Stirred, Not Shaken
Authors: Joshua Wynne
Journal: Annals of Internal Medicine (2002)

Editorials5 February 2002Stirred, Not ShakenJoshua Wynne, MD, MBAJoshua Wynne, MD, MBAWayne State University; Detroit, MI 48201Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-136-3-200202050-00013 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The effect of alcohol on the cardiovascular system has been studied and debated for over 150 years (1), but a specific cardiomyopathy related to excessive alcohol consumption has been recognized only for the past half century (2). The putative effect of alcohol on the heart has been clouded and confounded by cardiovascular damage due to simultaneous nutritional deficiency as a consequence of beriberi, the toxic effects of additives such as cobalt, and the lack of a good large-animal model of alcoholic cardiomyopathy (3). We now know that alcohol can directly affect the cardiovascular system, but the precise mechanism of damage remains controversial (4, 5). Two studies in this issue (6, 7) add to our understanding of this association. While they may raise almost as many questions as they answer, taken together they can be stirred into our understanding of alcohol's effects on the heart without fundamentally shaking the foundations of our knowledge.That alcohol can affect the heart in humans would seem to be beyond doubt, although some would argue that a firm causal relationship has not been proven (8). Clear and persuasive data show that long-term alcohol use may be associated with left ventricular dysfunction and overt congestive heart failure, a variety of supraventricular and ventricular arrhythmias, sudden death, and hypertension. Alcohol is believed to be the causal agent in 3% to 40% of all patients with otherwise unexplained (idiopathic) dilated cardiomyopathy (9). Even short-term, acute ingestion of alcohol may result in transient left ventricular dysfunction and arrhythmias (10, 11). The cessation of alcohol consumption in patients with presumed alcoholic cardiomyopathy is associated with an improvement in left ventricular function and a reduction in scintigraphic evidence of myocardial damage (12). Long-term alcohol consumption produces a pattern of dilated cardiomyopathy in several animal models, although the lack of a good large-animal model has hindered study (3, 4). The recent description of a stable avian model of alcoholic cardiomyopathy may accelerate progress in our understanding of alcohol-mediated cardiovascular damage (3).In this issue, Nicolás and colleagues further document improved left ventricular function with the reduction or cessation of alcohol consumption, as well as a progressive worsening of left ventricular function in patients who continue to drink heavily (6). In a 4-year prospective study, the authors found that persons with chronic alcoholism who continued to drink heavily demonstrated progressive deterioration in noninvasively measured left ventricular systolic function, while function improved in those who ceased or reduced their alcohol intake. One interesting finding was that ventricular performance improved even in patients who continued to consume a moderate amount of alcohol. This may be the consequence of a threshold effect, where toxicity is seen only above a certain level of alcohol consumption. Moderate alcohol consumption might also have other effects on the cardiovascular system beyond causing myocardial depression. It is important not to infer a change in muscle function from a change in ejection fraction, since the ejection-phase indices depend on the particular loading conditions of the ventricle.While alcoholic cardiomyopathy has been recognized for many years, interest in other manifestations of alcoholic heart disease was stimulated by observations in the 1970s and 1980s regarding the apparent association between excessive alcohol consumption and the appearance of a variety of arrhythmias and sudden death. In one syndrome, termed the holiday heart syndrome because affected patients typically present with arrhythmia after binge drinking on a holiday, patients may have no other manifestations of end-organ damage and usually do not have left ventricular dysfunction or congestive heart failure. Several types of arrhythmias have been seen, most commonly atrial fibrillation but also atrial flutter and premature ventricular depolarizations (13). A study reported two decades ago used electrophysiologic testing to demonstrate that even modest doses of alcohol could produce rhythm disturbances in persons with a long-term history of alcohol abuse, most of whom had evidence of some form of heart disease (14). In the study by Nicolás and colleagues, 10 of 55 alcoholic men died during follow-up; all 10 men had continued to drink heavily (6). This finding highlights the potential importance of alcohol-related arrhythmias.The study by Walsh and associates in this issue is intriguing because it did not show the expected association of heavier drinking with increased risk for congestive heart failure (7). Studying the well-established Framingham cohort, the investigators used a clinical scoring method to identify patients who developed congestive heart failure during follow-up. They found that the risk for congestive heart failure was not associated with heavier alcohol consumption; in fact, moderate alcohol use actually appeared to have a protective effect. What are we to make of these findings?Several methodologic issues need to be considered before we discard our concept of alcohol-mediated heart damage. The first is the duration of alcohol use in these patients. Regan (10) and others have emphasized that alcoholic cardiomyopathy typically is seen after at least a decade of consistent consumption of at least 80 g of alcohol per day; the study by Nicolás and colleagues required a minimum of 10 years' consumption of at least 100 g/d (6). This information is not available in the study by Walsh and associates, and thus patients may not have had enough toxic exposure to cause heart failure during the study. In addition, the Walsh study did not include a direct measure of left ventricular function, such as echocardiography or nuclear techniques. Objective measures of cardiac performance usually are considered necessary to supplement clinical heart failure scores and reduce the false-positive rate (15, 16). We do not know how many patients actually had asymptomatic ventricular dysfunction that may become symptomatic at some point in the future. These issues notwithstanding, the Walsh study is well done and challenges some of our established principles. Whether the methodologic issues raised account for the results remains unclear. It should be emphasized that this study is not the only one to question the association of left ventricular systolic dysfunction and alcohol consumption. In a previous study, left ventricular function did not differ in 89 asymptomatic patients with chronic alcoholism compared with controls, although the alcoholic patients did have more evidence of left ventricular diastolic dysfunction (17).The Walsh study further supports the concept that some degree of alcohol consumption may actually be protective and beneficial; similarly, the Nicolás study showed improvement in left ventricular function even with continued moderate alcohol consumption. Several epidemiologic studies have suggested a U-shaped mortality curve as a function of alcohol use, with moderate alcohol consumption associated with reduced mortality. Perhaps most interesting is the so-called French paradox: In France, despite risk factors for coronary artery disease that are no lower and perhaps higher than usual (such as a diet high in saturated fats), persons have much lower mortality rates for coronary heart disease than in most other European countries, a phenomenon that has been attributed to the consumption of red wine (18, 19).What to do with this kind of information is, of course, problematic. Are we really to encourage the use of moderate alcohol consumption, even though we are aware of its multiple (potential) deleterious effects? I think not, particularly given that while the cardiovascular mortality rate is significantly lower in France than in other European countries, the overall mortality rate is not (20). It has been suggested that part of the reason for this dichotomy is a higher rate of alcohol-mediated noncardiovascular mortality (19). Given the widespread use of alcoholic beverages in the western world, let us hope that the provocative studies reported in this issue will stir researchers to gain further understanding of the cardiovascular effects of alcohol.References1. Klatsky AL. Alcohol and cardiovascular diseases: a historical overview. Novartis Found Symp. 1998;216:2-12. [PMID: 9949784] MedlineGoogle Scholar2. Brigden W. Alcoholic cardiomyopathy. Cardiovasc Clin. 1972;4:187-201. [PMID: 4568938] MedlineGoogle Scholar3. Morris N, Kim CS, Doye AA, Hajjar RJ, Laste N, Gwathmey JK. A pilot study of a new chicken model of alcohol-induced cardiomyopathy. Alcohol Clin Exp Res. 1999;23:1668-72. [PMID: 10550000] CrossrefMedlineGoogle Scholar4. Liang Q, Carlson EC, Borgerding AJ, Epstein PN. A transgenic model of acetaldehyde overproduction accelerates alcohol cardiomyopathy. J Pharmacol Exp Ther. 1999;291:766-72. [PMID: 10525098] MedlineGoogle Scholar5. Preedy VR, Richardson PJ. Alcoholic cardiomyopathy: clinical and experimental pathological changes. Herz. 1996;21:241-7. [PMID: 8805004] MedlineGoogle Scholar6. Nicolás JM, Fernández-Solà J, Estruch R, Paré JC, Sacanella E, Urbano-Márquez A, et al . The effect of controlled drinking in alcoholic cardiomyopathy. Ann Intern Med. 2002;136:192-200. LinkGoogle Scholar7. Walsh CR, Larson MG, Evans JC, Djousse L, Ellison RC, Vasan RS, et al . Alcohol consumption and risk for congestive heart failure in the Framingham Heart Study. Ann Intern Med. 2002;136:181-91. LinkGoogle Scholar8. McKenna CJ, Codd MB, McCann HA, Sugrue DD. Alcohol consumption and idiopathic dilated cardiomyopathy: a case control study. Am Heart J. 1998;135:833-7. [PMID: 9588413] CrossrefMedlineGoogle Scholar9. Gavazzi A, De Maria R, Parolini M, Porcu M. Alcohol abuse and dilated cardiomyopathy in men. Am J Cardiol. 2000;85:1114-8. [PMID: 10781762] CrossrefMedlineGoogle Scholar10. Regan TJ. Alcohol and the cardiovascular system. JAMA. 1990;264:377-81. [PMID: 2194048] CrossrefMedlineGoogle Scholar11. Spodick DH, Pigott VM, Chirife R. Preclinical cardiac malfunction in chronic alcoholism. Comparison with matched normal controls and with alcoholic cardiomyopathy. N Engl J Med. 1972;287:677-80. [PMID: 5055416] CrossrefMedlineGoogle Scholar12. Ballester M, Martí V, Carrió I, Obrador D, Moya C, Pons-Lladó G, et al . Spectrum of alcohol-induced myocardial damage detected by indium-111-labeled monoclonal antimyosin antibodies. J Am Coll Cardiol. 1997;29:160-7. [PMID: 8996309] CrossrefMedlineGoogle Scholar13. Ettinger PO, Wu CF, De La Cruz C, Weisse AB, Ahmed SS, Regan TJ. Arrhythmias and the “Holiday Heart”: alcohol-associated cardiac rhythm disorders. Am Heart J. 1978;95:555-62. [PMID: 636996] CrossrefMedlineGoogle Scholar14. Greenspon AJ, Schaal SF. The “holiday heart”: electrophysiologic studies of alcohol effects in alcoholics. Ann Intern Med. 1983;98:135-9. [PMID: 6824246] LinkGoogle Scholar15. Mosterd A, Deckers JW, Hoes AW, Nederpel A, Smeets A, Linker DT, et al . Classification of heart failure in population based research: an assessment of six heart failure scores. Eur J Epidemiol. 1997;13:491-502. [PMID: 9258559] CrossrefMedlineGoogle Scholar16. Marantz PR, Tobin JN, Wassertheil-Smoller S, Steingart RM, Wexler JP, Budner N, et al . The relationship between left ventricular systolic function and congestive heart failure diagnosed by clinical criteria. Circulation. 1988;77:607-12. [PMID: 3342491] CrossrefMedlineGoogle Scholar17. Lazarević AM, Nakatani S, Nesković AN, Marinković J, Yasumura Y, Stojicić D, et al . Early changes in left ventricular function in chronic asymptomatic alcoholics: relation to the duration of heavy drinking. J Am Coll Cardiol. 2000;35:1599-606. [PMID: 10807466] CrossrefMedlineGoogle Scholar18. Vinson JA, Teufel K, Wu N. Red wine, dealcoholized red wine, and especially grape juice, inhibit atherosclerosis in a hamster model. Atherosclerosis. 2001;156:67-72. [PMID: 11368998] CrossrefMedlineGoogle Scholar19. Law M, Wald N. Why heart disease mortality is low in France: the time lag explanation. BMJ. 1999;318:1471-6. [PMID: 10346778] CrossrefMedlineGoogle Scholar20. Criqui MH, Ringel BL. Does diet or alcohol explain the French paradox? Lancet. 1994;344:1719-23. [PMID: 7996999] CrossrefMedlineGoogle Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: Wayne State University; Detroit, MI 48201Corresponding Author: Joshua Wynne, MD, MBA, Division of Cardiology, Harper Hospital, 3990 John R Street, Detroit, MI 48201; e-mail, [email protected]org. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoAlcohol Consumption and Risk for Congestive Heart Failure in the Framingham Heart Study Craig R. Walsh , Martin G. Larson , Jane C. Evans , Luc Djousse , R. Curtis Ellison , Ramachandran S. Vasan , and Daniel Levy The Effect of Controlled Drinking in Alcoholic Cardiomyopathy Josep María Nicolás , Joaquim Fernández-Solà , Ramon Estruch , Joan Carles Paré , Emilio Sacanella , Alvaro Urbano-Márquez , and Emanuel Rubin Metrics Cited ByAlcohol consumption and risk of dementia 5 February 2002Volume 136, Issue 3Page: 247-249KeywordsAlcohol consumptionAlcoholicsAlcoholsArrhythmiaCardiomyopathiesDeath ratesHeartHeart failureLongitudinal studiesMortality ePublished: 5 February 2002 Issue Published: 5 February 2002 CopyrightCopyright © 2002 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...