Faculty Bibliography

BACKGROUND: Patients with severe atheromatous aortic disease (AAD) undergoing coronary artery bypass grafting (CABG) have increased operative risks. The 'off-pump' CABG (OPCAB) technique was evaluated in patients given the diagnosis of severe AAD by routine transesophageal echocardiography. METHODS: A total of 5737 patients underwent CABG, with 913 having transesophageal echocardiography findings of severe AAD. Of the patients with severe AAD, 678 (74.3%) had conventional CABG and 235 (25.7%) had OPCAB. RESULTS: Hospital mortality was 8.7% for conventional CABG and 5.1% for OPCAB (P =.08). Multivariate analysis revealed that increased mortality was significantly associated with acute myocardial infarction, conventional CABG, age, renal disease, history of stroke, and ejection fraction < 30%. Neurologic complications occurred in 6.3% of patients undergoing CABG and in 2.1% undergoing OPCAB (P =.01). Freedom from any complication was significantly greater with OPCAB. CONCLUSION: Routine intraoperative transesophageal echocardiography identifies patients with severe AAD. In these patients, OPCAB technique is associated with a lower risk of death, stroke, and all complications

OBJECTIVE: To analyze the effectiveness of new techniques of mitral valve reconstruction (MVR) that have evolved over the last decade, such as aggressive anterior leaflet repair and minimally invasive surgery using an endoaortic balloon occluder. SUMMARY BACKGROUND DATA: MVR via conventional sternotomy has been an established treatment for mitral insufficiency for over 20 years, primarily for the treatment of patients with posterior leaflet prolapse. METHODS: Between June 1980 and June 2001, 1,195 consecutive patients had MVR with ring annuloplasty. Conventional sternotomy was used in 843 patients, minimally invasive surgery in 352 (since June 1996). Anterior leaflet repair was performed in 374 patients, with increasing use over the last 10 years. Follow-up was 100% complete (mean 4.6 years, range 0.5-20.5). RESULTS: Hospital mortality was 4.7% overall and 1.4% for isolated MVR (1.1% for minimally invasive surgery vs. 1.6% for conventional sternotomy; =.4). Multivariate analysis showed the factors predictive of increased operative risk to be age, NYHA functional class, concomitant procedures, and previous cardiac surgery. The 5-year results for freedom from cardiac death, reoperation, and valve-related complications among the 782 patients with degenerative etiology are, respectively, as follows ( >.05 for all end points): for anterior leaflet repair, 93%, 94%, 90%; for no anterior leaflet repair, 91%, 92%, 91%; for minimally invasive surgery, 97%, 89%, 93%; and for conventional sternotomy, 93%, 94%, 90%. CONCLUSIONS: These findings indicate that late results of MVR after minimally invasive surgery and after anterior leaflet repair are equivalent to those achievable with conventional sternotomy and posterior leaflet repair. These options significantly expand the range of patients suitable for mitral valve repair surgery and give further evidence to support wider use of minimally invasive techniques

BACKGROUND: This study analyzes a single institutional experience with minimally invasive mitral valve operations of 6 years, reviewing short-term morbidity and mortality and long-term echocardiographic follow-up data. METHODS: Seven hundred fourteen consecutive patients had minimally invasive mitral valve procedures between November 1995 and November 2001; concomitant procedures included 91 multiple valves and 18 coronary artery bypass grafts. Of these 714 patients, 561 patients had isolated mitral valve operations (375 repairs, 186 replacements). Mean age was 58.3 years (range, 14 to 96 years; 30.1% > 70 years), and 15.4% of patients had previous cardiac operations. Arterial cannulation was femoral in 79.0% and central in 21%, with the port access balloon endo-occlusion used in 82.3%. Cardioplegia was transjugular retrograde (54.1%) or antegrade (29.4%). Right anterior minithoracotomy was used in 96.6% and left posterior minithoracotomy in 2.2%. RESULTS: Hospital mortality for primary isolated mitral valve repair was 1.1% and 5.8% for isolated mitral valve replacement. Overall hospital mortality was 4.2% (30 of 714). Mean cross-clamp time was 92 minutes and mean cardiopulmonary bypass time was 127 minutes. Postoperatively, median ventilation time was 11 hours, intensive care unit time was 19 hours, and total hospital stay was 6 days. Complications for all patients included permanent neurologic deficit (2.9%), aortic dissection (0.3%); there was no mediastinal infection (0.0%). Follow-up echocardiography demonstrated 89.1% of the repair patients had only trace or no residual mitral insufficiency. CONCLUSIONS: This study demonstrates that the minimally invasive port access approach to mitral valve operations is reproducible with low perioperative morbidity and mortality and with late outcomes that are equivalent to conventional operations

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