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Author: Admin | 2025-04-28
Adjusted for baselineFramingham risk score and level of electrocardiographic left ventricular hypertrophyTable 3 shows the results for the primary composite endpoint and the individual endpoints. The primary endpoint was the first occurrence of stroke, myocardialinfarction or cardiovascular death, analyzed using an ITT approach. The table shows the number of events for each component in two different ways. The Componentsof Primary Endpoint (as a first event) counts only the events that define the primary endpoint, while the Secondary Endpoints count all first events of a particular type,whether or not they were preceded by a different type of event.Table 3: Incidence of Primary Endpoint Events COZAAR Atenolol Risk Reduction* 95% CI p-Value N (%) Rate† N (%) Rate† Primary Composite Endpoint 508 (11) 23.8 588 (13) 27.9 13% 2% to 23% 0.021 Components of Primary Composite Endpoint (as a first event) Stroke (nonfatal) 209 (5) 286 (6) Myocardial infarction (nonfatal) 174 (4) 168 (4) Cardiovascular mortality 125 (3) 134 (3) Secondary Endpoints (any time in study) Stroke (fatal/nonfatal) 232 (5) 10.8 309 (7) 14.5 25% 11% to 37% 0.001 Myocardial infarction (fatal/nonfatal) 198 (4) 9.2 188 (4) 8.7 -7% -13% to 12% 0.491 Cardiovascular mortality 204 (4) 9.2 234 (5) 10.6 11% -7% to 27% 0.206 Due to CHD 125 (3) 5.6 124 (3) 5.6 -3% -32% to 20% 0.839 Due to Stroke 40 (1) 1.8 62 (1) 2.8 35% 4% to 67% 0.032 Other‡ 39 (1) 1.8 48 (1) 2.2 16% -28% to 45% 0.411 * Adjusted for baseline Framingham risk score and level of electrocardiographic left ventricular hypertrophy † Rate per 1000 patient-years of follow-up ‡ Death due to heart failure, non-coronary vascular disease, pulmonary embolism, or a cardiovascular cause other than stroke or coronary heart disease Although the LIFE study favored COZAAR over atenolol with respect to the primary endpoint (p=0.021), this result is from a single study and, therefore, is lesscompelling than the difference between COZAAR and placebo. Although not measured directly, the difference between COZAAR and placebo is compelling becausethere is evidence that atenolol is itself effective (vs. placebo) in reducing cardiovascular events, including stroke, in hypertensive patients.Other clinical endpoints of the LIFE study were: total mortality, hospitalization for heart failure or angina pectoris, coronary or peripheral revascularization procedures,and resuscitated cardiac arrest. There were no significant differences in the rates of these endpoints between the COZAAR and atenolol groups.For the primary endpoint and stroke, the effects of COZAAR in patient subgroups defined by age, gender, race and presence or absence of isolated systolic hypertension(ISH), diabetes, and history of cardiovascular disease (CVD) are shown in Figure 3 below. Subgroup analyses can be difficult to interpret and it is not known whetherthese represent true differences or chance effects.Figure 3: Primary Endpoint Events† within Demographic Subgroups Symbols are proportional to sample size. #Other include Asian,Hispanic,Asiaric,Multi-race,Native American,European. †Adjusted for baseline Framingham risk score and level of electrocardiographic left ventricular hypertrophy Nephropathy In Type 2 Diabetic PatientsThe RENAAL study was a randomized, placebo-controlled, double-blind, multicenter study conducted worldwide in 1513 patients with
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