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Preventive Cardiology  
1999 Guide to Preventive Cardiology for Women                                                                                        
AHA/ACC Scientific Statement: Consensus Panel Statement 1999  
(Circulation. 1999;99:2480-2484.)

2000 AHA Scientific Statement
Beyond Secondary Prevention :
Identifying the High-Risk Patient for Primary Prevention : Executive Summary   (Circulation. 2000;101:111.)

1999 AHA Scientific Statement
Diabetes and Cardiovascular Disease
: A Statement for Healthcare Professionals From the AHA
(Circulation 1999; 100: 1132-1133. )

Hormone Replacement Therapy and Cardiac Prevention Response - Beth L. Abramson, etc.
(Circulation 2000; 101: e223-e224.)

Hormone Replacement Therapy and Incidence of Acute Myocardial Infarction
A Population-Based Nested Case-Control Study   -  Cristina Varas-Lorenzo, etc. (Spain)
(Circulation. 2000;101:2572.)

Background—Epidemiological studies suggest a decreased risk of coronary heart disease (CHD) in healthy women taking hormonal replacement therapy (HRT). Whether this effect is shared by oral and transdermal preparations is unknown.

Methods and Results—We conducted a population-based case-control study nested in a cohort of women 50 to 74 years of age without cardiovascular disease history in the United Kingdom. Among 164 769 women from the General Practice Research Database (January 1, 1991, to December 31, 1995), we identified 1242 first acute myocardial infarctions (AMI) and confirmed 1013 after medical record review. We randomly selected 5000 age-frequency–matched control subjects. AMI incidence was 1.6 per 1000 person-years; 13% and 17% of cases and control subjects used HRT within 6 months before the index date. Risk factor and comorbidity–adjusted OR of AMI for current-recent HRT users compared with nonusers was 0.72 (95% CI 0.59 to 0.89). The OR was similar within 30 days before the index date. The beneficial effect was present after 1 year of use (OR 0. 68; 95% CI 0.53 to 0.86), with no increase in risk within the first year. ORs for unopposed and opposed therapy were 0.52 (95% CI 0.35 to 0.78) and 0.79 (95% CI 0.59 to 1.08); 79% and 21% used oral and transdermal therapy.

The protective effect was present at medium-high doses of estrogens with ORs for oral and transdermal therapy of 0.63 (95% CI 0.46 to 0.86) and 0.62 (95% CI 0.37 to 1.06) and ceased after 2 to 3 years since stopping HRT.

Conclusions—Results are consistent with those previously reported in women without CHD who were taking oral HRT and, although based on few users, suggest that transdermal therapy might have similar cardioprotective effects.  

Current Perspectives on Statins -  David J. Maron, etc.(Vanderbilt University)
(Circulation. 2000;101:207.)

Abstract—Statins (HMG-CoA reductase inhibitors) are used widely for the treatment of hypercholesterolemia. They inhibit HMG-CoA reductase competitively, reduce LDL levels more than other cholesterol-lowering drugs, and lower triglyceride levels in hypertriglyceridemic patients. Statins are well tolerated and have an excellent safety record. Clinical trials in patients with and without coronary heart disease and with and without high cholesterol have demonstrated consistently that statins reduce the relative risk of major coronary events by 30% and produce a greater absolute benefit in patients with higher baseline risk.

Proposed mechanisms include favorable effects on plasma lipoproteins, endothelial function, plaque architecture and stability, thrombosis, and inflammation. Mechanisms independent of LDL lowering may play an important role in the clinical benefits conferred by these drugs and may ultimately broaden their indication from lipid-lowering to antiatherogenic agents.

1999 AHA Science Advisory  
Antioxidant Consumption and Risk of Coronary Heart Disease:

Emphasis on Vitamin C, Vitamin E, and ß-Carotene  -  Diane L. Tribble
(Circulation. 1999;99:591-595.)

Two particularly illustrative prospective cohort studies were published as companion papers in 1993.19 20 The first, by Stampfer et al,19 involved analyses of data from >85 000 Nurses' Health Study participants who were followed up for periods of 8 years. Risk of major coronary disease was lowest in women within the highest compared with those within the lowest quintile of reported vitamin E intake after adjustment for age and smoking status (relative risk, 0.66; 95% CI, 0.50 to 0.87).  Lower risk was associated with levels of vitamin E intake that were achievable only by supplementation. Subsequent analyses revealed a 43% lower risk for vitamin E supplement users versus nonusers and an inverse relationship between risk and duration of supplement use. The second study, by Rimm et al,20 described a similar benefit for vitamin E based on data from >39 000 male participants of the Health Professionals Follow-up Study (HPFS) who were followed up for 4 years.

A major case in point is the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a randomized trial that tested the effects of daily doses of 50 mg (50 IU) of vitamin E (all-racemic -alpha-tocopheryl acetate), 20 mg of ß-carotene, both, or placebo for 5 to 8 years in a population of >29 000 male smokers.26 The major end point was lung cancer, but the investigators also evaluated coronary heart disease. No reduction in risk of lung cancer or major coronary events was observed with any of the treatments. Moreover, with vitamin E supplementation, there was an unexpected increase in risk of death from hemorrhagic stroke, and with ß-carotene supplementation, there were unexpected increases in mortality from lung cancer and ischemic heart disease.

Secondary Prevention Trials
Results from secondary prevention trials have been more supportive of the potential health benefits of antioxidants. The Cambridge Heart Antioxidant Study (CHAOS) tested the effects of high doses (400 or 800 IU/d) of -tocopherol on subsequent cardiovascular events in patients with angiographic evidence of coronary atherosclerosis.33 On the basis of the combined results for the 2 dose levels, risks of myocardial infarction (MI) and all cardiovascular events were reduced by 77% and 47%, respectively, in the treatment group, with a delay in the onset of treatment benefit of 200 days. Similar reductions were not observed for fatal cardiovascular end points. Although there are some concerns regarding the design of the CHAOS trial, including the use of 2 vitamin E doses, similar results have been obtained in other recent trials. Less impressive but consistent with the CHAOS study were results from a secondary analysis of the ATBC Study.34 In individuals with a history of MI at the start of the study, risk of subsequent nonfatal MI was reduced by 38% in the -tocopherol group; in contrast, risk of fatal coronary end points was not reduced. As in the larger study, risk of fatal coronary end points was increased with ß-carotene supplementation (both with and without -tocopherol).

The apparent benefits of vitamin E (-tocopherol) in individuals with existing coronary disease are not consistent with the proposed role of oxidants in initiating lesions. Recent results from subgroup analyses of the Cholesterol Lowering Atherosclerosis Study (CLAS) suggest that high vitamin E intake could inhibit lesion progression.35 36 Consideration of this effect as well as other possible effects of vitamin E on the clinical expression of cardiovascular disease is warranted.

Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study. Lancet. 1996;347:781–786.[Medline]

Rapola JM, Virtamo J, Ripatti S, Huttunen JK, Albanes D, Taylor PR, Heinonen OP. Randomised trial of -tocopherol and ß-carotene supplements on incidence of major coronary events in men with previous myocardial infarction.
Lancet. 1997;349:1715–1720.[Medline]

Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary heart disease in women. N Engl J Med. 1993;328:1444–1449.

Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med. 1993;328:1450–1456.