Search

Prediction of late clinical events was studied in a series of 145 patients who had control angiographic studies at one year and between two and 14 years after saphenous vein coronary artery bypass graft surgery. During a mean observation interval of 7.4 years, new narrowing or occlusion occurred in grafts of 59% of the patients and progression in non-bypassed arteries was observed in 66%. One or several of the following events were observed in 56% of the patients: recurrent or worse effort angina, unstable angina, myocardial infarction and heart failure. Unstable angina during follow-up was more frequent in young patients and in those who had this clinical presentation before surgery. The incidence of myocardial infarction was likewise greater in patients who had preoperative unstable angina and in those with four to five risk factors for coronary artery disease, as well as those having a lesser number of inserted grafts. Heart failure was predicted independently by either four to five risk factors, a low left ventricular contraction score or fewer grafts placed at surgery. The number of inserted grafts correlated inversely with any one of the late clinical events.

Diazepam (0.1 mg. per kilogram) was given intravenously to 12 patients with hemodynamic left ventricular failure at the time of cardiac catheterization. Anxiety was effectively relieved in 10 patients. Systemic and coronary hemodynamic parameters were assessed before and 5 and 15 minutes after diazepam. Heart rate, cardiac index, and left ventricular stroke-work index did not change significantly. Mean aortic pressure decreased in all patients (average of 10 mm. Hg) and left ventricular end-diastolic pressure (LVEDP) decreased from a mean +/- S.E.M. of 24.3 +/- 3 mm. Hg at rest to 16 +/- 2.1 at 5 minutes (p less than 0.001) and 15.8 +/- 2.1 at 5 minutes (p less than 0.002). Left ventricular angiography performed 30 minutes after diazepam did not increase LVEDP above the pre-diazepam control value. Systolic ejection period and tension-time index also decreased significantly after diazepam. Coronary hemodynamics and myocardial metabolism were unaltered by diazepam. The fall in LVEDP induced by diazepam is probably secondary to a decrease in arterial pressure (afterload) possibly associated with a decrease in venous return (preload). Our data therefore suggest that diazepam exerts a beneficial action on depressed left ventricular function and, thus, may be a sedative agent of choice in patients with myocardial infarction and heart failure.

In 72% of 143 patients undergoing a second coronary bypass grafting, mural or occlusive late thrombosis was observed histologically in 69% of 173 resected grafts. Late thrombosis was particularly prevalent in atherosclerotic grafts (80.2% vs. 40.4% in nonatherosclerotic grafts) and was always noted in 16 grafts with aneurysmal dilation. Multivariate analysis of risk factors contributing to late thrombosis indicated that graft atherosclerosis and smoking after graft surgery played important roles. Univariate analysis also showed significantly higher ratios of serum total cholesterol/HDL cholesterol and of serum LDL cholesterol/HDL cholesterol in patients whose grafts were affected by late thrombosis. To prevent late thrombosis of saphenous vein aortocoronary grafts, it appears reasonable that decreasing the ratios of total cholesterol/HDL cholesterol and of LDL cholesterol/HDL cholesterol, refraining from smoking, and controlling other risk factors for atherosclerosis should be advised.

Improvement of effort angina following pure aortocoronary bypass graft surgery was related to postoperative control angiographic studies of grafts and coronary arteries in 75 unselected patients. Clinical and angiographic evaluations were carried out at approximately 1 year and at 5 to 7 years after surgery. At 1 year, 61 (81.3%) were improved (52 without angina and 9 with partial improvement by at least two functional classes), whereas 14 were unimproved (18.7%). At approximately 6 years, loss of improvement (reappearance of angina or aggravation by at least two functional classes) was observed in 22 of the 61 improved patients, representing an attrition of 36.1% over a 5-year period. Graft occlusion or a narrowing of over 50% was observed in two of the 39 patients in whom improvement had continued (5.1%), whereas it was found in six of the 22 patients (27.3%) whose results deteriorated (p less than 0.05). Similarly, progression to occlusion of a preexisting stenosis of over 50% or appearance of a new stenosis of over 50% in a major coronary artery (distal to a graft or in an unbypassed artery) was observed in five of the 39 patients with continued improvement (12.8%) and in 11 of the 22 patients whose condition deteriorated (p less than 0.01). Changes in a graft or in a coronary artery were noted in 63.6% (14/22) of the patients with loss of improvement as compared to only 18% (7/39) of the patients whose improvement did not deteriorate. Improvement of angina was also evaluated in all survivors among our first 500 cases who had preoperative effort angina and pure bypass surgery with or without angiographic studies. Of these 260 patients, 70.4% were angina-free or improved by two to three functional classes at 1 year, and only 41.9% at 7 years after surgery. It is concluded that the effect of aortocoronary bypass graft surgery is transient in a high proportion of patients and that deterioration of results is related to late graft modifications and progression of atherosclerosis, particularly in ungrafted coronary arteries.