Objective Mitral valve repair (MVR) is the definitive therapy for mitral myxomatous degeneration. Median sternotomy has been the traditional approach to repair until the advent of the da Vinci Surgical System (Intuitive Surgical, Inc., Sunnyvale, CA). Minimally invasive surgical approaches for mitral repair have been slow to gain acceptance in cardiac surgery. We review the MVR results from our single-institution academic robotic program. Methods From August 2004 through April 2008, patients who underwent a robotic-assisted (RA) MVR were identified. RA technique included a 4-cm right minithoracotomy, femoral cardiopulmonary bypass with transthoracic aortic occlusion, and RA-MVR. Repair types were combinations of quadrangular/triangular leaflet resection, sliding plasty, chordal transfer/replacement, and edge-to-edge approximation, with band annuloplasty in all cases. Postrepair echocardiography and morbidity follow-ups were completed in all patients. Our primary outcome was adequacy of repair, and secondary outcome was major complications. Results There were 43 patients (29 male and 14 female) who underwent RA-MVR for severe (4 +) mitral regurgitation during the 4-year review. Average operative time was 272.26 minutes. Only one patient had mild postoperative mitral regurgitation, whereas 20 had trace and 22 had no regurgitation after repair. Mean ventilator time was 32.1 hours, and length of stay was 5.7 days. One third of the patients (33%) received postoperative-packed red blood cell transfusions (average: 2.4 units per patient). Twenty-eight percent of patients developed atrial fibrillation after repair. Most of the patients (95.3%) were discharged home. There were no 30-day mortalities. Conclusions Based on our small single-institution experience, RA-MVR provides an effective treatment for severe mitral valve regurgitation. Although procedure durability is slowly being established, preliminary results are promising. Careful programmatic advances with an integrated team approach can facilitate acceptable postoperative outcomes and excellent MVR.
Surfactant dysfunction is a primary pathophysiologic component in patients with adult respiratory distress syndrome (ARDS). In this study we tested the efficacy of aerosolized surfactant (Sf ) replacement in a severe lung injury model of endotoxin-induced ARDS. Twenty-one certified healthy pigs were anesthetized, surgically prepared for measurement of hemodynamic and lung function, then randomized into one of four groups: (1) control (n = 5), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 6), infused with Escherichia coli LPS (100 μ g/kg) without positive end- expiratory pressure (PEEP) and ventilated with a nonhumidified gas mixture of 50% N2O and 50% O2; (3) LPS + PEEP (n = 4), infused with LPS, placed on PEEP (7.5 cm H2O), and ventilated with a humidified gas mixture; and (4) LPS + PEEP + Sf (n = 6), infused with LPS, placed on PEEP, and ventilated with aerosolized Sf (Infasurf, ONY, Inc.). All animals were studied for 6 h. Arterial Po 2 significantly decreased in both the LPS and LPS + PEEP groups (LPS + PEEP = 74 ± 19 mm Hg; LPS = 74 ± 19 mm Hg, p < 0.05) while venous admixture (Q˙ s/Q˙ t) increased in these groups (LPS + PEEP = 43.3 ± 3.9%; LPS = 47.7 ± 11%, p < 0.05) as compared with the control group. PEEP + Sf reduced the fall in Po 2 (142 ± 20 mm Hg) and rise in Q˙ s/Q˙ t (15.1 ± 3.6%) caused by LPS. Delayed induction of PEEP (2 h following LPS) did not significantly improve any parameter over the LPS group without PEEP in this ARDS model. LPS without PEEP (3.4 ± 0.2 cells/6,400 μ m2) caused a marked increase in the total number of sequestered leukocytes in the pulmonary parenchyma as compared with the control group (1.3 ± 0.1 cells/6,400 μ m2). LPS + PEEP + Sf (2.3 ± 0.2 cells/6,400 μ m2) significantly decreased while LPS + PEEP significantly increased (4.0 ± 0.2 cells/6,400 μ m2) the total number of sequestered leukocytes as compared with the LPS without PEEP group. In summary, aerosolized surfactant replacement decreased leukocyte sequestration and improved oxygenation in our porcine model of endotoxin-induced lung injury.
Cardiopulmonary bypass (CPB) causes a systemic inflammatory response syndrome (SIRS), which can progress to an acute lung inflammation known as postperfusion syndrome. We developed a two-phase hypothesis: first, that SIRS, as indicated by elevated cytokines post-CPB, would be correlated with postoperative pulmonary dysfunction (Phase I), and second, that the cytokine interleukin-6 (IL-6) is predominantly released from the heart in CPB patients (Phase II). Blood samples were collected from patients undergoing CPB for elective cardiac surgery. In seven patients (Phase I), arterial samples were drawn before, during (5 minutes and 60 minutes), and after CPB. In 14 patients (Phase II), samples were collected from the coronary sinus, superior vena cava, and a systemic artery at the times indicated previously. Samples were analyzed with enzyme-linked immunosorbent assay: IL-1, IL-6, IL-8, IL-10, and tumor necrosis factor-α were assessed in Phase I and IL-6 assessed in Phase II. In Phase I, IL-6, IL-8, and IL-10 were elevated after CPB, but only IL-6 concentrations correlated with lung function. In summary, Phase I data demonstrate that increased IL-6 levels at the end of CPB correlate with reduced lung function postoperatively. In Phase II, IL-6 elevation was similar at all sample sites suggesting that the heart is not the major source of IL-6 production. We suggest that IL-6 be implemented as a prognostic measure in patient care, and that patients with elevated IL-6 after CPB be targeted for more aggressive anti-inflammatory therapy to protect lung function.
Left ventricular masses are rare entities that often require surgical excision when diagnosed due to the risk of embolization. We report 2 separate patients presenting with evidence of cerebral embolization both of whom were diagnosed with isolated left ventricular masses and underwent surgical excision through a robot-assisted approach. Microscopic pathology revealed a myxoma and hemangioma, respectively. Both cases demonstrate that left ventricular masses can be feasibly excised through a robot-assisted minithoracotomy approach.
While blood:crystalloid cardioplegia is the clinical standard for patients undergoing cardiopulmonary bypass (CPB), it has been postulated that whole blood minicardioplegia may benefit the severely injured heart by reducing cardioplegic volume, thereby reducing myocardial edema. To test this hypothesis, we compared the cardioprotection of a popular 4:1 blood:crystalloid cardioplegia to whole blood minicardioplegia (WB) in a porcine model of acute myocardial ischemia. Yorkshire pigs ( n = 20) were placed on atriofemoral bypass and subjected to 30 minutes of global normothermic ischemia. Animals were randomized to receive either 4:1 cold cardioplegia ( n = 10) or WB cold cardioplegia ( n = 10) delivered antegrade continuously for 90 minutes. Baseline (BL) echocardiographic determination of left ventricular mass (LVM) was compared within groups for cardiac edema (%) measured by histologic morphometrics. All (100%) animals receiving WB were successfully weaned off CPB, whereas only 40% of animals receiving 4:1 were successfully weaned off CPB. Cardiac edema percentage ( p < .004) and LVM ( p < .05) were significantly decreased in the WB group compared with 4:1. WB cardioplegia increases the number of hearts successfully weaned from CPB and decreases cardiac edema in our porcine model of acute myocardial ischemia. This finding implies whole blood cardioplegia may be more protective in a select group of patients undergoing extended CPB time by decreasing myocardial edema.
