Recent randomized trials of hormone replacement therapy (HRT) in postmenopausal women are not consistent with the decrease in cardiovascular risk seen in observational studies of hormone therapy users compared with nonusers. Emerging evidence indicates that HRT use in some women with established coronary heart disease may be associated with prothrombotic effects or proinflammatory effects leading to adverse events. In healthy women, the decision to use HRT should be based primarily on noncardiac factors until more data becomes available that is relevant to this population. Several alternatives to HRT, including phytoestrogens and selective estrogen receptor modulators, have favorable effects on cardiovascular risk factors, but their impact on clinical outcomes remains to be determined.

Coronary Disease↗

PubMed2002

Postmenopausal hormone replacement therapy and atherosclerosis.

The role of postmenopausal hormone replacement therapy (HRT) in the prevention of cardiovascular disease (CVD) has evolved since estrogen was first proposed to be vasoprotective. The discovery of novel molecular signaling pathways involving the estrogen receptor in vascular cells and the elucidation of numerous biologic mechanisms have suggested that HRT may exert its potentially beneficial or adverse cardiovascular effects through multiple mechanisms. Estrogen has genomic, as well as rapid nongenomic, effects that alter vasodilation, coagulation, inflammation, and the vascular injury response, some of which may have potentially beneficial or adverse cardiovascular consequences. Current guidelines do not support the use of HRT in the secondary prevention of CVD, and recent results of primary prevention trials show evidence of increased early cardiovascular risk and no overall health benefit with combination estrogen-progestin treatment. The role of estrogen alone in the primary prevention of CVD awaits the results of ongoing trials. The key to the use of estrogen replacement therapy for the prevention of CVD may be to target therapy before atherosclerosis is evident, and to identify women with genetic susceptibility who may be at increased risk for an adverse outcome associated with therapy.

Age Factors↗

PubMed2002

Lipid-lowering therapies in the management of acute coronary syndromes.

Despite the significant advances made in the treatment of acute coronary syndromes (ACS) with antiplatelet and antithrombotic therapy, the risk of serious complications remains high, especially in the first few months following an acute coronary event. Although lipid-lowering therapy in patients with significant risk factors (primary prevention) or stable coronary disease (secondary prevention) is known to improve long-term survival, patients with a recent ACS were specifically excluded from the early statin trials. However, the use of lipid-lowering agents (principally statins) during hospitalization or in the period immediately following an acute coronary event has recently been studied. Statin therapy in this setting has been shown to reduce angina, rehospitalization, and mortality. Improved outcomes associated with lipid-lowering therapy in ACS may be mediated through beneficial effects on plaque stabilization, endothelial function, inflammation, and thrombus formation. This paper reviews the evidence supporting the potential benefits and mechanisms of statin therapy in the management of ACS. Clinical guidelines to achieve optimal lipid management are also discussed.

Acute Disease↗

PubMed2002

Carotid artery reactivity to isometric hand grip exercise identifies persons at risk and with coronary disease.

BACKGROUND: The change in brachial artery diameter (DBA(d)) following release of an occluding cuff (BAO(cclR)) has been used to characterize local endothelial function and coronary risk. We designed a study to determine the CA diameter (CA(d)) response to exercise (IHG), whether the response is influenced by coronary risk, and compare it with the BAO(cclR) method. METHOD AND RESULTS: High resolution ultrasound was used to detect the DCA(d) in response to120 s of 33% of maximum and DBA(d) was measured 60 s following release of an occluding cuff. There was no change in CA(d) during IHG. At 90 s following release, CA(d) dilated >0.1 mm in 95% of volunteers with average risk (mean 0.42+/-0.25 mm or 5.97+/-3.5%). There was no change or constriction in 62% of high risk (0.01+/-0.28 mm, 0.0+/-3.6%), and predominantly constriction in CAD subjects (-0.22+/-0.23 mm, -0.01+/-3.2%), P=0.0001 for trend and 0.01 between groups. The %DCA(d) following IHG and %DBA(d) following OcclR were highly correlated, r=0.66, P=0.0001. The major determinant of response to each stressor was group (%DBA(d) R(2)=0.55 and %DCA(d) R(2)=0.52). CONCLUSIONS: The reactivity of the carotid artery to IHG is highly influenced by coronary risk, and may be an additional modality to characterize pre-clinical CAD and assess treatment strategies.

Adult↗

PubMed2002

Antioxidant nutrient supplementation and brachial reactivity in patients with coronary artery disease.

Epidemiologic studies have shown a correlation between antioxidant intake and coronary artery disease (CAD); however, the results of clinical trials have been inconsistent. We evaluated the effect of combined antioxidant supplementation on endothelial function and its correlation with change in low-density lipoprotein cholesterol (LDLC) oxidation in patients with established CAD. In a double-blind, placebo-controlled 12-week trial, 18 nonsmoking, nondiabetic patients (mean age 62.4 +/- 8.1 years) were randomized to receive placebo or antioxidant supplementation consisting of (a) 400 IU of vitamin E, 500 mg of vitamin C, and 12 mg of beta-carotene; or (b) 800 IU of vitamin E, 1000 mg of vitamin C, and 24 mg of beta-carotene daily. Endothelial function was evaluated on the basis of percent and absolute changes in brachial artery diameter in response to reactive hyperemia induced by occlusion-release. Baseline and 12-week values of LDL oxidation (measured on the basis of lag phase), endothelial function, dietary composition, serum antioxidants, and lipids were measured. We noted a significant between-group difference at 12 weeks for change in plasma concentrations of alpha-tocopherol, vitamin C, and beta-carotene between the placebo and antioxidant groups (p <.05). Both placebo and treatment groups demonstrated a significant improvement in lag phase; however, the treatment group achieved a greater, although nonsignificant, magnitude of change compared with the placebo group (181.3 +/- 177.8 minutes vs 80.6 +/- 63.0 minutes, P =.06). Within-group change in brachial reactivity from baseline to follow-up in the treatment group did not reach statistical significance (1.7% +/- 3.2% and 0.07 mm +/- 0.13 mm, P =.08 and P =.09, respectively), whereas an improved change in brachial reactivity was observed in the placebo group (2.2% +/- 1.9%, 0.09 mm +/- 0.06 mm, P <.05). No significant correlation was found between change in lag phase and change in endothelial function. On adjustment for confounders, antioxidant supplementation was found not to be a significant predictor of brachial reactivity. We conclude that antioxidant supplementation did not significantly alter brachial reactivity, despite significantly increased plasma levels of antioxidants and improved lag phase. These data should be confirmed in larger-scale trials and examined in studies evaluating individual dietary antioxidant supplementation.

Antioxidants↗

PubMed2002

Cholesterol predicts stroke mortality in the Women's Pooling Project.

BACKGROUND AND PURPOSE: Cholesterol is emerging as a risk factor for stroke; however, few data are available regarding the relation of cholesterol and stroke mortality in women and ethnic minorities. METHODS: We evaluated the risk of death caused by total stroke, nonhemorrhagic stroke, and hemorrhagic stroke by race, age, and cholesterol quintile in 24 343 women with no previous cardiovascular disease who were participating in 8 US longitudinal, prospective, cohort studies included in the Women's Pooling Project. RESULTS: We observed 568 stroke deaths (461 nonhemorrhagic, 83 hemorrhagic) for women > or =30 years of age without previous cardiovascular disease during 339 215 person-years of follow-up. In multivariate models, black women <55 years of age had a 76% increased risk of death caused by stroke compared with white women [relative risk (RR), 1.76; 95% confidence interval (CI), 1.10 to 2.81]. For black women <55 years of age, the top compared with the lowest cholesterol quintile (Q5 versus Q1) remained an independent predictor of stroke mortality (RR, 2.58; 95% CI, 1.05 to 6.32) in multivariate models. For white women <55 years of age, Q5 versus Q1 cholesterol did not predict stroke mortality with significance (RR, 1.47; 95% CI, 0.57 to 3.76). In analogous multivariate models, we found a positive relation between continuous cholesterol and nonhemorrhagic stroke death in women <55 years of age (RR, 1.23; 95% CI, 1.02 to 1.49). CONCLUSIONS: Our results show that cholesterol is a risk factor for nonhemorrhagic stroke death in women <55 years of age and is more strongly associated with mortality in black women <55 years of age than in white women. These data document the importance of cholesterol in addition to established risk factors for predicting stroke mortality in young women and may guide prevention strategies.

Adult↗

PubMedDate not supplied

Epidemiology of coronary heart disease in women.

Cardiovascular disease (CVD) is the leading cause of mortality in women and a major cause of morbidity. Coronary heart disease (CHD) accounts for nearly half of all CVD deaths. Gender differences in CHD include a later age of onset for women, a greater prevalence of comorbid diseases, and differences in the initial manifestations of the disease. Traditional risk factors for CHD include tobacco use, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, and atherogenic diet. More recently identified risk factors in women include high sensitivity C-reactive protein (hsCRP), homocysteine, and lipoprotein (a). Appropriate management of risk factors is associated with a reduced incidence of CHD, yet poor implementation in women is widely documented. Barriers to optimal risk factor management in women should be identified and overcome in an effort to maximize the cardiovascular health of women.

Age of Onset↗

PubMedDate not supplied

The association between educational level and risk of cardiovascular disease fatality among women with cardiovascular disease.

BACKGROUND: The inverse relation of socioeconomic status with incident cardiovascular diseases (CVDs) has been well established. However, few data are available describing this relation among ethnically diverse women with prevalent CVD. Using education as a proxy for socioeconomic status, we examined its relation to CVD mortality among women with established CVD. SUBJECTS: Data from 2,157 women with CVD at baseline, who participated in nine long-term U.S. cohort studies, were pooled. METHODS: Cox regression models adjusted for history of diabetes mellitus, total cholesterol, systolic and diastolic blood pressure, body mass index, smoking, race/ethnicity, and age at baseline were used to estimate hazard ratios for CVD mortality between non-high school graduates and high school graduates. RESULTS: During a mean follow-up time of 11.5 years, 615 CVD deaths were observed. There was an age-dependent (p = .003) inverse association between education and CVD mortality among women with CVD. At age 60, the risk of dying due to CVD among non-high school graduates was more than twice greater than that of high school graduates (hazard ratio = 2.34; 95% CI 1.27-4.29). At age 65, the hazard ratio decreased to 1.31 (95% CI 1.00-1.71). By age 70, there was no difference in the hazard of dying between high school graduates and nongraduates (hazard ratio = 1.01; 95% CI .85-1.21). CONCLUSIONS: Our results show that among women with CVD, educational level was a significant, and age-dependent, predictor of fatal CVD independent of other traditional risk factors. These women are an important high-risk population to target secondary prevention and educational efforts.

Adult↗

PubMedDate not supplied

Waist circumference predicts cardiometabolic and global Framingham risk among women screened during National Woman's Heart Day.

PURPOSE: To evaluate the cardiometabolic risk profiles of 6938 women (mean age 49.2 +/- 14.6 years) attending the 2005 Sister to Sister: Everyone Has a Heart Foundation free public health standardized cardiovascular disease (CVD) risk factor screening events in 12 cities across the United States by race/ethnicity and waist circumference. MAIN FINDINGS: Among women without a history of CVD or diabetes (n = 6327), 90% were found to have at least one major modifiable CVD risk factor, with one-third of women having three or more major risk factors. Nearly half of all women with elevated total cholesterol (> or = 200 mg/dL) or low high-density lipoprotein (HDL)-cholesterol (< 50 mg/dL) did not report a known history of abnormal cholesterol. Among women with no history of hypertension, 16% had a blood pressure > or = 140/90 mm Hg. Unrecognized diabetes and glucose intolerance were striking among fasting women (n = 1218; 9% had a blood glucose > or = 126 mg/dL and 43% had a blood glucose > or = 100 mg/dL). In adjusted logistic regression models, women with a waist circumference > or = 35 inches were more likely to have blood pressure > or = 140/90 (OR = 1.9, p < 0.0001), total cholesterol > or = 200 mg/dL (OR = 1.2, p = 0.006), HDL-cholesterol < 50 mg/dL (OR = 2.5, p < 0.0001), fasting glucose > or = 100 mg/dL (OR = 2.0, p < 0.0001), and Framingham global risk score > or = 10%, CVD or diabetes (OR = 2.0, p < 0.0001). Waist circumference was significantly correlated with Framingham global risk (r = 0.24, p < 0.001) and number of risk factors (r = 0.24, p < 0.0001). Increased clustering of risk factors was predictive of waist size > or = 35 inches vs. < 35 inches in logistic models (p for trend > 0.0001). Among a subsample of women who underwent standardized screening for stress and depression, 62% had stress levels associated with increased cardiac risk, and 27% met criteria for clinical depression. CONCLUSIONS: Hypertension, dyslipidemia, and/or impaired fasting glucose were newly identified in approximately half the women screened. Waist size significantly correlated with clustering of risk factors, global Framingham risk score, CVD and diabetes, suggesting it may be an easily measured surrogate for women at increased risk of future cardiovascular clinical events who may benefit from further assessment and intervention.

Adult↗

PubMedDate not supplied

Self-reported physical activity and myocardial flow reserve in postmenopausal women at risk for cardiovascular disease.

BACKGROUND: Regular exercise protects against coronary heart disease (CHD) events and improves vascular reactivity. Exercise effects on myocardial flow reserve (MFR) are not well studied. METHODS: We performed dynamic N-13 ammonia positron emission tomography (PET) in 16 postmenopausal women (60 +/- 6 years) to measure myocardial blood flow (MBF) and MFR. We also obtained information from each woman on her self-reported physical activity. RESULTS: Of the 16 patients, 6 reported moderate regular physical activity, and 10 did not. Women who reported regular, at least moderate physical activity had a higher percentage increase in adenosine MBF from rest compared with women who did not exercise (268% vs. 129%, p = 0.04) and had a significantly higher mean maximal MFR (3.68 vs. 2.29, p = 0.04). CONCLUSIONS: These findings provide further mechanistic support for the beneficial cardiovascular effects of exercise.

Aged↗

PubMedDate not supplied

Limitations of current cardiovascular disease risk assessment strategies in women.

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Cardiovascular Diseases↗

PubMedDate not supplied

Physical activity and coronary heart disease: prevention and effect on risk factors.

The general public recommendation to accumulate 30 minutes of daily physical activity on most, preferably all, days of the week was recently modified by the National Academy of Science Institute of Medicine to at least 60 minutes of cumulative daily physical activity to maintain cardiovascular health at a maximal level. Data suggest that regular physical activity, even as little as 30 minutes daily, can positively impact cardiovascular health by improving many of the major risk factors associated with coronary heart disease, including hypertension, dyslipidemia, obesity, insulin resistance, and endothelial function. With the recent and rapid rise in the rate of obesity in the United States, a doubling of the dose of physical activity daily may help offset the trend of increased caloric intake that has contributed to this epidemic. We briefly review the evidence regarding the amount and intensity of physical activity necessary to alter these cardiovascular risk factors with the goal of reducing coronary events.

Coronary Disease↗