Stage 1 palliation of hypoplastic left heart syndrome: implications of blood gases.

OBJECTIVE: To estimate ratios of pulmonary-to-systemic blood flows (Qp/Qs) after stage I palliation (Norwood operation) for hypoplastic left heart syndrome and to determine whether early postoperative death can be associated with abnormalities of Qp/Qs ratios. DESIGN: Retrospective. SETTING: University hospital. PARTICIPANTS: Patients who underwent stage I palliation (Norwood operation) for hypoplastic left heart syndrome (n = 76). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The results of the last intraoperative blood gas analysis were compared between patients who survived the day of operation (58 of 76) and the patients who died intraoperatively or within 4 hours after operation (18 of 76). Qp/Qs ratios were calculated using the Fick principle from arterial and venous oxygen saturations at estimated pulmonary venous oxygen saturation of 95%. A lower arterial oxygen saturation (SaO(2), 69.0 +/- 20.5% v 77.3 +/- 8.5%; p < 0.05) and more marked metabolic acidosis (pH, 7.244 +/- 0.115 v 7.298 +/- 0.095; p < 0.05; base excess, -6.8 +/- 4.4 v -3.0 +/- 4.2; p < 0.05) were observed in nonsurvivors. Calculated Qp/Qs ratios ranged between 0.2 and 6.5 in survivors and between 0.6 and 1.9 in nonsurvivors. CONCLUSIONS: Postoperative excessive pulmonary blood flow was not implicated as a cause of death based on blood gas data and Qp/Qs ratios. In nonsurvivors, low cardiac output and hypoxemia were assumed to be major problems.

Incidence and risk factors of perioperative cerebral complications. Heart transplantation compared to coronary artery bypass grafting and valve surgery.

OBJECTIVE: The aim of this study was to define the neurologic risk of heart transplantation compared to coronary artery bypass grafting (CABG) and valve surgery. DESIGN: A retrospective study. SETTING: A university hospital. PATIENTS: 8001 patients undergoing heart transplantation, CABG and valve surgery. MEASURES: The incidences of perioperative central nervous system (CNS) complications were compared between different procedures. Risk factors were analysed using univariate and multivariate methods. RESULTS: The overall incidence of CNS complications was 19.8% (78/393) in heart transplantation, 3.1% (176/5734) in elective CABG, 9.5% (161/1689) in elective valve surgery, 10.3% (15/146) in emergency CABG and 51.3% (20/39) in emergency valve surgery. Most powerful predictors of CNS complications were preoperative intra-aortic counterpulsation (IABP) in the heart transplantation group, age >65 years in the CABG group and preoperative use of catecholamine in the valve group. CONCLUSIONS: CNS complications occur much more frequently after heart transplantation than elective CABG and valve surgery. The high incidence of CNS complications after emergency operations as well as preoperative catecholamine and IABP as powerful contributing factors suggest that preoperative cerebral hypoperfusion due to a compromised hemodynamic state facilitates postoperative CNS complications and this may partly explain the high incidence of CNS complications after heart transplantation.

Studies on the mechanism of action of the hypoglycemic agent, 2-(3-methylcinnamylhydrazono)-propionate (BM 42.304).

A new hypoglycemic agent, 2-(3-methylcinnamylhydrazono)-propionate MCHP (BM 42.304) was shown to be an inhibitor of the transfer of long-chain fatty acids across the mitochondrial inner membrane. The following data support this conclusion: the drug, at already 5 microM, inhibited ketogenesis from oleate but not from octanoate in the perfused guinea-pig liver; likewise, ketogenesis from L-(-)-palmitoylcarnitine and palmitoyl-CoA + L-(-)-carnitine, but not from octanoate, was depressed in isolated guinea-pig liver mitochondria. Oxigraphic measurements of the oxygen uptake by isolated mitochondria showed that the drug impaired oxygen uptake with the long-chain fatty acid derivatives but not with octanoate. Finally, in vivo effects of the drug such as hypoketonemia and an increased concentration of free fatty acids in blood are in agreement with the above formulated mechanism of action. A comment is given on the relationships between fatty acid oxidation and gluconeogenesis in the guinea-pig liver.