LEFT-VENTRICULAR FUNCTION AND CORONARY-ARTERY DISEASE PROGRESSION EARLY AFTER CORONARY-BYPASS GRAFTING

To investigate the effects of coronary artery disease progression on l eft ventricular function in patients who suffer angina early after cor onary artery bypass grafting, we studied the progression of coronary s tenoses, the occurrence of graft occlusions, and measured left ventric ular ejection fraction (regional and global) in 34 consecutive patient s who underwent repeat angiography 25.2 +/- 3.5 (standard error of the mean) months postoperatively, from a total population of 550 patients who underwent bypass grafting. Resting left ventricular function and stenosis severity were assessed using a computerized, quantitative ana lysis system. Coronary stenosis progression was defined as an increase in the percentage of the stenotic occlusion by 30% or more, any incre ase in lesion severity that resulted in total coronary artery occlusio n, or the occurrence of a new stenosis that occluded the artery by 50% or more. Group 1 comprised 21 patients with all grafts patent and gro up 2 comprised 13 patients with one or more grafts occluded (20 of 34 grafts). Coronary artery disease progressed in all patients in group 1 , and this involved 22 of 54 (41%) grafted vessels and 3 of 15 (20%) n ongrafted vessels (p < 0.05). Coronary artery disease progressed in 11 patients in group 2, involving 15 of 32 (47%) grafted vessels and 1 o f 6 (17%) nongrafted vessels (p < 0.01). An increased collateral circu lation was observed in both groups. The left ventricular ejection frac tion remained unchanged in both groups (group 1, 0.60 +/- 0.03 versus 0.62 +/- 0.03; group 5 0.62 +/- 0.05 versus 0.62 +/- 0.04 before and a fter bypass, respectively; p = not significant) and there was no diffe rence between the groups. We conclude from our findings that, in patie nts with angina that recurs within 5 years of the bypass procedure, le ft ventricular function is preserved despite coronary artery disease p rogression and graft occlusion. This is probably due to the developmen t of a collateral circulation, albeit insufficient to prevent exercise -induced myocardial ischemia.