[Repeat thrombolysis in acute myocardial infarction]. / Ismételt thrombolysis acut myocardialis reinfarctusban.

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.

Clinical application of the nitroglycerin lingual spray.

The effect of sublingually administered nitrate spray was investigated with noninvasive methods. During 3 months, 82 patients were entered into the study: 40 with angina pectoris, 15 with acute myocardial infarction, 18 with hypertensive crisis, and 9 with left ventricular failure or acute pulmonary edema. The hemodynamic effects of two jets of nitroglycerin spray (0.8 mg Nitrolingual spray; Pohl-Boskamp, Hohenlocksted, Germany) was measured on heart rate, blood pressure, and flow velocity at baseline and 1, 5, and 10 minutes after drug administration. Flow velocities were measured through the left ventricular outflow tract and the mitral valve (early diastolic wave and atrial wave) with bedside Doppler echocardiography. The time to improvement and occurrence of adverse events was analyzed. Heart rate was constant after the therapy (75 +/- 8, 75 +/- 10, 75 +/- 10, and 75 +/- 9 beats per min; not significant), and systolic blood pressure decreased significantly 1 minute after administration and remained decreased throughout the examination (135 +/- 27, 124 +/- 21, 125 +/- 19, and 124 +/- 22 mm Hg, respectively; p < 0.001). The diastolic blood pressure was also significantly decreased (82 +/- 17, 79 +/- 14, 78 +/- 12, 78 +/- 14 mm Hg; p < 0.001). A significant increase in flow velocities in the left ventricular outflow tract was detected (90 +/- 8, 101 +/- 10, and 114 +/- 13 cm/s; p < 0.001) concomitantly with a significant increase in the early diastolic flow (46 +/- 4, 65 +/- 6, and 76 +/- 8 cm/s; p < 0.001) and the atrial wave (101 +/- 9, 110 +/- 10, and 118 +/- 9 cm/s; p < 0.001). This increase of flow velocity was less pronounced through the mitral valve than through the left ventricular outflow tract.

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.

Association between total cholesterol and thromboxane B2 levels in offspring of parents suffering from premature coronary artery disease.

Relationship between plasma thromboxane B2 concentration and serum total cholesterol level was studied in 129 healthy 3 to 18 years old children, 77 girls and 52 boys, without any family history of premature coronary artery disease and in 181 offspring, 105 girls and 76 boys, of parents suffering from acute myocardial infarction before the age of 45. It was identified an enhancement in serum total cholesterol level of endangered children, and an elevated release of thromboxane A2 in affected girls. A significant negative correlation was found between serum total cholesterol concentration and plasma thromboxane B2 level in healthy girls. However, there was no correlation between serum total cholesterol level and plasma thromboxane B2 concentration in the children whose parents had premature coronary artery disease. It appears, from our results, that this in an alteration of thromboxane A2 release of platelets in children of families with high risk of cardiovascular diseases.

[Plasma prostacyclin and thromboxane concentration in healthy children and in offspring of parents suffering from myocardial infarct]. / Plazma prosztaciklin és tromboxán koncentráció egészséges gyermekeken és fiatalkori myocardialis infarctusban megbetegedett szülök utódaiban.

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.