Journal of Addictions Nursing, 15:75–79, 2004Copyright c© International Nurses Society on AddictionsISSN: 1088-4602 print / 1548-7148 onlineDOI: 10.1080/10884600490450209

Cardiovascular Disease in Alcohol Abusers

Susan Beyer, MSN, APRN, PMHNP, BCPsychiatric Mental Health Nurse Practitioner in private practice of Hadi Tajani, MD,Bedford, Texas, USA

Moderate alcohol use (two or fewer drinks daily) may offer somedegree of protection from coronary artery disease and stroke. Anypotential benefit must be weighed against an individual’s risk pro-file for alcohol abuse or dependence and the associated health andsocial consequences. Health costs of alcohol abuse are well into thebillions. Heavy alcohol consumption is associated with cardiomy-opathy, arrhythmias, hypertension, stroke, and sudden death. Al-cohol is the major cause of nonischemic cardiomyopathy in theWestern world. In any health care setting, education about the po-tential risks and benefits of alcohol use must be provided with healthpromotion and maintenance strategies tailored to the individual.

Keywords Alcohol, Cardiovascular Disease

Heart disease in the United States is the number one causeof death followed by cancer and stroke (Anderson, Hsiang-Ching, Murphy, & Kochanek, 2003). Observations from pop-ulation studies (Friedman, 1998) show that moderate alcoholuse (Table 1) appears to offer some degree of risk reductionfor coronary artery disease and stroke. Moderate use appearsto favorably influence levels of high-density and low-densitylipoprotein cholesterol and inhibit platelet aggregation (Rimm,Williams, Fosher, Criqui, & Stampfer, 1999) thus decreasingplaque accumulation and associated inflammatory processes inthe arteries. Alcohol appears to decrease the level of C-reactiveprotein, a marker of inflammation (Scott, Arch, & Gilbert, 2002).

The antioxidant properties of wine appear to confer morebenefit than other spirits (Gronbaek et al., 2000). Antioxidantswork to decrease the level of free radicals, which are asso-ciated with cell damage. However, this finding was not sup-ported in a large longitudinal study over 12 years following38,077 male health professionals. No single beverage offeredany added benefit to cardiovascular health (Mukamal et al.,2003). Medical complications of excessive alcohol use are wellknown, including diseases of the cardiovascular system, liver,

Address correspondence to Susan Beyer, 1604 Hospital Parkway,# 507, Bedford, TX 76022. E-mail: Sbbeyer@charter.net

gastrointestinal tract, and cancer (Figueredo, 1997; Gronbaeket al., 2000; Hanna, Chou, & Grant, 1997; Lorimier, 2000; Saccoet al., 1999; Sesso et al., 2000). The large body of evidence re-garding morbidity and mortality related to alcohol argues againstany recommendation for encouraging its use for health benefits(Friedman, 1998).

ECONOMIC AND MEDICAL CONSEQUENCESIn addition to the health risks of excessive alcohol use, the

costs to society are significant. An estimated 107,000 prematuredeaths and $66 billion in annual losses related to productivity andemployment are attributed to alcohol abuse. Insurance costs areover $600 million. Treating the health consequences of alcoholabuse runs over $13 billion (Henrick, Fountain, & Livermore,1998). Medical consequences associated with the abuse of alco-hol doubles that of other abused substances. Cardiomyopathy,cardiac arrhythmias, sudden coronary death, hypertension, coro-nary heart disease, and stroke have a direct or indirect associationwith heavy alcohol consumption.

A REVIEW OF THE CARDIOVASCULAR SYSTEM

StructureThe heart muscle propels blood throughout the body ensur-

ing the transportation of oxygen and substances essential to cellmetabolism. Byproducts generated by cellular metabolism alsoare transported via the cardiovascular system for detoxificationand removal through the kidneys and liver. The four chambers ofthe heart, the atria, and ventricles serve as a pumping system andare separated by a series of valves. The heart typically movesfour to eight liters of blood every minute (cardiac output). Theatria are low pressure chambers providing storage and conduitfunctions for blood emptied through the vena cavae and pul-monary veins. The ventricles, larger with thicker walls, propelblood into the pulmonary and systemic circulation. The rightventricle ejects large volumes of unoxygenated blood into thepulmonary circulation system for reoxygenation. The left ven-tricle, larger and most muscular, propels oxygenated blood from

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TABLE 1What is moderate drinking?

Men: Two drinks per dayWomen: One drink per dayA drink

12 ounces of regular beer5 ounces of wine1.5 ounces of 80-proof distilled spirits

Source: United States Department of Agri-culture Home and Garden Bulletin No. 232,5th ed., 2000.

the lungs out into systemic circulation via the aorta. Approxi-mately 60–70% of blood contained in the ventricles is ejectedwith each contraction (ejection fraction). The pumping actionconsists of contraction (systole) and relaxation (diastole). Onecycle of contraction and relaxation is the cardiac cycle. A normalcardiac cycle (heart rate) occurs about 70 times per minute.

The chambers of the heart do not directly provide blood flowto the cells of the heart. The branch of the systemic circulation’sarteries and veins supplying the heart is termed coronary circu-lation. Occlusions in these vessels deprive the heart muscle ofmuch needed oxygen with deprivation of blood flow (ischemia)or infarction (tissue death due to local lack of oxygen). Depend-ing on the degree of damage and cell death, structural and func-tional changes can occur including alterations in contractility,dysrythmias, and heart failure.

The Conduction SystemThe heart is able to initiate and conduct electrical impulses

to the myocytes (muscle cells) in the atria and ventricles to pro-duce contraction. When activated (depolarized), cardiac musclefibers contract. In the healthy heart, electrical impulses originatein the sinoatrial (SA) node and spread through the atria. The SAnode contains clusters of spontaneously depolarizing cells andis the heart’s dominant pacemaker (Gettes, 2000). To reach theventricles, the impulse must then travel to the atrioventricular(AV) node and through a specialized connecting system com-prised of the bundle of His, bundle branches, and Purkinje fibers(Goldschlager, 2000) (Figure 1). An electrocardiogram (ECG)measures the heart’s electrical activity.

The generation and movement of electrical impulses from onecardiac myocyte to the next is necessary to generate the forceneeded to produce the rhythmic shortening and relaxing of thecardiac muscle fibers that produce the cardiac cycle. Electricalactivation and conduction depends primarily on the movement ofsodium, calcium, and potassium ions across the cell membrane.Sodium and calcium ions are involved in cell depolarizationand contractile force. The movement of potassium ions allowsa momentary relaxation where the cells reset for the next waveof impulse generation. This rhythmical emission of electricalimpulses creates the forces that allow the contraction (systole)and relaxation (diastole) of the heart muscle.

FIG. 1. The conduction system. Source: The Circulatory System @http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookcircSYS.htmlText c©1992, 1994, 1997, 1998, 2000, 2001, by M. J. Farabee, all rights reserved.Use for educational purposes is encouraged. E-mail: mj.farabee@emcmail.maricopa.edu

CARDIOVASCULAR EFFECTS OF ALCOHOLCardiac muscle lacks the enzyme necessary to metabolize

alcohol—alcohol dehydrogenase. “Alcohol and its direct metabo-lite acetaldehyde are direct cardiotoxins acutely and chronically”(Stevenson, 2000, p. 340). Alcohol depresses myocardial con-tractility even at low blood alcohol concentrations impairingthe heart’s ability to pump effectively. While the specific in-teraction of factors producing decreased contractility is not yetknown, cellular processes involved in calcium transport (essen-tial to cardiac contractile function), protein synthesis (essentialto the regulation of ion flow across the cell membrane), and theproduction of free radicals (highly reactive byproducts of cellmetabolism capable of producing cell damage and death) areimplicated (Friedman, 1998; Kloner & Rezkalla, 1998).

While not yet fully understood, alcohol affects blood flow.Acutely, there is an increase in skin, viscera, and cerebral bloodflow with a decrease to the pancreas and muscles of the ex-tremities. Ischemia may be a factor in the etiology of alcoholicpancreatitis. Heart rate and blood pressure increase with alcoholingestion with a concomitant increase in oxygen requirements.The impact on coronary blood flow is even less well defined butbelieved to be one of vasodilation. Increased myocardial bloodflow appears to distribute blood supply more to the arterioles ofnonischemic rather than ischemic myocardium increasing therisk of injury to any existing diseased tissue (Friedman, 1998).

Excessive exposure to cobalt is a known toxin to the thy-roid and the cardiovascular and pulmonary systems. It is a traceelement essential to the production of vitamin B12 (hydroxo-cobalamin) and ingested in necessary amounts through a typicaldiet. In the 1960s cobalt was used as an additive in the productionof beer in Canada. It was found to be responsible for a syndromeknown as beer drinker’s cardiomyopathy, characterized by peri-cardial effusion, elevated hemoglobin concentrations, and con-gestive heart failure (Barceloux, 1999). Cobalt is no longer usedin the production of alcoholic beverages.

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CARDIOVASCULAR DISEASE IN ALCOHOL ABUSERS 77

CHRONIC HEAVY ALCOHOL USE ANDCARDIOVASCULAR DISEASE

Alcoholic Dilated CardiomyopathyIn dilated cardiomyopathy (see Figure 2), the chambers of

the heart become dilated, the left ventricular wall thickens, andthe myocardium becomes flabby and loses contractile function(Table 2). Cardiac output and ejection fraction are decreased.Dyspnea on exertion, orthopnea, fatigue, peripheral edema, andjugular venous distention are typical symptoms reflecting thediminished contractile ability of the heart (congestive heart fail-ure). Chest x-ray shows cardiomegaly (hypertrophy of the heart)and pulmonary congestion. Arrythmias may be evident on ECG.Diagnostically, echocardiography reveals the dilated chambersof the heart (Kloner & Rezkalla, 1998).

Although cardiomyopathy may result from viral, bacterial,or parasitic infections as well as thiamine deficiency (beri beri)(Kloner & Rezkalla, 1998), it is the most prevalent form of alco-hol related heart disease. It is associated with long-term heavydrinking. Ten to 20 years of heavy drinking increases the riskfor heart muscle disease even in those with no other cardiovas-cular illness risk factors such as hyperlipidemia, hypertension,or diabetes. Susceptible individuals may be at higher risk drink-ing six drinks (four ounces of pure ethanol) daily over five toten years. Binge drinking also may be implicated (Stevenson,2000). Every chronic drinker does not develop cardiomyopathy,so biological predisposition may play a role (Friedman, 1998).

There is a clear relationship between the toxic effects of pro-longed alcohol exposure and loss of myocardial contractility,even though the exact etiological mechanism is yet to be fully un-derstood. The pathophysiology producing the clinical manifes-tations of cardiomyopathy may involve the interplay of increasedlevels of circulating catecholamines, hypertension, tachycardia,

FIG. 2. A Heart in dilated cardiomyopathy. Source: Alcohol Health &Research World, Vol. 14, No. 4, 1990 in National Institute on Alcohol Abuseand Alcoholism (2001) Bethesda, Maryland. http://www.niaaa.nih.gov/gallery/cardiovascular/rubinhtm.htm

TABLE 2Pathophysiologic effects of alcoholic

cardiomyopathy

Fatigue, weakness, dyspneaMarked to moderate cardiomegalyLeft ventricular hypertrophyDecreased left ventricular functionValvular incompetenceIntraventricular conduction defectsTachycardia and atrial fibrillationSystemic or pulmonary thromboembolismDecreased cardiac outputDecreased ejection fractionLeft heart failure

infection, and nutritional deficiencies often evident in chronicalcoholism (Friedman, 1998).

Continued drinking results in disease progression and even-tual death, most often from congestive heart failure or fatal dis-turbances in heart rhythm. Complete reversibility is rare. Earlydetection and medical treatment are essential to halting diseaseprogression. Medical intervention to relieve the symptoms ofcongestive heart failure involves salt restriction, angiotension-coverting enzyme inhibitors, and diuretics (Kloner & Rezkalla,1998). Digitalis and anticoagulants may be necessary tostrengthen the force of ventricular contraction and reduce therisk of thrombus formation. Abstinence, always a goal in addic-tion treatment, is vital to improving the outcome in the treatmentof alcoholic cardiomyopathy.

Cardiac Arrythmias and Sudden DeathHeart rhythm changes can occur with chronic or acute alcohol

use. “Holiday heart syndrome” is a sudden and abrupt elevationin heart rate that sends individuals to emergency rooms aroundthose times of the year associated with holiday or social cele-brations or on Mondays after a weekend binge. Binge drinkingcan precipitate atrial fibrillation, the most common arrythmiaassociated with alcohol use. Heart rate can increase to over 300beats per minute. Typically there are no lasting sequellae in oth-erwise healthy individuals. In alcoholics an episode of holidayheart syndrome may be the earliest manifestation of cardiomy-opathy. Atrial fibrillation can occur in alcoholics with or withouta dilated cardiomyopathy. Elevated ventricular rates can followatrial fibrillation. Left undetected and untreated this increasedventricular activity may eventually result in a dilated heart andsubsequent impaired contractile function (Friedman, 1998).

Physiologic events associated with increased autonomic out-flow in alcohol withdrawal may play a role in promoting condi-tions favorable to potentially deadly arrhythmias. Tachycardiaand hypertension occur as the withdrawal state produces a hyper-adrenergic response of the autonomic nervous system with highlevels of excitatory circulating catecholamines, epinephrine, and

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norepinephrine. Oxygen demand in the myocardium increasesand ischemia, infarction, and lethal arrhythmias are potentialconsequences. In alcoholics with existing coronary artery dis-ease, the risk for sudden death is even greater (Friedman, 1998).

HypertensionHypertension is defined as a blood pressure exceeding 140/90.

Alcoholics have a higher prevalence of hypertension, regard-less of age, weight, or smoking. Hypertension is a prominentrisk factor for myocardial infarction and stroke. Alcohol pro-duces an excitatory response in the sympathetic nervous system.Chronic alcohol use seems to reset blood pressure to higher lev-els. Even weeks after withdrawal, there is a residual sensitivityin the sympathetic nervous system (Friedman, 1998). The ex-act mechanism is not yet understood. In those heavy drinkerswho also have essential hypertension, effective managementbecomes more difficult. The risks of untreated hypertension in-clude stroke, kidney failure, myocardial infarction, and conges-tive heart failure.

Coronary Artery Disease and StrokeAlcohol is associated with coronary artery disease and stroke

related morbidity and mortality. It plays an interrelated role withother risk factors. Smoking and poor dietary habits often gohand in hand with alcoholism. In one large study over a seven-year period, adjusting for other risk factors, those who increasedtheir drinking more than two drinks a day had a 63% increasein coronary heart disease and stroke risk (Sesso et al., 2000).

Most cardiovascular and cerebrovascular events associatedwith alcohol use can be understood by recognizing the relation-ship between alcohol and hypertension. Hypertension is a majorrisk factor for the development of cardiovascular disease andstroke. Alcohol increases myocardial oxygen requirements byelevating blood pressure and increasing heart rate. It can evokecoronary vasospasm and increase myocardial ischemia by re-distributing blood flow away from ischemic tissues (Friedman,1998). Stroke is strongly associated heavy alcohol use (Hart,Smith, Hole, & Hawthorne, 1999; Hillborn, 1998; Sacco et al.,1999; Sesso et al., 2000). Blood pressure elevation and increasedcerebral blood flow associated with alcohol ingestion may be theetiologic factors in hemorrhagic stroke. While not necessarily adirect causative agent, traumatic hemorrhagic strokes occur as aresult of falls and assaults suffered while intoxicated. There ap-pears to be a temporal relationship between recent heavy drink-ing and the rupture of cerebral aneurysms. The precise mech-anism is not known (Hillborn, 1998). Thrombus formation canoccur in alcoholic cardiomyopathy, atrial fibrillation, and otherarrythmias and precipitate an ischemic stroke.

SUMMARYWhen one thinks about the health risks of alcoholism, gas-

trointestinal and liver disease may first come to mind. While

serious and potentially lethal, it is important for nurses workingwith any patient or client population to have an understandingof the impact of alcohol on cardiovascular health. Two of thetop three killers of Americans are heart disease and stroke. Withalcohol’s well-documented relationship to cardiovascular mor-bidity and mortality, exploring patterns of alcohol use should bea fundamental part of any health assessment. The general pub-lic has been informed via the print and electronic media of anapparent relationship between moderate drinking and cardiovas-cular health. Few details have been provided and even less hasbeen presented about alcohol’s damaging effects to cardiovas-cular health. As nurses and health educators we focus on healthpromotion and illness prevention. We have an obligation to re-main adequately informed so that we may accurately interpretthe latest research about the risks and benefits associated withalcohol use particularly related to cardiovascular health.

REFERENCESAnderson, A. E., Hsiang-Ching, K., Murphy, S. L., & Kochanek, K. D.

(2003). Deaths: Final data for 2002. National Vital Statistics Reports, 52(3).Hyattsvill, MD: National Center for Health Statistics.

Barceloux, D. G. (1999). Cobalt. Journal of Toxicology Clinical Toxicology,37(2), 201–206.

Figueredo, V. M. (1997). The effects of alcohol on the heart: Detrimental orbeneficial? Postgraduate Medicine, 101(2), 165–176.

Friedman, H. S. (1998). Cardiovascular effects of alcohol. In M. Galanter(Ed.), Recent developments in alcoholism: The consequences of alcoholism(Vol. 14, pp. 135–139). New York: Plenum.

Gettes, L. S. (2000). Principles of electrophysiology. In L. Goldman & J. C.Bennett (Eds.), Cecil textbook of medicine (21st ed., pp. 226–230).Philadelphia: W.B. Saunders.

Goldschlager, N. (2000). Electrocardiography. In L. Goldman & J. C. Bennett(Eds.), Cecil textbook of medicine (21st ed., pp. 185–191). Philadelphia: W.B.Saunders.

Gronbaek, M., Becker, U., Johansen, D., Gottschau, A., Schnohr, P., Hein, H. O.,Jensen, G., & Sorensen, T. I. (2000). Type of alcohol consumed and mortal-ity from all causes: Coronary heart disease, and cancer. Annals of InternalMedicine, 133, 411–419.

Hanna, E. Z., Chou, P., & Grant, B. F. (1997). The relationship between drinkingand heart disease morbidity in the United States: Results from the NationalHealth Survey. Alcoholism: Clinical and Experimental Research, 21(1), 111–118.

Hart, C. L., Smith, G. D., Hole, D. J., & Hawthorne, V. M. (1999). Alcoholconsumption and mortality from all causes, coronary heart disease, and stroke:Results from a prospective cohort study of Scottish men with 21 years offollow up. British Medical Journal, 318, 1725–1729.

Henrick, H., Fountain, D., & Livermore, G. (1998). The economic costs ofalcohol and drug abuse in the United States, 1992 (NIH Publication No.98-4327). Bethesda, MD: National Institute on Drug Abuse.

Hillborn, M. (1998). Alcohol consumption and stroke: Benefits and risks. Alco-holism: Clinical and Experimental Research, 22(7), 352S–358S.

Kloner, R. A., & Rezkalla, S. (1998). Substance abuse and the heart. InE. J. Topol (Ed.), Textbook of cardiovascular medicine (pp. 947–970).Philadelphia: Lippincott-Raven.

Lorimier, A. A. (2000). Alcohol, wine, and health. The American Journal ofSurgery, 180, 357–361.

Mukamal, K. J., Conigrave, K. M., Mittleman, M. A., Camargo, C. A., Stampfer,M. J., Willett, W. C., & Rimm, E. B. (2003). Roles of drinking pattern andtype of alcohol consumed in coronary heart disease in men. New EnglandJournal of Medicine, 348, 109–118.

Rimm, E. B., Williams, P., Fosher, K., Criqui, M., & Stampfer, M. J. (1999).

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11/2

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For

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onal

use

onl

y.

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Moderate alcohol intake and lower risk of coronary heart disease: Meta-analysis of effects on lipids and haemostatic factors. British Medical Journal,319(1), 523–1528.

Sacco, R. L., Elkind, M., Boden-Albala, B., Lin, I. F., Kargman, D. E., Hauser,W. A., Shea, S., & Paik, M. C. (1999). The protective effect of moderatealcohol consumption on ischemic stroke. The Journal of the American MedicalAssociation, 281, 53–60.

Scott, H. S., Arch, G. M., & Gilbert, G. (2002). Relation between alcohol con-sumption and C-reactive protein levels in the adult U.S. population. Journalof the American Board of Family Practice, 15(6), 437–442.

Sesso, H. D., Stampfer, M. J., Rosner, B., Hennekens, C. H., Manson, J. E., &Gaziano, J. M. (2000). Seven-year changes in alcohol consumption and sub-sequent risk of cardiovascular disease in men. Archives of Internal Medicine,160, 2605–2612.

Stevenson, L. W. (2000). Diseases of the myocardium. In L. Goldman &J. C. Bennett (Eds.), Cecil textbook of medicine (21st ed., pp. 336–346).Philadelphia: W.B. Saunders.

U.S. Department of Agriculture and U.S. Department of Health and HumanServices. (2000). Home and Garden Bulletin No. 232, 5th ed. Nutrition andYour Health. Dietary Guidelines for Americans.

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