Epidemiology and prevention of coronary heart disease in families

被引:59
作者
Higgins, M
机构
[1] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48104 USA
[2] Univ Michigan, Sch Publ Hlth, Dept Internal Med, Ann Arbor, MI 48104 USA
关键词
D O I
10.1016/S0002-9343(99)00409-X
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although family histories are used primarily to aid in diagnosis and risk assessment, their value is enhanced when the family is considered as a unit for research and disease prevention. The value of a family history of coronary heart disease (CHD) is increased when the age, sex, number of relatives, and age at onset of disease are incorporated in a quantitative family risk score. Medical and lifestyle risk factors that aggregate in families include dyslipidemia, hypertension, obesity, hyperfibrinogenemia, diabetes mellitus, smoking habits, eating patterns, alcohol consumption, physical activity, and socioeconomic status. Advances in detecting and understanding interactions between genetic susceptibility and modifiable risk factors should lead to improvements in prevention and treatment. However, working with families can be difficult. In the United States, families are usually small, are often widely dispersed, and may not be intact. Family histories may be unknown, affected relatives may be dead, and secular trends mask similarities among generations. Many exposures occur outside the home, and families change over time. Ethical, legal, and social issues arise when dealing with families. Nevertheless, opportunities are missed when research, clinical practice, and prevention focus on individual patients. Greater emphasis on families is needed to reduce the burden of CHD. Am J Med. 2000;108:387-395. (C) 2000 by Excerpta Medica, Inc.
引用
收藏
页码:387 / 395
页数:9
相关论文
共 61 条
[1]  
*AM HEART ASS, AM HEART ASS 1 HEART
[2]  
[Anonymous], 1994, BMJ, V308, P313
[3]  
[Anonymous], 1997, FINAL REPORT TASK FO
[4]  
Bensen JT, 1999, GENET EPIDEMIOL, V16, P165, DOI 10.1002/(SICI)1098-2272(1999)16:2<165::AID-GEPI4>3.0.CO
[5]  
2-H
[6]  
Bensen JT, 1999, GENET EPIDEMIOL, V17, P141, DOI 10.1002/(SICI)1098-2272(1999)17:2<141::AID-GEPI4>3.0.CO
[7]  
2-Q
[8]   A QUANTITATIVE ASSESSMENT OF PLASMA HOMOCYSTEINE AS A RISK FACTOR FOR VASCULAR-DISEASE - PROBABLE BENEFITS OF INCREASING FOLIC-ACID INTAKES [J].
BOUSHEY, CJ ;
BERESFORD, SAA ;
OMENN, GS ;
MOTULSKY, AG .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1995, 274 (13) :1049-1057
[9]   THE RESPONSE TO LOVASTATIN TREATMENT IN PATIENTS WITH HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA IS MODULATED BY APOLIPOPROTEIN-E POLYMORPHISM [J].
CARMENA, R ;
ROEDERER, G ;
MAILLOUX, H ;
LUSSIERCACAN, S ;
DAVIGNON, J .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1993, 42 (07) :895-901
[10]   FAMILIAL AGGREGATION OF FACTORS ASSOCIATED WITH CORONARY HEART DISEASE [J].
DEUTSCHER, S ;
EPSTEIN, FH ;
KJELSBERG, MO .
CIRCULATION, 1966, 33 (06) :911-+