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Background: Internal thoracic artery (ITA) conduits are known to provide long-term patency and increased patient survival with low morbidity after coronary artery bypass grafting (CABG). Excellent clinical results with the ITA have stimulated interest in additional arterial grafts., Methods and Results: To review our experience and evaluate postoperative complications associated with these new conduits, from May 1985 to September 1993, we studied 290 patients who underwent CABG using additional arterial conduits. The right gastroepiploic artery (GEA) was used in 152 patients and the inferior epigastric artery (IEA) was used in 130 patients. Eight patients with both GEA and IEA grafts were excluded. Patient records were analyzed as to preoperative characteristics, angiographic findings, operative data, and postoperative complications. Statistical analysis was done using the Pearson chi 2 statistic and the t test. Ninety-eight percent of patients received one concomitant ITA graft, and the majority of patients in both groups had bilateral ITA grafts. The GEA group had a higher proportion of reoperations (GEA group, 54%; IEA group, 16%; P < .001), previous myocardial infarction (MI) (GEA group, 67%; IEA group, 50%; P = .004) and New York Heart Association class IV (GEA group, 28%; IEA group, 6%; P = .001). The IEA group was generally slightly older (IEA group, 56 years; GEA group, 52 years; P = .001). Hospital mortality (GEA group, 4%; IEA group, 0.8%) and postoperative morbidity (mediastinal bleeding, infection, stroke, MI, and low cardiac output) were not significantly different between the two groups or from our experience with routine CABG using the ITA. Three intraabdominal complications occurred in the GEA group: 2 episodes of bleeding and 1 of pancreatitis. One patient in the IEA group had abdominal wall bleeding. With overall short follow-up, angiographic patency in a small number of patients has been good: 80% for the GEA group and 85.7% for the IEA group., Conclusions: We conclude that the morbidity associated with these additional arterial conduits is low and is comparable with that associated with routine CABG using the ITA. Currently we use the ITA for primary targets and alternative arterial conduits for vessels of secondary importance or when the ITA and/or saphenous vein is not available.

This retrospective analysis tests the hypothesis that topical cardiac hypothermia is an unnecessary adjunct to intraoperative myocardial protection and an avoidable cause of pulmonary morbidity in patients with coronary disease receiving blood cardioplegia. The hospital records of 150 nonrandomized consecutive patients undergoing elective and emergency isolated coronary revascularization were reviewed. All patients received multidose cold blood cardioplegia followed by warm blood cardioplegic reperfusion distributed through grafts. Fifty patients received iced slush, 50 received topical 4 degrees C saline, and no topical cooling was used in 50 others. Patients groups were comparable in number of grafts (3.7 versus 3.5 versus 3.5) and crossclamp time (61 versus 62 versus 61 minutes). More emergency operations were performed in the patients receiving no topical hypothermia (12/50 versus 8/50 versus 7/50). Postoperative x-ray films were reviewed by a radiologist who did not know of patient grouping. Postoperative results were comparable in hemodynamics, inotropic requirements (10/50 ice versus 8/50 saline versus 5/50 no cooling), myocardial infarction (1/50 versus 2/50 versus 2/50), and enzymes (aspartate aminotransferase myocardial band creatine kinase). No patient died. Ice topical hypothermia (versus no topical cooling) was associated with more left pleural effusions (25/50 versus 9/50; p less than 0.05), atelectasis (33/50 versus 18/50; p less than 0.05), elevated left hemidiaphragms (13/50 versus 0/50; p less than 0.05), and longer postoperative hospitalization (11.2 versus 8.5 days; p less than 0.05). Topical 4 degrees C saline reduced diaphragmatic elevation and pleural effusion (versus topical ice) but was associated with more atelectasis (34/50 versus 18/50; p less than 0.05) than no topical cooling. These data suggest that routine topical hypothermia is an unnecessary adjunct to blood cardioplegic protection in patients with coronary disease, since supplemental topical cooling does not improve postoperative hemodynamics or reduce inotropic requirements, enzyme release, or prevalence of postoperative myocardial infarction, and it increases pulmonary morbidity, which can be reduced by its avoidance.

This study tests the hypothesis that surgical revascularization (i.e., simulating coronary artery bypass grafting) with control of reperfusion conditions (total vented bypass) and of reperfusate composition (substrate-enriched blood cardioplegic solution) produces better recovery than is possible in the non-surgical setting (i.e., normal blood in beating, working hearts to simulate streptokinase and angioplasty). Eighteen dogs underwent 2 hours of left anterior descending coronary artery ligation (35% of the left ventricle at risk) followed by 2 hours of reperfusion. In five dogs the ligature was released to simulate streptokinase thrombolysis and angioplasty in working hearts (medical). In 13 dogs, surgical reperfusion was accomplished during total vented bypass, where six dogs received normal blood and seven others received substrate-enriched blood cardioplegic solution with 1 additional hour of aortic clamping (i.e., a total of 3 hours of ischemia). Segmental shortening with ultrasonic crystals, tissue water content, and vital staining (triphenyltetrazolium chloride) were assessed. Ischemia produced severe systolic bulging (-42% of control systolic shortening, p less than 0.05). Medical reperfusion resulted in failure to restore regional contractility (-27% systolic shortening, p less than 0.05), severe edema (82.4% H2O content, p less than 0.05), and extensive transmural nonstaining (44%, p less than 0.05). In contrast, surgical reperfusion with substrate-enriched blood cardioplegic solution during total vented bypass restored regional contraction to 46% of control values (p less than 0.05) and resulted in less edema (80.6% H2O content, p less than 0.05), and only mild nonstaining (21%, p less than 0.05) restricted to the subendocardial region. Surgical revascularization with controlled reperfusion conditions and reperfusate composition produces better myocardial salvage than is possible in the medical setting, despite a longer period of ischemia.

Triphenyltetrazolium chloride has been used to detect irreversibly damaged tissue after regional ischemia and reperfusion. We used this staining technique in our studies of myocardial ischemia and reperfusion and found that a transmural triphenyltetrazolium chloride nonstaining pattern is not an accurate predictor of myocardial necrosis: functional recovery occurs despite nonstaining. Mongrel dogs (n = 91) were anesthetized and made ischemic by ligation of the left anterior descending coronary artery. Regional myocardial function was assessed by means of ultrasonic crystals. Following 2, 4, or 6 hours of ischemia, the ligature was removed, and each heart was reperfused either in the working state or during total bypass with either normal blood or substrate-enriched blood cardioplegic solution of differing composition. The hearts were then removed and incubated in triphenyltetrazolium chloride at 37 degrees C for 20 to 40 minutes. The pattern of nonstaining in the area at risk varied from patchy subendocardial, to confluent subendocardial, to transmural and did not correlate with the recovery of regional contraction following ischemia. Mitochondrial ultrastructure was altered minimally in nonstained muscle, which regained contractile function after 6 hours of ischemia. Fifty-two of sixty-five hearts (80%) showing a transmural nonstaining pattern in the area of ultrasonic crystal placement recovered the capacity to shorten systolically immediately after controlled reperfusion during total vented bypass. These results show that the triphenyltetrazolium chloride staining method does not predict myocardial necrosis and that appropriate reperfusion following 2 to 6 hours of ischemia will result in recovery of myocardial shortening despite transmural nonstaining.

This study evaluates the capacity of regional substrate-enriched blood cardioplegic reperfusion (without bypass) to salvage cardiac muscle subjected to 40 minutes of regional ischemia. Results are compared with those obtained by normal blood reperfusion at either systemic or reduced perfusion pressure (i.e., simulating acute angioplasty or streptokinase thrombolysis). All studies were carried out in beating, working hearts when the conditions of reperfusion were not controlled. The results show that regional cardioplegic reperfusion without cardiopulmonary bypass reduces the incidence of perfusion ventricular fibrillation (15% versus 55%, p less than 0.05), increases recovery of subendocardial creatine phosphate (35.3 versus 14.0 mumol/gm, p less than 0.05) and adenosine triphosphate (6.0 versus 3.1 mumol/gm, p less than 0.05), reduces histochemical damage evaluated by triphenyltetrazolium chloride (0% versus 43% transmural nonstaining, p less than 0.05), and improves myocardial contractile reserve capacity (91% versus 41%, p less than 0.05). Normal blood reperfusion restored immediate systolic shortening in only 3 of 18 hearts (17%), and regional cardioplegic reperfusion without bypass produced early recovery of regional systolic shortening in only 10 of 16 hearts (63%, p greater than 0.05). Thus the value of controlling reperfusate composition without simultaneous control of reperfusion conditions is limited.

This study assesses the regional oxygen requirements of muscle segments that are beating and working, beating and empty, arrested and decompressed, and nonischemic that move dyskinetically. Regional oxygen demands were evaluated by producing a dyskinetic segment by infusing regional cardioplegic solution through a left anterior descending coronary artery catheter with and without extracorporeal circulation. The results show that the O2 demands of the perfused dyskinetic cardiac muscle segment (4 to 8 ml/100 gm/min) are approximately 55% of the contracting (beating, working) segment (7 to 12 ml/100 gm/min) and are fivefold more than when the same muscle segment is arrested and decompressed by total vented bypass (0.8 to 1.2 ml/100 gm/min). Additional studies showed that ischemia for 2 hours (left anterior descending coronary artery ligation) produced severe dyskinesia (-24% control systolic shortening), which failed to recover after reperfusion with the heart in the beating, working state. In contrast, lowering O2 demands by reperfusion during bypass restored occasional contractile function as a consequence of left ventricular decompression. Dyskinetic muscle segments have a high oxygen requirement that may affect their capacity to be salvaged if reperfusion is conducted without left ventricular decompression. These observations suggest that the value of revascularization in the working heart (i.e., streptokinase with or without angioplasty) may be limited unless the left ventricle is decompressed during reperfusion and provide an explanation for the delayed recovery of mechanical function in hearts reperfused surgically with normal blood during cardiopulmonary bypass.

This study tests the hypotheses that postischemic adenosine triphosphate levels are unreliable predictors of functional recovery, myocardial adenosine triphosphate concentration of less than 2 mumol/gm does not indicate irreversible damage, mitochondrial adenosine triphosphate generating capacity can be nearly normal despite low levels of tissue adenosine triphosphate and the failure to replenish adenosine triphosphate after ischemia is due to depletion of the adenosine nucleotide pool, which can be replenished partially by exogenous precursors (e.g., 5-amino-4-imidazolecarboxamide ribotide [AICAR]). Myocardial adenosine triphosphate was depleted to less than 2 mumol/gm by either global ischemia (37 degrees C aortic clamping) or regional ischemia (acute coronary occlusion). Reperfusion was either with normal blood or with substrate-enriched blood cardioplegic solution during total vented bypass. Tissue adenosine triphosphate content and mitochondrial adenosine triphosphate generating capacity were measured, and functional recovery was determined by right heart bypass function curves or regional segmental shortening (ultrasonic crystals). Hearts undergoing 15 minutes of global ischemia and normal blood reperfusion had impaired functional recovery (stroke work index = 58 +/- 5%; p less than 0.05 of control) despite adenosine triphosphate concentration greater than 2 mumol/gm. Transmural mitochondrial State 3 respiration averaged 83% of control values despite adenosine triphosphate levels of 1 mumol/gm in hearts undergoing 45 minutes of 37 degrees C global ischemia and 2 additional hours of aortic clamping with multidose glutamate-enriched blood cardioplegia. AICAR increased adenosine triphosphate to 2 mumol/gm (p less than 0.05), but functional recovery was nearly complete (stroke work index = 94 +/- 2% of control) and was comparable with and without AICAR. Hearts undergoing 4 hours of regional ischemia recovered 31 +/- 5% systolic shortening after controlled reperfusion despite tissue adenosine triphosphate less than 0.5 mmol/gm (15% of control), and they retained 63% adenosine triphosphate generating capacity. Postischemic adenosine triphosphate levels correlate poorly with functional recovery, and adenosine triphosphate levels less than 2 mumol/gm do not indicate irreversible ischemic injury. Low postischemic levels may be repleted partially by adenine nucleotide precursor supplementation (AICAR).(ABSTRACT TRUNCATED AT 400 WORDS)