[Intracranial hemorrhage following thrombolytic therapy in acute myocardial infarct]. / Hemorragia intracraneal tras la terapéutica trombolítica en el infarto agudo de miocardio.

INTRODUCTION: Intracranial hemorrhage in acute myocardial infarction, under thrombolytic therapeutic, ranges from 0.3 to 3% in different trials. We carried out a study to stabilised the incidence of this complication in ours patients, as well as to analyze its characteristics and asses the presence the predictive factors. METHODS: We retrospectively reviewed 997 consecutive patients with acute myocardial infarction treated with thrombolytic agents. We used two different protocols in two consecutive periods of time. Protocols differ in the age of the patients, the thrombolytic agent and its interval of applications. We analyze the intracranial hemorrhage incidence rate in each period, as well as its relations with the age of the patients, the sex and the thrombolytic agent used. We also analyze the possible predictive risk factors: cerebral-vascular disease, hypertension, diabetes, etc. RESULTS: The overall rate of intracranial hemorrhage was 1.6%, higher in the patients of the second period (0.9% vs 1.9%, p = NS). The age over 70 years don't show a significant increase of this incidence (1.7% vs 1.5%). The APSAC group have shown a greater rate of hemorrhage (4%) than streptokinase (0.8%) and rTPA (1.2%). Cerebral-vascular disease and hypertension background were the two factors more frequently related to hemorrhage. The mortality rate was 68.7%. CONCLUSION: The intracranial hemorrhage is a severe complication of thrombolytic therapy with a relative low incidence, but in our experience, higher than described in multicenter studies. There are several factors related that we would to take into account when is applied this therapy.

[Thrombolytic therapy in acute myocardial infarct. New performance protocols. Their influence on mortality and the incidence of complications]. / Terapéutica trombolítica en el infarto agudo de miocardio. Nuevos protocolos de actuación. Su influencia en la mortalidad e incidencia de complicaciones.

The new protocols of actuation in acute myocardial infarction thrombolysis have increased the number of patients treated, and have changed their characteristics. To assess the influence that this event has had in the complications incidence and mortality rate, we revise 704 infarcts treated with thrombolytic in a coronary unit, during 8 years. We separate two groups: 1) Patients treated since november 1983 to december 1988 following the established protocol at the beginning of this therapeutic (n = 328). 2) Patients treated since this date to july 1991, with a new protocol that include older than 70 years patients, moore than 6 hours of therapeutics delay and use of another thrombolytics, moreover streptokinase (n = 376). These changes have increased the number of thrombolysis in the second group (24.6 vs 49.1%; p < 0.001). Nevertheless being a higher group of risk we have found neither a significant mortality increase (6.40 vs 7.71%; p = NS), nor complications related to the thrombolysis: The incidence of major hemorrhages were 2.13 vs 1.06% (p = NS), cerebral hemorrhages 0.91 vs 1.6% (p = NS), hypotension related to the thrombolytics 15.55 vs 5.85% (p < 0.001). Neither has had significant difference in the incidence of reinfarcts (6.42 vs 5%; p = NS). In conclusion, the great number of thrombolysis realized nowadays, due to the actuation protocols changes, have increased significantly, neither the complications related with this therapeutic, nor the mortality rate, nor the reinfarcts number.

Effects of early use of captopril on haemodynamics and short-term ventricular remodelling in acute anterior myocardial infarction.

To determine whether ventricular short-term enlargement following acute myocardial infarction is related to increased left filling pressures and whether early treatment with captopril alters this process we studied 68 patients with a first acute myocardial infarction. Forty patients with a pulmonary capillary pressure equal or above 17 mmHg were randomized to treatment with conventional therapy plus captopril (n 20) or placebo (n 20), in a double blind fashion. The remaining 28 patients (non-dysfunction group) were treated conventionally. During the first 72 h, afterload showed a prompt decrease in the captopril group as compared to placebo. Changes from baseline to 14 days in end-diastolic and end-systolic left ventricular volume indexes determined by radionuclide ventriculography were: non-dysfunction, 85.6 (+/- 21) vs 88 (+/- 20) and 44 (+/- 17) vs 44 (+/- 17) ml.m-2; captopril (n 20), 96.6 (+/- 18) vs 99 (+/- 19) and 66 (+/- 22) vs 65 (+/- 22) ml.m-2; placebo (n 20), 96 (+/- 25) vs 113 (+/- 19) (P < 0.001) and 63 (+/- 18) vs 74 (+/- 22) ml.m-2 (P < 0.01). This study indicates that short-term ventricular enlargement is related to the degree of ventricular dysfunction and that captopril may improve this process.