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Biomedical subjects

S Timár

Publications and source records attributed to S Timár.

5 recordsLinked to original sources

[Repeat thrombolysis in acute myocardial infarction].

During two years period (Jul. 97-Aug. 99) data of patients suffering from recurrent acute myocardial infarct within 6 days were compared by retrospective analysis. In this interval authors treated 58 patients with recurrent myocardial infarct. 22 patients were transmitted to a catheterisation lab, data of the other 36 patients were compared. There were two treatment groups: 18 patients received repeated thrombolysis (IT group), and 18 patients got conventional therapy (HT group). In the thrombolytic group 15 patients received streptokinase infusion again, and urokinase infusion was administred in 3 patients at second time. The patients were not transferred to a cath lab, because of their older ages (10 patients), or capacity problems (13 patients), or in absence of their signed consent (13 patients). Comparisons were made on the basis of non invasive diagnostic procedures (reperfusion signs suggested by ECGs and enzymatic changes, and left ventricular ejection fraction at discharge), bleeding rate, and frequency of recurring angina at the 3 months visit, and on the basis of mortality. Ejection fractions and reperfusion signs were better in the repeated thrombolytic group (time of maximal level ST elevation: IT 19.70 +/- 6.00 min, HT 23.17 +/- 5.15 min, p = 0.26 NS; T wave inversion time within six hours: IT 168 +/- 45.17 min, HT 170 +/- 58.99 min, p = 0.94; reperfusion arrhythmia: IT 7, HT 3, p = 0.15; CK peak time: IT 16.89 +/- 6.94 hour, HT 20.00 +/- 6.72 hour, p = 0.18 NS; CK-MB peak time: IT 12.22 +/- 7.19 hour, HT 16.67 +/- 6.17, hour, p = 0.55; > 3 x CK peak time: IT 14.18 +/- 6.03 hour, HT 20.00 +/- 7.37 hour, p = 0.06, > 3 x CK-MB peak time: IT 8.80 +/- 4.54 hour, HT 15.20 +/- 6.19 hour, p = 0.02, ECHO EF: IT 48.53 +/- 6.81%, HT 43.14 +/- 4.90%, p = 0.02, Isotope ventriculography EF: IT 50.87 +/- 5.45%, HT 44.57 +/- 4.89%, p = 0.003), however the bleeding rate was moderately higher (minor bleeding: IT 7, HT 3, p = 0.15, major bleeding: IT 3, HT 1). The frequency of ischemic episodes at 3-month visit, and 3-month mortality were similar in the two groups (episodes of angina: IT 2.00 +/- 1.57, HT 2.42 +/- 1.88, p = 0.55; mortality: IT 4, HT 6, p = 0.46). Repeated thrombolysis is an effective therapeutical tool in centres without cath lab--according to the risk-benefit ratio too--in the case of early repeated myocardial infarct.

Electrocardiography↗

Balance of prostacyclin and thromboxane in offspring of parents with premature coronary arterial disease.

6-keto-prostaglandin F1a and thromboxane B2 were determined in order to obtain more information about the prostacyclin synthesis and thromboxane A2 release in 3- to 18-year-old healthy children and in offspring of parents who have had an acute myocardial infarction before the age of 45. The authors demonstrated a reduction of plasma prostacyclin synthesis in children with a positive family history of premature coronary arterial disease. Thromboxane levels in the affected adolescent boys were significantly lower compared with the controls. The ratio of thromboxane:prostacyclin in endangered children did not show a significant difference from that of healthy controls. These data indicate that prostaglandins are a definitive marker for identifying cardiovascular risk children. It must be supposed that in adolescence, only in boys, with a positive family history of premature coronary arterial disease, a compensatory mechanism exists to protect them from developing an imbalance in the regulation of prostaglandins.

6-Ketoprostaglandin F1 alpha↗

[Plasma prostacyclin and thromboxane concentration in healthy children and in offspring of parents suffering from myocardial infarct].

6-keto-prostaglandin F1a and thromboxane B2 were determined by radioimmunoassay in 135 healthy children, as a control group, and in 125 offsprings of parents suffering from premature coronary artery disease. Plasma prostacyclin concentration had decreased in children with a positive family history of coronary artery disease. It was demonstrated a strong reduction of thromboxane level in boys from age 11 in endangered group while the thromboxane/prostacyclin ratio did not differ from the control. It was supposed that in adolescent sons of parents who have had an acute myocardial infarction before the age of 45, a compensatory mechanism exists to protect them from disturbances in regulation of the balance between prostacyclin and thromboxane.

Adolescent↗