Faculty Bibliography

BACKGROUND: A recent report suggested that a thoracotomy approach for reoperative mitral valve (MV) procedures was associated with an equivalent mortality and an unacceptable risk of stroke. We assessed these outcomes in a single institution's experience. METHODS: From 1992 through 2007, 905 patients underwent reoperative MV procedures. The approach was a median sternotomy in 612 (67.6%), right anterior thoracotomy in 242 (26.7%), and left posterior thoracotomy in 51 (5.6%). Concomitant procedures in 411 patients (67.6%) included aortic procedures in 189, tricuspid procedures in 170, and coronary artery bypass grafting in 90. Hypothermic fibrillation was used in 65 patients. Logistic analysis was used to analyze risk factors and outcomes. RESULTS: Overall mortality was 12.7% (115 of 905), 6.7% (25 of 371) for first time isolated MV reoperations, and 10.1% (50 of 494) for all isolated MV operations. Overall incidence of stroke was 3.8% (34 of 905); 10.9% (9 of 82) with retrograde arterial perfusion and 3.0% (25 of 824) with central aortic cannulation (p < 0.001). For isolated MV reoperations, the incidence of stroke was 4.3% (21 of 494): 2.9% (7 of 241) for antegrade perfusion and 5.5% (14 of 253) for retrograde perfusion (p = 0.15). Risk factors for death were age (p < 0.001), renal failure (p < 0.01), tricuspid valve disease (p < 0.001), chronic obstructive pulmonary disease (odds ratio [OR], 2.9; 95% confidence interval [CI], 1.8 to 4.9; p < 0.001), emergency procedure (OR, 2.9; 95% CI, 1.2 to 6.9; p = 0.02), and ejection fraction less than 0.30 (OR, 1.9; 95% CI, 1.1 to 3.3, p = 0.018). Risk factors for stroke were retrograde perfusion (OR, 4.4; 95% CI, 1.8 to 10.3; p < 0.01) and ejection fraction below 0.30 (OR, 2.1; 95% CI, 0.9 to 5.0; p = 0.09). CONCLUSIONS: The incidence of stroke in reoperative MV operations is associated with perfusion strategies, not with the incisional approach. Reoperative sternotomy and minithoracotomy with central cannulation are both useful for reoperative MV procedures and are associated with low stroke rates

BACKGROUND: Elderly patients requiring reoperative cardiac surgery for valve disease are considered high risk for immediate outcomes, but little is known about their long-term survival. It is often conjectured that medical therapy provides equivalent late survival in this population, which may dissuade both patient and surgeon from considering reoperation. We analyzed a cohort of such patients undergoing reoperative valve surgery to determine their long-term survival. METHODS: From 1992 through 2007, 363 patients aged 75 years or more underwent reoperative isolated valve surgery; 211 (58%) had aortic valve replacement and 152 (42%) had mitral valve surgery. Mean age was 80.5 years. Hospital outcomes were prospectively recorded. Survival from all-cause death was determined from the Social Security Death Index. RESULTS: Hospital mortality was 13.8% (12.8% for aortic and 15.1% for mitral valve operations; p = 0.52). Multivariable predictors of hospital death were New York Heart Association functional class III or IV heart failure (odds ratio = 3.19, p = 0.012), dialysis (odds ratio = 15.63, p = 0.003), and more than one reoperation (odds ratio = 2.59, p = 0.058). At 5 years, overall survival was 62% +/- 3% for all patients (66% +/- 4% for aortic and 56% +/- 4% for mitral valve patients). For aortic valve patients aged 80 years or more, 5-year survival was 60% +/- 0.6%. Life expectancy table analysis predicted a 5-year survival of 57% for an age-matched and sex-matched comparison group. CONCLUSIONS: Reoperative surgery for elderly patients with isolated aortic or mitral valve pathology is associated with excellent long-term survival, particularly when treating aortic valve disease. While in-hospital mortality is higher among the elderly than among younger patients, specific predictors of poor outcome can be identified preoperatively to risk stratify these patients

OBJECTIVE: Vein graft arterialization results in activation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinases-1 and -2 (ERK1/2), which have been implicated in cell proliferation, migration, and apoptosis. The goal of our study was to characterize the effect of MAPK inhibition on intimal hyperplasia (IH) in arterialized vein grafts in hypercholesterolemic rabbits. METHODS: Reversed bilateral jugular vein to common carotid artery interposition grafts were constructed in 16 New Zealand White rabbits. The veins were incubated for 30 min prior to grafting with either the synthetic ERK1/2 activation inhibitor UO126 or the control vehicle. Vein graft and control jugular vein were harvested 3 h, 1 d, and 28 d after arterialization for histological and biochemical analyses. RESULTS: Treatment with UO126 was associated with 31% reduction in mean intimal area (1.68 +/- 0.78 mm(2)versus 2.44 +/- 1.65 mm(2); mean +/- SD; P = 0.036) relative to controls. The intima-to-media ratio of UO126-treated vein grafts decreased by 29% (0.53 +/- 0.04 versus 0.74 +/- 0.06; mean +/- SD; P < 0.01) compared to controls, vehicle-treated vein grafts. There was also significant increase in apoptosis in UO126-treated vein graft medial cell layer at 1 d. CONCLUSION: Topical administration of UO126 before vein grafting significantly decreases IH in arterialized vein grafts in hypercholesterolemic rabbits. These results may have significant implications for the development of strategies aimed at blocking or reducing IH in bypass grafts. Therefore, further evaluation of this simple strategy to improve vein graft patency following coronary artery or peripheral vascular bypass surgery is warranted

BACKGROUND: Short-term results with minimally invasive approaches for mitral valve repair in degenerative disease have been encouraging, with potential for diminishing blood loss and hospital length of stay. Little is known, however, about the long-term efficacy of this approach. This report analyzes a single institution's results over 12 years with minimally invasive mitral repair. METHODS: Since 1986, 3,057 patients have undergone mitral valve repair; 1,601 patients had degenerative disease and are the subject of this report. Minimally invasive mitral repair was done in 1071 patients with a right anterior minithoracotomy and direct vision. Clinical and echocardiographic variables were entered prospectively into a database. RESULTS: Hospital mortality was 2.2% for all patients (36 of 1601); 1.3% for isolated minimally invasive (9 of 712) and 1.3% (3 of 223) for isolated sternotomy mitral valve repair; and 3.6% (24 of 666) for valve repair plus a concomitant cardiac procedure. For isolated valve repair, 8-year freedom from reoperation was 91% +/- 2% for sternotomy and 95% +/- 1% for minimally invasive (p = 0.24), and 8-year freedom from reoperation or severe recurrent insufficiency was 90% +/- 2% for sternotomy and 93% +/- 1% for minimally invasive (p = 0.30). Eight-year freedom from all valve-related complications was 86% +/- 3% for sternotomy and 90% +/- 2% for minimally invasive (p = 0.14). CONCLUSIONS: These data indicate that long-term outcomes after minimally invasive mitral repair are excellent and equivalent to results achieved with sternotomy. In view of previously published advantages of short-term morbidity, minimally invasive approaches to mitral valve surgery deserve expanded use

OBJECTIVE: The inflammatory process of aortic stenosis involves the differentiation of aortic valve myofibroblasts into osteoblasts. Osteopontin, a proinflammatory glycoprotein, both stimulates differentiation of myofibroblasts and regulates the deposition of calcium by osteoblasts. Osteopontin levels are increased in patients with such conditions as end-stage renal disease, ectopic calcification, and autoimmune disease. We hypothesized that increased plasma osteopontin levels might be associated with the presence of aortic valve calcification and stenosis. METHODS: Venous blood from volunteers older than 65 years undergoing routine echocardiographic analysis or aortic valve surgery for aortic stenosis was collected. Plasma osteopontin levels were measured by means of enzyme-linked immunosorbent assay. The presence of aortic stenosis was defined as an aortic valve area of less than 2.0 cm(2). Aortic valve calcification was assessed by using a validated echocardiographic grading system (1, none; 2, mild; 3, moderate; 4, severe). Comparisons were performed with nonpaired t tests. RESULTS: Aortic stenosis was present in 23 patients (mean age, 78 years) and was absent in 7 patients (mean age, 72 years). Aortic valve calcification scores were 3.5 +/- 0.6 and 1.3 +/- 0.5 in patients with and without aortic stenosis, respectively (P < .001). Patients with no or mild aortic valve calcification had lower osteopontin levels compared with patients with moderate or severe aortic valve calcification (406.1 +/- 165.8 vs 629.5 +/- 227.5 ng/mL, P = .01). Similarly, patients with aortic stenosis had higher osteopontin levels compared with patients without aortic stenosis (652.2 +/- 218.7 vs 379.7 +/- 159.9 ng/mL, P < .01). CONCLUSION: Increased levels of plasma osteopontin are associated with the presence of aortic valve calcification and stenosis. These findings suggest that osteopontin might play a functional role in the pathogenesis of calcific aortic stenosis

The fgf-2 gene encodes low molecular weight (LMW, 18 kDa) and high molecular weight (HMW, 22-24 kDa) forms that originate from alternative translation of a single mRNA and exhibit diverse biological functions. HMW fibroblast growth factor-2 (FGF-2) inhibits cell migration and induces cell transformation or growth arrest in a cell type- and dose-dependent fashion. Conversely, LMW FGF-2 upregulates both cell proliferation and migration in most cell types. Although transcriptional and translational regulation of HMW and LMW FGF-2 has been extensively investigated, little is known about post-translational control of their relative expression. Here we report that thrombin, a key coagulation factor and inflammatory mediator, cleaves HMW FGF-2 into an LMW FGF-2-like form that stimulates endothelial cell migration and proliferation. The effect of thrombin on these cell functions requires HMW FGF-2 cleavage. This post-translational control mechanism adds a novel level of complexity to the regulation of FGF-2, and links the activities of thrombin and FGF-2 in patho-physiological processes in which both molecules are expressed

BACKGROUND: Disparities associated with race, particularly African-American race, in access to medical and surgical care for patients with cardiac disease have previously been documented. The purpose of this study was to determine the presentation, etiology, and hospital outcome differences between African-American patients and white patients with regard to surgically corrected mitral valve disease. METHODS: All 1,425 adult patients who underwent first time, isolated mitral valvuloplasty or mitral valve replacement by the same group of surgeons at New York University Medical Center and Bellevue Hospital Center between 1993 and 2003 were studied. RESULTS: African Americans (n = 123, 8.6%) were significantly younger (45.6 +/- 14.4 versus 60.5 +/- 15.3 years) and had significantly higher incidences of diabetes mellitus, renal failure, congestive heart failure, endocarditis, and rheumatic mitral disease; whereas whites (n = 1,302, 91.4%) more commonly had degenerative mitral disease. African Americans were less likely to undergo mitral valvuloplasty. There were no significant differences in the incidences of postoperative complications or hospital mortality (2.4% African American versus 5.1% white, p = 0.19). CONCLUSIONS: African Americans present for mitral valve surgery at a significantly younger age than whites and with higher incidences of many risk factors. Whether presentation at a significantly earlier age in African Americans is a result of failures in primary care or an enhanced susceptibility to the process of mitral disease and comorbidities remains to be determined. African Americans were less likely to undergo mitral valvuloplasty, which may have an effect on long-term outcome. Improved screening in this racial group will facilitate earlier referral, increasing the potential for mitral valvuloplasty

OBJECTIVES: This study analyzed the differences in clinical presentation, etiology, and hospital outcome between Hispanic and non-Hispanic patients who underwent surgical correction of mitral valve disease at a large urban medical center. DESIGN: All adult patients undergoing isolated mitral valve repair or replacement surgery at two hospitals between 1993 and 2003 were studied. Patients were grouped according to ethnicity as reported to the New York State Cardiac Surgery Reporting System. Preoperative variables compared included age, congestive heart failure (CHF), etiology, and pertinent medical and surgical histories, while perioperative variables included type of operation, mortality, and hospital complications. RESULTS: A total of 1683 patients (135 Hispanic,1548 non-Hispanic) underwent mitral valve surgery. Hispanic patients were younger (48.3+/-16.0 vs 59.7+/-15.9 years, P<.001) and had higher incidences of CHF (48.9% vs 35.3%, P=.002), endocarditis (8.9% vs 5.0%, P=.05), and rheumatic disease (12.6% vs 5.4%, P<.001). Non-Hispanic patients had a higher incidence of degenerative disease (68.0% vs 54.8%, P<.01). No differences in hospital mortality (Hispanic 5.9% vs 5.3%, P=.76) or perioperative complications were observed between the two groups, although Hispanic patients were less likely to undergo mitral valve repair than mitral valve replacement (35.6% vs 61.2%, P<.001). CONCLUSIONS: In the urban population studied, Hispanic patients presented for mitral valve surgery at a younger age and with a higher prevalence of CHF and rheumatic disease. Public health strategies to prevent rheumatic fever among Hispanics are needed, and improved screening might facilitate earlier referral for Hispanic patients, increasing the potential for benefitting from mitral valve repair