[Comparison of 2 treatment strategies with prednisone and interferon in chronic hepatitis B]. / Comparación de dos esquemas de tratamiento con prednisona interferón en la hepatitis crónica por virus B.

Twenty patients with chronic B hepatitis and viral replication were included in a randomized study comparing the efficacy of sequential treatment with prednisone for 6 weeks followed by alpha-2a interferon (IFN) for 6 months (group A, 9 cases), versus concomitant administration of both drugs (group B, 11 cases). There were no significant differences between the two groups regarding age, sex, AST, ALT, DNA-VHB values, index of histological activity or type of underlying chronic hepatitis. Two patients from each group were excluded. The mean follow-up of the patients was 22.2 months. In group A, four responses were achieved (57.1%), of which 2 were complete and 2 partial. The overall response rate in group B was 77.7% (7 cases), 6 of them were complete responses (66.7%). Among HBsAg-positive patients from group B, one seroconverted to anti-HBs. A total of 7 patients with anti-HBe were included in the study. Two belonged to group A, in which a partial response was achieved, and another 5 were in group B, with 4 reaching a complete response and one reaching a partial response. There were no statistical differences with regards to the type of response in both groups. The AST, ALT values, as well as the pre-treatment levels of DNA-VHB, showed a significant statistical association with the response (p < 0.05). In all patients responding to treatment a histological improvement was observed that became even more evident in the biopsy performed 12 months after IFN withdrawal. In conclusion, concomitant therapy with prednisone and IFN is as effective as sequential therapy in the treatment of chronic B hepatitis. The results achieved with concomitant therapy suggest that new controlled trials are need to establish if this therapeutic schedule is the elective treatment in chronic B hepatitis.

Readmission in unstable angina.

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.

Effects of enalaprilat on hemodynamics and ventricular activation duration in hypertensive patients with left ventricular hypertrophy: clinical evidence of improved excitation-contraction coupling with angiotensin converting enzyme inhibition in human hypertension.

Hypertension is a major risk factor for the development of heart failure. Despite significant progress in our knowledge of the physiopathology of heart failure, the cause for decompensation in patients with left ventricular hypertrophy (LVH) is still obscure. The angiotensin converting enzyme inhibitor enalaprilat has been found to improve electromechanical coupling of heart cells in animal models. To assess the effects of enalaprilat on ventricular electromechanical coupling in humans, we studied the His bundle electrograms and hemodynamics in 22 hypertensive patients with LVH. Patients received either 2.5 mg enalaprilat or saline placebo intravenously in a double-blind protocol. There were no significant changes in heart rate, and atrioventricular and His-Purkinje conduction times. Ventricular activity duration was reduced from 110 +/- 11 msec to 88 +/- 13 msec after enalaprilat administration (P < .01). Enalaprilat decreased peak-systolic and end-diastolic left ventricular pressures, and arterial and pulmonary pressures, as well as pulmonary and systemic vascular resistances. End-systolic wall stress decreased 18% (P < .01), ejection fraction increased 11% (P < .01), and end-diastolic pressure-volume ratio decreased 50% (P < .001) after enalaprilat administration. There were no significant changes in these parameters after saline infusion. It is concluded that enalaprilat reduces ventricular activation duration and improves ventricular performance in hypertensive patients with LVH. Data suggest that enalaprilat significantly improves excitation-contraction coupling in these patients.

Effects of enalapril on ventricular volumes and neurohumoral status after inferior wall myocardial infarction.

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.

Prevalence of ectopic ventricular activity after left ventricular mass regression.

To assess the effects of left ventricular mass reduction on the prevalence of ventricular ectopic activity, we conducted a double-blind, placebo-controlled trial measuring ambulatory 48 h premature ventricular depolarizations in 27 patients with mild-to-moderate hypertension and an increased left ventricular mass index. Data was obtained at baseline and 6 +/- 2 months after randomization to either 25 mg captopril or placebo twice a day. Patients on captopril attained reduction in blood pressure from 167 +/- 11/103 +/- 6 to 136 +/- 10/85 +/- 5 mm Hg (P = .001), left ventricular mass index regression from 149 +/- 17 to 96 +/- 23 g/m2 (P = .001), and ventricular ectopic activity reduction from 413 +/- 172 to 77 +/- 27 ventricular extrasystoles/day (P = .001). Patients on placebo had no significant change in blood pressure (from 162 +/- 11/101 +/- 6 at baseline to 160 +/- 8/100 +/- 8 mm Hg after 6 months; P = NS). In the placebo group left ventricular mass index increased from 155 +/- 40 to 182 +/- 51 g/m2 (P = .01), and ventricular ectopic activity decreased from 634 +/- 293 to 562 +/- 260 ventricular extrasystoles/day (P = NS). Eight out of 14 patients on captopril (57%) and 1 out of 13 patients on placebo (8%) achieved reduction > 85% in ventricular ectopic activity per day (P = .004). Using multivariate logistic regression analysis, left ventricular mass index regression and reduction in systolic blood pressure were the most important correlates for this effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduction in cardiac conduction velocity delay by angiotensin converting enzyme inhibition in hypertensive patients with left ventricular hypertrophy. Detection by signal averaged electrocardiography.

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.

Effects of enalapril on heart failure in hypertensive patients with diastolic dysfunction.

Ten hypertensive patients with symptoms of heart failure and normal systolic function but with diastolic dysfunction were treated with 10 mg enalapril twice a day for 9 +/- 3 months to evaluate the effects of this agent alone on heart failure induced by diastolic dysfunction. After therapy, all patients improved and echocardiographic parameters of diastolic dysfunction became normalized. It is concluded that enalapril appears to be useful in the treatment of heart failure in hypertensive patients with normal systolic function and diastolic dysfunction.

Usefulness of a systemic hypertension in-hospital educational program.

The effects of an educational program on compliance and blood pressure (BP) control were assessed in 47 hypertensive patients hospitalized for nonhypertension-related diseases. Patients were randomized to receive either a questionnaire and an educational program (group I, 25) or questionnaire only (group II, 22). Baseline clinical characteristics, admission diagnoses and antihypertensive medications were similar between the groups. Antihypertensive medications used by patients before the trial were not changed. Eight weeks after the initial intervention, patients in group I showed a significant reduction in both systolic and diastolic BP (137/89 vs 154/98 mm Hg, p = 0.005 and 0.006, respectively) and improved compliance (96 vs 36%, p = 0.04), compared with patients in group II. An education program in patients with high BP is an effective method to improve compliance and BP control in the short-term.