RESUMEN
Exercise testing (ET) has been used for assessing the arrhythmogenic tendency of myocardium in patients (pts) with coronary heart disease. It has been suggested that coronary patients with left ventricular (LV) dyssynergy are prone to present ventricular extrasystolic arrhythmia (VA) during ET. We studied the functional status of the LV in a group of 25 coronary patients who presented VA during ET (Group A), and compared the results with a group of 87 patients without VA during ET (Group B). No statistically significant difference was found between the two groups in end-diastolic pressure, ejection fraction, and extent of dyssynergy of the LV. Furthermore, no significant difference was noted in the extent of development of the collateral circulation.
Asunto(s)
Complejos Cardíacos Prematuros/fisiopatología , Prueba de Esfuerzo , Hemodinámica , Presión Sanguínea , Circulación Colateral , Ventrículos Cardíacos , Humanos , Contracción Miocárdica , Volumen SistólicoRESUMEN
The net delta left ventricular ejection time index 4 minutes after exercise is prolonged in many patients with coronary artery disease. This prolongation is thought to be due to the lack of response of the ischemic myocardium to adrenergic stimulation and has been proposed as a measure of myocardial ischemia. In this study, the effect of beta adrenergic blockade on net delta left ventricular ejection time was studied in nine normal subjects (Group A) and in eight patients with stable angina and coronary artery disease (Group B). In Group A, a treadmill exercise test was performed for 10 minutes before and after administration of propranolol, 160 mg daily, for 2 days. The postexercise net delta left ventricular ejection time was significantly greater after propranolol (mean +/- standard error of the mean 12 +/- 4 versus 35 +/- 4 ms, p less than 0.01). In group B a maximal treadmill exercise test was performed before and after therapy with propranolol. Only patients with a normal net delta left ventricular ejection time before propranolol were selected. The net delta left ventricular ejection time again increased significantly after propranolol (11.5 +/- 4 versus 35.3 +/- 5 ms p less than 0.01). It is concluded that prolongation of postexercise net delta left ventricular ejection time cannot be used to diagnose ischemia in patients who are receiving propranolol therapy. Our data support the hypothesis that prolongation of net delta left ventricular ejection time after exercise is caused by an impaired myocardial response to catecholamines, whether due to ischemia or effective beta adrenergic blockade.
Asunto(s)
Gasto Cardíaco , Enfermedad Coronaria/fisiopatología , Corazón/efectos de los fármacos , Esfuerzo Físico , Propranolol/farmacología , Volumen Sistólico , Adulto , Angina de Pecho/tratamiento farmacológico , Angina de Pecho/fisiopatología , Presión Sanguínea/efectos de los fármacos , Enfermedad Coronaria/tratamiento farmacológico , Prueba de Esfuerzo , Frecuencia Cardíaca/efectos de los fármacos , Humanos , Persona de Mediana Edad , Propranolol/uso terapéuticoRESUMEN
The characteristics of premature ventricular beats predisposing to ventricular tachycardia or fibrillation were assessed by 24-h ambulatory monitoring and maximal treadmill exercise testing in 339 cardiac patients with premature ventricular beats. Premature ventricular beats were divided into early (Q-premature ventricular beat less than QT), late (within the last 20% of the cardiac cycle), and midcycle. Ventricular tachycardia was recorded in 45 patients and ventricular fibrillation, in three. The frequency of ventricular tachycardia or fibrillation was 32% in patients with late, 16% in patients with early, and 7% in patients with midcycle premature ventricular beats (P less than 0.05). Patients with frequent (less than 10/min) multiformed premature ventricular beats had a frequency of ventricular tachycardia or fibrillation of 44%, while only 13% of patients with frequent uniformed premature ventricular beats had ventricular tachycardia (P less than 0.05). Ambulatory patients with ventricular tachycardia or fibrillation have frequent multiformed premature ventricular beats, and the ventricular tachycardia or fibrillation is usually triggered by late premature ventricular beats.
Asunto(s)
Complejos Cardíacos Prematuros/diagnóstico , Adulto , Anciano , Atención Ambulatoria , Complejos Cardíacos Prematuros/complicaciones , Enfermedades Cardiovasculares/complicaciones , Prueba de Esfuerzo , Femenino , Humanos , Masculino , Persona de Mediana Edad , Monitoreo Fisiológico , Taquicardia/complicaciones , Fibrilación Ventricular/complicacionesRESUMEN
The time course of the blockade effect of propranolol on the sinus node (SN) and the atrioventricular node (AVN) was studied in six normal volunteers. Serial isoproterenol infusions were done before and after oral propranolol administration, 160 mg daily for two days. The inhibition by propranolol of the heart rate increases due to isoproterenol was used to assess the blockade of the sinus node, and the diminution by propranolol of the shortening in the PR interval due to isoproterenol was used to assess the blockade of the atrioventricular node. The blockade effects on the sinus node and the atrioventricular node were identical and persisted more than 24 hours. There was no good relationship between plasma propranolol and blockade effect on sinus node and/or atrioventricular node as propranolol was no longer detectable in the plasma 24 hours after the last dose. A transient hypersensitivity to isoproterenol was present 36 to 48 hours after propranolol withdrawal. The explanation of these phenomena most likely lies in the peculiar nature of beta-adrenergic receptors.