Heart Fail Rev (2009) 14:5155 DOI 10.

1007/s10741-007-9048-8

Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking
Christine E. Skotzko Alina Vrinceanu Lynnette Krueger Ronald Freudenberger

Published online: 22 November 2007 Springer Science+Business Media, LLC 2007

Abstract Alcohol use, abuse, and dependence have the potential to result in alcoholic cardiomyopathy (ACM). This distinct form of congestive heart failure (CHF) is responsible for 2136% of all cases of nonischemic dilated cardiomyopathy in Western society. Without complete abstinence, the 4-year mortality for ACM approaches 50%. Therefore, accurate and detailed assessment of alcohol use in congestive heart failure is essential. The prevalence of problematic alcohol use is unrecognized by many clinicians. Clinical assessment of alcohol intake is often reduced to a simple question such as, Do you drink? Denial and minimization are hallmarks of alcohol abuse, with many individuals underreporting their use of alcohol. Clinicians can overcome these hurdles by implementing practical history taking measures to improve the accuracy of self-reported alcohol use. The data regarding the dangers of ongoing alcohol use in individuals with ACM make attempts to engage individuals in treatment to support abstinence essential. Suggestions for detailed and accurate assessment are discussed. Keywords Alcohol Cardiomyopathy Congestive heart failure Assessment

Does drinking matter? Alcohol use is the third leading cause of preventable death in the US, after smoking and obesity [1]. Alcohol is consumed by two-thirds of the United States population and at least 10% are considered heavy drinkers [2]. The lifetime prevalence of alcohol abuse is estimated to be 1424%, and one in 13 Americans currently meet criteria for alcohol dependence [1, 3]. Furthermore, from 20 to 30% of patients admitted to a general medical hospital abuse alcohol [1, 4]. Given the prevalence and potential impact of alcohol abuse in the general medical population, it is important for clinicians to recognize and evaluate alcohol consumption in their patients. The negative effects of alcohol on human organ systems, including the heart, are well documented [1, 2, 4, 5], and persistent alcohol abuse might contribute to the onset and progression of heart failure. In fact, alcohol is the leading cause of nonischemic-dilated cardiomyopathy, accounting for 2136% of cases [2]. Some alcohol dependent individuals have subclinical abnormalities of the heart, and as a consequence of ongoing drinking, may develop cardiac symptomatology [5]. Heavy alcohol consumption leads to a signicantly increased risk for sudden cardiac death and cardiac arrhythmias [2, 4]. Post-operatively, in the intensive care unit, chronic alcoholics have up to ve times more cardiac complications, including arrhythmias and hypoxemia, presumably due to their limited cardiac reserve [4]. These complications are associated with biventricular dysfunction, which can be seen in conjunction with the occurrence of severe infections and septic shock. Alcoholic Cardiomyopathy (ACM), a distinct form of congestive heart failure (CHF), is associated with alcohol intake of greater than 80 g per day (one standard drink is 13.5 g of alcohol) or a six pack of beer a day for a

C. E. Skotzko A. Vrinceanu L. Krueger R. Freudenberger Departments of Psychiatry & Cardiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA C. E. Skotzko (&) Morristown Memorial Hospital, Atlantic Health System, 100 Madison Avenue, Box 28, Morristown, NJ 07960, USA e-mail: Christine.Skotzko@atlantichealth.org

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minimum of 10 years [2]. Alcohol damage to the heart may be evident within a shorter period of time when alcohol consumption exceeds 90100 g per day [4]. However, many physicians do not perform a comprehensive assessment of alcohol intake, even when patients present with CHF or a history of ACM.

Effects of alcohol on cardiomyocytes A search for the molecular mechanism underlying alcoholinduced end-organ dysfunction has lead to the discovery of a non-oxidative pathway for the metabolism of alcohol. This pathway is found in the human heart, brain, liver, and pancreas. It appears that non-esteried fatty acids are esteried in the presence of ethanol to produce fatty acid ethyl esters, uncharged molecules, that can accumulate in mitochondria and impair energy utilization of cells [6]. Also, it well known that ethanol interferes with lipid metabolism in general, affecting the fatty acid composition of the sarcolemma membrane, and the functional properties of the sarcoplasmic reticulum [7]. On a larger scale, acute ingestion of alcohol exerts a direct negative ionotropic effect by diminishing myocardial contractility. It also produces indirect positive effects through augmentation of cathecholamine release. This indirect effect results in increased blood pressure, heart rate, and contractility. An early response to heavy alcohol consumption is an increased ventricular wall thickness-todiameter ratio. With continued chronic alcohol use, cardiomegaly with 4-chamber dilatation and valvular regurgitation are often seen [2]. Individuals who continue to binge drink after the onset of heart failure usually suffer a progressively downhill course. Without complete alcohol abstinence, the 4-year mortality for ACM is 50% [2]. Cessation of alcohol early in the course of the disease may preserve cardiac function and allow reversal of some of the damage [2, 8]. In one series of studies, patients who became abstinent had a 4-year mortality that was persistently one-sixth that of the actively drinking group [9, 10].

Assessment of alcohol use The prevalence and potential consequences of alcohol abuse and dependence make it essential that clinicians be prepared to identify problematic alcohol consumption. Once identied, treatment referral can be pursued to assist the patient in obtaining abstinence. Early identication is of the utmost importance in the diagnosis and management of ACM, as the impact of ongoing drinking on mortality and morbidity is well documented [2, 9, 10].

The diagnosis of an alcohol problem is best made by history. It is important to be aware of the accuracy of selfreported measures of alcohol intake. Laboratory tests for detecting alcohol use have a sensitivity of no better than 50% [1]. In 33 methodological papers published between 1984 and 1999, alcohol intake was assessed by ve main methods: quantity frequency, extended quantity frequency, retrospective diary, prospective diary, and 24-h recalls. The mean level of alcohol intake differed by as much as 20% among these methods. It was also found that when researchers specically asked about intake of beer, wine, and liquor, consumption results were 20% higher than individuals originally reported. Methods that inquire about both the frequency and amount of beer, wine, and liquor consumed individually yield the most realistic levels of intake [11]. Addictions assessments, performed by psychiatrists, psychologists, social workers, and addictions counselors generally uncover a more extensive and/or more severe pattern of alcohol use than that initially diagnosed by the cardiologist. Additional screening, interventions, and treatment are almost always recommended as a result of such consultations. Formal recommendations facilitate understanding of current and past alcohol related issues and provide concrete ways for the clinician to assist the individual. Information and support is also provided to the individual with CHF to assist him or her in realizing the health impact that alcohol has had, and the potential for increased morbidity and mortality with ongoing alcohol use. Approximately 5090% of alcohol problems are missed in physicians ofces. Patients and health care providers share responsibility. Patients frequently deny they have a problem or may not link alcohol with its consequences. Physicians are often rushed and focus on the patientidentied problem. A study showed that, of patients visiting their doctor for alcohol related problems, only 50% were asked about their alcohol use [1]. A recent national survey of primary care physicians and psychiatrists on screening and interventions for alcohol problems found that 88% of the physicians asked their new outpatients, whether they drank alcohol. However, only 13% of the primary care physicians used formal validated screening instruments [12]. When used, ofce-based substance abuse assessments often lack sufcient detail to identify alcohol problems and rely on an individuals willingness to disclose use [11]. In fact, when comparing assessment methodologies used by admitting physicians and house ofcers at a tertiary care hospital and psychiatrists at our own institution, we found that admission screening assessment for alcohol use in the tertiary care hospital was very often limited to the general question, Do you drink?

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Denial and minimization are hallmarks of the substance abusing population, and patients often under report the use of drugs and alcohol [13, 14]. Clinicians can overcome these hurdles by implementing practical history taking measures. The successful treatment of ACM relies on an accurate diagnosis of prior alcohol consumption and ongoing attention to the importance of abstinence. The clinical course of ACM can be altered signicantly with proper interventions, especially when alcohol abuse or use is ongoing. The clinical vignettes that follow are intended to illustrate typical responses given by individuals admitted with CHF exacerbations. Appropriate additional queries are cited as well as the clinical information that was obtained by the consulting psychiatric provider.

The mimimizer Case 1. Do you drink? not much. A 30 year-old single male presented to the emergency room after 2 weeks of increasing shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea. He had initially been diagnosed with bronchitis and treated with antibiotics. He was found to have four-chamber cardiac dilatation and an estimated left ventricular ejection fraction of 15% on echocardiography. MUGA scan revealed moderate to marked left ventricular enlargement, mild right ventricular enlargement, severe global hypokinesis, and a calculated left ventricular ejection fraction of approximately 11%. Further evaluation with cardiac catheterization revealed normal coronaries. The patient was diagnosed with CHF and dilated cardiomyopathy, initially felt to be of a viral etiology. In the ofce, prior to admission, the patient had denied heavy alcohol intake. How many drinks do you have on a typical day when you are drinking? A 14-year history of drinking a six-pack of beer and/or a pint of liquor every other day was elicited. Upon further questioning he admitted to drinking a six-pack of beer plus a half pint of hard liquor daily (much [100 g daily). His last drink was 2 weeks prior to admission; around the time he began developing cough and shortness of breath. This additional history allowed his team to better educate him and recommend appropriate treatment, as well as counsel strict abstinence from all alcohol use.

pitting edema, and chronic renal failure secondary to low cardiac index. The patient was diagnosed with CHF less than 2 years earlier following a myocardial infarction with an episode of ventricular tachycardia. An automatic implantable cardiac debrillator was placed at that time. On admission, the patient was classied as having New York Heart Association (NYHA) class 4 CHF with an ejection fraction below 30%. When queried regarding his alcohol consumption he responded that he drank socially. How often are you social, and how many drinks do you have on a typical day? Yielded the history that the patient used to drink alcoholup to a fth of Amaretto per day prior to his myocardial infarction. Afterwards, he denied drinking other than on rare occasions. When was the last time you drank? Yielded the admission that these rare occasions occurred 12 times per week depending on the social situation. Exactly how much do you drink when you are drinking? Yielded that he consumed of two double shots of scotch (about 54 g) per event. Clarication of his history allowed alcohol use to be considered as a potential contributing factor to his present status. It also provided an opportunity for discussion of the importance of abstinence from alcohol that would otherwise have been missed.

The denier Case 3. Do you drink? no. The pattern changer: occasional use A 40-year-old female, with a history of nonischemic dilated cardiomyopathy for 9 years, was admitted for worsening shortness of breath, paroxysmal nocturnal dyspnea, chest pain, and fatigue. Cardiac catheterization at that time revealed no evidence of CAD and a calculated ejection fraction of 26%. An echocardiogram demonstrated severe left ventricular dilatation, severe decrease in left ventricular systolic function, mild mitral and mild tricuspid regurgitation, mild pulmonary hypertension, and an estimated left ventricular ejection fraction of 1520%. On admission it was documented that the patient does not drink alcohol. Did you ever drink alcohol? The patient reported drinking a half bottle of scotch and a six-pack of beer per weekend(much [100 g) until 6 years ago when she completely stopped drinking scotch because she lost the taste. She still reported drinking 34 beers per month. Diagnosis of prior alcohol abuse and ongoing use allowed for a re-conceptualization of underlying cardiomyopathy and referral for alcohol treatment.

Case 2. Do you drink? socially. A 56-year-old male was admitted with complaints of increasing shortness of breath, bilateral lower extremity

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Case 4. Do you drink? no. the hidden alcohol history A 70-year-old male with a history of a prior distant myocardial infarction (20 years ago), hypertension, and hypercholesterolemia was admitted with complaints of worsening shortness of breath. For the past 6 months, the patients condition required readmission every 24 weeks for acute shortness of breath caused by ash pulmonary edema. Five months prior to admission, after an episode of palpitations, the patient had electrophysiology studies that revealed inducible ventricular tachycardia, for which he underwent implantation of a cardiac debrillator. The current cardiac catherization showed the proximal left anterior descending artery had 100% stenosis, proximal circumex had 50% stenosis, and the distal right coronary artery had 80% stenosis and an ejection fraction of approximately 20%. Echocardiogram demonstrated fourchamber dilatation with signicantly decreased left ventricular systolic function, severe global hypokinesis, left atrial enlargement, and moderate mitral regurgitation. Ofce medical records, as well as admission history, indicated that he denied any cigarette smoking or alcohol abuse. Did you ever drink alcohol? Revealed that the patient had owned a bar for 40 years and drank a case of beer per day for 30 years. He had stopped drinking only 3 years ago, because the alcohol had begun to make him feel ill. This information allowed his cardiologist to respond appropriately when he asked if he should be drinking a glass of wine each evening.

drinking tend to deny use even if they stopped only days ago. This is particularly true if the assessment question only refers to current use. We recommend that the clinicians use the technique of normalization (symptom expectation) when inquiring about alcohol use: for example, instead of: Do you drink alcohol? We recommend asking: Did you ever drink alcohol? When did you last drink alcohol? How often do you drink alcohol? If the patient answers that he/she does not drink alcohol, the interviewer should pursue the subject by asking at least one of the following additional questions: When was the last time you drank? Have you ever drunk alcohol, beer, liquor or wine? Was there ever a period of time in the past when you did drink alcohol? After acknowledging that use has occurred, follow up with a simple question such as: How many drinks do you have on a typical day when you are drinking? Does a couple mean one or two or three or four? If a potential pattern of use or abuse is identied, the issue should be pursued further, by assessing the extent of the problem with one or more of the following questions: Are you always able to stop drinking when you want to? Has drinking ever created problems between you and your spouse or friends? Have you ever gotten into trouble at work because of drinking? Have you ever had any legal problems because of drinking? Do you nd that you have given up activities that you would otherwise be doing in favor of drinking? Denial and minimization are hallmarks of much of the population that uses alcohol be they abusers or true social drinkers. This is associated with social stigmatization of alcohol use. An astute clinician can better overcome these hurdles with detailed alcohol assessment. Pursuing these questions in a thorough fashion is of equal importance with gathering a detailed history regarding medication compliance, salt restriction, and exercise tolerance. The proper treatment of ACM relies on an accurate diagnosis of prior alcohol use. The clinical course of this disease process can be altered signicantly with proper interventions, especially when the abuse or use of alcohol is ongoing. The collaborative routine use of psychiatric and social services can assist in maximizing therapeutic interventions for the patient with ACM. While no studies have

Practical considerations: approaches to improved history taking It is signicant that in all of these clinical cases the alcohol abuse history was hidden despite denite, albeit supercial, assessment by the clinician. The CAGE questionnaire a 4item interview-based assessment of alcohol use has been demonstrated to have a sensitivity of 93% and a specicity of 76% for the identication of problem drinkers [15]. It assesses an individuals prior attempts to Cut down alcohol use; Annoyance with others comments about their drinking; experience Guilt regarding events associated with their alcohol use; and necessity of an Eye opener upon awakening for the day. While cited as a standard assessment, the above vignettes demonstrate how the CAGE can be ineffective as acknowledgement of alcohol consumption is required. Recognition of the reluctance of many to afrm or recognize alcohol consumption necessitates that follow up questions be pursued. As demonstrated, it is extremely important to inquire about both recent and past alcohol use. Patients who quit

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55 8. Pavan D, Nicolosi GL, Lestuzzi C, Burelli C, Zardo F, Zanuttini D (1987) Normalization of variables of left ventricular function in patients with alcoholic cardiomyopathy after cessation of excessive alcohol intake: an echocardiographic study. Eur Heart J 8(5):435440 9. Figueredo VM (1997) The effects of alcohol on the heart: detrimental or benecial? Postgrad Med 101(2):165167, 171, 172, 175,176 10. Fabrizio L, Regan TJ (1994) Alcoholic cardiomyopathy. Cardiovasc Drugs Ther 8(1):8994 11. Feunekes GI, van t Veer P, van Staveren WA, Kok FJ (1999) Alcohol intake assessment: the sober facts. Am J Epidemiol 150(1):105112 12. Saunders JB, Aasland OG, Bebor TF, De La Fuente JR, Grant M (1993) Development of the Alcohol Use Disorders Identication Test (AUDIT): WHO collaborative project on early detection of persons with harmful alcohol consumption II. Addiction 88:791 804 13. Fuller R, Lee K, Gordis E (1988) Validity of self-report in alcoholism research: results of a veterans administration cooperative study. Alcohol Clin Exp Res 12(2):201205 14. Morral A, McCaffrey D, Iguchi M (2002) Hardcore drug users claim to be occasional users: drug use frequency underreporting. Drug Alcohol Depend 57(3):193202 15. Bernadt MW, Mumford J, Taylor C, Smith B, Murray RM (1982) Comparison of questionnaire and laboratory tests in the detection of excessive drinking and alcoholism. Lancet 6(8267):325328

been done to document an impact on medical outcomes, the data regarding the dangers of ongoing alcohol use in individuals with ACM make attempts to engage individuals in treatment to support abstinence essential.
Acknowledgments Matthew J. Steiner, MD, Nina A. Cooperman, Psy.D. for assistance with literature review and manuscript preparation. Funded by NHLBI contract # HC 25197.

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