Objectives Activation of the neuroendocrine axis in congestive heart failure is of prognostic significance, and neurohumoral blocking therapy prolongs survival. The hypothesis that surgical reduction of left ventricular size and function decreases neuroendocrine activation is less established. We evaluated the neurohormonal response to left ventricular reconstruction surgery in ischemic cardiomyopathy. Methods Norepinephrine, plasma renin activity, and angiotensin II were measured in 10 patients before and 12 months after left ventricular reconstruction. In an additional 5 patients, brain natriuretric peptide was measured before and 3 months postoperatively. Three-dimensional cardiovascular imaging was used to assess ejection fraction and left ventricular end-diastolic volume index. Results Concurrent with improvements of New York Heart Association functional class (2.9 ± 0.5 preoperatively vs 2.0 ± 0.4 postoperatively, P < .001), ejection fraction (23.9% ± 6.6% vs 36.2% ± 6.2%, P < .01), and left ventricular end-diastolic volume index (140.8 ± 33.8 mL/m2 vs 90.6 ± 18.3 mL/m2, P < .01), considerable reductions were observed for median plasma profiles of norepinephrine (562.0 pg/mL vs 319.0 pg/mL, P < .05), plasma renin activity (5.75 μg/L/h vs 3.45 μg/L/h, P < .05), angiotensin II (41.0 ng/mL vs 23.0 ng/mL, P = .051), and brain natriuretric peptide (771.0 pg/mL vs 266.0 pg/mL, P < .05). The more plasma renin activity or angiotensin II decreased after left ventricular reconstruction, the higher was the increase in ejection fraction (R = -.745, P < .05 [plasma renin activity]; R = -.808, P < .05 [angiotensin II]). Conclusions Surgical improvements of ejection fraction and left ventricular end-diastolic volume index by left ventricular reconstruction were accompanied by improvement of both the neuroendocrine activity and the functional status in patients with congestive heart failure. Whether this favorable neurohormonal response is predictive of an improved survival requires further evaluation.
Bibliographical noteFunding Information:
Supported by the Department of Thoracic and Cardiovascular Surgery and the George M. and Linda H. Kaufman Center for Heart Failure at The Cleveland Clinic Foundation.