Cut-off levels based on deviation from standard negative control is better than moderate level based on fixed cut-off for ACA assessed using ELISA for the diagnosis of antiphospholipid syndrome.

AIM: To assess the consistency of the standard negative control of IgG and IgM ACA levels within runs and batches of tests, and levels of ACA agreement between those established according to deviation from standard negative control and those established based on a fixed level cut off. METHODS: Serum samples of 148 patients who presented an INR < 0.9 or prothrombin activity of > 130% or aPTT below 0.8 times control or thrombosis with aPTT below 1.2 times control were tested in a 22-time running test to determine IgG and IgM ACA levels using Quanta Lite ACA IgG (HRP) and Quanta Lite ACA IgM (HRP) commercial reagents. RESULTS: Coefficients of variant within runs and batches of standard negative control IgG and IgM ACA levels were 19.30% and 29.17% respectively. Using kappa statistics to determine degree of agreement between cut-off levels by deviation from standard negative control and fixed cut-off level of ACA identified using ELISA, the disagreement in IgM and IgG were k 0.30, and 95% CI of k 0.27 to 0.34 (z = 1.033, p = 0.3015), and k 0.63, and 95% CI of k 0.53 to 0.73 (z = 1.411, p = 0.1584) for cut-off levels based on deviations from standard negative control and fixed cut-off levels respectively. Cut-off levels based on deviation from standard negative control was more sensitive, with a 92% predictive true positive value, compared to a 69% predictive true positive value by fixed cut-off levels of IgM ACA detected using ELISA, and nearly equivalent to IgG ACA, with 84.4% and 87.1% predictive true positive values respectively. CONCLUSION: Cut-off points based on fixed levels of ACA detected using ELISA cannot be applied, because both IgG and IgM ACA levels of standard negative control were inconsistent among runs and batches. Cut-off points based on the deviation of 3 standard negative control levels for IgG ACA and based on deviations of 2.5 times from standard negative control levels for IgM ACA were better than cut off by fixed levels of ACA in producing true positive results.

Clinical Manifestation of Acute Myocardial Infarction in the Elderly.

A retrospective study were performed in patients with acute myocardial infarction (AMI) that hospitalized in ICCU Cipto Mangunkusumo hospital, Jakarta during the period of January 1994 until Decmber 1999. There were 513 patients hospitalized with MCI, 227 patients (44.2%) were classified as elderly, and 35.2% of them were female. Most of the elderly AMI patients reported typical chest pain just like their younger counterparts. Elderly AMI patients tend to come later to the hospital, and more Q-wave myocardial infarction were identified compared to non- Q-wave myocardial infarction. Risk factors of diabetes mellitus and hypertension were more common among the elderly. The prevalence of atrial fibrillation and the mortality rate were higher among elderly AMI patients.

Anti-thrombin III, Protein C, and Protein S deficiency in acute coronary syndrome.

The final most common pathway for the majority of coronary artery disease is occlusion of a coronary vessel. Under normal conditions, antithrombin III (AT III), protein C, and protein S as an active protein C cofactor, are natural anticoagulants (hemostatic control) that balances procoagulant activity (thrombin antithrombin complex balance) to prevent thrombosis. If the condition becomes unbalanced, natural anticoagulants and the procoagulants can lead to thrombosis. Thirty subjects with acute coronary syndrome (ACS) were studied for the incidence of antithrombin III (AT III), protein C, and protein S deficiencies, and the result were compare to the control group. Among patients with ACS, the frequency of distribution of AT-III with activity < 75% were 23,3% (7 of 30), and only 6,7% ( 2 of 30 ) in control subject. No one of the 30 control subject have protein C activity deficient, in ACS with activity < 70% were 13,3% (4 of 30). Fifteen out of the 30 (50%) control subjects had protein S activity deficiency, while protein S deficiency activity < 70% was found 73.3.% (22 out of 30). On linear regression, the deterministic coefficient of AT-III activity deficiency to the development ACS was 13,25 %, and the deterministic coefficient of protein C activity deficient to the development of ACS was 9,06 %. The cut-off point for AT-III without protein S deficiency expected to contribute to the development of vessel disease was 45%. On discriminant analysis, protein C activity deficiency posed a risk for ACS of 4,5 greater than non deficient subjects, and AT-III activity deficiency posed a risk for ACS of 3,5 times greater than non deficient subjects. On binary logistic regression, protein S activity acted only as a reinforcing factor of AT-III activity deficiency in the development of ACS. Protein C and AT III deficiency can trigger ACS, with determinant coefficients of 9,06% and 13,25% respectively. Low levels of protein C posed a greater risk of ACS than low levels of AT III. Protein S deficiency was a reinforcing factor on AT-III deficient to development of ACS. The cut-off point of AT-III without protein S deficiency expected to give single vessel disease was 45%, and 9,5% for the development of triple vessel disease.