Effect of Revascularization on Left Ventricular Remodeling in Patients With Heart Failure from Severe Chronic Ischemic Left Ventricular Dysfunction Roxy Senior, MD, Avijit Lahiri, MB, MRCP, and Sanjiv Kaul, MD Few data exist regarding the effect of revascularization on left ventricular (LV) geometry in patients with severe LV systolic dysfunction and viable myocardium. We hy- pothesized that patients with chronic ischemic LV dys- function but viable myocardium will have improved LV geometry after revascularization, which in turn will im- prove long-term outcome. Accordingly, 70 patients with severe ischemic LV dysfunction (LV ejection fraction <0.35) were studied at rest. They then either underwent revascularization (n 36) or were treated medically (n 34). Fifty-four patients had viable myocardium, and 16 did not. They were evaluated for change in LV function and geometry (size and shape) a mean of 21 months later. Further follow-up was performed for a mean of 3.5 years to determine outcome. Patients with viable myocardium had improvement not only in re- gional and global function, but also in LV geometry (shape and size), which was independent of and in- cremental to the improvement in function. On long- term follow-up, change in LV end-systolic volume was the only multivariate discriminator between 15 pa- tients who died and 55 who did not, irrespective of whether they had undergone revascularization. Thus, measurement of the effect of revascularization of vi- able myocardium in chronic ischemic heart disease should not only include improvement in resting re- gional and global LV function, but also LV geometry. Improvement in LV geometry contributes to better LV systolic function, which in turn is the best predictor of survival after revascularization. 2001 by Excerpta Medica, Inc. (Am J Cardiol 2001;88:624 – 629) T he beneficial effect of revascularization of dys- functional myocardium in chronic ischemic heart disease has traditionally been measured by its effect on improvement of resting regional and global left ventricular (LV) function. 1–4 It has been argued, how- ever, that because the endocardium is responsible for most of the wall thickening seen at rest, regional functional recovery may not occur after revasculariza- tion, even when most of the myocardium excluding the endocardium is viable. 5 In this situation, benefit from revascularization may be achieved by restoration of adequate flow to viable mid- and epimyocardium, which in turn will prevent infarct expansion and LV remodeling, and thus prevent heart failure and death. We recently reported the effect of revascularization of viable myocardium in a series of prospectively recruited patients with chronic ischemic heart disease whose main symptom was congestive heart failure. 6 We recorded a second echocardiogram in these pa- tients after revascularization to test the hypothesis that patients with viable myocardium will benefit from revascularization by favorably altering LV geometry as well as resting LV function. We further postulated that patients with improved LV function and geometry will have a better outcome than those whose LV function and geometry were unchanged or became worse. Although several studies have described the prognostic value of preoperative echocardiography for predicting survival after revascularization, 6–9 this is the first attempt to examine the value of both the pre- and postrevascularization echocardiogram for predict- ing long-term outcome. METHODS Study design: All patients underwent a baseline clinical assessment, rest echocardiography, low-dose dobutamine echocardiography, and coronary angiog- raphy. After these tests, the patients underwent either revascularization or were treated medically based on the physician’s preference. The results of the echocar- diogram were not divulged to the patient’s physician. At 21 8 months after the initial echocardiogram, a second echocardiogram was recorded to measure changes in the left ventricle caused by revasculariza- tion or the lack thereof. Patients were then followed for a mean of 3.5 1.8 years to determine outcome. Patient selection: This is a report of 70 patients from an original cohort of 87 consecutive patients who have been previously described. 6 These patients were se- From the Department of Cardiovascular Medicine, Northwick Park and St. Mark’s Hospitals and Institute of Medical Research, Harrow, United Kingdom; and the Cardiovascular Division, University of Vir- ginia, Charlottesville, Virginia. This study was supported in part by grants from Northwick Park Hospital Cardiac Research Fund, Harrow, United Kingdom; Dupont Pharmaceuticals, Wilmington, Delaware; and the Michael Tabor Grant, Harrow, United Kingdom. Dr. Kaul was supported by Grant HL-48890 from the National Institutes of Health, Bethesda, Maryland; an Established Investigator Award from the American Heart Association, Dallas, Texas; and a travel grant from Dupont Pharmaceuticals, Wilmington, Delaware. Manuscript received March 6, 2001; revised manuscript received and accepted May 4, 2001. Address for reprints: Roxy Senior, MD, Department of Cardiology, Northwick Park Hospital, Watford Road, Harrow, Middlesex HA1 3UJ, United Kingdom. E-mail: nphcardiology@netscapeonline.co.uk. 624 ©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matter The American Journal of Cardiology Vol. 88 September 15, 2001 PII S0002-9149(01)01803-3