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program outlined focuses on helping the smoker who wants to stop s moking . it demands a minimal amount of time from the physician and it is self-supporting . If these guidelines are followed, the physician should had that helping the smokers who want help to stop smoking is a productive and rewarding experience .

References I . Rosenberg L. Kaufman DW, Munich SP, Shapiro S . The risk of myocardial infarction after quitting smoking in men under 55 years ofage . N Engl J Med 1985 :313:151I-4. 1. Hertz At, Anderson A1 . Brooks HL. Menley JC, Parent UT, Barbonak it . The association of smoking with cordiomyepalhy . N Engl I Med 1use:311 :1201-6. 3. Slone D, Shapiro S, Rosenberg L . el al. Relation of cigarette smukim, to myocardial infarction in young women. N Engl J Mail 1978198 :1273-6. 4. Wilhelmsson C. Vedin IA, Elmfeldl D, Tibblin G . Wilhelmsen L . Smoking sad myocardial infarction. Lancer 1975:1:415-20. 5. Salonen JT. Stopping smoking and long-term mortality after acute myn cordial infarction . Br Heart J 1980 :43 :463-9. 6. Mulcahy R . Influence of cigarette smoking on morbidity and monaliry after myocardial infarction . Br Heart J 1983 ;49:410 .5 . 7. Hallstrom AP, Cobb LA, Ray R . Smoking as a risk factor for recurrence of sudden cardiac arrest . N Engl I Med 1986:314271-6. 8. Deanfield 1E. She, MI . Wilson RA, Horlock P . deLandshcere CM. Selwyn AP . Direct effects of smoking on the bean: silent ischemic disturbances of coronary raw . Am J Cordial 198657:1005-9. 9. Nonacid 1, Wright C, Knkler S, Ribeiro P . Fox K . Cigarette smoking and the treatment of angina with pmpranolol . alenalol. and nifed, line. N Eng1 J Med 1984:310:951-4.

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10. Myers KA . Relationship of smoking to peripheral unenul disease . Aug Fast Physician 1979;8:765-8 . IL McLaughlin PR, Bermun No . Morton RC, 33-metre L, Morch IE . Long-term angiogesphic a enl of the influence of coronary risk fact., on naive coronary circulation and sophenotss vein aonncoronary gears . Am Heart J 1977 ;93 :327-33. 12. Gillnm RF, Folsom A. Luepker RV . et al. Sodden death and acute myocardial infraction in a metropolitan area, 1970 .1960. The Minnesota Heart Survey . N End I Med 1963 ;309:1353-8. 13, Gomez-Marin 0, Folsom AR, Ranks TE, el al . Improvement in longterm survival among patients hospitalized will acute myocardial infarction, 19701o 1980 : The Minnesota Heart Survey . N Eng1J Med 1967 ;316: 1353-9 . 14. Keys A . Seven Countries: A Multivariate Analysis of Death and Core . nary Heart Disease. Cambridge: Harvard University Press, 1980 :65. 15. Kouke TE . Hill C, Heitzig C, et al. Smoke-free hospitals . Attitudes of patients, employees. and fatally . Mine Med 1985 :68 :53-5. 16. KnappJ,SileinG,SoremenG,strike TE .Cleanairhealth cam . Aguide to establish smoke frot health care facRICns . Minneapolis: Minnesota Coalition for a Smoke-Free Society 2000 . 1986 . 17 . Freidson E . Doctoring Together . A Study of Professional Social Control. New York : Elsevier Science Publishing, 1975 :257. 18 . AAFP stop smoking program. Physician and office staff manual, Kansas City, Kansas: American Academy of Family Physicians, 1987 . 19. Hughes JR, Koltke T . Doctors helping smokers. Real world tactics. Minn Med 1966 :69 :293-5. 20. The impact of providing physicians with quit-smoking materials for smoking patients . C A 1981:31 :75-8. 21 . Quit For Good. Bethesda, Maryland: National Cancer Institute, DHHS National lastilales of Health Publication No . IPHB) 85-1924 ..185-2494. 22 . AAFP slop smoking program . Patient stop smoking guide . Kansas City, Kansas: American Academy of Family Physicians, 1987 .

Identification of High Risk Relatives for Coronary Heart Disease RICHARD M . SCHIEKEN, MD, FACC Richmond, Virginia

The risk factors that have familial aggregation are as follows : I) cholesterol ; 2) lipoproteins ; 3) smoking; 4) hypertension; and 5) obesity .

Cholesterol Familial aggregation of hyperlipidemia . Familial hypercholesterolemia is an autosomal dominant disorder characterized by plasma low density lipoprotein levels, xanthomas

From the Medical college of Virginia, Richmond, Virginia. This study was supported in pan by Grant HL31010 from the National Institutes of Health, Bethesda, Maryland .

and premature atherosclerosis (1) . The estimated frequency of heterozygotes is 1/500 and that of homozygotes 1/ 1,000,000 (2) . In large part because of this underlying genetic abnormality, there is an increased frequency of ischemic heart disease in relatives of coronary heart disease patients compared with relatives of control subjects (3). Many case control studies have demonstrated that the family at risk can be identified. Fathers of patients with coronary heart disease have experienced more than twice the rate of coronary h,nsrt disease as have fathers of control patients. The father of young patients with coronary heart disease have an even greater relative risk for coronary heart disease ; mothers of patients have shown a significant increase in coronary heart



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disease compared with mothers of control subjects and siblings have shown even greater familial aggregation for coronary heart disease than have parents (4) . Prospective studies, unlike case control studies, eliminate recall bias that may exist . Results of such studies generally show that the rate of coronary heart disease tends to be highest in subjects whose parents died of coronary heart disease relatively early in life (5) . Moreover. coronary heart disease tends to occur relatively early in subjects whose parents had developed coronary heart disease early. If both parents had coronary heart disease at a young age, their offspring have a much higher risk for developing coronary heart disease than if only one or neither had coronary heart disease . Schrott et al . (5), who studied schoolchildren in the Muscatine study, classified the group according to their level of total serum cholesterol . In the high group were children with cholesterol levels >95th percentile for their age . In the middle group were children with levels between the 5th and 95th percentiles and in the low group were those with levels <5th percentile for age. The coronary mortality was determined from death certificates . The investigators found that children whose cholesterol was in the high group, that is >95th percentile for age, had male relatives who exhibited a twofold excess of increased coronary mortality as compared with the middle or low group of children . They concluded that the cholesterol levels of schoolchildren cluster with those of their family members and that persistent hypercholesterolemia in children identifies families at risk for coronary heart disease . Bodurtha et al. (6) divided a group of I1 year old children according to their level of high density lipoprotein (HDL) cholesterol . Children with a family history of premature cardiovascular death had lower levels of a subfraction of HDL cholesterol (HDL2 cholesterol) than did those without such a history . The white girls who reported a high level of physical activity had higher levels of HDL and HDL2 cholesterol than did their more sedentary peers. In general, children of mothers who smoked had lower HDL2 cholesterol than did the children of nonsmoking mothers . These data suggest that low levels of HDL2 cholesterol in children can identify families in which there is an increase of corn nary heart disease and that parental smoking may contribute to changes in this risk factor in the children of smokers as well as in the smokers themselves. Identifying families at risk. In summary, there is a familial aggregation of hyperlipidemia . Therefore, young victims of coronary heart disease identity families at risk . Their first degree relatives such as their siblings and children should have screening for hyperlipidemia . These individuals should be screened for low density lipoprotein (LDL) cholesterol and, if possible, the subfractions of HDL cholesterol . Elevated levels of LDL cholesterol clearly indicate future risk of a coronary heart disease event. Lower levels of HDL2

sCHiEKEN IDEN71I4CATION OF HIGH RISK RELATIVES

III/

cholesterol appear to indicate a family that is less protected from the adverse effects of LDL cholesterol . In children aged 10 to age 15 years, the 75th percentile of the total plasma cholesterol distribution is approximately 170 meedl . This corresponds to a level of 230, the 75th percentile for 40 to 44 year old white individuals (7) . Therefore, the risk of a child with a level of 170 mgldl approaches that of the 40 year old individual who faces a twofold excess risk of acquiring coronary heart symptomatic disease . Children of families at risk for premature cardiovascular death in the study of Bodurtha et al . had total 14DL cholesterol of 45.6 versus 50 .2 for the families without this risk . In addition the mean HDL2 cholesterol level was 10 .7 mgldl versus 14.4 mg/dl. There was no difference between groups in the HDL3 cholesterol levels . Those analyses were adjusted for sex, height, weight, race and tricep skinfold thickness. Therefore, school-age children whose total cholesterol is > 170 mg/dl, LDL cholesterol >105 mg/dl and HDL2 cholesterol


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progression from borderline or labile hypertension occurs more frequently when family history is positive for essential hyp%Artens ;on (21)) . Our data from families of twins (21) saggesi that there are different genes regulating rest and reactive blood pressure levels . Role of left ventricular hypertrophy . Left ventricular hypertrophy has been documented in adolescents and young adults early in the course of hypertension as well as in adults with well established hypertension (22) . Schieken and coworkers (23) showed that left ventricular mass when corrected for body size was increased in children whose blood pressures were in the upper quintile of a school-age population . The electrocardiogram (ECG) was a less sensitive measure of left ventricular hypertrophy and did not correlate well w;th blood pressure (24). Thus, in summary, children from families with a high prevalence of hypertension should have their blood pressure carefully monitored . In addition, if they have persistently elevated blood pressure, they should have an echocardiogram to evaluate the size of their left ventricle . The ECG appears to be a less sensitive method to evaluate left ventricular mass than the echocardiogram . Left ventricular hypertrophy may be an ;mportant predictor of .,re hypertension . In addition, siblings and parents of fur hypertensive patients should have their blood pressure monitored carefully . Initial therapy should include weight loss and increased dynamic exercise ; salt restriction may or may not contribute to this regimenCigarette Smoking Risk to the smoker, Cigarette smoking is the most preventable cause of excess death and disability from cardiovascular disease in the United States . Cigarette smoking appears to exert its effect on atherosclerotic coronary heart disease by increasing platelet adhesiveness and thus increasing the risk of a thrombotic event (25) . In addition to the effects on coagulation of cigarette smoking, carbon monoxide, which is found in cigarette smoke, lowers the threshold for the occurrence of ventricular fibrillation and increases the risk for sudden death (26) . Risk for family members of smokers. Members at risk in a family with a smoker may include not only the smoker, who has a definite excess risk, but also nonsmoking family members . After adjustment for age and other risk factors, the incidence of coronary heart disease among women with smoking husbands was approximately 15 times that of women with nonsmoking husbands (27). As part of the MCV Twin Study, Moskowitz et al : (28) studied II year old children classified according to membership in smoking or nonsmoking families. Children who were exposed to passive smoking had the following abnormalities: elevated whale blood 2.3-diphosphoglycerate (DPG), which was related in a dose-response curve to their level of thiocyanate, higher diastolic blood pressure at rest, a lower heart rate at rest and

reduced HDL2 cholesterol subtraction . Also, children exposed to passive cigarette smoke had a greater left ventricular wall thickness and left ventricular wall mass and a lower cardiac index than did children not exposed to passive smoking. The investigators speculate that passive smoking by unbalancing the ratio of myocardial oxygen supply to demand may increase coronary risk in prepubertal boys . Therefore, in summary, the family at risk with respect to smoking Is a family that has any member who smokes . Adults who smoke clearly have an increased risk of coronary heart disease . In addition, their nonsmoking spouses have an increased risk . Newer data now reveal that children exposed to smoking parents have abnormalities of their myocardial oxygen supply demand ratio that can adversely affect their coronary risk factors . The strongest associations of smoking adolescents versus nonsmoking adolescents are that smoking adolescents have a best friend, sibling or parent who is a smoker. Therefore, the number one preventive measure with respect to smoking is to prevent people from becoming addictive smokers, to enroll smokers in families in cessation programs and to educate small children about the risk of disease. Summary The family at increased risk for future coronary heart disease is the family with a member who has 1) had one or more myocardial infarctions before age 55 years ; 2) has levels of LDL cholesterol >75th percentile for age ; 3) has excessively low levels of HDL 2 cholesterol; 4) has hypertension or has had a stroke, or both ; 5) has excessive weight at any age and excessive weight gain during adulthood, or 6) smokes in the household .

References 1 . Goldstein JL, Brown MS. Familial hypercholesterolemia . In : Standsbury JB, et al ., ads, The Metabolic Basis of Inherited Diseases, 5th ed . New

York : McGraw-Hill, 1983 :672-712 . 2. Slack J. Inberttanre of familial hypercholesrerolemia . Atherosclerosis

Rev 19793:35. 3. Slack 1, Emus KA . The 1 .94tial risk ofdeath from trdxmic heart disease in first degree relatives of 121 men and 96 women with ischemic heart disease . 1 Mad Genet 19663 :239. 4 . Deutscher S, Epstein Fit. ttielsberg MO. Familial aggregation offactors associated with coronary heart disease . Circulation 1966 ;33:911-24 . 5 . Low EA . Sonic implications of mortality statistics relating to coronary

artery disease. J Chronic Dis 1957 :6:192-2a9. 6. Bodurtha JN . Schieken K, Soonest J, Nance WE. High-density lipnpru .

tein-cholesterol subtractions in adolescent twins . Pediatrics 1987 ;79:1819. 7. The LRC Study Data Book, Vol. 1 . The Prevalence Study . Betheeda.

Maryland :

U.S .

Department

of

Health and Human Services, National

Institutes of Health, July 1980, NIH publication no . 80 .1527 . 8. Feinteib M, Garrison IU . The contribution of family stcdiea to the partitioning of population variance of blood pressure . Pros Cun Biol Res

1979 ;32:653-73.

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9. Picketing Y. High Blood Pressure . 2nd ed. New Y,rk : Gorse & Stratton . 1968 . 10 . Boshani NO. Feinimb M, Garrison RJ. Christian JC. Rosenman RH . Generic variance in blood pressure . Act . Gone, Med Gemellol 1976 :25. 137-44 . 11 . Feinleib M, Garrison RJ . Borhani N . el al. Studies of Hypertension in Twins . In : Paulo . ed . Epidemiology and Control of Hypertension . New York: Grant & Stmnoer. 1975 :3-20. 12 . RonaR, .'.eresfordso .Themodeofinheriounceorblondpressurel-ds . J Epidemial Community Health 1950:34:160-73 . 13. Biron R, Mongeau J, Benmnd D . Familial Aggregation of Blood Pre-re in Adopted amt Natural Children. In: Peol 0 . ed. Epidemiolog , and Control of Hypertension. New York: Gmne & Stratoo. 1975 :397-104. 14. ZinnerSH, Levy PS, Karen EH. Familial aggregation of blood pressure in

childhood . N Engl J Med 1971 ;284:4922-4 . 15. Chiang BN, Per]- LV . Epstein PH. Overveigln and hypertension . Circulation 196939 :403-21 . 16. Karnel WB, Brand N . Skinner 1J Jr., Dawber TR . NeNamara PM. The relation of adiposity to blood pressure and the development of hypertension. Ann Intern Most 1967;67:48-59. 17. Freis ED. Sale. volume and the prevention of hypertension . Circulation 197653:589-95. 18. Pielinen PI, W„pg O, Altschul AM . Electrolyte output . blood pressure and family history of hypertemion . Am J Clio Not, 197932:997-1005 . 19. Falkner B, Orteso G, Angelakos ET. Fernandes M, Langman D . Cardioamender response to mental stress in normal adolescents with hypenenre parents. Hemodynamics and menal stress in adolescems . HypenenSon 1979 ; : :27-30.

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20. Paaenharger RS Jr-Thome MC. Wing AL . Chronic disease in former college students. VIII, Characteristics in young predisposing to hypederr scan in later nut,. Am 1 Epidemiol 196&03:25. 21 . Schieken Rdi, Eaves LS . nodunha 1M. The genetic of cardiovascular reaaivity . Circulation 1905 :72(snPpl 1171:111-258. 22 . Dunn FG . Chandramtna P. de Carvalho J0, Bash LL . Frohlich ED . Parhophysin!ogic assessment of hypertensive heart disease with ec!tocar Biography . Am 1 Ci rd of 19773938Y95 .

23 . Schieken RM . Clarke WR. Lauer RM . Left vemricular hypertrophy is children with bland pressure in the upper gainile of the distribution IMuscatine Study) . Hypertension 19813 :669-75. 24. Schieken RM, Clark, wit, Prineas R . Klein V . latter RM. Electrocardiographic measures oflol ventricular hypertrophy in children across the distribution of blood pressure : the Muscmine Study. Circulation 1982:66: 428-32 . 25. Aronnw WS . Ffiecl of cigarette smoking and of carhan monoxide on coronary heart disease . Chest 1976:70:514-8. 26. Betina DA. Banerjee CM . Birkhead NC, Greets, CH . Scott SD, WV . EBece, of carbon monoxide inhalation on ventricular 6bnllatlon H-. Arch Environ Health 197631:42-6 . 27. GadandC.Ba..u-ConnorE .SuarezL.CriquiMH,WingardDL.Effect, of pass; smoking on ischemic heart disease mortality of nonsmokers . A prosper[ no lady . A. J Epidermal 1995J21 :645-50. 28. Moskowitz WE, Masteiler M . Bossano R, Schieken RM . lions passive ,making increase heart disease risk in pubertal boys lulotel? Circulation 1987 :766mpplIV) :IV.359.

Reducing Community Risk of Heart Disease THOMAS E. KOTTKE, MD, FACC Rochester, Minnesota

Just as a straight line may not be the quickest way to traverse the distance between two points, targeting efforts to prevent heart disease to those at highest risk is neither the most effective nor the most efficient strategy . One reason is that

heart disease appears at all levels of risk for patients of

members of a group, "the patients I sea," The questions that arise with efforts to prevent coronary heart disease are: 1) Should the physician attempt to determine who is at highest risk of the disease and then focus the intervention on those individuals, or should the physician treat all risk factor

American physicians. A second reason is that the behaviors associated with coronary heart disease-smoking and eat-

elevations in all patients? 2) Should the physician address one risk factor with focused intensity, or should the physi-

ing-are social behaviors ; by definition, change in social

cian address multiple risk factors with diffused intensity? 3)

behavior requires change in the social reinforcement process. Clinicians usually view their patients as isolated individ-

Does the proposed intervention actually work? 4) What should the physician be doing in his or her practice?

uals . However, to prevent coronary heart disease, physicians must take the small step of seeing their patients as

Why the Community Approach Cardiac risk factors predict very well which population will get coronary heart disease but predict poorly which

From the Mayo Clinic, Rochester . Minnesota . This work was supported in part by Grant RR01632 and CA38361 from the National Insritutesed Health. Bethesda, Maryland.

individuals within the population will get the disease . If one has a group consisting of Japanese and Eastern Finnish men, it would not be difficult to guess which men will have the