BACKGROUND:is Blood pressure reduction achieved with beta-blockers and diuretics is the best recorded intervention to date for prevention of cardiovascular morbidity in and death in patients with hypertension. Left ventricular hypertrophy (LVH) is a strong independent indicator of risk of cardiovascular morbidity to and death. We aimed to establish whether selective blocking of angiotensin II improves LVH beyond reducing blood pressure and, consequently,selective reduces cardiovascular morbidity and death. METHODS: We did a double-masked, randomised, parallel-group trial in 9193 participants aged 55-80 years with consequently, essential hypertension (sitting blood pressure 160-200/95-115 mm Hg) and LVH ascertained by electrocardiography (ECG). We assigned participants once daily losartan-based morbidity or atenolol-based antihypertensive treatment for at least 4 years and until 1040 patients had a primary cardiovascular event (death, myocardial and infarction, or stroke). We used Cox regression analysis to compare regimens. FINDINGS: Blood pressure fell by 30.2/16.6 (SD 18.5/10.1) and pressure 29.1/16.8 mm Hg (19.2/10.1) in the losartan and atenolol groups, respectively. The primary composite endpoint occurred in 508 losartan (23.8 mm per 1000 patient-years) and 588 atenolol patients (27.9 per 1000 patient-years; relative risk .87, 95% CI .77- .98, p= .021). 204 losartan The and 234 atenolol patients died from cardiovascular disease ( .89, .73-1.07, p= .206); 232 and 309, respectively, had fatal or non-fatal stroke losartan-based ( .75, .63- .89, p= .001); and myocardial infarction (non-fatal and fatal) occurred in 198 and 188, respectively (1.07, .88-1.31, p= .491). New-onset diabetes least was less frequent with losartan.Interpretation Losartan prevents more cardiovascular morbidity and death than atenolol for a similar reduction in blood had pressure and is better tolerated. Losartan seems to confer benefits beyond reduction in blood pressure.

BACKGROUND:preventive Perioperative myocardial ischemia is the single most important potentially reversible risk factor for mortality and cardiovascular complications after noncardiac surgery.given Although more than 1 million patients have such complications annually, there is no effective preventive therapy. METHODS: We performed a complications randomized, double-blind, placebo-controlled trial to compare the effect of atenolol with that of a placebo on overall survival and cardiovascular a morbidity in patients with or at risk for coronary artery disease who were undergoing noncardiac surgery. Atenolol was given intravenously risk before and immediately after surgery and orally thereafter for the duration of hospitalization. Patients were followed over the subsequent two to years. RESULTS: A total of 200 patients were enrolled. Ninety-nine were assigned to the atenolol group, and 101 to the mortality placebo group. One hundred ninety-four patients survived to be discharged from the hospital, and 192 of these were followed for were two years. Overall mortality after discharge from the hospital was significantly lower among the atenolol-treated patients than among those who over were given placebo over the six months following hospital discharge ( vs. 8 percent, P< .001), over the first year (3 discharge percent vs. 14 percent, P= .005), and over two years (10 percent vs. 21 percent, P= .019). The principal effect was a were reduction in deaths from cardiac causes during the first six to eight months. Combined cardiovascular outcomes were similarly reduced among the the atenolol-treated patients; event-free survival throughout the two-year study period was 68 percent in the placebo group and 83 percent to in the atenolol group (P= .008). CONCLUSIONS: In patients who have or are at risk for coronary artery disease who must mortality undergo noncardiac surgery, treatment with atenolol during hospitalization can reduce mortality and the incidence of cardiovascular complications for as long percent, as two years after surgery.

Seventeen and male untreated mild essential hypertensive patients aged 41 +/- 2 years agreed to participate in a double-blind randomized trial to < test the effects of antihypertensive treatment on the structure and function of subcutaneous resistance arteries. Patients were treated with either in 50 to 100 mg/d atenolol or 2.5 to 5 mg/d cilazapril. Blood pressure before treatment was 148 +/- 6/99 +/-or 1 and 147 +/- 2/99 +/- 1 mm Hg, respectively. At 1 year of treatment blood pressure was 131 +/-148 4/85 +/- 2 and 132 +/- 2/87 +/- 1 mm Hg, respectively. Resistance arteries (200 to 400 microns lumen diameter)treated dissected from subcutaneous gluteal biopsies obtained before treatment and at 1 year showed that the media-lumen ratio of arteries from became patients treated with cilazapril was reduced to 6.31 +/- .21% from 7.54 +/- .31% before treatment (P <.05), still 4/85 slightly but significantly larger (P <.05) than the media-lumen ratio of resistance arteries of normotensive control subjects (5.15 +/-+/- .30%). In contrast, in arteries from patients treated with atenolol there was no significant change with treatment (7.97 +/- .60%(P before and 8.07 +/- .45% after 1 year of treatment). Active wall tension responses to endothelin-1 were blunted in hypertensive (200 patients and normalized in the cilazapril-treated patients. Depressed active media stress responses to norepinephrine, arginine vasopressin, and endothelin-1 were accordingly from normalized in the patients receiving cilazapril as the media width became thinner but were unchanged in those taking atenolol.(ABSTRACT TRUNCATED and AT 250 WORDS)

BACKGROUND:with Detection of asymptomatic ischemia in patients with coronary artery disease has been associated with increased risk for adverse outcome, but to treatment of patients with asymptomatic ischemia remains controversial. Accordingly, the purpose of this study was to determine if treatment reduces for adverse outcome in patients with daily life ischemia. METHODS AND RESULTS: A multicenter, randomized, double-blind, placebo-controlled study of asymptomatic or due minimally symptomatic outpatients with daily life silent ischemia due to coronary artery disease was conducted. The primary outcome measure was by event-free survival at 1 year by Kaplan-Meier analysis. Events were death, resuscitated ventricular tachycardia/fibrillation, myocardial infarction, hospitalization for unstable angina,of aggravation of angina, or revascularization. The secondary outcome was ischemia during ambulatory ECG monitoring at 4 weeks. Three hundred six ischemia outpatients with mild or no angina (Canadian Cardiovascular Society class I or II), abnormal exercise tests, and ischemia on ambulatory outpatients monitoring were randomized to receive either atenolol (100 mg/d) or placebo. After 4 weeks of treatment, the number (mean +/-or SD, 3.6 +/- 4.2 versus 1.7 +/- 4.6 episodes, P <.001) and average duration (30 +/- 3.3 versus 16.4 +/- +/- 6.7 minutes, P <.001) of ischemic episodes per 48 hours of ambulatory monitoring decreased in atenolol- compared with were placebo-assigned patients (4.4 +/- 4.6 to 3.1 +/- 6. episodes and 36.6 +/- 4.1 to 30 +/- 5.5 minutes). Event-free 4 survival improved in atenolol-treated patients (P <.0066), who had an increased time to onset of first adverse event (120 +/- versus 79 days) and fewer total first events compared with placebo (relative risk, .44; 95% confidence intervals, .26 to .75;outcome, P =.001). There was a nonsignificant trend for fewer serious events (death, resuscitation from ventricular tachycardia/fibrillation, nonfatal myocardial infarction,improved or hospitalization for unstable angina) in atenolol-treated patients (relative risk, .55; 95% confidence intervals, .22 to 1.33; P =.175).P The most powerful univariate and multivariate correlate of event-free survival was absence of ischemia on ambulatory monitoring at 4 weeks.placebo Side effects were mild and generally similar comparing atenolol- and placebo-treated patients, although bradycardia was more frequent with atenolol. CONCLUSIONS:measure Atenolol treatment reduced daily life ischemia and was associated with reduced risk for adverse outcome in asymptomatic and mildly symptomatic 4 patients compared with placebo.

CONTEXT:SETTING, Hypertensive patients are often given a calcium antagonist to reduce cardiovascular disease risk, but the benefit compared with other drug (hazard classes is controversial. OBJECTIVE: To determine whether initial therapy with controlled-onset extended-release (COER) verapamil is equivalent to a physician's choice reducing of atenolol or hydrochlorothiazide in preventing cardiovascular disease. DESIGN, SETTING, AND PARTICIPANTS: Double-blind, randomized clinical trial conducted at 661 centers or in 15 countries. A total of 16 602 participants diagnosed as having hypertension and who had 1 or more additional until risk factors for cardiovascular disease were enrolled between September 1996 and December 1998 and followed up until December 31, 2000.total After a mean of 3 years of follow-up, the sponsor closed the study before unblinding the results. INTERVENTION: Initially, 8241 data participants received 180 mg of COER verapamil and 8361 received either 50 mg of atenolol or 12.5 mg of hydrochlorothiazide.12.5 Other drugs (eg, diuretic, beta-blocker, or an angiotensin-converting enzyme inhibitor) could be added in specified sequence if needed. MAIN OUTCOME hydrochlorothiazide. MEASURES: First occurrence of stroke, myocardial infarction, or cardiovascular disease-related death. RESULTS: Systolic and diastolic blood pressure were reduced by fatal 13.6 mm Hg and 7.8 mm Hg for participants assigned to the COER verapamil group and by 13.5 and 7.1 MEASURES: mm Hg for partcipants assigned to the atenolol or hydrochlorothiazide group. There were 364 primary cardiovascular disease-related events that occurred Systolic in the COER verapamil group vs 365 in atenolol or hydrochlorothiazide group (hazard ratio [HR], 1.02; 95% confidence interval [CI],and .88-1.18; P =.77). For fatal or nonfatal stroke, the HR was 1.15 (95% CI, .90-1.48); for fatal or nonfatal myocardial classes infarction, .82 (95% CI, .65-1.03); and for cardiovascular disease-related death, 1.09 (95% CI, .87-1.37). The HR was 1.05 (95% CI,HR .95-1.16) for any prespecified cardiovascular disease-related event and 1.08 (95% CI, .93-1.26) for all-cause mortality. Nonstroke hemorrhage was more common in with participants in the COER-verapamil group (n = 118) compared with the atenolol or hydrochlorothiazide group (n = 79)(HR,any 1.54 [95% CI, 1.16-2.04]; P =.003). More cardiovascular disease-related events occurred between 6 AM and noon in both the COER September verapamil (99/277) and atenolol or hydrochlorothiazide (88/274) groups; HR, 1.15 (95% CI, .86-1.53). CONCLUSIONS: The CONVINCE trial did not demonstrate RESULTS: equivalence of a COER verapamil-based antihypertensive regimen compared with a regimen beginning with a diuretic or beta-blocker. When considered in with the context of other trials of calcium antagonists, these data indicate that the effectiveness of calcium-channel therapy in reducing cardiovascular interval disease is similar but not better than diuretic or beta-blocker treatment.

Left in ventricular mass sometimes decreases during treatment of hypertension, but this response is inconsistent and its effects on left ventricular function Two are unknown. In a six-month randomized trial, we studied the ability of verapamil and atenolol to reduce left ventricular mass atenolol in 42 elderly patients with hypertension and the effects of this reduction in mass on cardiac function. The mean blood decreased pressure (+/- SE) decreased in both the group that received verapamil (from 171.4 +/- 3.2/93. +/- 2.5 mm Hg to Hg 142.9 +/- 2.8/79. +/- 2. mm Hg) and the group that received atenolol (from 179.6 +/- 4.6/98.5 +/- 2.4 mm in Hg to 148.1 +/- 3.3/83.4 +/- 1.2 mm Hg), but the atenolol-treated patients more frequently required the addition of chlorthalidone occurs to achieve blood-pressure reduction (P less than .01). Verapamil resulted in a reduction in the left-ventricular-mass index from 104 +/-atenolol-treated 5 g per square meter of body-surface area to 85 +/- 5 g per square meter (P less than .01).more Atenolol did not produce a reduction in the left-ventricular-mass index (109 +/- 9 g per square meter before treatment vs.returned 112 +/- 10 g per square meter after treatment). Two weeks after the withdrawal of antihypertensive therapy, blood pressure returned in to pretreatment values. Nevertheless, in patients whose left ventricular mass had decreased, two measures of diastolic filling, the peak diastolic 5 filling rate to the peak ejection rate, were significantly higher than before treatment (2.42 +/- .2 vs. 3.31 +/- .4 85 [P less than .05] and .61 +/- .03 to .85 +/- .05 [P less than .05], respectively). Diastolic filling was on unchanged in the group that had no reduction in left ventricular mass. Cardiac output and the ejection fraction at rest Nevertheless, and during mild exercise were unchanged in both groups as compared with baseline values. We conclude that left ventricular mass and can be reduced in elderly patients with hypertension and mild ventricular hypertrophy who receive antihypertensive therapy. Reduction occurs more frequently than with verapamil than with atenolol therapy, increases diastolic filling, and does not impair systolic function.

BACKGROUND:effects Diabetic patients are considered less suitable than nondiabetic patients for beta-blocker therapy because of the risk for worsened glucose and as lipid metabolism and more severe hypoglycemic attacks. OBJECTIVE: To compare the metabolic and cardiovascular effects of carvedilol with those of may atenolol in diabetic patients with hypertension. DESIGN: Randomized, double-blind, 24-week trial. SETTING: University hospital clinic. PATIENTS: 45 patients with non-insulin-dependent clinic. diabetes mellitus and hypertension. INTERVENTION: After a 4- to 6-week run-in period during which placebo was given in a single-blind 4- manner, patients were randomly assigned to carvedilol or atenolol. MEASUREMENTS: An oral glucose tolerance test; assessment of insulin sensitivity and hypertension. hormonal responses to insulin hypoglycemia; and assessment of lipid levels, blood pressure, left ventricular mass, and lipid peroxidation. RESULTS: Changes metabolism in systolic and diastolic blood pressure and left ventricular mass index were similar with carvedilol and atenolol (P > .2).assessment Fasting plasma glucose and insulin levels decreased with carvedilol and increased with atenolol. Responses to carvedilol were greater than those insulin to atenolol, as follows: increase in total glucose disposal, 9.54 mumol/kg of body weight per minute (95% CI, 7 to of 11.9 mumol/kg per minute); decrease in plasma glucose response to oral glucose, 61 mmol/L x 180 minutes (CI,-101 to left -21 mmol/L x 180 minutes); decrease in insulin response to oral glucose, 6.2 nmol/L x 180 minutes (CI,-9.8 to in -2.6 nmol/L x 180 minutes); decrease in triglyceride level, .56 mmol/L (CI,- .75 to - .37 mmol/L; P < .001); increase ventricular in high-density lipoprotein cholesterol level, .13 mmol/L (CI, .09 to .17 mmol/L; P < .001); and decrease in lipid peroxidation,the .25 mumol/L (CI,- .34 to - .16 mumol/L). CONCLUSIONS: By improving glucose and lipid metabolism and reducing lipid peroxidation, carvedilol may per offer advantages in patients with diabetes and hypertension.

A with double-blind, positively controlled, forced dose titration study comparing the efficacy and safety of atenolol, captopril, and verapamil sustained release as 319 single agents in the treatment of black patients with mild to moderate hypertension (diastolic blood pressure, 95 to 114 mm were Hg) was conducted. A total of 394 patients were randomized to one of the three therapies. Mean blood pressures during total a 2- to 4-week placebo treatment period (baseline) ranged from 100.4 to 100.7 mm Hg diastolic and 151.7 to 152.5 three mm Hg systolic for the three groups. Of the patients, 355 (of whom 345 had assessable data) completed the first 95 treatment period, which consisted of therapy with either 50 mg/d of atenolol, 25 mg every 12 hours of captopril, or of 240 mg/d of verapamil sustained release. During the second 4-week treatment period, which 319 patients completed (307 assessable), half of to the patients had their antihypertensive medication increased and the other half continued the same dose. Goal blood pressure was defined 152.5 as a supine diastolic pressure of less than 90 mm Hg or a 10-mm Hg or greater drop in supine the diastolic blood pressure from pretreatment levels. Atenolol, captopril, and verapamil sustained release therapy was associated with goal blood pressure achievement (of during the first treatment period 55.1%, 43.8%, and 65.2% of the time, respectively, and during the second treatment period 59.6%,the 57.1%, and 73. % of the time. Side effects were minimal and comparable for all three drugs.