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Background Injury incurred while saphenous veins are being obtained results in poor graft patency and impairs the results of coronary artery bypass grafting. A novel method of obtaining veins, the no-touch technique, has shown improved long-term saphenous vein graft patency. Methods This randomized trial included 108 patients undergoing coronary artery bypass grafting and compared the patency of no-touch saphenous vein with that of radial artery grafts. Each patient was assigned to receive one no-touch saphenous vein and one radial artery graft to either the left or the right coronary territory to complement the left internal thoracic artery. Results Angiography was performed in 99 patients (92%) at a mean of 36 months postoperatively. Graft and grafted coronary artery patency was evaluated. The patency of grafts for no-touch saphenous vein and radial artery was 94% versus 82% ( p = 0.01), respectively. The patency of coronary arteries grafted with no-touch saphenous vein and radial artery grafts was 95% versus 84% ( p = 0.005), respectively. Eighty-nine of 96 (93%) left internal thoracic artery grafts were patent. Conclusions No-touch saphenous vein grafts showed a significantly higher patency rate than the radial artery grafts and the patency was comparable to the patency for left internal thoracic artery grafts. This highlights the improvement in saphenous vein graft quality with the no-touch technique and increases the number of situations in which saphenous veins may be preferable to radial artery grafts as conduits in coronary artery bypass grafting.

Background . The media of saphenous veins is composed of two cell populations: smooth muscle (SMC) and non-smooth muscle (NSMC) cells. Previous studies demonstrate a loss of SMCs by 3 days after grafting, despite an increase in cell proliferation. The purpose of this study is to determine the rates of apoptotic cell death versus cell proliferation for the two major cell populations of the media. Methods . Veins (six/time point) were examined at 0.5, 1, 2, 4, 8, 24, and 48 hours after grafting in crossbred pigs. Terminal transferase-mediated dUTP nick end labeling (TUNEL) and proliferating cell nuclear antigen (PCNA) stains were used to assess apoptosis and proliferation. Apoptosis was also corroborated with confocal and electron microscopy. Results . Apoptosis was high in both cell populations: at 8 hours, SMC and NSMC apoptosis peaked at 14.5% ± 3.5% and 49.9% ± 7.8%, respectively. In contrast, cell proliferation was different between the two populations. SMC proliferation was low at all time points, whereas NSMC proliferation rose to 22% ± 5.4% by 48 hours. Conclusions . Medial SMCs are removed through apoptosis and appear to be replaced by fibrous tissue (NSMCs) early after vein grafting. This reciprocal change between the medial SMC and NSMC populations may contribute to late vein graft degeneration.

We hypothesized that acute electrical stimulation of a latissimus dorsi cardiomyoplasty would augment the collateral blood flow delivered by the skeletal muscle to the heart. This hypothesis was tested in an animal model (13 goats) of coronary artery disease. Six weeks after a cardiomyoplasty was performed, myocardial collateral blood flow derived from the latissimus dorsi muscle was measured with colored microspheres when the muscle was at rest and during electrical stimulation of the thoracodorsal nerve at 1.25 Hz. The area at risk for ischemia averaged 13.37 +/- 2.08 g (mean +/- standard error), or 18.4% of left ventricular mass (n = 13). At rest, significant skeletal muscle-derived collaterals developed in 9 animals, and formed predominantly to chronic ischemic myocardium (mean +/- standard error, 0.07 +/- 0.02 mL.g-1 x min-1; n = 9), rather than infarct (0.03 +/- 0.02 mL.g-1 x min-1; n = 5), or normal myocardium (0.0005 +/- 0.0001 mL.g-1 x min-1; n = 9). Stimulation increased skeletal muscle-derived collateral blood flow to chronic ischemic areas to 0.38 +/- 0.09 mL.g-1 x min-1 (n = 9) (p0.05). During stimulation, the collateral flow was greater in the epicardium (0.46 +/- 0.11 mL.g-1 x min-1) than in endocardium (0.14 +/- 0.09 mL.g-1.min-1) (p0.05). This study demonstrates that electrical stimulation of a latissimus dorsi cardiomyoplasty increases extramyocardial collateral blood flow to chronic ischemic myocardium.

Background . Studies have demonstrated a high incidence of antibodies to heparin/platelet factor 4 complexes, the antigen in heparin-induced thrombocytopenia, in patients after cardiopulmonary bypass surgery. In many hospitals, beef lung heparin has been used historically for cardiopulmonary bypass, and there has been reluctance to change to porcine heparin despite concerns of an increased incidence of heparin-induced thrombocytopenia in patients receiving bovine heparin. Methods . A prospective randomized trial comparing bovine and porcine heparin in cardiopulmonary bypass surgery was conducted. Presurgery and postsurgery heparin antibody formation was studied using the serotonin release assay and a heparin/platelet factor 4 enzyme-linked immunosorbent assay. Results . Data available on 98 patients, randomized to receive either bovine or porcine heparin, revealed no significant difference in patient positivity by serotonin release assay (12% in both groups) or by the heparin/platelet factor 4 enzyme-linked immunosorbent assay (29% with porcine and 35% with bovine heparin) postoperatively. There were no significant differences between preoperative and postoperative platelet counts or thromboembolic complications. Conclusions . Our study does not support the belief that bovine heparin is more likely than porcine heparin to induce the development of antibodies to heparin/platelet factor 4.

Treatment of saphenous veins with c-myc antisense oligomers during preparation for grafting reduces medial cellular proliferation and macrophage infiltration, and preserves medial smooth muscle content at 3 days. Accordingly, the purpose of this study was to examine whether c-myc antisense oligomers have an impact on late vein graft remodeling.Sixty-two pigs underwent unilateral saphenous vein-carotid artery interposition grafting. Harvested veins were incubated either in saline (control group) or 20-micromol/L or 200-micromol/L concentrations of c-myc antisense oligomers (treated groups) for 30 minutes intraoperatively. Three months after surgery, vein graft histology was assessed.Forty-five of 62 randomized animals survived the experiment; no differences in animal survival or graft patency among the groups were observed (p = NS, chi2). C-myc antisense oligomers significantly decreased neointimal and wall thickness, as well as increased lumenal index, in treated groups (p0.04, p0.03, and p0.001, respectively, analysis of variance). In contrast, there was no difference in medial thickness or perivascular wound healing.Intraoperative treatment of saphenous veins with c-myc antisense oligomers decreased neointimal formation at 3 months after grafting. In conjunction with our previous reports, these findings suggest that early inhibition of cellular proliferation and inflammatory infiltration results in a sustained reduction in neointimal formation and favorable graft remodeling.

Injury to the smooth muscle cells of the media affects the remodeling process of vein grafts. The purpose of this study was to determine whether different techniques of surgical preparation influence the degree of medial smooth muscle injury.Carotid-saphenous vein interposition grafting was performed in crossbred pigs (n = 32), using distended (n = 16) or nondistended (n = 16) conduits. After 3 to 90 days, the media was evaluated for the presence of smooth muscle cells (desmin stains), myofibroblast formation (transient alpha-SM actin expression), and apoptosis (TdT-mediated dUTP nick end-labeling [TUNEL]).Smooth muscle loss was uniformly severe; only 5% +/- 5% (p0.01) and 14% +/- 9% (p0.01) of the medial area of distended and nondistended veins were desmin positive in comparison with 80% +/- 9% of controls. Apoptosis appeared to contribute to medial smooth muscle loss (5.7% +/- 4.3% in vein grafts versus 0.0% +/- 0.0% of TUNEL-positive cells in controls; p = 0.05). There was a time dependent increase in medial myofibroblast formation (p0.05).Severe medial smooth muscle loss occurs in vein grafts, even when prepared without distension. Apoptosis contributes to the early disappearance of smooth muscle cells. Adjunctive measures, in addition to ideal surgical techniques, should be developed to prevent medial muscle loss.

In the presence of myocardial ischemia, chronic electrical stimulation of a latissimus dorsi (LD) cardiomyoplasty enhances extramyocardial collateral blood flow. We postulated that basic fibroblast growth factor (bFGF) may mediate extramyocardial collateral formation. To test this hypothesis, LDs from goats with cardiomyoplasties were probed for the presence of bFGF by Western blot analysis and immunohistochemistry. Three groups were studied: static LD cardiomyoplasty (group 1); LD cardiomyoplasty stimulated at a 2-Hz frequency for 6 weeks (group 2); and LD cardiomyoplasty electrically stimulated and given human recombinant bFGF (group 3). There was no evidence of bFGF in the left LDs of group 1 by Western blot. Basic fibroblast growth factor-like immunoreactive evidence was found in the left LDs of group 2 goats by both Western blot and immunohistochemistry. In the right LDs of group 2, bFGF-like material was found by immunohistochemistry but not by Western blot, which suggests that the tissue concentrations were low (near the limits of detection). The left LDs of group 3 were positive for bFGF by Western blot and immunohistochemistry. Group 3 right LDs were positive for bFGF by immunohistochemistry. Immunohistochemical findings in group 2 indicate that bFGF is present in goat skeletal muscle. Western blot data from groups 1 and 2 suggest that bFGF may be increased in chronically stimulated cardiomyoplasties. From findings in group 3, we conclude that exogenous bFGF does not downregulate, and may upregulate, endogenous production. These results support the possibility that skeletal muscle bFGF is an important factor in extramyocardial collateral formation.