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During modern medical times, alcohol has had a Jekyl and Hyde reputation. For the most part, alcohol has been considered detrimental to the heart. In 1884, Dr. O. Bollinger, a pathologist, ascribed the term ?Munich beer heart? to the dilated hearts of former residents of Munich who were noted to have histories of heavy alcohol use. More recently, the World Health Organization and the International Society and Federation of Cardiology1, recognizing that alcohol abuse was the leading cause of non-ischemic cardiomyopathy in Western society, recommended that the term ?alcoholic heart muscle disease? be ascribed to this condition.

Yet there have been those who have supported the concept that alcohol, in moderation, may be cardioprotective. In 1904, Dr. R. Cabot found at autopsy that the amount of atherosclerotic coronary disease was less in those whose charts reported a previous history of drinking compared with the coronary arteries of abstainers. In 1974, Klatsky et al.2, in the Kaiser-Permanente study, found a statistically significant negative association between alcohol consumption and subsequent myocardial infarction. They also observed a U-shaped mortality curve relative to the amount of alcohol consumed by 2000 men and women over a ten year period. The decrease in mortality in mild to moderate ethanol users appeared primarily due to a decrease in the incidence of fatal coronary events. More recently, the Multicenter Study of Myocardial Infarction3 found that patients who consumed alcohol had improved outcomes after acute coronary events compared with abstainers.

Thus, there may be confusion for some physicians regarding the recommendations that they might make to patients as to whether alcohol is detrimental or beneficial to the heart. The purpose of this article is to 1) review the relationship between alcohol abuse and cardiovascular disease and 2) review the potential beneficial effects of moderate consumption on the heart.

Alcohol and the Heart: Detriment?

Alcohol abuse can result in any of several cardiovascular complications (Figure 1). Alcohol abuse is the major cause of non-ischemic cardiomyopathy in Western society. The incidence of cardiomyopathy secondary to alcohol abuse has been reported to range from 11 to 40% in one study from a greater metropolitan area4, 5. Yet, the majority of alcoholics are asymptomatic from a cardiac standpoint, although they may demonstrate subclinical abnormalities of systolic and diastolic function and hypertrophy. In one study of 250 chronic alcoholic men, only 9% had evidence for cardiomyopathy6. However, given the large number of alcoholics, this minority of abusers with cardiomyopathy represent a majority of all non-ischemic cardiomyopathies.

How much alcohol does one have to drink to develop cardiomyopathy? There is general agreement that at least 80 grams (5 ounces) per day for over ten years is necessary to put one at risk for developing cardiomyopathy. This is equivalent to drinking 6 beers, a pint of whiskey, or a bottle and a half of wine per day over ten years. Interestingly, there is a frequent absence of major abnormalities in other organs (i.e., cirrhosis) in alcoholics who develop a cardiomyopathy. It has been suggested that alcoholics who develop cardiomyopathy have an environmental or genetic predisposition. One example of a previously identified environmental predisposition was the addition of cobalt to beer. The practice of using cobalt to increase the ?head? on a beer from the tap, produced heart failure in a number of beer drinkers in Quebec, although the amount of cobalt used was insufficient to have toxic effects on its own. The finding of an increased frequency of the HLA-B8 antigen in alcoholics with cardiomyopathy compared to alcoholics with normal heart function, is one of several examples of a potential genetic predisposition to developing cardiomyopathy.

Alcoholic heart muscle disease is typical of other non-ischemic cardiomyopathies. Systolic and diastolic function are impaired, with subsequent four chamber dilatation and low output failure. Mild hypertrophy is often present which may be the result of hypertension due to, or complicated by, prolonged alcohol abuse. The mechanisms underlying the contractile dysfunction associated with alcoholic heart muscle disease remain uncertain. However, recent work from our laboratory7 suggest that there is an impaired calcium - pressure relationship at the level of the myofilament contractile apparatus, and not a decrease in intracellular calcium, which results in depressed contractility. Additional studies to understand the mechanisms of contractile dysfunction in alcoholic heart muscle disease are presently underway.

Once an alcoholic develops cardiomyopathy, persistent abuse results in a mortality rate of approximately 50% over four years8. However, as opposed to other non-ischemic cardiomyopathies, this four year mortality rate decreases to 9% in those who abstain following a diagnosis of alcoholic heart muscle disease8. This decreased mortality rate is believed to be primarily due to an improvement in cardiac function with abstention. In a 5 year follow-up study of 11 patients with alcohol-induced cardiomyopathy, who subsequently abstained, all 11 patients demonstrated improvement in left ventricular ejection fraction, with the majority returning to within the normal range9. Thus, unlike other non-ischemic cardiomyopathies, alcoholic heart muscle disease can be at least partially reversed.

Arrhythmias (especially atrial), as well as baseline electrocardiographic abnormalities, have been associated with alcoholic heart muscle disease. In 1974, Ettinger et al.10, reported a temporal relationship between the incidence of arrhythmias and heavy alcohol consumption occurring around the Christmas and New Year holidays, which they referred to as ?holiday heart?. Arrhythmias seen in the alcoholic patient are mostly of the supraventricular variety, and can be exacerbated by acute intoxication. The presence of ventricular arrhythmias with alcoholic heart muscle disease are suggested by an increased incidence of sudden death in alcoholics. Baseline electrocardiographic abnormalities are non-specific and can include conduction disturbances, prolonged QT intervals, and non-specific T wave abnormalities.

In addition to the potential for cardiomyopathy and arrhythmias, there are other negative cardiovascular aspects to alcohol abuse. The prevalence of hypertension is increased in alcoholics compared to moderate drinkers and non-drinkers. Furthermore, the coexistence of essential hypertension and heavy alcohol use makes successful therapy more difficult. It is likely that this hypertensive effect of alcohol contributes to the development of alcoholic heart muscle disease.

Alcohol abuse also increases the overall incidence of cerebral vascular accidents. While there is a significant increase in hemorrhagic strokes, this is partially offset by a decrease in the incidence of ischemic strokes. Mild to moderate drinkers may actually have a reduced incidence of cerebrovascular accidents compared to non-drinkers, in a manner analogous to their decreased incidence of ischemic heart disease.

Alcohol and the Heart: Benefit?

As Dr. Roger Lee stated at the American Medical Association meeting in 1925, ?it is an old saying that alcohol is a highly inflammable substance whether you apply a match or a word to it. Nevertheless, from time to time, some of us with more courage than caution may well venture to express our views concerning the place of alcohol in therapeutics?. Over the last century, the medical profession has primarily concentrated on the negative aspects of alcohol abuse. However, there were those who early on recognized that drinking in moderation was not necessarily a ?bad thing?. In 1892, Sir William Osler wrote ?in moderation wine, beer and spirits may be taken throughout a long life without impairing the general health?. Louis Pasteur said ?wine is the most healthful and hygienic of beverages?.

More recently, the 1995 Report on the Dietary Guidelines for Americans11 reported that ?current evidence suggests that moderate drinking...is associated with a lower risk of coronary heart disease in some individuals?. This conclusion was based on an abundance of data in the literature supporting a cardioprotective effect of mild to moderate alcohol consumption. For example, in 1979 St. Leger and colleagues12 reported an inverse relationship between mortality rates from ischemic heart disease in men aged 55 to 64 and total wine consumption in different countries. As the French are the leading consumers of wine in the world, this became known as the French Paradox. The French Paradox implies that there is a lower incidence of mortality from ischemic heart disease in France despite the fact that saturated fat intake, serum cholesterol, blood pressure and prevalence of smoking are no lower than elsewhere. Numerous epidemiologic studies have confirmed this cardioprotective effect of moderate alcohol consumption.

In the Health Professionals Follow-up Study13, the relative risk of coronary artery disease decreased with increasing amounts of alcohol consumed per day in 51,529 male health professionals followed over 10 years. This was confirmed in the Nurses Health Study were 85,709 women aged 34 to 59 were followed for 12 years14. In these women, light to moderate alcohol use was also associated with decreased cardiovascular mortality (as well as overall mortality). However, this decrease in mortality mostly occurred in women who had increased risk for coronary heart disease and those 50 years or older. A review of the literature by the Royal College of Physicians15 showed that numerous studies in many different cultures and populations uniformly demonstrated a decreased incidence of fatal events due to ischemic heart disease in moderate consumers of alcohol15.

What is moderate alcohol consumption? Moderation has been defined by the Dietary Guidelines Committee for Americans11 as less than or equal to one drink per day for women and less than or equal to two drinks per day for men (Figure 2). A drink is defined as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80 proof distilled spirits. Similarly, the Royal College of Physicians in United Kingdom recommends one to two drinks per day for women and one to three drinks per day for men15. The reason the recommendations for women are lower than that for men is due to the fact that women become more intoxicated than men at an equivalent dose of alcohol. This is the result of significant differences between the sexes in the activity of gastric alcohol dehydrogenase and in the fat to body water ratio. Alcohol is more soluble in water than in fat, so that a given amount of alcohol is more highly concentrated in a women?s body water than in a man?s.

How does alcohol protect the heart? Several possibilities are listed in Figure 1. Data from clinical and epidemiological studies have demonstrated that regular alcohol consumption reduces the risk of ischemic heart disease 30 to 60%. This protective effect of alcohol may be the result of increased levels of high-density-lipoprotein (HDL) cholesterol and its associated apolipoproteins AI and AII, increased fibrinolytic activity, and endogenous tissue plasminogen activator (tPA). Additionally, platelet aggregability is decreased in regular consumers of alcohol compared with non-drinkers. Increased HDL parameters might attenuate the development of atherosclerosis. Increased fibrinolytic activity and decreased platelet aggregability might inhibit thrombus formation in coronary arteries. Increased levels of endogenous tPA might promote natural thrombolysis. A combination of all or some of these factors likely accounts for the reduction of fatal coronary events in consumers of alcohol.

Several recent studies suggest that, in addition to decreasing the incidence of ischemic heart disease, regular alcohol use may also improve outcome following a myocardial infarction. Wannamethee et al.16 found that moderate drinking and high levels of physical activity were associated with increased survival after myocardial infarction. In the Multicenter Study of Myocardial Ischemia3, patients who regularly consumed alcohol had a significantly decreased incidence of death, reinfarction, or unstable angina during the 26 months following admission for acute myocardial infarction or unstable angina. Another study utilizing the National Institute of Alcoholism and Alcohol Abuse and National Institutes of Health Alcohol Epidemiologic Data System17, found that of 14,407 subjects followed over 20 years, ?those dying of acute myocardial infarction were less likely to be continuous drinkers and more likely to be continuous nondrinkers?.

How might regular alcohol consumption improve outcome following a myocardial infarction? It is well recognized that outcome is directly related to the amount of myocardial recovery following an ischemic event. Myocardial recovery can be increased if the injury associated with reperfusion after prolonged ischemia (ischemia-reperfusion injury) is attenuated. Preconditioning (i.e., brief episodes of ischemia and reperfusion prior to an ischemic event) is an experimental intervention that has been shown to attenuate ischemia-reperfusion injury. Activation of adenosine receptors (types A1 and A3) on myocytes is one mechanism by which preconditioning has been shown to occur. Interestingly, many of the effects of alcohol on cellular and organ function are also mediated by adenosine.

Recent work from our laboratory has been directed at answering the following questions: 1. Does regular ethanol consumption protect against myocardial ischemia-reperfusion injury? and 2. Is this protective effect mediated through activation of adenosine receptors? We found that following prolonged ischemia and reperfusion, hearts from guinea pigs subjected to ethanol (5 to 20% in their drinking water for 3 to 6 wks) demonstrated improved contractile recovery and decreased myocyte necrosis, as compared with non-drinking controls. In the presence of an inhibitor of the myocyte-predominant adenosine A1 receptor the protective effect of ethanol was abolished. An inhibitor of endothelium-predominant adenosine A2 receptors did not affect this protection. These data are consistent with the hypothesis that regular alcohol consumption attenuates the ischemia-reperfusion injury, and that this protection is mediated through activation of adenosine A1 receptors in a manner analogous to preconditioning. Importantly, this protection appears to be continually present with regular alcohol consumption, as opposed to the transient (hours) protection afforded by experimental preconditioning. Therefore, these findings raise the possibility that regular alcohol consumption produces a chronic preconditioning-like effect which improves myocardial recovery, and thereby survival, following myocardial infarction. Ongoing studies are determining, at the cellular and molecular levels, the mechanisms responsible for this cardioprotective effect of alcohol.

Moderate drinkers have either similar or lower blood pressure levels compared to nondrinkers. Whether this contributes to the cardioprotective effects of moderate alcohol consumption is yet to be determined.

Is Red Wine Better?

Most studies have shown that there the cardioprotective effect of different alcoholic beverages is similar13, 14. A notable exception is the recent Copenhagen City Heart Study which found that wine, and not beer or spirits, decreased cardiovascular mortality 18.

Why might wine drinkers have greater protection against ischemic heart disease than consumers of other types of alcoholic beverages? It has been suggested that wine drinkers have greater health consciousness, adhere better to dietary principles and consume their ethanol on a regular basis as opposed to bingeing. Additionally, there is experimental data from animal studies to suggest that red wine may have additional benefits over other alcoholic beverages. For example, in one study19 the percent of coronary arteries with atherosclerotic lesions in rabbits who were prone to atherosclerotic development was decreased 60% in animals that had red wine included in their diet. Other alcoholic beverages had less significant effects: 33% with white wine, 25% with ethanol, 17% with whiskey, and no difference in the development of atherosclerotic lesions between animals consuming beer and controls.

What is it about red wine that is different from other alcoholic beverages? As opposed to other alcoholic beverages, red wine contains phenolic and antioxidant compounds. The most well studied of the phenolics is trans-resveratrol. Phenolics are known to alter eicosanoid metabolism in a manner which results in decreased platelet aggregability and thrombus formation. The antioxidants in red wine, such as ?-tocopherol, may decrease oxidation of low-density lipoproteins (LDL). Decreased oxidation of LDL would attenuate the development of atherosclerotic plaques.

Clinical, epidemiologic, and bench work studies suggest that the compound ethanol has cardioprotective effects. This would suggest that any alcoholic beverage in moderation should have a therapeutic benefit. However, there is data to suggest that wine drinkers may derive additional benefit. This additional benefit is likely a combination of a healthier life style associated with wine drinkers and the presence of other protective compounds in wine in addition to ethanol. Future work will help to clarify this superiority of red wine over other alcoholic beverages in producing cardioprotection.

Regular Alcohol Consumption as a Public Health Policy?

Should a public health recommendation be made for the general population to regularly consume alcohol? I believe the answer to this is no. Unfortunately, the potential complications associated with alcohol abuse may ultimately outweigh the benefits of cardioprotection. Some would take this recommendation as an excuse to increase their present drinking to abusive levels. Others who did not previously drink might turn out to have a predisposition to alcoholism. These increases in drinking levels would exacerbate hypertension. The number of hemorrhagic cerebral vascular accidents would increase. Alcohol-related accidents and violent crimes would increase, especially in younger males. There would be an increase in malignancies (e.g., breast and colon) and the potential for birth defects if drinking during pregnancy. Thus, the risks of recommending regular alcohol consumption as a public health policy may outweigh the benefits of cardioprotection.

Similarly, I believe a public health recommendation to abstain from alcohol is no more responsible than a recommendation which indiscriminately advocates drinking. Heart disease is the number one killer in the United States. Therefore, regular alcohol consumption may offer a cardioprotective effect for a large proportion of the adult population. Thus, as stated in the 1995 Report on the Dietary Guidelines for Americans11, alcohol in moderation may have a therapeutic benefit in some individuals.

Who may benefit from regular alcohol use? Middle aged and older males (40 and older), who are at increased risk for ischemic heart disease, would most likely benefit from regular alcohol consumption. Younger males (less than 30 to 40), who are not yet at increased risk for ischemic heart disease, would likely not benefit. This is the population which is primarily associated with alcohol-related accidents and violent acts. In premenopausal females (less than 40 to 50), it is questionable whether regular alcohol consumption would be beneficial. While there is a decrease in ischemic heart disease, there is an offsetting increased incidence of breast cancer. Exceptions to this would be women with significant risks for ischemic heart disease and no family history of breast cancer. For postmenopausal females (50 and older), where there is an increase in the incidence of ischemic heart disease, there may be a benefit from regular alcohol consumption. Interestingly, regular alcohol consumption has been found to augment estrogen levels in postmenopausal women 20

Conclusions

Within the medical field, alcohol has had an appropriate Jekyl and Hyde reputation. Alcohol abuse is a substantial public health problem of which the cost financially and otherwise are staggering. Prolonged abuse of alcohol can result in cardiomyopathy in a minority of alcoholics. However, due to the large number of alcoholics, alcohol is the major cause of non-ischemic cardiomyopathy in Western societies.

However, there is now substantial evidence to suggest that alcohol consumption in moderation has cardioprotective effects. Not only does mild to moderate alcohol consumption reduce the incidence of ischemic heart disease, but it also improves outcome in patients who have other risks for coronary events who do go on to have myocardial infarctions.

Your recommendations to regularly consume alcohol will be as individualized as are your patients. Personally, I regularly have a glass of wine with dinner, given my family history. Similarly, I approve of my patients drinking in moderation if they have risk factors for ischemic heart disease. However, I never tell previously abstinate patients to start drinking for their health unless they express interest and appear to understand the benefits and risks of drinking. Somewhat appropriate, as that famous philosopher Anonymous once said, ?God in His goodness sent the grape to cheer both great and small. Little fools drink too much and great fools none at all.?

REFERENCES

1. Report on the WHO/ISFC task force on the definition and classification of cardiomyopathies. Br Heart J 1980; 44:672-673.

2. Klatsky AL, Friedman GD, Siegelaub AB. Alcohol consumption before myocardial infarction. Ann. Int. Med. 1974; 81:294-301.

3. Nakamura Y, Kawai C, Kinoshita M, Moss AJ, for the Multicenter Study of Myocardial Ischemia Research Group. Moderate ethanol intake and outcome after an acute coronary event. Circulation 1995; 92(8):I-708 (abstr.).

4. Andersson B, Waagstein F. Spectrum and outcome of congestive heart failure in a hospitalized population. Am Heart J 1993; 126:632-40.

5. Roberts WC, Siegel RJ, McManus BM. Idiopathic dilated cardiomyopathy: analysis of 152 necropsy patients. Am J Cardiol 1987; 60:1340-55.

6. Estruch R, Nicolas JM, Villegas E, Junque A, Urbano-Marquez A. Relationship between ethanol-related diseases and nutritional status in chronically alcoholic men. Alcohol Alcohol 1993; 28:543-50.

7. Figueredo VM, Zhou HZ, Baker AJ, Weiner MW, Camacho SA. Faster isovolumic relaxation in rat hearts chronically exposed to ethanol. Circulation 1995; 92:I-182 (abstr.).

8. Demakis JG, Proskey A, Rahimtoola SH, et al. The natural course of alcoholic cardiomyopathy. Ann Intern Med 1974; 80:293-7.

9. Francis GS, Johnson TH, Ziesche S, Berg M, Boosalis P, Cohn JN. Marked spontaneous improvement in ejection fraction in patients with congestive heart failure. Am J Med 1990; 89:303-7.

10. Ettinger PO, Wu CF, De La Cruz C, Jr., Weisse AB, Ahmed SS, Regan TJ. Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders. Am Heart J 1978; 95:555-62.

11. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans. Washingtonn D.C.: United States Department of Agriculture, 1995.

12. St. Leger AS, Cochrane AL, Moore F. Factors associated with cardiac mortality in developed countries with particular reference to the consumption of wine. Lancet 1979; 1:1017-20.

13. Rimm EB, Giovannucci EL, Willett WC, et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet 1991; 338:464-8.

14. Fuchs CS, Stampfer MJ, Colditz GA, et al. Alcohol consumption and mortality among women. N Engl J Med 1995; 332:1245-50.

15. Alcohol and the heart in perspective. Sensible limits reaffirmed. A Working Group of the Royal Colleges of Physicians, Psychiatrists and General Practitioners. J R Coll Physicians Lond 1995; 29:266-71.

16. Wannamethee G, Whincup PH, Shaper AG, Walker M, MacFarlane PW. Factors determining case fatality in myocardial infarction "who dies in a heart attack"? Br Heart J 1995; 74:324-31.

17. Dufour MC, Caces MF, Whitmore CC, Hanna EZ. Alcohol consumption and death from acute myocardial infarction in a national longitudinal cohort. Alcohol Clin Exp Res 1996; 20:97A (abstr.).

18. Gronbaek M, Deis A, Sorenson TIA, Becker U, Schnohr P, Jensen G. Mortality associated with moderate intakes of wine, beer, or spirits. Br Med J 1995; 310:1165-1169.

19. Klurfeld DM, Kritchevsky D. Differential effects of alcoholic beverages on experimental atherosclerosis in rabbits. Exp Mol Pathol 1981; 34:62-71.

20. Felson DT, Zhang Y, Hannan MT, Kannel WB, Kiel DP. Alcohol intake and bone mineral density in elderly men and women. The Framingham Study. Am J Epidemiol 1995; 142:485-92.

FIGURE 1

ALCOHOL AND THE HEART: DETRIMENT 1. cardiomyopathy (alcoholic heart muscle disease) 2. arrhythmias (?holiday heart?) 3. hypertension

ALCOHOL AND THE HEART: BENEFIT 1. decreased ischemic heart disease 2. improved outcome following myocardial infarction 3. ? lower blood pressure

FIGURE 2

WHAT IS MODERATION?

Moderation is defined as = 1 drink per day for women and = 2 drinks per day for men. A drink is defined as:

1. 12 ounce glass of beer 2. 5 ounce glass of wine 3. 1.5 ounces (jigger) of 80 proof distilled spirits

From the Report of the Dietary Guidelines Committee on the Dietary Guidelines for Americans, 1995

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