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Should Your Family History of Coronary Heart Disease Scare You?

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Should Your Family History of Coronary Heart Disease Scare You? MOUNT SINAI JOURNAL OF MEDICINE 79:721–732, 2012 721 Should Your Family History of Coronary Heart Disease Scare You? Dorairaj Prabhakaran, MD, DM, FRCP1,2 and Panniyammakal Jeemon, MPH, PhD Fellow1,3,4 1Centre for Chronic Disease Control, New Delhi, India 2Centre of Excellence in Cardio-metabolic Risk Reduction in South Asia, New Delhi, India 3Public Health Foundation of India, New Delhi, India 4Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK OUTLINE Family History in Primary Prevention of Coronary Heart Disease FAMILY HISTORY AS RISK FACTOR FOR FUTURE RESEARCH RECOMMENDATIONS CORONARY HEART DISEASE CONCLUSION FAMILY HISTORY AND SUBCLINICAL ATHEROSCLEROSIS OTHER ISSUES RELEVANT TO FAMILY HISTORY AND ABSTRACT ITS ASSOCIATION WITH Traditional risk factors explain most of the risk CORONARY HEART DISEASE Family History and associated with coronary heart disease, and after Risk of Coronary Heart Disease: adjustment for risk factors family history was believed Role of Age of Onset of Disease to contribute very little to population-attributable Are There Differences in risk of coronary heart disease. However, the Risk Associated with Paternal and INTERHEART study demonstrated an independent Maternal History of association of family history of coronary heart Coronary Heart Disease? disease with acute myocardial infarction. To assess this relationship more comprehensively in multiple Family History and Risk of datasets in different populations, we carried out Coronary Heart Disease: Are There a detailed review of the available evidence. Case- Any Differences Related to control studies involving 17,202 cases and 30,088 Race/Ethnicity? controls yielded a pooled unadjusted odds ratio Is It Oversimplifying to Dichotomizethe (random-effects model, overall I 2 = 64.6%, P = FamilyHistoryVariable? 0.000) of 2.03 (95% confidence interval: 1.79–2.30), Issues in Interpretation of whereas cohort studies that included 313,837 Family History of individuals yielded an unadjusted relative risk Coronary Heart Disease and Variations for future coronary heart disease (random-effects in Definitions of Family History model, overall I 2 = 88.7%, P = 0.000) of 1.60 Ethical Issues in (95% confidence interval: 1.44–1.77). Although the Collecting Family History presence of family history of coronary heart disease Family History in Coronary indicates a cumulative exposure of shared genes and Heart Disease Risk Prediction environment, the risk estimates for family history did not attenuate significantly after adjustment for conventional coronary heart disease risk factors in several studies. It is probably an oversimplification to dichotomize the family history variable into a Address Correspondence to: simple ‘‘yes’’ or ‘‘no’’ risk factor, as the significance of Dorairaj Prabhakaran family history is influenced by several variables, such Centre for Chronic Disease Control as age, sex, number of relatives, and age at onset New Delhi, India of disease in the relatives. Moreover, a quantitative Email: [email protected] risk-assessment model for the family history variable, such as the ‘‘family risk score,’’ has a positive linear Published online in Wiley Online Library (wileyonlinelibrary.com). DOI:10.1002/msj.21348 © 2012 Mount Sinai School of Medicine 722 D. PRABHAKARAN AND P. JEEMON:FAMILY HISTORY OF CORONARY HEART DISEASE relationship with coronary heart disease. More studies clinical utility of incorporation of family-oriented are warranted to assess the benefits and risks of preventive cardiology into standard clinical practice. intensive interventions, both targeted individually and at the family level, among individuals with a valid family history and borderline elevated risk FAMILY HISTORY AS RISK FACTOR FOR factors. Mt Sinai J Med 79:721–732, 2012. © 2012 CORONARY HEART DISEASE Mount Sinai School of Medicine Clinically relevant sources of evidence on associ- Key Words: coronary heart disease, family history, ation of family history and CHD include data from risk factors. observational studies, such as case-control and cohort studies. We identified 24 case-control or cohort stud- Although cardiovascular diseases (CVD) accounted ies reporting the association of family history and for <10% of all deaths worldwide at the beginning CHD through MEDLINE, PubMed, and Embase search of the 20th century, it was responsible for nearly from 1966 to 2011 and by searching cross-references one-half of all deaths in the developed world and from published articles. Some of the common epi- more than a quarter in the developing world dur- demiological terms used in this article and their ing the first decade of the 21st century.1 Of the definitions are provided in Table 1. Of the identified 16.7 million CVD deaths in 2002, 7.2 million were studies, 12 were case-control studies16– 27 and the due to coronary heart disease (CHD).2 Although CHD remaining 12 were cohort studies.28– 39 We were able is decreasing in many industrialized countries, it is to extract data for pooled estimate of odds ratio (OR) increasing in developing and transitional countries,3 or relative risk (RR) imposed by family history from partly as a result of increasing longevity, urbanization, all identified studies. Case-control studies involving and lifestyle changes. 17,202 cases and 30,088 controls (Figure 1) yielded a Traditional risk factors such as elevated blood pooled unadjusted OR (random-effects model, over- pressure, adverse lipid profile, smoking, and diabetes all I 2 = 64.6%, P = 0.000) of 2.03 (95% confidence explain most of the CHD mortality and morbidity interval [CI]: 1.79–2.30), whereas the cohort studies, burden and have been used in risk-prediction which included 313,837 individuals (Figure 2) yielded models.4 However, a higher concordance for CHD an unadjusted RR for future CHD (random-effects 2 trait and CHD risk factors among monozygotic model, overall I = 88.7%, P = 0.000) of 1.60 (95% twins, as demonstrated in the studies from Denmark, Sweden, and Norway, highlights the potential Table 1. Definitions. genetic contributions to CHD.5–9 Furthermore, the Familial aggregation: Any trait more common in relatives importance of family history in premature CHD is of an affected individual than in the general population well studied, and familial aggregation (as defined in due to genetic factors or shared environment. Table 1) has been frequently cited as evidence for Family risk score: A quantitative risk score for CHD the role of genetic factors in the development of computed from observed and expected CHD events 10– 14 using family data. CHD. Odds ratio: A measure of effect size describing the Although family history is an accepted risk strength of association. It is the ratio of the probability factor for CHD and is independent of common of an event occurring in one group to the probability of CHD risk factors, it has not been used in several it occurring in another group. of the available risk-prediction tools.15 Accurate P value: The probability that a variable would assume a value greater than or equal to the observed value strictly assessment of cardiovascular risk is essential for by chance. clinical decision-making, because the benefits, risks, Meta-analysis: A statistical method to compile the results and costs of alternative management strategies must of several studies that address a set of common or be weighed to choose the best treatment options for related hypothesis. individual patients. Deeper understanding of patterns Random-effects model in meta-analysis: In this model, we assume that the true effect could vary from study to of CHD risk in families may help to identify a study. The studies included in the analysis are assumed subset of the population that is at high risk for to be a random sample of the relevant distribution of CHD events. There is need for creation of concrete effects, and the combined effect estimates the mean evidence to promote family-based risk assessment effect in the distribution. and prevention. In this regard, we systematically Fixed-effect model in meta-analysis: In this model, we assume that there is one true effect size that is shared by reviewed the available evidence on the magnitude all individual studies. and strength of association between family history and prevalent or incident CHD and assessed the Abbreviation: CHD, coronary heart disease. DOI:10.1002/MSJ MOUNT SINAI JOURNAL OF MEDICINE 723 CI: 1.44–1.77). However, we did not have access to Although the presence of family the original data to do a meta-regression and dissect out the independent effect of family history over and history of coronary heart disease above the traditional risk factors of CHD. indicates a cumulative exposure of shared genes and environment, Case-control studies involving only a small fraction of the 17,202 cases and 30,088 controls familial aggregation of coronary yielded a pooled unadjusted odds heart disease was accounted for ratio (random-effects model, by the familial aggregation of overall I 2 = 64.6%, P = 0.000)of traditional risk factors. The risk 2.03 (95% confidence interval: estimates for family history of 1.79–2.30), whereas the cohort coronary heart disease did not studies, which included 313,837 attenuate significantly after individuals, yielded an adjusting for the traditional risk unadjusted relative risk for future factors of coronary heart disease. coronary heart disease Evidence for familial aggregation of premature (random-effects model, overall CHD also comes from a large study carried out in I 2 = 88.7%, P = 0.000)of1.60 the state of Utah, in the United States.45 In this study (95% confidence interval: involving 121,555 families, familial aggregation was documented using a quantitative family risk score 1.44–1.77). (FRS). The FRS was calculated for each family by comparing the observed number of affected persons in the family with the number expected, based on Natural-history studies of atherosclerosis have applying total number of age-specific and sex-specific demonstrated higher serum concentrations of person-years of experience calculated from 167,447 lipoproteins and homocysteine and higher blood adults aged ≥30 years.
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