Redo sternotomy for cardiac reoperations using peripheral heparin-bonded cardiopulmonary bypass circuits without systemic heparinization: technique and results.

OBJECTIVE: Cardiac reoperations are challenging and time-consuming and incur a high incidence of perioperative complications because of injuries to cardiac structures, bleeding, and hemodynamic instability. Some centers are using extracorporeal circulation with heparinization at the time of resternotomy, but it leads to prolonged anticoagulation, platelet dysfunction, fibrinolysis, coagulopathy, and morbidity. The authors routinely perform resternotomy in complex surgery with the support of heparinless cardiopulmonary bypass with heparin-bonded circuits (HBCs). The authors describe their technique, indication, and results. METHODS: The femoral artery or axillary artery and femoral veins are cannulated before sternotomy, and cardiopulmonary bypass is instituted using an HBC without systemic heparinization. Systemic heparin (200-300 U/kg) is administered when all structures are isolated before aortic cross-clamping (activated coagulation time >400 seconds). RESULTS: Between 1996 and 2008, 336 patients underwent redo sternotomy using the HBC for complex cardiac procedures, with 29 deaths (8.6% deaths within 30 days). Only 5 (1.5%) of 336 patients sustained injury to the right ventricle, aorta, bypass grafts, or ventricular fibrillation during re-entry without hemodynamic deterioration; and underwent uneventful repair and outcomes. There was no online HBC thrombosis. CONCLUSIONS: This study shows that HBC without systemic heparinization during resternotomy can be used safely in complex redo cardiac surgery. The heart is completely decompressed during the resternotomy, allowing easy dissection, less likely injury to vital structures, and less bleeding without compromising the hemodynamics.

The hemodynamic effects of methylene blue when administered at the onset of cardiopulmonary bypass.

Hypotension occurs during cardiopulmonary bypass (CPB), in part because of induction of the inflammatory response, for which nitric oxide and guanylate cyclase play a central role. In this study we examined the hemodynamic effects of methylene blue (MB), an inhibitor of guanylate cyclase, administered during cardiopulmonary bypass (CPB) to patients taking angiotensin-converting enzyme inhibitors. Thirty patients undergoing cardiac surgery were randomized to receive either MB (3 mg/kg) or saline (S) after institution of CPB and cardioplegic arrest. CPB was managed similarly for all study patients. Hemodynamic data were assessed before, during, and after CPB. The use of vasopressors was recorded. All study patients experienced a similar reduction in mean arterial blood pressure (MAP) and systemic vascular resistance (SVR) with the onset of CPB and cardioplegic arrest. MB increased MAP and SVR and this effect lasted for 40 minutes. The saline group demonstrated a persistently reduced MAP and SVR throughout CPB. The saline group received phenylephrine more frequently during CPB, and more norepinephrine after CPB to maintain a desirable MAP. The MB group recorded significantly lower serum lactate levels despite equal or greater MAP and SVR. In conclusion, administration of MB after institution of CPB for patients taking angiotensin-converting enzyme inhibitors increased MAP and SVR and reduced the need for vasopressors. Furthermore, serum lactate levels were lower in MB patients, suggesting more favorable tissue perfusion.

Prototype anionic detergent technique used to decellularize allograft valve conduits evaluated in the right ventricular outflow tract in sheep.

BACKGROUND AND AIM OF THE STUDY: Biodegradable polymeric materials or extracellular matrix scaffolds are used in tissue-engineered heart valve designs, with the expectation of replicating the anatomic, histological and biomechanical characteristics of semi-lunar valves. The study aim was to evaluate the extent of in-vivo recellularization and the explant pathology findings of a prototype anionic, non-denaturing detergent and endonuclease technique used to decellularize allograft (homograft) valve conduits implanted in the right ventricular outflow tract (RVOT) of sheep, and to identify possible risks associated with tissue-engineered heart valve conduits based on decellularized allograft semilunar valve scaffolds. METHODS: Valve conduits were decellularized using a solution of N-lauroylsarcosinate and endonucleases, rinsed in lactated Ringers solution, and stored in an antibiotic solution at 4 degrees C until implanted. Explanted valves and unimplanted controls were examined macroscopically, radiographically (for calcification) and histologically using immunohistochemistry (IHC), routine and special histological stains, transmission electron microscopy (TEM) and polarized light microscopy (evaluation of collagen crimp). RESULTS: Cells and cellular remnants were uniformly absent in the decellularized cusps, but occasional focal sites of arterial wall smooth muscle cells and to a greater extent subvalvular cardiac myocytes were variably retained. The trilaminar histological structure of the cusp was preserved. Valve conduit-related pathology consisted of intracuspal hematoma formation, collagen fraying, thinning of the conduit wall, and inflammatory cells associated with cardiac myocyte remnants. Cuspal calcification was not seen, but elastic fibers in the conduit wall and retained subvalvular cardiac myocyte remnants were liable to calcification. Fibrous sheath formation was present on the luminal surface of the conduit and extended over the cuspal surfaces to a variable extent. Myofibroblast-like cells repopulated the conduit wall and the basal region of the cusp. Re-endothelialization was variably present on the cuspal surfaces. CONCLUSION: Explant pathology findings showed that in-vivo recellularization occurred, but was focally limited to regions of the arterial wall and cusp base. Safety concerns related to detergent and endonuclease use were identified. Methods to eliminate the potential for structural deterioration and enhance the rate and extent of recellularization of valve conduit tissue are required. Pathology findings showed implantation of valve conduits in the RVOT of juvenile sheep for 20 weeks to be a reliable animal model for the initial in-vivo assessment of decellularized valves. A 20-week period may be insufficient however to evaluate the long-term safety and effectiveness of a tissue-engineered valve conduit, as these depend on effective and phenotypically appropriate recellularization accompanied by sustained cell viability and function.

Endovascular vein harvest: systemic carbon dioxide absorption.

OBJECTIVE: Endovascular vein harvest (EDVH) requires CO(2) insufflation to expand the subcutaneous space, allowing visualization and dissection of the saphenous vein. The purpose of this study was to assess the extent of CO(2) absorption during EDVH. DESIGN: Prospective observational study. SETTING: Single tertiary care hospital. PATIENTS: Sixty patients (30 EDVH and 30 open-vein harvest) undergoing isolated coronary artery bypass graft surgery. METHODS: Hemodynamic, procedural, and laboratory data were collected prior to (baseline), during, and at it the conclusion (final) of vein harvesting. Data were also collected during cardiopulmonary bypass (CPB). Data were compared by using t tests, analysis of variance, and correlation statistics when needed. RESULTS: There were significant increases in arterial CO(2) (PaCO(2), 35%) and decreases in pH (1.35%) during EDVH. These were associated with increases in heart rate, mean blood pressure, and cardiac output. Within the EDVH group, greater elevations (>10 mmHg) in PaCO2 were more likely during difficult harvest procedures, and these patients exhibited greater increase in heart rate. Elevated CO(2) persisted during CPB, requiring higher systemic gas flows and greater use of phenylephrine to maintain desired hemodynamics. CONCLUSION: EDVH was associated with systemic absorption of CO(2). Greater absorption was more likely in difficult procedures and was associated with greater hemodynamic changes requiring medical therapy.