Hypercoagulability affecting early vein graft patency does not exist after off-pump coronary artery bypass.

OBJECTIVE: Hypercoagulability may compromise the patency of bypass grafts. The authors hypothesized that perioperative in vitro platelet responses to varying agonists (eg, thrombin, platelet activating factor, collagen, adenosine diphosphate) correlate with early graft thrombosis after off-pump coronary artery bypass grafting (OPCAB). DESIGN AND PARTICIPANTS: Prospective study of 78 OPCAB patients with 151 venous bypass grafts treated with perioperative aspirin and intraoperative heparin (250 U/kg). SETTING: Tertiary, academic medical center. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Hypercoagulability, defined by TEG (maximum amplitude [MA]>70 mm), whole-blood aggregometry (>15 ohms after 5 mcl/mL collagen) or hemoSTATUS (Ch5CR>0.5), was serially assessed around OPCAB. An immediate decline in platelet function after surgery and on postoperative day 1 returned to normal by postoperative day 3 in most patients. Graft blood flow was analyzed intraoperatively, and vein biopsies were analyzed for endothelial disruption. Graft patency was assessed by multichannel computed tomography coronary angiography on postoperative day 5. No differences in any of the platelet function assays were noted for the 8 patients with graft thrombosis (n=8 grafts) versus the 68 patients with all patent grafts (n=129 grafts). Ten patients developed a rise in platelet function postoperatively >1 SD above baseline; only 1 developed graft thrombosis (p=not significant v patients with normal platelet function). CONCLUSIONS: OPCAB is not associated with a significant activation in postoperative platelet function. This study suggests that if hypercoagulability exists after OPCAB, it is not involved in the pathogenesis of arterial thrombotic events such as early bypass graft failure.

Incidence of and risk factors for perioperative optic neuropathy after cardiac surgery.

BACKGROUND: Visual loss from optic neuropathy rarely occurs in the perioperative period in patients who have undergone nonocular surgery. We performed a retrospective, matched, case-control study to determine the incidence of perioperative optic neuropathy (PON) after cardiac surgery with the use of cardiopulmonary bypass (CPB) and to determine risk factors that may lead to this potentially devastating complication. METHODS: Medical records of all patients undergoing cardiac surgery during a 9-year period were reviewed retrospectively to identify visual loss from acute unilateral and bilateral optic neuropathy during the perioperative period that had developed in patients. Data were collected from these patients and compared with data from control subjects matched for age, gender, risk factors for vascular disease, and type of surgery to determine the incidence of and potential risk factors for PON. RESULTS: Of 9701 surgical patients requiring CPB, 11 patients (0.113%) with PON were identified. Although both the absolute and relative drop in hemoglobin during the perioperative period approached statistical significance, no other putative risk factors were identified. CONCLUSIONS: The risk of PON associated with cardiac surgery in which CPB is used is low but substantial. The factors that lead to the condition remain unknown, although the presence of systemic vascular disease and both the absolute and relative drop in hemoglobin during the perioperative period seem to be important. Because PON often causes profound permanent visual loss, we recommend that patients, particularly those with systemic vascular disease, for whom cardiac surgery with CPB is planned, be made aware of this potential complication.

Myocardial reperfusion injury: etiology, mechanisms, and therapies.

Reperfusion of ischemic myocardium is required for tissue survival; however, reperfusion elicits pathologic consequences. Myocardial reperfusion injury is a multifarious process that is mediated in part by oxygen free radicals, neutrophil-endothelium interactions, apoptosis, and intracellular calcium overload. The oxygen paradox describes the contradictory need to delivery oxygen to ischemic tissue and the resultant reduction of oxygen to form free radicals that are involved in macromolecule oxidation, membrane disfunction, apoptosis, and damaged calcium sequestering ability, which results in hypercontracture. These cell-damaging crises are amplified by the excessive activation of neutrophils, which promote the formation of proinflammatory mediators, oxygen radicals, and the reduction of endothelial nitric oxide formation, leading to increased neutrophil-endothelium interactions and capillary occlusion. Neutrophil action is twofold, however, because it is required for necrotic debris removal after severe ischemia. The oxygen radicals produced by neutrophils, endothelium, and myocytes may also play a role in activating the apoptotic cascade. Although the role of apoptosis in reperfusion injury is controversial, apoptotic cells are found in infarcted tissue. One of the key mediators may be increased inner mitochondrial membrane permeability, resulting in reduced ATP formation, release of cytochrome c, and caspase activation, which is key to promotion of apoptosis. Increased mitochondrial membrane permeability occurs during exposure to supraphysiological calcium concentrations. This occurs because of compensatory Na+/Ca2+ exchange to remove the excess intracellular sodium resulting from decreased Na+/K+ pumping during ischemia and increased Na+/H+ exchange following reperfusion. Supraphysiological calcium elicits hypercontracture and cellular damage. The various therapies being developed to diminish myocardial reperfusion injury involve inhibition of the processes described above as well as others. Although single therapies have shown some promise, the complexity of the response to reperfusion has made dramatic improvement elusive. Effective treatment will most likely require multifaceted antagonism of the numerous pathological cascades initiated by reperfusion.

Nonheparinized partial cardiopulmonary bypass for repair of traumatic aortic rupture.

Traumatic aortic rupture requires rapid, definitive repair for optimal outcome, particularly with respect to distal neurologic function. Over the past 10 years, the R Adams Cowley Shock Trauma Center of the University of Maryland has used partial cardiopulmonary bypass without systemic heparization exclusively for all repairs of the descending aorta. A heparin-bonded circuit allows for controlled distal perfusion and obviates the need for heparinization. Excellent outcome with minimal morbidity has been achieved using this technique. Our protocol and perfusion apparatus are discussed within.

Feasibility of off-pump ASD closure using real-time 3-D echocardiography.

BACKGROUND: If surgeons could "see " through blood and cardiac chamber walls, it would ultimately be unnecessary to open the heart or use cardiopulmonary bypass to perform procedures such as atrial septal defect (ASD) closure or mitral valve repair. Conventional echocardiography generates cross-sectional images that are not satisfactory as the only visualization for surgical procedures, and current 3-Dimensional (3-D) CT and echo systems take several minutes to compose and process a single still frame. Recently, however, the first system for real-time 3-D echocardiography has been developed. This study examines whether real-time 3-D echocardiography can provide images of sufficient anatomic definition, depth perception, and image resolution to substitute for optical visualization in performing ASD closures. METHODS: A prototype Volumetrics 3-D echocardiographic system was evaluated in a water bath on a complex-surfaced standard reference model to determine the image resolution and define the ideal imaging parameters. A static image and views of sutures being placed with an endoscopic needle driver and two commercial suture placement devices were evaluated at multiple angles and distances from the target. The resulting images were graded by a blinded reviewer. Once the best imaging parameters were determined, five porcine ASDs were closed with interrupted sutures, running sutures, or a pursestring suture using only echo visualization. RESULTS: The highest quality images were obtained with the probe at a distance of 4-6 cm and at angles perpendicular or 45 degrees forward to the target. Spatial and temporal resolutions were adequate to suture all ASDs closed under only echo guidance. CONCLUSIONS: The evaluated real-time 3-D echo system provided adequate spatial and temporal information to act as a guide for surgical procedures.

Cardiovascular responses to repetitive defibrillation during implantable cardioverter-defibrillator testing.

OBJECTIVE: To study the effects of electrical applications and subsequent postshock hypotension on myocardial performance and vascular tone during implantable cardioverter-defibrillator (ICD) placement. DESIGN: Prospective, blinded, observational investigation. SETTING: Single, university-affiliated institution. PARTICIPANTS: Twenty patients undergoing elective ICD placement and testing under general anesthesia. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Serial measurements were made of hemodynamic variables, left ventricular end-systolic (ESA) and end-diastolic (EDA) areas, fractional-area-of-contraction (FAC), time of hypoperfusion (when mean arterial pressure < or =50 mmHg postshock), and applied conversion energy. Multiple linear regression was performed to determine correlations among collected variables, and repeated measures analysis of variance was used to compare mean values. Minimal changes were detected in mean values of arterial, pulmonary, and central venous pressures; cardiac output; heart rate; and mixed venous saturation during repeated testing. Percentage changes in cardiac index (CI) rose and systemic vascular resistance index (SVRI) fell, however, as the number of shocks increased, reaching significance at the seventh and eighth shocks (v baseline; both p = 0.015). The percentage change in CI was linearly related to hypoperfusion time and accumulated energy (%deltaCI = 1.553 + [0.068 x sigma hypoperfusion time [sec]], r = 0.92, p < 0.001; %deltaCI = 0.326 + [0.125 x sigma Energy [J]], r = 0.94, p < 0.001). The percentage change in SVRI was inversely related to hypoperfusion time and accumulated energy (%deltaSVRI = 2.195 - [0.122 x sigma energy [J]], r = 0.79, p = 0.004; %deltaSVRI = 0.542 - [0.0634 - sigma hypoperfusion time [sec]], r = 0.73, p = 0.01). Echocardiographic EDA, ESA, and FAC were not significantly changed but showed substantial variability. CONCLUSION: Hemodynamic stability was generally well maintained during ICD placement and testing. Increases in CI were associated with concurrent reductions in systemic afterload, rather than enhanced FAC. Increasing postshock hypotension and applied energy were associated with decreases in CI and systemic afterload. Insignificant, but highly variable, changes were noted echocardiographically.