chronic heart failure is characterized by a progressive left ventricular (LV) dilation and a reduction in contractility. The Acorn CorCap (Acorn Cardiovascular, St. Paul, MN) cardiac support device (CSD) was designed to prevent further LV dilation, and LV end-diastolic volume was reduced in both preclinical and clinical trials of the Acorn CSD [1–4]. Surprisingly, there was also evidence of increased systolic function. Specifically, the Acorn CSD in the canine model of serial intracoronary microsphere-induced cardiomyopathy was associated with a leftward shift of the end-systolic pressure volume relationship [3], and in clinical studies, systolic dimensions and volumes were reduced and LV ejection fraction was increased or unchanged [1, 2, 4]. Unfortunately, in the initial randomized clinical trial, a survival benefit with the Acorn CSD could not be demonstrated [2].
The report by Speziale and colleagues [5] in this issue of The Annals of Thoracic Surgery is illustrative. The authors report the results of a single-center prospective series of 39 patients with dilated cardiomyopathy treated with the Acorn CSD, alone or with cardiac resynchronization therapy (CRT). The primary outcomes were echocardiographic indicators of LV reverse remodeling and perceived health and quality of life. Sixteen patients received CRT. Operative mortality was 5.1%. Two patients died at a mean follow-up of 13.3 ± 2.5 months: 1 of refractory heart failure and the other of pancreatic cancer. All sections of the Short Form 36 questionnaire, except body pain, were improved.
Similar to previous studies, systolic function was improved. Specifically, Speziale and colleagues found that the Acorn CSD was associated with a reduction in LV end-diastolic and end-systolic volume (21% and 31%, respectively), and ejection fraction increased from 25% to 36%. At the cellular level, the Acorn CorCap CSD is associated with improved calcium cycling within the sarcoplasmic reticulum, downregulation of stretch response proteins, attenuation of cardiomyocyte hypertrophy, and restoration of α-myosin and β-myosin heavy chain isoform ratios [3]. However, it remains unclear whether the reduction in end-diastolic volume per se or the prevention of further dilation drives the improvement in systolic function. Further work along these lines is warranted.
This report of the effects of CRT in patients receiving the Acorn CSD shows that in this small subgroup, there was no difference in outcomes between those receiving CSD alone vs CSD plus CRT, suggesting that the effects of CSD and CRT are not cumulative. Further investigation into whether CRT may be synergistic with CSD in patients with significant baseline electromechanical dyssynchrony is needed.
Although intraoperative transesophageal echocardiography has been used in the studies of CSD to date to ensure a 10% or less reduction in LV end-diastolic diameter, reduced LV compliance with resultant diastolic dysfunction and possible constrictive physiology remain a concern. The authors report a limited number of echocardiographic variables to show no significant change in LV filling pressure (E/e') or compliance (mitral E/A ratio). Invasive hemodynamic and pressure-volume assessment in an earlier study of a small subset of patients after CSD showed no evidence of constriction or diastolic dysfunction [6]. However, further study in larger groups with thorough echocardiographic and possibly invasive hemodynamic assessment of LV diastolic function is needed to better address this issue.
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