Primary and secondary coronary heart disease prevention using statins: is targeting Adam or Eve equally effective?
ABSTRACT Women differ from men in terms of their cardiovascular disease risk. The existing data suggest that primary cardiovascular disease prevention treatment with a statin could be cost effective for women and men with a high cardiovascular disease risk. In secondary cardiovascular disease prevention both men and women seem to benefit equally from statin treatment. However, the relatively small number of women included in several statin trials has limited the evidence available. With regard to the question of whether Eve is becoming Adam, the answer is not yet: we need more evidence!
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ABSTRACT: Little is known about the potential of statin-induced high-density lipoprotein cholesterol (HDL-C) increase to improve renal function in coronary heart disease (CHD) patients. In thispost hocanalysis of the GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) Study we investigated the effect of HDL-C increase after statin treatment on renal function. From a total of 1,600 patients, 880 were on various statins (mainly atorvastatin) and 720 were not. Other secondary prevention therapies were similar in the 2 groups. After a 3 year follow up, the lipid profile was unchanged in the statin untreated group and estimated glomerular filtration rate (eGFR) was reduced by 5.1% compared with baseline (P<0.0001). In contrast, in the statin treated group non-HDL-C was reduced by 43%, HDL-C was increased by 7% and there was a significant increase in eGFR compared with baseline by 9.8% (P<0.0001). In multiple regression analysis, the mean 7% increase in HDL-C in the treated arm during the entire study was associated with a 5.6% increase in eGFR recorded after the 6(th) week of treatment. The odds ratio of eGFR increase with every 5% statin-induced rise in HDL-C was 1.78 (95% confidence interval 1.19-3.34; P=0.001). Statin treatment significantly improved renal function. Statin-induced HDL-C increase significantly and independently contributed to this improvement. This finding supports the concept that improving lipid variables other than low density lipoprotein cholesterol is also beneficial to preserving renal function.The Open Cardiovascular Medicine Journal 01/2007; 1:8-14.
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ABSTRACT: A National Heart, Lung, and Blood Institute (NHLBI) Conference was held October 9-10, 1990, to review and discuss existing data on U-shaped relations found between mortality rates and blood total cholesterol levels (TC) in some but not other studies. Presentations were given from 19 cohort studies from the United States, Europe, Israel, and Japan. A representative of each study presented its findings and also submitted tables of proportional hazards regression coefficients for entry TC levels in regard to death, and these were incorporated into a formal statistical overview adjusted for age, diastolic blood pressure, cigarette smoking, body mass index, and alcohol intake, as available. The U-shape for total mortality in men and the flat relation in women resulted largely from a positive relation of TC with coronary heart disease death and an inverse relation with deaths caused by some cancers (e.g., lung but not colon), respiratory disease, digestive disease, trauma, and residual deaths. Risk for combined noncardiovascular, noncancer causes of death decreased steadily across the range of TC. The conference considered possible explanations for the statistical associations found between low TC levels or active TC lowering and certain causes of death. One is that TC is lowered by some disease conditions themselves, such as wasting in chronic pulmonary disease or reduced production and secretion of cholesterol-bearing lipoproteins with liver disease. In this sort of situation, the TC:mortality association found in observational studies may be due to preexisting disease. This was addressed by excluding early deaths from the analysis, which did not change the results. The conference considered as well the biological function of cholesterol, which, if seriously deranged, might hypothetically cause a wide variety of diseases and dysfunction. The conference also considered the biological functions that might provide plausible mechanisms for the associations found. Definitive interpretation of the associations observed was not possible, although most participants considered it likely that many of the statistical associations of low or lowered TC level are explainable by confounding in one form or another. The conference focused on the apparent existence and nature of these associations and on the need to understand their source rather than on any pertinence of the findings for public health policy. Further research is recommended to explain the observed associations of low TC levels (and TC lowering) with certain noncardiovascular diseases. This includes studies of the time course of TC change in disease, the relation of TC to morbidity, further studies of possible epidemiological confounding, monitoring of population trends in TC and mortality, further studies of the relations in women, auditing of noncardiovascular events in trials, studies of cell membrane, genetic and molecular links to cholesterol metabolism, TC level and disease, studies of disease manifestations in specific lipid disorders, and further study of the proposed causal mechanisms linking low TC and hemorrhagic stroke.Circulation 10/1992; 86(3):1046-60. · 15.20 Impact Factor
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ABSTRACT: The objective of our study was to examine age-specific mortality rates from coronary heart disease (CHD), particularly those among younger adults. Trends for obesity, diabetes, blood pressure, and metabolic syndrome among young adults raise concerns about the mortality rates from CHD in this group. We used mortality data from 1980 to 2002 to calculate age-specific mortality rates from CHD for U.S. adults age > or =35 years. Overall, the age-adjusted mortality rate decreased by 52% in men and 49% in women. Among women age 35 to 54 years, the estimated annual percentage change (EAPC) in mortality was -5.4% (95% confidence interval [CI] -5.8 to -4.9) from 1980 until 1989, -1.2% (95% CI -1.6 to -0.8) from 1989 until 2000, and 1.5% (95% CI -3.4 to 6.6) from 2000 until 2002. Among men age 35 to 54 years, the EAPC in mortality was -6.2% (95% CI -6.4 to -5.9) from 1980 until 1989, -2.3% (95% CI -2.6 to -2.1) from 1989 until 2000, and -0.5% (95% CI -3.7 to 2.9) from 2000 until 2002. Among women and men age > or =55 years, the estimated annual percentage decrease in mortality from CHD accelerated in more recent years compared with earlier periods. The mortality rates for CHD among younger adults may serve as a sentinel event. Unfavorable trends in several risk factors for CHD provide a likely explanation for the observed mortality rates.Journal of the American College of Cardiology 11/2007; 50(22):2128-32. · 14.09 Impact Factor