Drinking and coronary heart disease: The Albany Study

Volume

110

Number

2

diastolic

8. Fouad FM, Tarazi RC. Gallagher JH, Macintyre WJ, Cook SA: Abnormal left ventricular relaxation in hypertensive patients. Clin Sci 59:411s, 1980. 9. Inouye IK, Massie B, Loge D, Topic N, Silverstein D, Simpson P, Tubau J: Abnormal left ventricular filling: An early finding in mild to moderate systemic hypertension. Am .J Cardiol 53:120, 1984. 10. Hanrath P. Mathey DG, Siegert R, Bleifeld W: Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study. Am .J Cardiol 45:15, 1980. 1 I. Honow RO, Rosing DR. Bacharach SL, Green MV, Kent KM, Lipson I,(‘. Maron BJ, Leon MB, Epstein SF: Effects of verapamil on left ventricular systolic function and diastolic filling in patients with hypertrophic cardiomyopathy. Circulation 64587. 1981. 12. Bonow RO, Frederick TM, Bacharach SL, Green MV, Goose PW. Maron B.J. Rosing DR: Atria1 systole and left ventricular

Drinking and coronary Albany Study

13.

14.

15.

16. 17.

filling in cnr~mng’

disease

filling in hypertrophic cardiomyopathv: F:tfect of Verapamil. Am J Cardiol 51:1986, 1983. Peterson KL, Ricci D, Tsuji ,J, Sasayama S. I
heart disease:

The

The relation of alcohol consumption to coronary heart disease (CHD) was examined in a cohort of 1910 employed men aged 38 to 55 years enrolled in the Albany Study, a prospective investigation of factors related to cardiovascular disease. Two follow-up periods were examined, one between 1953-54 and 1971-72, the other after 1971-72. In the initial period, there was no clear evidence of a relation between the rate of alcohol consumption and CHD incidence. In the later period, men whose monthly consumption was 60 ounces or more had a lower than average CHD incidence rate. A negative relationship with drinking held for all manifestations of CHD. Other CHD risk factors were examined, special attention being given to cigarette smoking and HDL-cholesterol. The fact that drinking is a matter of choice may introduce some confounding factors. The absence of a relation between drinking and CHD risk in the earlier follow-up suggests the need for caution in interpreting the results. (AM HEART J 110:331, 1985.)

Tavia Gordon

and Joseph T. Doyle, M.D. Washington, D.C., and Albany, N.Y.

A number of studieP have reported that persons who drink moderate amounts of alcoholic beverages have a lower than average incidence of coronary heart disease (CHD). However, not all reports agree, and there is in addition some question of the impact of very heavy drinking on CHD risk and some question also whether alcohol consumption is related in the same way to all manifestations of CHD. Since CHD is the major cause of death in most Fr( m George

Supported

Washington

LJniversit?:

by the National

(‘ontract

83MO

Kecvzived

tu

and

Institutes

Albany

Medical

on Alcohol

Abuse

College. and

Alcoholism,

.515-9:18-01D. publication

Reprint request\: NY 1’208.

Joseph

Feb.

7. 1985;

T. Doyle.

M.D.,

accepted Albany

March Medical

8, 198.5. College.

Albany.

industrial societies and most men drink some alcoholic beverages, additional information on the subject is of interest. This report describes findings from the Albany Study. METHODS Population. The study cohort consisted of men who were civil service employees of the State of Kew York. The initial examinations took place mostly in 1953-54. Since then the cohort has been recalled for examination at regular intervals. At each examination members of the cohort are given a standardized cardiovascular examination. CHD was characterized by the findings on these routine examinations supplemented by information from personal physicians, hospitals, family members, friends, and death reports. Ascertainment was assisted by a peri331

August,

332

Gordon

and Doyle

American

Table I. Incidence of CHD by rate of alcohol consumption: Albany Study, l&year follow-up after 1953-54 18-year Alcohol consumed (ounces/month) None 1-9 10-19 20-2s 30-5s 60-89 so+

Total

Population at risk 569 364 296 161 168 95 55 1708

Table II. Incidence of CHD tion: Albany Study, lo-year

Number of cases

Rate (%I)

143 58 51 27 26 24 19 348

25.1 15.9 17.2 16.8 15.5 25.3 34.5 20.4

Note: The trend in rates was not statistically significant (t = 0.68, univariate). “None” includes 353 men so designated with an incidence rate of 20.1’(, and 216 “occasional” drinkers with an incidence rate of 33.3”(.

odic mail inquiry made of nonrespondents and by a routine examination of the death certificates filed with the State of New York. Alcohol histories. Alcohol histories were obtained at the time of the initial examination in 1953-54 from 1755 men then 38 to 55 years old. Another history was obtained in 1971-72 from those returning at that time. Thus, there are two follow-up periods, one covering the first 18 years of the study, the other covering 10 years after the 1971-72 examination. The number of cans of beer consumed each week or equivalent (A), the number of glasses of Wine (B), and the number of glasses of spirits (C) were recorded. This information was converted into ounces of alcohol/month using a formula developed by the Framingham Study investigators: (0.40A + 0.67B + C) 30/7. Coronary risk factors. At the same time that the alcohol histories were obtained, a smoking history was also completed. Other characteristics were measured as well. Details respecting the diagnosis of CHD are given elsewhere.? Men were weighed and their height was measured without clothes or shoes. Blood pressure was measured by mercury sphygmomanometer in the left arm with the subject seated. Serum total cholesterol was measured by the method of Abel1 et al.* In 1971-72 cholesterol in the lipoprotein fractions was measured by the method of Fredrickson et a1.g Statistics. Incidence rates by level of alcohol consumption were calculated. This analysis was supplemented by use of logistic regression.“’ Two-sided tests of significance were employed. RESULTS Incidence of coronary disease-18 year follow-up. Of the 1755 men for whom alcohol histories were obtained at entry, 1708 were then free of CHD. In the next 18 years, 348 of these men developed CHD, a rate of 20.4 % . There was a suggestion that the risk was greatest among men whose monthly alcohol consumption was 90 ounces or more, but there was

Population at risk

None 1-S 10-19 20-29 30-59 60-89 90+ Total Note: The univariate).

trend

1985 Journal

by rate of alcohol consumpfollow-up after 1971-72

incidence Alcohol consumed (ounces/month)

Heart

198 142 91 77 158 89 68 823 in rates was not statistically

IO-year

incidence

Number of cases

Rate cc’;)

42 32 18 9 35 14 9 159 significant

21.2 22.5 19.8 11.7 22.2 15.7 13.2 19.3 (t = -1.67.

also a clear excess among occasional drinkers (Table I). However, if nondrinkers and occasional drinkers are put aside, there was a significantly greater CHD risk at increasing consumption levels (p < 0.05). This was chiefly due to the fact that heavier drinkers tended to smoke more. Cigarette smoking is an important CHD risk factor. When that fact is taken into account, the trend of incidence on the rate of alcohol consumption is no longer statistically significant. Incidence

of coronary

disease-

10 year follow-up.

Among the 823 survivors taking the 1971-72 examination and still free of CHD at that time, 159 (19.3%) developed CHD in the next 10 years. This was double the rate for the first 10 years of the study. Thus, the fact that the cohort was now 18 years older than at entry to the study had produced a dramatic increase in the CHD incidence rate. In this later follow-up, the risk of CHD appeared to be less at higher rates of alcohol consumption than at lower consumption rates (Table II). However, this trend was also short of statistical significance, although, as we will note later, when other factors are taken into consideration, the trend is actually statistically significant, despite the small number in the remaining cohort. Manifestation of coronary disease. Four categories of CHD were analyzed by logistic regression: myocardial infarction (MI), heart attacks (MI or CHD death), CHD death, and angina pectoris as the first manifestation of CHD (APU). No form of CHD in either the initial follow-up (between 1953-54 and 1971-72) and the later follow-up (after 1971-72) was significantly associated with the rate of alcohol consumption in univariate regression analysis, although the regression coefficients for the followup after 1971-72 were consistently negative for all manifestations of CHD (Table III). Multivariate analysis. Because of the possibility

"olume

t 10

Number

2

Alcohol

III. Standardized logistic regressioncoefficients for various manifestations of CHD according to rate of alcoho:~consumption: Albany Study, follow-up after 1953-54 and 1971-72 Table

I ‘niraritrtr~ cot’ficifnts CHIJ munifcstntirin ‘Total CHD IHeart attack API MI (:HD death

consumption

lncidcnce 19.5344

C’haractpristic

after

O.lbl 0.0 1 -0.1’2 o.i):l 0.0::

-0.18

-0.06

-0.2:3*

-0.17

-0.08

-0.29 -0.17 -0.26

-0.06 -(LOS

-0.24 -0.26 -0.23

1971.72

-0.13 -0.36 _. Nrdr: incidence after 1953-54 was f;n IX years: after 1971-72 for ICI years. The multivariate t’urwtiuns included as cwariates with the rate of’ alcohol con+~mpt ion (wnces/month) the following: cigarettes/day, systolic blood pre:+ure. relative weight, age. and serum cholesterol (initial follow-up) or Iuw density lipoprotein cholesterol (later tallow-up). Ablneviations: (‘HI) = coronary heart disease; APU = angina pectoris as Ihe hrst mantf’estation (XCHD; MI = myocardial inl’arction. These categories are not exclusive. ‘p .: lJ.05.

that associated variables may have affected the apparent relation of drinking to CHD, multivariate logistic regressions were estimated for the two periods of follow-up. The variables considered, besides rate of alcohol consumption, were cigarettes smoked/day, systolic blood pressure, relative weight, age, and either serum cholesterol (initial follow-up) or plasma low density lipoprotein cholesterol (LDLC) (later follow-up). The multivariate logistic regression coefficients for CHD incidence on these variables are given in Table IV. In the first 17 years of follow-up, all of the variables other than the rate of alcohol consumption cited above were statistically significant risk factors for CHD. The rate of alcohol consumption at entry was not itself a statistically significant risk factor for CHD when these other variables are taken into consideration. On the other hand, the rate of alcohol consumption in 19’71-72 was significantly but negatively related to subsequent CHD incidence when covariates were taken into account (p < 0.05). For this older cohort, men consuming more alcohol/month tended to have lower CHD incidence rates. Of the other variables, all except re!ative weight were statistically significant CHD risk factors for the followup after 1971-72. Another variable that was measured in 1971-72 was high density lipoprotein cholesterol (HDL-C). If this variable is added to the regression equation, neither it nor the rate of alcohol consumption is statistically significant. When the rate of alcohol consumption is removed from the equation, HDL-C

333

IV. Multivariate standardized logiwic regression coefficients for CHD according to various characteristics: Albany Study, follow-up after 195354 and 1971-72 -_ IX-Jvar l/l- l’ear

COefjiCifTltS

after 1971-72

:li:wa.w

Table

Multicariatc~

Inwrdrnw 1953-5-I

and coronar>’

incidcarlccs aftfr lW-S-l

I rlcidPncr~ lf!iv- 1971-2

Alcohol consumption (oz/mo) Cigarettes/day Systolic blood pressure Relative weight Serum cholesterol LDL-cholesterol Age LDI, = low density ‘p < 0.n.~. tp < 0.01.

lipoprotein.

:p < o.nlll.

is a statistically significant inverse CHD risk factor (p < 0.05). Thus, either factor alone, but not both together, are significant variables in the regression equation. This is explained in statistical terms by the fact that both are negative CHD risk factors but are positively intercorrelated. It should be noted, as well, that when LDL-C and HDL-C are entered jointly into the multivariate regression equation (but the rate of alcohol consumption is omitted), both are significant CHD risk factors in this older cohort of men. The multivariate coefficients for the various CHD risk factors were also examined separately for each manifestation of CHD (heart attack, APU, MI, CHD death). While the resulting analysis was too voluminous to include here, the conclusion was that in general there was no important difference among these different manifestations of CHD in the relevant risk factors. The one important exception was with respect to APU. When angina was the first evidence of CHD, there is no indication that cigarette smoking played any role in precipitating the event. In fact, the regression coefficient for the effect of cigarette smoking on the risk of APU is slightly negative, although not statistically significant. The major difference in the risk factors associated with CHD incidence in the earlier and later follow-up has already been noted: the rate of alcohol consumption was a statistically significant negative risk factor for CHD in the later follow-up but was not a significant CHD risk factor in the initial follow-up. DISCUSSION Initial follow-up. The findings from the Albany Study with respect to the relation of drinking with CHD incidence are ambivalent. In the initial follow-

August,

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Gordon

and Doyle

up there was no significant relation of incidence with the rate of consumption when associated factors are taken into account. There was some suggestion in that initial follow-up of a higher CHD incidence among nondrinkers than among those drinking less than 60 ounces of alcohol/month, but a formal multivariate analysis did not confirm this. Men drinking 60 ounces of alcohol or more per month at entry had higher CHD incidence rates than average, but the apparent upward trend to CHD incidence with higher levels of consumption, while statistically significant when only drinkers were considered, was no longer significant even among this group of drinkers when other variables (particularly cigarette smoking) were taken into consideration. Occasional drinkers. There was also a high incidence rate among “occasional” drinkers in the initial follow-up. It is possible, of course, that this group included a large number of heavy drinkers who failed to report that fact. The internal evidence does not bear this out. Conceivably, some had previously been heavy drinkers and had reduced their consumption for health reasons. While we have no direct evidence on this point, it is an article of faith that heavy drinkers must quit completely in order to control their drinking, and hence are unlikely to become “occasional” drinkers. We could find no evidence that would serve to explain even in part the high CHD incidence in this group, but in terms of their reported alcohol consumption rates they were essentially nondrinkers and were treated as nondrinkers in all the regression analyses. Later follow-up. In contradistinction to the absence of a discernible relation between drinking and CHD incidence in the initial follow-up, there was an inverse relation between the rate of alcohol consumption reported in 1971-72 and subsequent CHD incidence rates. This was statistically significant (p < 0.05) when other variables are taken into account. There is some suggestion that this inverse relation may be due in part to the fact that drinking raises the level of HDL-C and that a higher level of HDL-C appears to be protective against CHD. This conclusion, which has been suggested by other studies, is based primarily on the logic of the multivariate analysis. However, the conclusion remains moot.” Moreover, it is impossible to rule out the possibility that the findings for the Albany cohort reflect (at least in part) some other factors associated with the choice by individuals of how much to drink or whether to drink at all; that is,

American

Heart

1985 Journal

some possible gratuitous consequence of self-selection. Conclusions. Other prospective studies have yielded varying results, some reporting a positive association of drinking with CHD risk,*“-l4 some a negative assOciation,l-fi and some no association at a11.15 The Albany Study seems to be ambivalent itself. Thus, the question of the relation of drinking and CHD risk still seems unresolved and an explanation for the diverse findings from different studies remains to be found. REFERENCES

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14. Wilhelmsen L, Wedel H, Tibblin G: Multivariate analysis of risk factors for coronary heart disease. Circulation 48:950, 1978. 15. Morris JN, Kagan A, Pattison DC, Gardner M: Incidence and prediction of ischemic heart-disease in London busmen. Lancet 2:553. 1966.