Treatment of dyslipidemia in pre- and postmenopausal women with and without known atherosclerotic cardiovascular disease.

Division of Cardiovascular Disease, University of Alabama at Birmingham, UAB Station - LHR 310, Birmingham, AL 35294, USA.
Current Cardiology Reports 10/2001; 3(5):401-7. DOI: 10.1007/s11886-001-0057-2
Source: PubMed

ABSTRACT Cardiovascular disease is the primary cause of death among women in the United States, in part due to a very high prevalence of dyslipidemia. Clinical trials have shown that low-density lipoprotein cholesterol-lowering therapy can decrease angiographic progression of coronary disease and decrease clinical events among women and men. Although hormone replacement therapy has beneficial effects on the lipoprotein profile, its role in cardiovascular disease prevention remains unclear. The recently released Third Report of the National Cholesterol Education Program Expert Panel provides detailed guidelines for the management of dyslipidemia in women, with a focus on low-density lipoprotein cholesterol and intensity guided by risk of cardiovascular events.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although cholesterol-reducing treatment has been shown to reduce fatal and nonfatal coronary disease in patients with coronary heart disease (CHD), it is unknown whether benefit from the reduction of low-density lipoprotein cholesterol (LDL-C) in patients without CHD extends to individuals with average serum cholesterol levels, women, and older persons. To compare lovastatin with placebo for prevention of the first acute major coronary event in men and women without clinically evident atherosclerotic cardiovascular disease with average total cholesterol (TC) and LDL-C levels and below-average high-density lipoprotein cholesterol (HDL-C) levels. A randomized, double-blind, placebo-controlled trial. Outpatient clinics in Texas. A total of 5608 men and 997 women with average TC and LDL-C and below-average HDL-C (as characterized by lipid percentiles for an age- and sex-matched cohort without cardiovascular disease from the National Health and Nutrition Examination Survey [NHANES] III). Mean (SD) TC level was 5.71 (0.54) mmol/L (221 [21] mg/dL) (51 st percentile), mean (SD) LDL-C level was 3.89 (0.43) mmol/L (150 [17] mg/dL) (60th percentile), mean (SD) HDL-C level was 0.94 (0.14) mmol/L (36 [5] mg/dL) for men and 1.03 (0.14) mmol/L (40 [5] mg/dL) for women (25th and 16th percentiles, respectively), and median (SD) triglyceride levels were 1.78 (0.86) mmol/L (158 [76] mg/dL) (63rd percentile). Lovastatin (20-40 mg daily) or placebo in addition to a low-saturated fat, low-cholesterol diet. First acute major coronary event defined as fatal or nonfatal myocardial infarction, unstable angina, or sudden cardiac death. After an average follow-up of 5.2 years, lovastatin reduced the incidence of first acute major coronary events (1 83 vs 116 first events; relative risk [RR], 0.63; 95% confidence interval [CI], 0.50-0.79; P<.001), myocardial infarction (95 vs 57 myocardial infarctions; RR, 0.60; 95% CI, 0.43-0.83; P=.002), unstable angina (87 vs 60 first unstable angina events; RR, 0.68; 95% CI, 0.49-0.95; P=.02), coronary revascularization procedures (157 vs 106 procedures; RR, 0.67; 95% CI, 0.52-0.85; P=.001), coronary events (215 vs 163 coronary events; RR, 0.75; 95% CI, 0.61-0.92; P =.006), and cardiovascular events (255 vs 194 cardiovascular events; RR, 0.75; 95% CI, 0.62-0.91; P = .003). Lovastatin (20-40 mg daily) reduced LDL-C by 25% to 2.96 mmol/L (115 mg/dL) and increased HDL-C by 6% to 1.02 mmol/L (39 mg/dL). There were no clinically relevant differences in safety parameters between treatment groups. Lovastatin reduces the risk for the first acute major coronary event in men and women with average TC and LDL-C levels and below-average HDL-C levels. These findings support the inclusion of HDL-C in risk-factor assessment, confirm the benefit of LDL-C reduction to a target goal, and suggest the need for reassessment of the National Cholesterol Education Program guidelines regarding pharmacological intervention.
    JAMA The Journal of the American Medical Association 06/1998; 279(20):1615-22. · 30.39 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Physical inactivity contributes to weight gain, but only 22% of Americans are regularly active. To examine short- and long-term changes in weight, body composition, and cardiovascular risk profiles produced by diet combined with either structured aerobic exercise or moderate-intensity lifestyle activity. Sixteen-week randomized controlled trial with 1-year follow-up, conducted from August 1995 to December 1996. Forty obese women (mean body mass index [weight in kilograms divided by the square of height in meters], 32.9 kg/m2; mean weight, 89.2 kg) with a mean age of 42.9 years (range, 21-60 years) seen in a university-based weight management program. Structured aerobic exercise or moderate lifestyle activity; low-fat diet of about 1200 kcal/d. Changes in body weight, body composition, cardiovascular risk profiles, and physical fitness at 16 weeks and at 1 year. Mean (SD) weight losses during the 16-week treatment program were 8.3 (3.8) kg for the aerobic group and 7.9 (4.2) kg for the lifestyle group (within groups, P<.001; between groups, P = .08). The aerobic group lost significantly less fat-free mass (0.5 [1.3] kg) than the lifestyle group (1.4 [1.3] kg; P = .03). During the 1-year follow-up, the aerobic group regained 1.6 [5.5] kg, while the lifestyle group regained 0.08 (4.6) kg. At week 16, serum triglyceride levels and total cholesterol levels were reduced significantly (P<.001) from baseline (16.3% and 10.1% reductions, respectively) but did not differ significantly between groups and were not different from baseline or between groups at week 68. A program of diet plus lifestyle activity may offer similar health benefits and be a suitable alternative to diet plus structured aerobic activity for obese women.
    JAMA The Journal of the American Medical Association 01/1999; 281(4):335-40. · 30.39 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Randomized trials have established statin treatment as secondary prevention in coronary artery disease, but it is unclear whether early treatment with statins following acute myocardial infarction (AMI) influences survival. To evaluate the association between statin treatment initiated before or at the time of hospital discharge and 1-year mortality after AMI. Prospective cohort study using data from the Swedish Register of Cardiac Intensive Care on patients admitted to the coronary care units of 58 Swedish hospitals in 1995-1998. One-year mortality data were obtained from the Swedish National Cause of Death Register. Patients with first registry-recorded AMI who were younger than 80 years and who were discharged alive from the hospital, including 5528 who received statins at or before discharge and 14 071 who did not. Relative risk of 1-year mortality according to statin treatment. At 1 year, unadjusted mortality was 9.3% (1307 deaths) in the no-statin group and 4.0% (219 deaths) in the statin treatment group. In regression analysis adjusting for confounding factors and propensity score for statin use, early statin treatment was associated with a reduction in 1-year mortality (relative risk, 0.75; 95% confidence interval, 0.63-0.89; P =.001) in hospital survivors of AMI. This reduction in mortality was similar among all subgroups based on age, sex, baseline characteristics, previous disease manifestations, and medications. Early initiation of statin treatment in patients with AMI is associated with reduced 1-year mortality. These results emphasize the importance of implementing the results of randomized statin trials in unselected AMI patients.
    JAMA The Journal of the American Medical Association 05/2001; 285(4):430-6. DOI:10.1016/S1062-1458(01)00231-8 · 30.39 Impact Factor
Show more