Asunto(s)
Infarto del Miocardio/etiología , Deficiencia de Proteína C/complicaciones , Deficiencia de Proteína S/complicaciones , Adulto , Electrocardiografía , Femenino , Fibrinolíticos/administración & dosificación , Fibrinolíticos/uso terapéutico , Humanos , Infarto del Miocardio/sangre , Infarto del Miocardio/diagnóstico , Proteína C/análisis , Deficiencia de Proteína C/sangre , Proteína S/análisis , Deficiencia de Proteína S/sangre , Estreptoquinasa/administración & dosificación , Estreptoquinasa/uso terapéutico , Resultado del TratamientoRESUMEN
The study included 100 patients with acute inferoposterior myocardial infarction consequently admitted to hospital. Both the standard ECG in 12 leads as well as additional V7-V9 and Slapak & Partilla leads were recorded in each patient. Two-dimensional echo at rest was performed to evaluate regional wall motion. The criterion of dividing patients into any MI subgroup was the presence of abnormal Q wave in any system leads. Posterior + inferior MI was found in 88%, limited posterobasal--in 2% and diaphragmal (inferior)--in 10% of patients. Good correlation of Q-wave in II, aVF and S1-S4, V7-V9 and S1-S4 was found. The more abnormal Q waves were revealed in lead systems the more was necrosis size as assessed by echo. We conclude, that additional lead systems are of value in revealing necrosis size and its location in patients with damaged posterior wall.
Asunto(s)
Electrocardiografía/métodos , Sistema de Conducción Cardíaco/fisiopatología , Infarto del Miocardio/diagnóstico , Infarto del Miocardio/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
The action of the synthetic antioxidant aemoxipin, 3-oxypyridime derivative on platelet aggregation was studied in 8 patients with ischemic heart disease and cardialgias. An hour later after an intravenous injection in a dose of 5-10 mg/kg, aemoxipin reduced platelet aggregation by 25% (p < 0.05), inhibited the reaction of "release" and spontaneous platelet aggregation. The same effect of the drug was demonstrated in the aggregation caused by ADP action on platelets preliminarily activated by minimum adrenaline concentrations in a tube. Our results are in agreement with the data of other investigators concerning a direct, non-specific nature of aemoxipin action on cellular membranes.
Asunto(s)
Antioxidantes/farmacología , Picolinas/farmacología , Inhibidores de Agregación Plaquetaria/farmacología , Adenosina Difosfato/farmacología , Angina de Pecho/sangre , Angina de Pecho/tratamiento farmacológico , Antioxidantes/administración & dosificación , Relación Dosis-Respuesta a Droga , Humanos , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/tratamiento farmacológico , Picolinas/administración & dosificación , Agregación Plaquetaria/efectos de los fármacos , Inhibidores de Agregación Plaquetaria/administración & dosificaciónAsunto(s)
Circulación Coronaria/efectos de los fármacos , Fibrinólisis/efectos de los fármacos , Infarto del Miocardio/tratamiento farmacológico , Estreptoquinasa/uso terapéutico , Terapia Trombolítica , Adulto , Anciano , Circulación Coronaria/fisiología , Femenino , Fibrinólisis/fisiología , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/fisiopatologíaRESUMEN
Intracoronary streptokinase (250.000 units over 60-90 min) was administered within 7.8 +/- 0.4 hrs after the onset of myocardial infarction symptoms to 85 patients, and intravenous streptokinase (500.000 units over 5-10 min) was given within 4.8 +/- 0.4 hrs to 46 myocardial infarction patients. Coronary angiography was conducted 1 to 3 hours after intravenous streptokinase administration. Coronary arterial reperfusion was achieved in 62% of patients in the former group, and in 66% in the latter one. Reperfusion was seen in 84% of patients in the first 3 hours after the onset of infarction, and in 60-66% at later dates. Hypofibrinogenemia did not become critical and persisted for one more day in cases of intravenous streptokinase infusions, as compared to the intracoronary route. Intravenous administration of 500.000 units streptokinase at the rate of 100.000-50.000 U/min is an effective and safe method for the treatment of myocardial infarction, and its prospective application in health practices appears quite promising.