(Circulation. 1999;100:944-950.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Moderate Alcohol Consumption and the Risk of Sudden Cardiac Death Among US Male Physicians
From the Division of Preventive Medicine (C.M.A., J.E.M., N.R.C, U.A.A., J.M.G., C.H.H) and Cardiovascular Medicine (J.M.G.), Department of Medicine, Brigham and Women's Hospital; the Cardiac Unit (C.M.A.), Department of Medicine, Massachusetts General Hospital; and the Departments of Ambulatory Care and Prevention (C.H.H., N.R.C) and Epidemiology (C.H.H, J.E.M.), Harvard Medical School, Boston, Mass.
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Abstract |
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Background—Individuals who consume high amounts of alcohol (>5 drinks/d) have increased risks of ventricular arrhythmia and sudden cardiac death (SCD). However, the relationship is less clear for drinkers of light-to-moderate amounts.
Methods and Results—We prospectively assessed whether
light-to-moderate alcohol drinkers have a decreased risk of SCD among
21 537 male participants in the Physicians Health Study who were free
of self-reported cardiovascular disease and provided
complete information on alcohol intake at study entry. Over 12 years of
follow-up, 141 SCDs were confirmed. After control for multiple
confounders, men who consumed 2 to 4 drinks/wk (RR=0.40; 95% CI, 0.22
to 0.75; P=0.004) or 5 to 6 drinks/wk (RR=0.21; 95% CI,
0.08 to 0.56; P=0.002) at baseline had significantly
reduced risks of SCD compared with those who rarely or never consumed
alcohol. The relationship for SCD was U-shaped
(P=0.002), with the risk approaching unity at 
2
drinks/d. In contrast, the relationship of alcohol intake and nonsudden
CHD death was L-shaped or linear (P for trend=0.02).
Conclusions—In these prospective data, men who consumed light-to-moderate amounts of alcohol (2 to 6 drinks/wk) had a significantly reduced risk of SCD compared with those who rarely or never consumed alcohol.
Key Words: alcohol • death, sudden • arrhythmia • coronary disease • epidemiology
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Introduction |
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Sudden cardiac death (SCD) accounts for 250 000 deaths in the United States every year1 ; therefore, identification of modifiable risk factors for SCD continues to be an important public health goal. One modifiable risk factor, alcohol consumption, may have a differential effect on the risk of sudden versus nonsudden coronary heart disease (CHD) death.2 It is well established that heavy alcohol consumption (>5 drinks/d) is associated with an increased risk of SCD3 4 ; however, the results of studies addressing light-to-moderate alcohol consumption and SCD have not been consistent. Prospective studies have found either no5 6 7 or a positive8 association, whereas case-control studies have reported inverse linear associations.9 10 11 In men, SCD is associated with underlying CHD in >90% of cases,12 and because light-to-moderate alcohol consumption has been associated with lower risks of other CHD end points,13 14 15 16 17 18 19 we hypothesized that men who drink light-to-moderate amounts of alcohol would have a lower risk of SCD. The Physicians' Health Study of 22 071 apparently healthy men followed up for an average of 12 years presented a unique opportunity to explore whether individuals who consume light-to-moderate amounts of alcohol have a lower risk of SCD and whether risks differ for SCD compared with other forms of CHD death.
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Methods |
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The methods of the Physicians' Health Study have been described in detail elsewhere.20 Briefly, 22 071 male physicians who were 40 to 84 years old in 1982 and had no history of myocardial infarction (MI), stroke, transient ischemic attacks, and cancer were assigned to aspirin and/or ß-carotene in a randomized, double-blind, placebo-controlled 2x2 factorial design. At baseline, the physicians completed questions on health status, risk factors for cardiovascular disease (CVD), alcohol consumption, antioxidant vitamin use, dietary intake of selected foods, and frequency of vigorous exercise. At baseline and at 84 months of follow-up, the physicians were asked, "How often do you usually consume alcoholic beverages (beer, wine, or liquor)?" The 7 possible response categories (2+/d, daily, 5 to 6/wk, 2 to 4/wk, 1/wk, 1 to 3/mo, and never/rare) were interpreted as the number of drinks consumed per unit of time.
Population for Analysis
Because the development of preclinical CVD symptoms may
influence the reporting of alcohol consumption, we chose to exclude
from the primary analyses men who reported nonfatal CVD
endpoints before ascertainment of alcohol intake. A total of 534 men
who reported angina or coronary
revascularization before randomization or who had
missing data on alcohol consumption were excluded, leaving 21 537
participants for the baseline analysis. Participants
contributed follow-up time from study entry to date of death or to the
scheduled end of the randomized ß-carotene component on December 31,
1995, whichever came first.
Endpoint Ascertainment and Definitions
Information on cardiovascular events was updated
every 6 months for the first year and annually thereafter. The
ascertainment of CVD events was by self-report on follow-up
questionnaires, and deaths were generally reported by postal
authorities or next of kin. All such events were reviewed by an
Endpoints Committee of physicians for confirmation by medical
records obtained from hospitals and attending physicians. The next
of kin were interviewed regarding the circumstances surrounding the
death if not adequately documented in the medical record. Deaths in
which there was evidence of CHD at or before death and in which
a noncoronary cause of death was not found were classified as
CHD deaths (ICD-9 codes 410 to 414). Cases of nonfatal MI were
confirmed by use of the World Health Organization
criteria.21
To ascertain the specific end point of SCD, medical records and reports from next of kin for all cardiovascular deaths (excluding strokes) were rereviewed by 2 cardiologists unaware of exposure status, and agreement was reached. SCD was defined as death within 1 hour of symptom onset and/or a witnessed cardiac arrest or abrupt collapse not preceded by more than 1 hour of symptoms that precipitated the terminal event. Information from the death certificate was not used in the determination of the timing of death. To increase our specificity for "arrhythmic death," we excluded anyone who had evidence of collapse of the circulation (hypotension, exacerbation of congestive heart failure, and/or altered mental status) before the disappearance of the pulse.22
Unwitnessed deaths with no information on timing but with an autopsy consistent with arrhythmic cardiac death (ie, acute coronary thrombosis or severe coronary artery disease without myocardial necrosis or other pathological findings to explain death) were considered possible SCDs, and the analysis was performed both including and excluding these deaths. Deaths (often unwitnessed) in which the timing could not be accurately determined from the available information were not classified as sudden or nonsudden.
Statistical Analysis
Age-adjusted means or proportions of baseline risk factors and
treatment group assignment were computed for the 7 levels of reported
alcohol consumption. The significance of associations was tested by the
Mantel-Haenszel 
2 test for trend for
categorical variables and linear regression for continuous
variables. Relative risks (RRs) were computed with Cox proportional
hazards models,23 controlling for age and randomized
aspirin and ß-carotene assignment. A multivariate Cox
proportional hazards model was used to control for potential
confounders simultaneously (see legend of Table 2
).
Participants with missing data (3.5%) on covariates included in the
multivariate model were excluded from analysis.
Because fish consumption was ascertained at 12 months, deaths within
the first year were excluded from the multivariate
analyses because of missing data on fish consumption.
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In our primary analyses, the information on baseline alcohol
intake was modeled categorically in the original 7 response categories,
with the men who answered never/rare as the reference group. Alcohol
intake was also modeled as a continuous variable by assignment of
the midpoint value to each response category. Tests for linear and
nonlinear trend were performed using this value. To test for a
curvilinear association, a quadratic term (average intake squared) was
added to the linear term in a separate model.24 To
investigate whether the effect of alcohol differed for nonarrhythmic
CHD endpoints, similar analyses were performed for nonsudden
CHD death and nonfatal MI. To further explore whether alcohol intake
was associated with mode of death (sudden versus nonsudden), a logistic
regression model restricted to patients who died was constructed with 4
levels of alcohol intake (rarely/never, 
1/wk, 2 to 6/wk,
daily).
For SCD, we also performed secondary analyses using baseline alcohol exposure but excluding deaths in the first 4 years of follow-up to address the possibility that undiagnosed, preexisting CVD could have been present in these men at the time of study entry. In addition, to address potential misclassification of intake due to changing alcohol consumption over time, we repeated the analysis using the updated measure of exposure at 7 years in a time-varying covariate Cox model. The other covariates were also updated at 7 years with the most recently reported information. To maintain a population free of CVD at the time alcohol intake was assessed, 3093 participants who reported nonfatal CVD end points before ascertainment of alcohol consumption on the 84-month questionnaire were excluded from the time-varying analysis at 84 months.
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Results |
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Alcohol Intake
The alcohol intake of the 21 537 participants was fairly evenly distributed across categories, with the exception of the highest. Only 667 men (3.1%) reported consuming
2 drinks/d. Table 1 shows age-adjusted baseline risk
factors according to level of alcohol intake. Baseline alcohol was
directly associated with age, smoking, hypertension, physical activity,
and fish consumption (ascertained at 12 months), as well as inversely
with diabetes and antioxidant vitamin use. At 84 months, 32.7% of the
cohort had decreased their alcohol intake by at least 1 category, and
15.1% increased their level. The proportion of participants who
reported a change in their alcohol intake at 84 months did not differ
significantly between the participants who had previously reported
nonfatal CVD and those who had not.
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Sudden Cardiac Deaths
Over 12 years, 141 SCDs (121 definite and 20 probable) were
documented. The relationship of alcohol intake at baseline with
subsequent risk of SCD is displayed in Figure 1. The relationship between moderate
alcohol consumption and SCD was U-shaped in both age- and
treatment-adjusted as well as multivariate
analyses. The nadir was apparent at 5 to 6 drinks/wk, and the
risk again approached unity at 2 drinks/d (Table 2
). Participants who consumed 2 to 4
drinks/wk had a 60% reduced risk of SCD (P=0.004), and
those who consumed 5 to 6 drinks/wk had a 79% reduced risk of SCD
(P=0.002) compared with those who rarely or never consumed
alcohol. The RRs in both these categories of light-to-moderate
consumption were also significantly reduced compared with those who
consumed 2 drinks/d. To assess the linear and nonlinear relations
between alcohol intake and SCD, we performed analyses in which
a continuous variable for alcohol (created by assigning the
midpoint value to each response category) was entered into the
multivariate model as both a linear and a quadratic
term. There was no evidence for a linear trend when the linear term was
entered alone (P=0.43). However, when the quadratic term was
entered into the model to test for nonlinear trend, the results were
significant (P=0.002), consistent with the observed
U-shaped relation.
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Although we excluded men with reported CVD at baseline, the subgroup
who rarely or never consumed alcohol could include men who refrained
from drinking because of early symptoms of CVD. If so, the higher SCD
rate in this group could be due, at least in part, to undiagnosed
preexisting disease. To address this issue, we repeated our
analyses after excluding deaths in the first 4 years of
follow-up. The multivariate RRs from this
analysis and their 95% CIs are displayed in Table 3. The U-shaped relationship defined by
the multivariate RRs were essentially unchanged after
the first 4 years of events were excluded.
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Because 
50% of this cohort increased or decreased their level of
intake over time, we repeated the multivariate
analysis using the updated measure of alcohol intake
ascertained at year 7 to address potential misclassification in the
baseline analyses. The multivariate RRs and
95% CIs from the time-varying analyses are displayed in Table 3. The U-shaped relationship defined by the
multivariate RRs persisted after the exposure was
updated (P for the quadratic term=0.02) despite updating of
potential confounders, even those that might be in the causal
pathway.
To explore whether the effect of alcohol differed by mode of death
(sudden versus nonsudden), we analyzed the relationship of
baseline moderate alcohol consumption with nonsudden CHD death. The
results of the age-adjusted and multivariate
analysis involving the 157 cases of nonsudden CHD death are
displayed in Table 2. In contrast to the U-shaped relationship
with SCD, the relationship with nonsudden CHD death appeared to be more
inversely linear or L-shaped (P for linear trend=0.02).
Table 4 displays the relative odds of
sudden versus nonsudden CHD death at 4 levels of alcohol intake among
the physicians who died of CHD. Compared with men who consumed alcohol
less than monthly, the risk of dying suddenly was significantly lower
in the men who consumed 2 to 6 drinks/wk, suggesting an added benefit
on SCD at this level of alcohol intake. Although limited, the results
of this subgroup analysis are consistent with a
differential effect of alcohol on SCD versus nonsudden CHD death. Like
the relationship observed with nonsudden CHD death, the relationship
between alcohol intake and nonfatal MI was inversely linear (Figure 2) and not U-shaped. The lowest risks
were found in those who consumed 2 drinks/d (RR, 0.50; 95% CI, 0.30
to 0.83), a level of consumption that was associated with an apparent
increase in the RR for SCD.
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Discussion |
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In this large, prospective cohort study of apparently healthy male physicians who were free of reported MI, stroke, or angina at study entry, alcohol consumption had a U-shaped association with SCD (P for quadratic term=0.002). Compared with those who rarely or never consumed alcohol, the nadir in risk occurred in those who reported consuming 5 to 6 drinks/wk (RR, 0.21; 95% CI, 0.80 to 0.56). The RR of SCD was also significantly decreased among those consuming 2 to 4 drinks/wk (RR, 0.40; 95% CI, 0.22 to 0.75). The RRs in both of these categories of light-to-moderate consumption were also significantly reduced compared with those who consumed
2 drinks/d.
These results were similar when baseline alcohol intake was used alone,
when this measure was updated by the value obtained at 84 months of
follow-up, or when the first 4 years of SCDs were excluded from the
analysis.
Most prospective studies have suggested that moderate alcohol intake
was not associated with a reduction in the risk of SCD despite observed
reductions in the risk of other CHD end points.5 6 7 The
small numbers of SCDs in these previous studies, 50% of the number
in this study, may have limited the power to detect an association. In
addition, previous studies tested only for linear and not quadratic
associations. However, 1 prospective study from Finland reported a
positive association between moderate alcohol intake (200 g/mo, 3
to 5 drinks/wk) and SCD.8 The disparate results of their
study might have been due, at least in part, to the Finnish pattern of
heavy consumption at less frequent settings per week (binge drinking),
which was probably uncommon in the US physicians.
In contrast to previous prospective studies, retrospective case-control
studies have reported a reduced risk of SCD at all levels of moderate
alcohol intake.9 10 11 In the present prospective cohort
study, the risk of SCD was no longer reduced among men who consumed 2
drinks/d. Our results may be compatible with these case-control
studies. The open-ended highest intake category (2 drinks/d) includes
both moderate and excessive drinking, and several studies have
documented the increased risk of SCD associated with heavy alcohol
consumption (>5 to 6 drinks/d).3 4 The elevated risks in
the highest intake category may have been limited to the heavy drinkers
and may not apply to more moderate drinkers.
The results of previous prospective studies have raised the concern that even low doses of alcohol may have an adverse effect on arrhythmogenesis, thereby diminishing the magnitude of the beneficial effects of alcohol on atherogenesis and possibly thrombosis, resulting in a neutral or increased risk of SCD. Our data do not support this possibility. We found reduced risks of SCD at consumption levels up to 1 drink/d, suggesting that up to these levels, the arrhythmogenic effect of alcohol is minimal and is outweighed by other beneficial effects. In fact, although the confidence bounds were wide, the odds ratio for sudden compared with nonsudden CHD death among the men who died was significantly lower at 2 to 6 drinks/wk, suggesting an added benefit of moderate alcohol consumption on SCD. This possible added benefit against SCD could be mediated by the beneficial effects on plaque rupture19 or thrombosis25 often documented on autopsies of SCD victims26 27 or through effects on the autonomic nervous system.28
In contrast to the findings for SCD, the relationship with nonfatal MI and nonsudden CHD death was linear, without an increase in RR at the highest level of intake. In addition, risks are not significantly reduced for nonfatal MI until consumption levels reach 1 drink/d, the same level at which risk for SCD begins to increase. Presumably the differential effect on SCD is due to the superimposed effect of alcohol (perhaps U- or J-shaped) on arrhythmogenesis on a background effect on atherogenesis and thrombosis. Although it is difficult to classify the mechanism of death, the definition of SCD used in this study was designed to be as specific as possible for death due to arrhythmia, based on the methods of Hinkle and Thaler.22
Several limitations of the present study warrant consideration. In this study population, alcohol intake was self-reported, raising the possibility of misclassification, which, if random, would tend to underestimate the magnitude of benefit or risk. However, health professionals have been found to reliably report alcohol use.29 Furthermore, the previously reported positive association between alcohol intake and HDL cholesterol (P for trend <0.001) supports the rank-order validity of the self-reported alcohol intake.16 Another limitation of our measure of alcohol is the lack of information on beverage type or drinking pattern. Therefore, we cannot comment on whether the association with SCD differs for beer, spirits, or wine, and we are unable to distinguish between the effects of intermittent binge drinking versus regular modest alcohol intake with meals. The observed association in this population most likely reflects the latter pattern of drinking, because binge drinking was probably rare in this population. The effects of drinking pattern may be particularly important with respect to SCD, given the known acute increased risk of arrhythmias associated with drinking binges (holiday heart).30 Finally, as with any observational study, the association between self-selection for alcohol consumption and SCD could be due, at least in part, to residual confounding by other dietary habits and lifestyle factors, although controlling for those available had little impact on risk estimates.
With respect to generalizability, the findings of our study are limited by the selective nature of the cohort: healthy male physicians free of known CVD enrolled in a randomized trial. The biggest impact may be a shift in the distribution of alcohol to far lower levels than in the general population, and therefore the curve in the general population may be J- rather than U-shaped. Physicians also differ in their access to medical care and above-average standard of living, as demonstrated by the total CHD mortality rate, which was only 22% of that of a comparable population.16 In addition, the observed relationship in men may not be generalizable to women. For these reasons, the study findings may be most applicable to healthy men free of known CVD.
In summary, this large prospective cohort study suggests that
light-to-moderate alcohol consumption (2 to 6 drinks/wk) among
apparently healthy men is associated with a significantly reduced risk
of SCD compared with nondrinkers as well as with those who consumed 2
drinks/d. This level of alcohol consumption does not appear to have
proarrhythmic effects, as had been suggested by some previous
prospective studies. In fact, light-to-moderate levels of alcohol (2 to
6 drinks/wk) may have additional benefits on SCD beyond those observed
for nonfatal MI and nonsudden CHD death. Furthermore, in contrast to
nonfatal events, the risk of SCD again increases at levels of alcohol
consumption associated with significantly reduced risk of nonfatal MI
in this same cohort (2 drinks/d). These data may help to explain the
observed U-shaped relationship with total
cardiovascular death in some
populations13 14 15 16 despite inverse linear or L-shaped
relationships with MI in other populations.17 18 19
SCD is the most common cause of death in adults <65 years old31 and therefore is a major public health problem in the United States and other industrialized countries. Because only 25% of out-of-hospital ventricular fibrillation arrest victims will survive to hospital discharge,32 any substantial reduction in the incidence of SCD will require effective preventive interventions. Further research directed at understanding the underlying mechanism by which alcohol may protect against SCD specifically and CHD in general could lead to the development of preventive therapeutics that have the benefits of alcohol without the accompanying risks.
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Acknowledgments |
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This study was supported by grants CA-34944, CA-40360, HL-26490, and HL-34595 from the NIH. Dr Albert is supported by a Mentored Clinical Scientist Development Award from the NHLBI (1-K08-HL-03783).
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Footnotes |
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Reprint requests to Dr Christine Albert, Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave E, Boston, MA 02215-1204.
Received March 9, 1999; revision received May 25, 1999; accepted June 2, 1999.
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 J. de Leiris, M. de Lorgeril, and F. Boucher Ethanol and cardiac function Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1027 - H1028. [Full Text] [PDF]
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E. Ruttmann, L. J. Brant, H. Concin, G. Diem, K. Rapp, H. Ulmer, and the Vorarlberg Health Monitoring and Promotion Pro {gamma}-Glutamyltransferase as a Risk Factor for Cardiovascular Disease Mortality: An Epidemiological Investigation in a Cohort of 163 944 Austrian Adults Circulation, October 4, 2005; 112(14): 2130 - 2137. [Abstract] [Full Text] [PDF]
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M. de Lorgeril, P. Salen, P. Defaye, P. Mabo, and F. Paillard Dietary prevention of sudden cardiac death Eur. Heart J., February 2, 2002; 23(4): 277 - 285. [Full Text] [PDF]
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 A. H. Glassman and J. T. Bigger Jr. Antipsychotic Drugs: Prolonged QTc Interval, Torsade de Pointes, and Sudden Death Am J Psychiatry, November 1, 2001; 158(11): 1774 - 1782. [Abstract] [Full Text] [PDF]
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N. Sotoodehnia, A. Zivin, G. H Bardy, and D. S Siscovick Reducing mortality from sudden cardiac death in the community: lessons from epidemiology and clinical applications research Cardiovasc Res, May 1, 2001; 50(2): 197 - 209. [Abstract] [Full Text] [PDF]
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 J. L. Abramson, S. A. Williams, H. M. Krumholz, and V. Vaccarino Moderate Alcohol Consumption and Risk of Heart Failure Among Older Persons JAMA, April 18, 2001; 285(15): 1971 - 1977. [Abstract] [Full Text] [PDF]
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B. Halliwell Lipid peroxidation, antioxidants and cardiovascular disease: how should we move forward? Cardiovasc Res, August 18, 2000; 47(3): 410 - 418. [Full Text] [PDF]
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