Faculty Bibliography

The formation of blood capillaries from preexisting vessels (angiogenesis) and vascular remodeling secondary to atherosclerosis or vessel injury are characterized by endothelial cell migration and proliferation. Numerous growth factors control these cell functions. Basic fibroblast growth factor (FGF-2), a potent angiogenesis inducer, stimulates endothelial cell proliferation, migration, and proteinase production in vitro and in vivo. However, mice genetically deficient in FGF-2 have no apparent vascular defects. We have observed that endothelial cell migration in response to mechanical damage in vitro is accompanied by activation of the extracellular signal-regulated kinase (ERK) pathway, which can be blocked by neutralizing anti-FGF-2 antibodies. Endothelial cells from mice that are genetically deficient in FGF-2 neither migrate nor activate ERK in response to mechanical wounding. Addition of exogenous FGF-2 restores a normal cell response, which shows that impaired migration results from the genetic deficiency of this growth factor. Injury-induced ERK activation in endothelial cells occurs only at the edge of the wound. In addition, FGF-2-induced ERK activation mediates endothelial cell migration in response to wounding without a significant effect on proliferation. These data show that FGF-2 is a key regulator of endothelial cell migration during wound repair

BACKGROUND: Repair of functional ischemic mitral regurgitation (MR) due to annular deformity and leaflet restriction remains a challenge for the surgeon and lacks well-documented outcomes. We investigated outcomes in the treatment of functional ischemic MR corrected by annuloplasty techniques alone. METHODS: From May 1980 to July 1999, 174 patients underwent repair for functional ischemic mitral insufficiency with annuloplasty alone (128 ring annuloplasty; 46 suture annuloplasty). Acute insufficiency was present in 25 (14.4%). Concomitant procedures included CABG (n = 152; 87.4%). Patients were studied longitudinally with annual follow-up and echocardiograms. RESULTS: Overall hospital mortality was 17.8% and was increased by NYHA Class 4 (23.8% vs. 8.7%; p = 0.011), diabetes (25.0% vs. 13.6%; p = 0.059), and chronic mitral insufficiency (16.4% vs. 8.0%; p = 0.070). Multivariate analysis revealed age (beta = 0.099; p = 0.049) and ejection fraction < 30% (beta = 1.260; p = 0.097) as significant predictors of hospital death. Mean postoperative mitral insufficiency was 0.84 +/- 0.86 (scale of 0-4). NYHA Class 4 (beta = 2.33; p = 0.034) and simple suture annuloplasty (beta = 2.08; p = 0.07) were associated with increased risk of late cardiac death. Cumulative incidence of mitral reoperation was 7.7% at 5 years. At follow-up, 89.7% of patients were in NYHA Class 1 or 2 with 83.4% having none or only mild mitral insufficiency. CONCLUSIONS: Ring annuloplasty is associated with a survival benefit when compared to simple suture repair in ischemic patients who require annuloplasty alone to correct the MR. Mitral reconstruction with a ring annuloplasty offers durable results in this homogeneous subset of functional ischemic MR patients. Ischemic mitral insufficiency is associated with significant late mortality

Minimally invasive cardiac surgery has allowed surgeons to perform valve procedures with a morbidity and mortality comparable with conventional resternotomy approaches while reducing postoperative ventilatory and intensive care unit requirements and overall hospital length of stay. Additionally, patient satisfaction with rapid recovery, earlier return to work, and improved cosmetic results has pushed the pendulum of reoperative valve surgery towards minimally invasive techniques. We reviewed our institutional data consisting of 129 patients requiring reoperative valve surgery over the past 4 years, which was accomplished using these minimally invasive approaches

BACKGROUND. Heparin bonding of the cardiopulmonary bypass (CPB) pump circuit decreases complement activation and fibrinolysis. It is not known whether inflammatory cytokines produced during CPB can also be modulated by the more biocompatible heparin-coated circuit. METHODS. This initial study evaluated the impact of heparin-bonded CPB circuits on production of the cytokines interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-a), IL-6, and IL-8 in adults undergoing complex cardiac operations with prolonged CPB. Twenty patients had blood samples drawn immediately before and at hourly intervals after the start of CPB using either a conventional oxygenator and circuit (n = 14) or a covalently bonded heparin oxygenator and circuit (n = 6). Levels of IL-1, TNF-a, IL-6, and IL-8 were measured in all serum samples using a 'sandwich' enzyme-linked immunosorbent assay. RESULTS. The levels of IL-6 and IL-8 increased in a time-dependent fashion in both groups, but the response was significantly less over time in the heparin-bonded group (p < 0.05) for both IL-6 and IL-8. Levels of IL-1 and TNF-a were not significantly elevated with lengthening bypass interval in either group. CONCLUSIONS. These data indicate that the use of heparin-coated bypass pump circuits results in lower serum levels of the inflammatory cytokines IL-6 and IL-8 than standard circuits. Biocompatible materials that decrease the inflammatory response to CPB may ultimately reduce the morbidity associated with cardiac operations