RESUMEN
To determine the characteristics of patients re-admitted after unstable angina (UA) pectoris, 120 consecutive patients hospitalized due to primary UA pectoris were prospectively studied 22 +/- 3 months after discharge. The patients were grouped based on the readmission rate. Those in group A (50) had recurrent admissions (mean 2.6, range 2 to 5). Seventy patients (group B) did not have readmissions during the follow-up period. All patients underwent coronary angiogram and symptoms-limited exercise stress test before discharge. The univariate characteristics for readmission were: age over 70 years (p = 0.02), nondiagnostic exercise stress testing (p = 0.03), angiographically diffuse coronary artery disease (p = 0.004), and non-interventional management (P < 0.001). Patients readmitted had increased incidence of myocardial infarction (p = 0.004) but similar survival at 2 years. By regression analysis, important variables for readmission were non-interventional management (Chi-Square = 7.6, p = 0.01), non diagnostic treadmill test (Chi-Square = 6.9, p = 0.03) and diffuse coronary artery disease (Chi-Square = 6.2, p = 0.04). It is concluded that in the interventional era the most important factor for readmission after primary UA pectoris is non-interventional management. Coronary revascularization should not be denied solely on the basis of age.
Asunto(s)
Angina Inestable/diagnóstico , Readmisión del Paciente , Anciano , Anciano de 80 o más Años , Angina Inestable/terapia , Distribución de Chi-Cuadrado , Unidades de Cuidados Coronarios/estadística & datos numéricos , Femenino , Estudios de Seguimiento , Humanos , Masculino , Persona de Mediana Edad , Readmisión del Paciente/estadística & datos numéricos , Estudios Prospectivos , Puerto Rico , Recurrencia , Análisis de RegresiónRESUMEN
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system and its beneficial modification with the use of angiotensin-converting enzyme inhibin after inferior wall myocardial infarction (MI) was evaluated. Fifty patients with acute inferior MI were randomly assigned to receive 5 mg per day of either enalapril or placebo after admission. Blood tests for neurohormone levels and echocardiograms were performed at initial examination and 4 weeks later. Baseline characteristics were similar in the two groups. Four weeks after randomization, patients treated with enalapril had lower end-diastolic volume (146 +/- 29 vs 167 +/- 15 ml; p = 0.04), end-systolic volume (56 +/- 18 vs 107 +/- 17 ml; p = 0.03), serum norepinephrine levels (320 +/- 93 vs 465 +/- 77 pg/ml; p < 0.01), angiotensin II levels (18 +/- 6 vs 54 +/- 11 pg/ml; p < 0.01), and atrial natriuretic polypeptide levels (106 +/- 9 vs 122 +/- 17 pg/ml; p = 0.05) than patients given placebo. The incidence of heart failure after MI was also lower in this group (4% vs 16%; p = 0.009). Results show that there is early neurohumoral activation in the course of acute inferior wall MI. Enalapril reduces neurohumoral levels and preserves ventricular volumes. These effects were associated with a reduction in the incidence of heart failure 4 weeks after MI in these patients.
Asunto(s)
Volumen Cardíaco/efectos de los fármacos , Enalapril/uso terapéutico , Infarto del Miocardio/tratamiento farmacológico , Función Ventricular Izquierda/efectos de los fármacos , Anciano , Aldosterona/sangre , Angiotensina II/sangre , Método Doble Ciego , Femenino , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/fisiopatología , Norepinefrina/sangreRESUMEN
Hypertensive patients with left ventricular hypertrophy (LVH) have increased prevalence of ventricular arrhythmias. Slow conduction velocity at the level of hypertrophic myocardial cells has been one of the postulated mechanisms for these arrhythmias. To assess the effects of angiotensin converting enzyme inhibition on modification in ventricular conduction velocities, we studied 25 hypertensive patients with LVH using signal averaged electrocardiography (SAECG) in a randomized double-blind placebo controlled and cross-over trial. Data were acquired at baseline and 10 min after a double-blind intravenous infusion of saline placebo or 2.5 mg enalaprilat. Sequential cross-over was done the next day. Root mean square vector was 55 +/- 5 microV at baseline, 55 +/- 5 microV after placebo and 54 +/- 4 microV after enalaprilat (P = NS). Low amplitude signal < 40 msec was 45 +/- 4 msec at baseline, 45 +/- 4 msec after placebo, and 43 +/- 4 msec after enalaprilat (P = NS). There was no change in filtered QRS (fQRS) duration between baseline (113 +/- 10 msec) and placebo (113 +/- 11 msec) measurements. However, after enalaprilat infusion, there was a significant reduction in fQRS to 106 +/- 7 msec (P = .04), and five patients (20%) with late potentials had normalization of this feature (P = .001). The data suggest that angiotensin converting enzyme inhibition with enalaprilat reduces conduction velocity delay in hypertensive patients with LVH.