Bilateral mammary grafting. Clinical, functional and angiographic assessment in 400 consecutive patients.

Between October 1985 and September 1991, 400 patients benefited from bilateral internal mammary artery (BIMA) grafting. Of these, 354 (88.5%) were male and the average age was 57.4 years. There were 132 (33%) urgent procedures, 55 in diabetic patients (14%) and 15 in end-stage renal failures (4%). An average of 3.9 distal anastomoses (AN) per patient was undertaken, 2.8 using arterial grafts. Two hundred sixty-nine patients (67.2%) received exclusively arterial grafts. Right internal mammary artery (RIMA) grafts were predominantly directed to the left coronary system (348 AN = 78%) and particularly to the circumflex (CX) area. Postoperative myocardial infarction was diagnosed in 16 patients (4%). Reoperation was required for early myocardial ischemia in 12 patients (3%) and for excessive bleeding in 23 patients (5.8%). Sternal complications occurred in 18 patients (4.1%), 5 in diabetic patients (9%) and 3 in renal patients (20%). The hospital mortality was 2% (8 patients, 3 cardiac causes). Follow-up averages 37.7 months. Late mortality was 3% (12 patients, 4 cardiac causes). Angina recurred in 12 patients (3.1%). The maximal stress test at a mean interval of 9 months was abnormal in 7.4% (21 patients). One hundred eighty-one patients (47%) consented to an angiographic restudy at an average of 13 months postoperatively. Pedicled RIMA patency rates equal those of pedicled LIMA (95.1 vs 96.7, NS) and the grafted vessel does not alter the patency rates of IMA AN. A pedicled IMA graft is preferable to a free IMA graft (96.1 vs 79.6, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial revascularization in patients on renal replacement therapy.

Coronary disease is the main cause of mortality and morbidity among long-term survivors on renal replacement therapy (RRT). Despite the additional risk factors, myocardial revascularization has been recently attempted with various success in some patients on RRT. We report on 26 patients (13 dialyzed and 13 transplanted, mean age: 50 years [range 38-66]) who have undergone either surgical aorto-coronary bypass (CABG) (n = 16) with mammary artery grafts, or percutaneous coronary angioplasty (PTCA) (n = 9), or both procedures (n = 2). Indication was angina pectoris in all but three patients with painless ischemia. Eight patients had unstable angina (NYHA class IV). A previous myocardial infarction was documented in 11 cases. Coronary angiography disclosed mainly multiple vessel disease (81%). Post CABG complications consisted of severe intrathoracic bleeding (n = 3) resulting in death in 2 cases. PTCA entailed no major complication. After the critical postoperative period, the long-term survival was the same as that of non-uremic patients and the clinical improvement, according to the NYHA classification, was highly satisfactory at 6 months and persists up to 2 years. We conclude that coronary angiography and myocardial revascularization should be considered in patients on long-term RRT developing coronary disease.

Increased platelet aggregability and prostacyclin biosynthesis induced by intense physical exercise.

Changes in platelet aggregability during maximal bicycle ergometry were studied in healthy untrained subjects. Ex vivo platelet aggregation in response to ADP and collagen was measured in whole blood by impedance aggregometry or by direct electronic counting in an Ultra-Flo 100 platelet counter. This last method revealed that the platelet aggregation induced by low concentration of ADP (0.5 - 1.0 microM) was significantly enhanced during exercise. The plasma level of beta-thromboglobulin and the urinary excretion of 2,3--dinor-6-keto prostaglandin F1 alpha were also increased. These data indicate that an intense physical exercise enhances the aggregability of human platelets and induces a compensatory increase in prostacyclin biosynthesis.

Effects of inhibition of fatty acid oxidation on myocardial kinetics of 11C-labeled palmitate.

The effects of glucose and lactate infusion on palmitate oxidation were compared with the effect of 2-tetradecylglycidic acid (TDGA), an irreversible inhibitor of the carnitine acyltransferase I, in normoxic canine myocardium. The initial capillary transit retention fraction of [1-11C]palmitate and its fractional distribution between oxidation and esterification in myocardium were measured by the residue detection method after intracoronary tracer injection, as well as by effluent measurements of 11CO2, the end product of palmitate oxidation. TDGA reduced the initial capillary transit retention fraction (from 56 +/- 13% to 37 +/- 6%; p less than 0.001) and oxidation of palmitate (n = 19), as also evidenced by the decrease in the fraction of tracer released as 11CO2 from 28 +/- 5% to 6 +/- 3% (p less than 0.001). Infusion of carbohydrate (glucose or lactate; n = 6) reduced 11CO2 production from 30 +/- 7% to 7 +/- 4% (p less than 0.05) but did not alter the initial capillary transit retention fraction of tracer (59 +/- 5% vs. 56 +/- 10%; NS). The latter was due to increased esterification into neutral lipids (41 +/- 11% of injected palmitate after carbohydrate infusion versus 21 +/- 12% in control conditions), as measured from multiexponential curve fittings. When carbohydrates were given after inhibition of palmitate oxidation by TDGA (n = 7), the 11C tissue clearance kinetics were strikingly similar to those observed after carbohydrate infusion alone. Thus, enhanced metabolic trapping of [1-11C]palmitate in myocardium resulted in initial capillary transit retention fractions that were not different from control conditions (41 +/- 5% vs. 48 +/- 12%; NS) despite inhibition of oxidation. The results show that the intracellular metabolism of palmitate contributes to the control of its uptake by myocardium. The findings are consistent with inhibition of palmitate oxidation by carbohydrates occurring at the same site as TDGA.

Sustained nonoxidative glucose utilization and depletion of glycogen in reperfused canine myocardium.

Ischemically injured reperfused myocardium is characterized by increased 18F-fluorodeoxyglucose uptake as demonstrated by positron emission tomography. To elucidate the metabolic fate of exogenous glucose entering reperfused myocardium, D-[6-14C] glucose and L-[U-13C] lactate were used to determine glucose uptake, glucose oxidation and the contribution of exogenous glucose to lactate production. The pathologic model under investigation consisted of a 3 h balloon occlusion of the left anterior descending coronary artery followed by 24 h of reperfusion in canine myocardium. The extent and severity of myocardial injury after the ischemia and reperfusion were assessed by histochemical evaluation (triphenyltetrazolium chloride and periodic acid-Schiff stains). Thirteen intervention and four control dogs were studied. The glucose uptake in the occluded/reperfused area was significantly enhanced compared with that in control dogs (0.40 +/- 0.14 versus 0.15 +/- 0.10 mumol/ml, respectively). In addition, a significantly greater portion of the glucose extracted immediately entered glycolysis in the intervention group (75%) than in the control dogs (33%). The activity of the nonoxidative glycolytic pathway was markedly increased in the ischemically injured reperfused area, as evidenced by the four times greater lactate release in this area compared with the control value. The dual carbon-labeled isotopes showed that 57% of the exogenous glucose entering glycolysis was being converted to lactate. Exogenous glucose contributed to greater than 90% of the observed lactate production. This finding was confirmed by the histochemical finding of sustained glycogen depletion in the occlusion/reperfusion area. The average area of glycogen depletion (37%) significantly exceeded the average area of necrosis (17%). These data demonstrate enhanced and sustained activity of the nonoxidative glycolytic pathway after a prolonged occlusion with reperfusion in canine myocardium. Because glycogen stores remain depleted, exogenous glucose becomes an important myocardial substrate under these pathologic conditions.

Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty.

The effects of balloon inflation on myocardial perfusion and metabolism were studied during aortic valvuloplasty in 17 patients with aortic stenosis, including 6 with associated coronary artery disease. Coronary sinus flow and blood samples were obtained before and during the first inflation, and 5 to 10 minutes after the last inflation. During inflation, coronary blood flow decreased (272 +/- 111 standard deviation to 166 +/- 92 ml/min; p less than 0.05), myocardial oxygen uptake fell and transcardiac lactate handling shifted from extraction to production (35 +/- 54 to -41 +/- 48 mumol/min; p less than 0.01). At the end of the procedure, aortic valve area had increased from 0.51 +/- 0.22 to 0.81 +/- 0.48 cm2 (p less than 0.002). Coronary sinus flow increased slightly above control values (+6%; difference not significant) and myocardial oxygen and lactate uptakes were back to control values. However, myocardial alanine production had increased from -3.6 to -6.6 mumol/min (p less than 0.05) and glutamine production was reduced or replaced by extraction (-3.3 +/- 2.1 to 3.5 +/- 3.8 mumol/min; p less than 0.05). Recovery of coronary flow, oxygen and lactate uptakes was not significantly different in patients with or without coronary artery disease, although the former patients tended to have less glutamine extraction and less improvement in their ejection fraction at the end of the procedure. Thus, aortic balloon valvuloplasty produces brief episodes of low-flow ischemia. Recovery of oxidative metabolism is almost immediate after deflation and no detrimental effect seems to persist at the end of the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic value of symptom limited exercise testing in men with a high prevalence of coronary artery disease.

In order to evaluate the independent prognostic information provided by exercise testing in populations with a high prevalence of coronary artery disease, survival rates were calculated with the life table method in 372 men, mean age 48 years, referred for coronary arteriography. The prevalence of angiographic coronary artery disease was 82%. During a mean follow-up of 29 months (1 to 8 years), 32 patients died and 27 patients had a nonfatal event (acute infarction or hospitalization for disabling angina). Both the history (presence or absence of typical angina pectoris or of a previous myocardial infarction) and the exercise test results (abnormal if angina and/or ST segment changes greater or equal to 0.1 mV occurred) had a significant prognostic value for the 5 year survival rate (P less than 0.001). In patients with a positive history, the 5 year cumulative survival rate was 76% if the exercise test was abnormal versus 94% if it was normal (P less than 0.001). The following 8 noninvasive and 2 invasive variables were submitted to a Cox regression analysis: age, typical angina pectoris, previous myocardial infarction, maximal heart rate and workload, maximal ST segment depression and elevation, angina pectoris during exercise testing, number of diseased vessels, and wall motion score on contrast ventriculography. By univariate analysis, the age and the maximal workload reached during exercise were the only noninvasive predictive variables for survival or cardiac events (P less than 0.05). By multivariate analysis, and combining all noninvasive and invasive variables, survival was predicted by the wall motion score, the presence or absence of 3 vessel disease, and age.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence and prognostic implications of severe ventricular arrhythmias during maximal exercise testing.

Among 7,500 consecutive maximal exercise tests (MET), we have observed 6 cases of ventricular fibrillation (VF) and 40 cases of ventricular tachycardia (VT); 13 patients had a sustained VT and 27 patients had a single short run of VT. No patient died immediately but 11 patients died during the follow-up. The prognosis was determined by the underlying disease (most often coronary artery disease) and the type of arrhythmia. The 5-year survival rate was 84% in patients with a short run of VT and only 43% in patients with VF or sustained VT.