title: Effect of coronary bypass grafting onto the site of old myocardial infarction and the recovery of cardiac function.
abstract: This study investigated whether or not revascularization to the site of old myocardial infarction can bring beneficial effects on postoperative cardiac function. Thirty-two patients without a history of old myocardial infarction and 71 with a history of old myocardial infarction were included. The mean number of grafts bypassed were 2.7 and 2.8, and the mean duration of aortic clamping was 99 min and 105 min in non-old myocardial infarction and old myocardial infarction patients, respectively. All the patients underwent simple coronary artery bypass grafting electively. The left ventricular stroke work index in non-old myocardial infarction and old myocardial infarction were 40.8 g-m/m2 and 38.9 g-m/m2 preoperatively, and this was recovered to 41.4 g-m/m2 and 38.7 g-m/m2, respectively, at 24 hours after reperfusion (NS). Subgroups of old myocardial infarctions had high ejection fractions of more than 50% (49) and low ejection fractions of less than 50% (22). The left ventricular stroke work index in high and low ejection fractions was 39.7 g-m/m2 and 36.7 g-m/m2 preoperatively (NS). Recovery rates in both high and low ejection fractions were reduced to 74.2% and 84.3% at 3 h after reperfusion (P < 0.001 and P < 0.05 versus preoperative value), but were increased in the low ejection fraction by up to 102.7% and 108.5% at 6 and 12 h after reperfusion, while still remaining reduced in the high ejection fraction at 88.8% and 88.2%, respectively (P < 0.01). At 24 h after reperfusion, left ventricular stroke work index in the low ejection fraction was improved to 44.3 g-m/m2 or 130% of the preoperative value, and the high ejection fraction was 37.5 g-m/m2 or 100% (NS). This showed that a chief cause of reduced cardiac function in the low ejection fraction was mainly reversible myocardial damage or hibernation. Preoperative mean left ventricular ejection fractions in non-old myocardial infarctions and old myocardial infarctions were 73.1% and 55.9%, and these returned to 73.7% (NS) and 61.8% (P < 0.001) at 1 month post-coronary artery bypass grafting. A similar trend towards a significant improvement was shown in both end-diastolic volume indices and end-systolic volume indices of patients with an old myocardial infarction (P < 0.001). Regional wall motion according to AHA classification in patients with old myocardial infarctions was estimated from biplane left ventriculogram as normal, reduced, none, dyskinetic and aneurysmal, and scored as 0, 1, 2, 3 and 4, respectively. Summated scores in old myocardial infarctions was improved from 5.2 to 4.1 after coronary artery bypass grafting (P < 0.05). There was a significant improvement of summated scores from 8.17 to 6.28 in the low ejection fraction (P < 0.05); however, this was not reflected in the high ejection fraction (3.76 to 3.0; NS). The regional wall motion in the old myocardial infarctions that were heart bypassed to the left anterior ascending artery (n = 67) or to the circumflex artery (n = 40) were significantly improved at regions 2 (P < 0.05), 3 (P < 0.05) and 7 (P < 0.05), and that bypassed to right coronary artery (n = 50) was also improved at regions 3 (P < 0.05), 5 (P < 0.05) and 7 (P < 0.001). This shows that augmentation of regional blood flow by coronary artery bypass grafting will contribute to awakening the hibernated myocardium even in the old myocardial infarction.
authors.affiliation: Cardiovascular Surgery, Cardiac Center, Iizuka Hospital, Fukuoka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Ando
authors.forename: J
authors.initials: J
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Hisahara
authors.forename: M
authors.initials: M
authors.lastname: Umesue
authors.forename: T
authors.initials: T
authors.lastname: Shirota
mesh_terms: D016022:Case-Control Studies; D001026:Coronary Artery Bypass / Q000379:methods; D003326:Coronary Circulation / Q000502:physiology; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000503:physiopathology / Q000601:surgery*; D017682:Myocardial Stunning / Q000503:physiopathology* / Q000601:surgery; D013318:Stroke Volume / Q000502:physiology