Does CABG improve left ventricular ejection fraction in patients with ischemic cardiomyopathy, and does it matter?

The study of Bax et al. (1) that is reported in this issue of The Journal of Nuclear Medicineaddresses an important clinical issue. Specifically, in the setting of left ventricular failure with markedly reduced ejection fraction (mean6 SD, 30 6 6 in this study), selection of patients with ischemic heart disease who will benefit from coronary revascularization often is problematic. The authors correctly note that coronary artery bypass grafting (CABG) carries increased risk in this patient group. In the Coronary Artery Surgery Study registry, for instance, surgical mortality was as much as threefold greater and 5 y survival was one third less for patients with reduced left ventricular ejection fraction (LVEF) than for patients with normal LVEF (2). However, in a more recent series, operative mortality was only 3.8% and actuarial survival was 94%, 82%, and 68% at 1, 2, and 5 y, respectively, after surgery in 79 consecutive patients with a mean LVEF of 18% 6 5% (3). Nevertheless, physicians are understandably reluctant to recommend surgery for these patients if the prospects for benefit are limited. The search for myocardial viability typically commences at this juncture. If substantial viable myocardium is present, the benefits logically outweigh the risks of CABG and are widely believed to do so. However, more precise framing of the question of benefit, and consideration of mortality versus symptomatic status, are important. Indeed, several authors have suggested that recruitable contractile reserve is an important determinant of improvement after CABG in ischemic heart disease patients who undergo surgery primarily for heart failure (4). Patients without such reserve are less likely to benefit symptomatically from CABG, whereas those with reserve are. Further, studies have shown that ischemic heart disease patients with a low LVEF who undergo surgery primarily for angina are more likely to obtain symptomatic benefit than are those who undergo surgery primarily for heart failure (3,5). Mortality data, however, generally focus on all comers with ischemic heart disease and low LVEF and typically show benefit relative to historic control subjects who are medically treated (3,5). Mickleborough et al. (3) reported no difference in longterm survival between patients who underwent surgery primarily for angina and patients who underwent surgery primarily for heart failure. A prospective, randomized clinical trial with endpoints of mortality and symptoms in this patient group, however, has not been performed and clearly is required to address these issues more definitively. In the absence of such a trial, the study of Bax et al. (1) and related investigations (6–12) represent efforts at fine tuning the selection process to identify those patients most likely to benefit from CABG. Two approaches have been used. One relies on preoperative evaluation of contractile function, typically with dobutamine echocardiography (9,13), although radionuclide ventriculography would work equally well (14) and possibly better, especially in patients with difficult acoustic windows. The other approach, used by numerous investigators (8,10,11,15–18) including Bax et al. (1), involves a combination of myocardial perfusion imaging and assessment of some cellular metabolic function, be that retention of thallium, sestamibi, or18F-FDG. Bax et al. focus on myocardial perfusion–glucose metabolism mismatching as the criterion for viability and conclude that if at least 30% of the left ventricular myocardium remains viable, CABG will improve the LVEF and functional class of the patient. Bax et al. present no data on mortality. Although their conclusions have intuitive appeal and are in accord with the results of some (8,11) but not all (14,19) prior studies, it is worth considering why matters may be more complex than they appear at first glance. First, a point or two is to made concerning data analysis in this study. Figure 2 of Bax et al. (1) and an associated multiple regression analysis provide the basis for their conclusion. Their figure, however, shows the expected amount of scatter and an r2 of 0.62, meaning that only approximately 60% of the change in LVEF after CABG is explained by the number of viable dysfunctional segments present preoperatively. Moreover, as is well known, correlation cannot establish causation; thus, neither the simple nor the multiple regression analysis should be construed as proving a causal relationship between increased LVEF and the number of preoperatively viable segments. As shown in Figure 2 of Bax et al., many instances of three or fewer viable segments were associated with a decline in LVEF after CABG. There is Received Jul. 10, 2000; revision accepted Jul. 27, 2000. For correspondence or reprints contact: Henry Gewirtz, MD, Cardiac Unit/Vincent Burnham 3, Massachusetts General Hospital, Boston, MA 02114.