Aims and Objectives: Postoperative atrial fibrillation (POAF) is the most common arrhythmia after coronary artery bypass grafting (CABG) surgery. The identification of patients at risk for POAF would be helpful to guide prophylactic therapy. Presently, there is no simple preoperative scoring system available to predict patients at higher risk of POAF. In a retrospective observational study, we evaluated the usefulness of CHA ₂ DS ₂ -VASc score to predict POAF after CABG. Materials and Methods: After obtaining approval from Institutional Review Board, 729 patients undergoing CABG on cardiopulmonary bypass (CPB) were enrolled. Patients were followed in the postoperative period for POAF. A multiple regression analysis was run to predict POAF from various variables. The area under the receiver operating characteristic (ROC) curve was calculated to test discriminatory power of CHA ₂ DS ₂ -VASc score to predict POAF. Results: POAF occurred in 95 (13%) patients. The patients with POAF had higher CHA ₂ DS ₂ -VASc scores than those without POAF (4.09 ± 0.90 vs. 2.31 ± 1.21; P < 0.001). The POAF rates after cardiac surgery increased with increasing CHA ₂ DS ₂ -VASc scores. The odds ratio for predicting POAF was highest with higher CHA ₂ DS ₂ -VASc scores (3.68). When ROC curve was calculated for the CHA ₂ DS ₂ -VASc scores, area of 0.87 was obtained, which was statistically significant (P < 0.0001). Conclusions: The CHA ₂ DS ₂ -VASc score was found useful in predicting POAF after CABG. This scoring system is simple and convenient to use in the preoperative period to alert the clinician about higher probability of POAF after CABG surgery.

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Objective: The aim was to compare various pre-and post-operative parameters and to identify the predictors of mortality in neonates, infants, and older children undergoing Modified Blalock Taussig shunt (MBTS). Materials and Methods: Medical records of 134 children who underwent MBTS over a period of 2 years through thoracotomy were reviewed. Children were divided into three groups-neonates, infants, and older children. For analysis, various pre-and post-operative variables were recorded, including complications and mortality. Results: The increase in PaO ₂ and SaO ₂ levels after surgery was similar and statistically significant in all the three groups. The requirement of adrenaline, duration of ventilation and mortality was significantly higher in neonates. The overall mortality and infant mortality was 4.5% and 8%, respectively. Conclusion: Neonates are at increased risk of complications and mortality compared with older children. Age (<30 days), weight (<3 kg), packed red blood cells transfusion >6 ml/kg, mechanical ventilation >24 h and post shunt increase in PaO ₂ (P _Diff ) <25% of baseline PaO ₂ are independent predictors of mortality in children undergoing MBTS.

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Studies in cardiac surgical patients have shown an association of hyperglycemia with increased incidences of sepsis, mediastinitis, prolonged mechanical ventilation, cardiac arrhythmias and longer intensive care and hospital stay. There is considerable controversy regarding appropriate glycemic management in these patients and in the definition of hyperglycemia and hypoglycemia or the blood sugar levels at which therapy should be initiated. There is also dilemma regarding the usage of "tight glycemic control" with studies showing conflicting evidences. Part of the controversy can be explained by the differing designs of these studies and the variable definitions of hyperglycemia and hypoglycemia.

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Hypertrophic cardiomyopathy (HCM) poses many unique challenges regarding the conduct of anesthesia and surgery. Adequate preload, control of sympathetic stimulation, heart rate, and increased afterload are required to decrease the left ventricular outflow tract obstruction. Comprehensive intraoperative transesophageal echocardiography (TEE) examination confirms the diagnosis, elucidates the pathophysiology, and identifies the various anomalies of mitral valve apparatus and allows assessment of the adequacy of surgery. In this review, we focus on the preoperative assessment, conduct of anesthesia and comprehensive TEE examination of patients presenting for surgery with HCM. The various surgical options are extended myectomy and resection, plication and release.

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Objective: We studied effects of phenylephrine (PHE) on postischemic functional recovery and myocardial injury in an ischemia-reperfusion (I-R) experimental model. Materials and Methods: Rat hearts were Langendorff-perfused and subjected to 30 min zero-flow ischemia (I) and 60 min reperfusion (R). During R PHE was added at doses of 1 μM (n = 10) and 50 μM (n = 12). Hearts (n = 14) subjected to 30 and 60 min of I-R served as controls. Contractile function was assessed by left ventricular developed pressure (LVDP) and the rate of increase and decrease of LVDP; apoptosis by fluorescent imaging targeting activated caspase-3, while myocardial injury by lactate dehydrogenase (LDH) released during R. Activation of kinases was measured at 5, 15, and 60 min of R using western blotting. Results: PHE did not improve postischemic contractile function. PHE increased LDH release (IU/g); 102 ± 10.4 (Mean ± standard error of mean) control versus 148 ± 14.8 PHE (1), and 145.3 ± 11 PHE (50) hearts, (P < 0.05). PHE markedly increased apoptosis. Molecular analysis showed no effect of PHE on the activation of proapoptotic c-Jun N-terminal kinase signaling; a differential pattern of p38 mitogen activated protein kinase (MAPK) activation was found depending on the PHE dose used. With 1 μM PHE, p-p38/total-p38 MAPK levels at R were markedly increased, indicating its detrimental effect. With PHE 50 μM, no further changes in p38 MAPK were seen. Activation of Akt kinase was decreased implying involvement of different mechanisms in this response. Conclusions: PHE administration during reperfusion does not improve postischemic recovery due to exacerbation of myocardial necrosis and apoptosis. This finding may be of clinical and therapeutic relevance.

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Protein S (PS) along with activated protein C plays an important role in the down-regulation of in vivo thrombin generation. Its deficiency can cause abnormal and inappropriate clot formation within the circulation necessitating chronic anticoagulation therapy. The risk of developing thrombotic complications is heightened in the perioperative period in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Heparin resistance is very rare in these patients, especially when antithrombin levels are near normal. Management of CPB in this scenario is quite challenging. We report the perioperative management, particularly the CPB management, of a patient with type I PS deficiency and incidentally detected heparin resistance, who underwent coronary artery bypass grafting with CPB.

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Thirty seven year old asymptomatic male underwent routine medical examination which revealed an abnormal mass in the right atrium. Family history was not suggestive of any cardiac or malignant disease. Detailed investigation detected deficiency of protein S, which is a vitamin K dependent protein and a cofactor for activated protein C mediated cleavage of factor Va and VIIIa. The deficiency of protein S predisposes to venous thrombosis. Further investigation revealed that it was an organized calcified thrombus in right atrium occupying almost whole of the cavity. Various approaches including surgical excision, thrombolysis and anticoagulation has been used to manage such thrombosis. However therapeutic approach is still a question of debate. Atriotomy and excision of mass was done using cardiopulmonary bypass.

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In patients with a right to left intracardiac shunt, air embolism results in an obligatory systemic embolization. Nonembolization of entrained air is described in a child with a single ventricle physiology who had earlier undergone bidirectional Glenn shunt construction and Damus-Kaye-Stansel anastomosis. The air entrainment was detected by intra-operative transesophageal echocardiography. The combined effect of a "diving bell" phenomenon and mild aortic valve regurgitation are suggested as the reasons for the confinement of air into the ventricle preventing catastrophic systemic embolization.

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