Study of leukocytic hydrolytic enzymes in patients with acute stage of coronary heart disease.

BACKGROUND: Coronary heart disease (CHD) is a major killer worldwide. Atherosclerosis, which is the basis of CHD, is believed to be an inflammatory disorder. Though various aspects of atherosclerosis are extensively studied, leukocytic hydrolytic enzymes are not studied very well with respect to CHD. AIM: This study was planned to assess changes associated with leukocytic hydrolases in CHD patients. SETTING AND DESIGN: A tertiary care hospital; case-control study. MATERIALS AND METHODS: 106 patients with acute myocardial infarction, 60 patients with unstable angina and 45 healthy controls were included in the study. Acid phosphatase, lysozyme, adenosine deaminase (ADA) and cathepsin-G levels were estimated from leukocytes. Reduced glutathione (GSH) and malondialdehyde (MDA) levels were measured. STATISTICAL ANALYSIS: Statistical comparison of data was done using student's t-test (unpaired). Correlation difference was calculated by using Pearson correlation coefficient. RESULTS: Significantly higher levels of acid phosphatase, lysozyme, ADA with lower levels of cathepsin G in leukocytes were observed in CHD group. We also found significantly higher levels of serum MDA with lower concentrations of blood GSH in CHD group. In diabetic CHD group, significantly higher levels of leukocytic acid phosphatase, lysozyme, ADA and serum MDA with lower levels of cathepsin G and blood GSH were observed. CONCLUSIONS: Our study indicates that leukocyte hydrolytic enzymes, mainly acid phosphatase, lysozyme and ADA were more active in CHD patients and may contribute to inflammation related with CHD. Its also indicates that leukocyte cathepsin-G may have antiinflammatory role.

Blood lactate levels during cardiopulmonary bypass for valvular heart surgery.

Cardiopulmonary bypass (CPB) is widely used to maintain systemic perfusion and oxygenation during open-heart surgery. Tissue hypoperfusion with resultant lactic acidosis during CPB, may occur during hypothermia, extreme haemodilution, low flow CPB, and excessive neurohormonal activation. There has been no documentation of the correlation between blood lactate level elevations in the perioperative period, and its relation to preoperative New York Heart Association (NYHA) classification and the use of ionotropic support during weaning from CPB, duration of postoperative ventilatory support and perioperative mortality. We studied the perioperative blood lactate levels in 82 patients undergoing valvular heart surgery. Arterial blood samples were collected at different stages of CPB. The observed mean baseline lactate levels were 1.9+/-0.8 mmol/L (normal range of 0.9 to 1.7 mmol/L). The mean circulating lactate levels at 15 min and 45 min after institution of CPB increased to 7.01+/-2.6 mmol/L and 9.92+/-3.5 mmol/L. A progressive decline in the mean lactate level, was seen during rewarming (at 35 degrees C), immediately off-bypass, 24 hours and 48 hours postoperatively with mean lactate levels being 7.01+/-3.2 mmol/L, 4.75+/-1.01 mmol/L, 3.06+/-1.1 mmol/L, and 2.10+/-1.05 mmol/L respectively. Comparison of mean lactate levels in NYHA class I, II, III, and IV patients showed that in the intraoperative period and immediately after CPB, the elevation in lactate levels were statistically significant (p< 0.001) in patients in NYHA Class IV. However the values, in all classes, were similar at 24 and 48 hours after CPB. Also, patients with lactate levels >4 mmol/ L required prolonged inotropic and ventilatory support.

Glutaric aciduria type I associated with learning disability.

The authors report a 7-year-8-months-old boy with glutaric aciduria type I who had associated dyslexia, dysgraphia and dyscalculia. The diagnosis of glutaric aciduria type I was confirmed on the basis of characteristic neuroimaging and biochemical findings. Axial T1-weighted magnetic resonance imaging scan of the brain showed fronto-temporal atrophy, open opercula and bat-wing dilatation of the sylvian fissures. Axial T[2]-weighted and FLAIR imaging showed hyperintense signal abnormality in both putamen and in the fronto-parietal deep white matter. Urinary aminoacidogram by thin layer chromatography revealed a generalized aminoaciduria. Urinary organic acid analysis by gas chromatography- mass spectroscopy revealed a marked excretion of glutaric acid. Psychoeducational testing was used to diagnose the learning disability. We postulate that the accumulation of glutaric acid and other metabolites was responsible for the child developing the associated learning disability.