CVD risk watchtower

CVD risk watchtower

Preventive Medicine 43 (2006) 353 – 355 This Month in Preventive Medicine All along the CHD/CVD risk watchtower It is ...

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Preventive Medicine 43 (2006) 353 – 355

This Month in Preventive Medicine

All along the CHD/CVD risk watchtower It is now well established that Western women are just as susceptible as men to coronary heart disease (CHD). In the US, nearly half a million women die each year from CHD as opposed to a quarter of a million women who die from all types of cancer, including breast cancer, combined (Mensah et al., 2005). It is intriguing that women are much less aware of their risk than men (Anonymous, 2005). In 1997 only 30% of US women recognized that cardiovascular disease (CVD) was their leading cause of death (Mosca et al., 2006). A US nationally representative sample of 1008 women selected through random-digit dialing has provided a mixed update: in 2003 more than half (55%) were aware of their CVD risk, almost a doubling of the 30% observed in 1997, but still a far cry from the 80% goal for 2010 (US Department of Health and Human Services, 2000). Another interesting aspect of that edifying report is that the most frequently cited barrier to engaging in healthy lifestyles was, for 49% of the women, “too much confusion in the media.” Can we blame them? There is too much confusion and they can't get no relief! For example, as discussed by Rothstein (2006) in his review article on the relation between dietary fat and health in this issue of PM, in the absence of clear-cut evidence, the content of the corresponding public health messages has fluctuated substantially over the last 100 years, from positive (because associated with not being poor) to negative (because associated with not being slim) to neutral (because clinical trials did not observe a deleterious effect). Similar yo-yo stories could be told for the health risks of oral contraceptives or of hormone replacement therapy. There is a long-standing controversy over whether epidemiologic studies based on confounded comparisons of exposed and non-exposed cohorts or of cases and controls should be considered the culprits for these shortcomings (Pocock and Elbourne, 2000). Observational studies are always presumed guilty of inferior validity compared to randomized controlled trials (RCTs). Nonetheless, RCTs also have their problems (Shapiro, 2003). As mentioned by Rothstein (2006), large RCTs tend to enroll unrepresentative samples of highly motivated, health-conscious, well-educated, higher income, and nonsmoking volunteers and tend to test costly lifestyle intervention techniques that are not economically feasible in the community. Even more important is the fact that RCTs often fail to provide definitive answers. Is there any alternative between the Charybdisian observational study and the Scyllan RCT? There must be some way out of here! At least for us, community-based intervention studies subject to the dual constraints of having to be viable in the real world and conducted with scientific rigor are the best solution. They can re-orient health policy by making their way through to peer-reviewed journals. We welcome publishing more research studies of this type in PM. Three more articles in this issue are concerned with expanding our understanding of CHD/CVD risk factors. In the prospective community-based Groningen Longitudinal Aging Study of incident CHD and 7-year mortality, Van Jaarsveld et al. (2006) found that men with congestive heart failure or acute myocardial infarction (AMI) had survival rates worse than those of women, yet mortality risk factors were similar by gender, with the exception of diabetes, which was a risk factor only among women with AMI. One explanation concerns gender-related differences in the prevalence of CHD risk factors such 0091-7435/$ - see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.ypmed.2006.09.009


This Month in Preventive Medicine

as smoking, body mass index, and comorbidity (Yusuf et al., 2004). A second explanation is that CHD risk factors may have differential effects by gender. A meta-analysis showed that the impact of diabetes on CHD mortality was greater for women (Lee et al., 2000), while men showed greater effects of disability, high cholesterol, and smoking (Janghorbani et al., 1993; Kattainen et al., 2004; Marang-van de Mheen et al., 2001). The 2001 National Cholesterol Education Program Adult Treatment Panel report (NCEP ATP III) recommends that clinicians calculate 10-year CHD risk using multivariable methods only for adults with two or more risk factors. Using data on 4,097 individuals 20–79 years of age without diagnosed CVD or diabetes from the 1999–2002 National Health and Nutrition Examination Survey, Persell et al. (2006) extrapolated that relying on the ATP III risk factor counting method rather than determining 10-year CHD risk using multivariable methods in all patients would result in misclassifying over 5 million US adults (mostly middle-aged and older men) as being at low CHD risk when they actually had at least a moderately high risk. The third article along the CHD/CVD risk watchtower takes the middle-way between Charybdis and Scylla, in keeping with our call for papers mentioned above. In the Dutch Hartslag Limburg project, Harting et al. (2006) performed a multiple risk factor/multiple component high-risk approach intervention RCT for CVD prevention among 25 general practices (12 intervention vs. 13 control (usual care) practices). The results were based on multilevel analyses of the data collected from over 1000 individuals who had at least a 20% risk of incurring a cardiovascular event within 10 years at baseline and at 4 and 18 months post-intervention. The statistical models were adjusted for age, gender, educational level, smoking status, and body mass index, included variance components to account for clustering within general practices and for practitioners within practices, and also included interaction terms for investigating possible subgroup effects. The main research question was whether the high-risk approach led to positive changes in saturated fat intake, smoking, and physical activity. The main findings were that the intervention produced a meaningful decrease in saturated fat consumption at 4 months that declined but remained modest at 18 months, a promising increase in physical activity but only among individuals who were obese at the baseline, and had no effect on smoking. The authors end the article with a thorough discussion further buttressed with useful process evaluation data and a consideration of the potential limitations to internal and external validity that conservatively cautions against the wholesale real-world implementation of the intervention in its current form. What a refreshing relief! References Anonymous, 2005. Disparities in screening for and awareness of high blood cholesterol—United States, 1999–2002. JAMA 293, 1849–1850. Harting, J., van Assema, P., van Limpt, P., et al., 2006. Cardiovascular prevention in the Hartslag Limburg project: effects of a high-risk approach on behavioral risk factors in a general practice population. Prev. Med. 43, 372–378 (this issue). Janghorbani, M., Hedley, A.J., Jones, R.B., Zhianpour, M., Gilmour, W.H., 1993. Gender differential in all-cause and cardiovascular disease mortality. Int. J. Epidemiol. 22, 1056–1063. Kattainen, A., Reunanen, A., Koskinen, S., Martelin, T., Knekt, P., Aromaa, A., 2004. Disability predicted mortality in men but not women with coronary heart disease. J. Clin. Epidemiol. 57, 513–521. Lee, W.L., Cheung, A.M., Cape, D., Zinman, B., 2000. Impact of diabetes on coronary artery disease in women and men: a meta-analysis of prospective studies. Diabetes Care 23, 962–968. Marang-van de Mheen, P.J., Smith, G.D., Hart, C.L., Hole, D.J., 2001. Are women more sensitive to smoking than men? Findings from the Renfrew and Paisley study. Int. J. Epidemiol. 30, 787–792. Mensah, G.A., Brown, D.W., Croft, J.B., Geenlund, K.J., 2005. Major coronary risk factors and death from coronary heart disease: baseline and follow-up mortality data from the Second National Health and Nutrition Examination Survey (NHANES II). Am. J. Prev. Med. 29 (5Sl), 68–74. Mosca, L., Mochari, H., Christian, A., et al., 2006. National study of women's awareness, preventive action, and barriers to cardiovascular health. Circulation 113, 525–534. Persell, S.D., Lloyd-Jones, D.M., Baker, D.W., 2006. National Cholesterol Education Program risk assessment and potential for risk misclassification. Prev. Med. 43, 368–371 (this issue). Pocock, S.J., Elbourne, D.R., 2000. Randomized trials or observational tribulations? N. Engl. J. Med. 342, 1907–1909. Rothstein, W.G., 2006. Dietary fat, coronary heart disease, and cancer: a historical review. Prev. Med. 43, 356–360 (this issue).

This Month in Preventive Medicine Shapiro, S., 2003. Risks of estrogen plus progestin therapy: a sensitivity analysis of findings in the Women's Health Initiative randomized controlled trial. Climacteric 6, 302–310. US Department of Health and Human Services, 2000. Healthy People 2010. (conference ed., 2 vols., Washington, DC). Van Jaarsveld, C.H.M., Ranchor, A.V., Kempen, G.I.J.M., et al., 2006. Gender-specific risk factors for mortality associated with incident coronary heart disease—A prospective community-based study. Prev. Med. 43, 361–367 (this issue). Yusuf, S., Hawken, S., Ounpuu, S., et al., 2004. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 364, 937–952.

Alfredo Morabia, M.D., Ph.D. Center for the Biology of Natural Systems, Queens College–CUNY, 163-03 Horace Harding Expressway, Flushing, NY 11365, USA E-mail address: [email protected] Michael C. Costanza, Ph.D. Geneva University Hospitals, Division of Clinical Epidemiology, 25, Rue Micheli-du-Crest, CH-1211 Geneva 14, Switzerland


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