ABSTRACTS

INFLUENCE ON LATE SURVIVAL OF GRAFT STATUS AND DEGREE OF CORRECTION FOLLOWING AORTOCORONARY BYPASS GRAFT SURGERY Jacques Hermann, MD; Frederic0 Corbara, MD; Jacques Lespkance, MD; Martial G. Bourassa, MD, FACC; Lucien Campeau, MD, FACC, Montreal Heart Institute, Montreal, Quebec, Canada

In 807 patients (pts) having pure aortocoronary bypass graft surgery among our first 1000 pts, the 6 year late survival (excluding deaths within the first month) was not influenced by the degree of correction. It was sus- pected that this might be explained by the high graft at- trition of 25% during the first year. Survival was there- fore determined after the first year in 65 pts in whom correction was still optimal as determined by angiographic studies obtained 1 year after surgery (all coronary ar- teries with stenosis >,70% successfully bypassed), and in 267 pts with incomplete correction at angiography (N156) or at the time of surgery (Nlll). The 6 year late survival (6 yr LS) was 98.4+3.2% for the pts with optimal correc- tion as compared to 83.2+6.4% for pts with incomplete cor- rection (pcO.025). The 6 yr LS (after the first yeas) was 94.1C4.6% in 113 pts in whom all grafts were patent, as compared to 70.4?16.8% in 38 pts whose grafts were all oc- cluded (p<O.Ol). 40 pts with at least 1 graft patent and 1 occluded had a 6 yr LS of 87.2+12.0%.

In conclusion, late survival is greatly influenced by the degree of correction and graft status 1 year after surgery.

LONG-TERM BENEFITS OF MYOCARDIAL RBVASCULARIZATION 04R) Denis H. Tyras, MD; Hendrick 8. Barner, MD, FACC; George C. Kaiser, MD, FACC; John E. Codd, MD; Hillel Laks, MD, FACC; Vallee L. Willman, MD, FACC. Saint Louis University, St. Louis, MO.

From January, 1970 through June, 1977, 1541 patients received isolated coronary artery bypass grafts. Operative mortality was 2.6%. Actuarial five-year sur- vival was 92.8%. Cumulative graft patency rates were 92.3% at one month, 85.8% at one year, 82.4% at three years and 70.5% at five years. Survival rate for single vessel disease was 97.7%. In multivessel dis- ease, survival increased with the number of grafts used: single (90.6X), double (91.7X), triple or more (92.9%). Late myocardial infarction occurred in 3.3% of patients. Not only does MR appear to be of long- term benefit in relief of angina, but also it appears to offer favorable results in longevity and low inci- dence of late myocardial infarction.

MONDAY, MARCH 6, 1978 PM

ANGINA PECTORIS: CLASSICAL AND VARIANT

3:30 to 5:30

DECREASE IN MYOCARDIAL OXYGEN SUPPLY AS A MECHANISM IN RESTING AND NOCTURNAL ANGINA WITH ST DEPRESSION: HEMODYNAMIC EVIDENCE Jaime Figueras, MD; William Ganz, MD, FACC; Bramah N. Singh, MD, FACC; Yzhar Charuzi, MD; H.J.C. Swan, MD, FACC, Cedars-Sinai Medical Center, Los Angeles, California

The mechanism of resting or nocturnal angina (AR) with ST depression (ST+) is uncertain relative to a primary change in myocardial oxygen (MOz) supply or demand. The temporal sequence of changes in systemic (BP) and pulmonary artery (PAP) pressures and lead V5 of the ECG, continuously re- corded on tape for 11-43 hrs in 18 patients (pts) with history of AR and exertional angina, was therefore anal- yzed. Cardiac index (CI) was measured by Swan-Ganz ther- modilution catheter every 2 hrs and at onset and at relief of AR. In 7 pts with >75% obstruction in 2-3 major coron- ary vessels and chest pain acceptable and treated as isch- emit, there were no ECG or hemodynamic changes during pain. The nature of pain in these pts remains uncertain; it may be nonischemic in origin. Its response to nitro- glycerin was poor, delayed and variable. In contrast, in each of the remaining 11 pts, AR was preceded by ST+ and by marked increases in systolic PAP (25+1.1 vs 48+4.0 mmHg; p<O.OOl) and diastolic PAP (llkD.8 vs 27+1.7 mmHg, P<O.OOl). Stroke index was decreased at onset of pain (32.1~2.5 vs 27.7k1.9 ml/beat/m2, p0.001). In 7 of these pts BP increased significantly coincident with the ECG changes. In 4 pts who had the highest systemic vascular resistance (SVR), BP fell or did not change; 3 of these 4 pts had the lowest CI. Heart rate (HR) did not change significantly. Pain was relieved promptly in all cases by nitroglycerin, Since the HRxBP product (index of MO2 de- mand) did not increase prior to the onset of ischemia, the -- data suggest that these cases of AR are due to a primary decrease in MO2 supply.

HYPOXIC CORONARY CONTRACTION MEDIATED BY BETA2 ADRENERGIC RECEPTORS Philip D. Henry, MD, FACC; Mitsuhiro Yokoyama, MD; Steven Fisher, Washington University, St. Louis, Missouri

Hypoxia has been shown to produce in isolated canine cor- onary arteries transient relaxation and subsequent sus- tained contracture. To define the mechanism underlying contracture, helical coronary arterial strips (n = 61) mounted isometrically for tension recording were equili- brated in deoxygenated Krebs buffer for 5 min and exposed to cumulative concentrations of adrenergic antagonists or agonists. The a-blockers phenoxybenzamine (5 arteries), phentolamine, and prazosin (10 arteries each) did not attenuate contracture in concentrations up to lo-' M. The a-agonists phenylephrine and methoxamine up to 5~10~~ M did not enhance contracture. In contrast, L-propranolol, a nonselective B-blocker, and butoxamine, a vasoselective (B2) blocker, evoked dose-dependent relaxations and, at a concentration of 10m6 M, completely suppressed the con- tractures (15 arteries). Isoproterenol, a nonselective B-agonist, and soterenol and salbutamol, !&-selective agonists, augmented contracture in a dose-dependent man- ner between lo-' and 10m6 M, the highest doses produc- ing at least threefold increases in tone (20 arteries). The cardioselective (B1) blockers practolol, metoprolol, and paraoxprenolol failed to reduce contracture in con- centrations up to lOa M (11 arteries). Thus, coronary arteries possess Bz-receptors which mediate hypoxic con- tracture. Results help to explain why propranol, but not practolol, increases perfusion in acutely ischemic canine myocardium.

February 1975 The Amorlcan Journal ol CARLMOLOOY Volume 41 357