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Alcohol use and congestive heart failure: incidence, importance,
and approaches to improved history taking
Christine E. Skotzko Æ Alina Vrinceanu Æ
Lynnette Krueger Æ Ronald Freudenberger
Published online: 22 November 2007
Ó 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 21–36% 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 clini-
cians. 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 con-
sumed 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 14–24%, 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 21–36% of cases [2].
Some alcohol dependent individuals have subclinical
abnormalities of the heart, and as a consequence of ongo-
ing drinking, may develop cardiac symptomatology [5].
Heavy alcohol consumption leads to a significantly
increased risk for sudden cardiac death and cardiac ar-
rhythmias [2, 4]. Post-operatively, in the intensive care
unit, chronic alcoholics have up to five times more cardiac
complications, including arrhythmias and hypoxemia,
presumably due to their limited cardiac reserve [4]. These
complications are associated with biventricular dysfunc-
tion, 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
123
Heart Fail Rev (2009) 14:51–55
DOI 10.1007/s10741-007-9048-8
minimum of 10 years [2]. Alcohol damage to the heart may
be evident within a shorter period of time when alcohol
consumption exceeds 90–100 g per day [4]. However,
many physicians do not perform a comprehensive assess-
ment 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 alcohol-
induced 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-esterified fatty acids are
esterified 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-to-
diameter ratio. With continued chronic alcohol use, cardi-
omegaly 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 identified, treatment referral can be pursued to assist
the patient in obtaining abstinence. Early identification 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 self-
reported 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 five 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 specifically 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 indi-
vidual. 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 50–90% of alcohol problems are missed
in physician’s offices. 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 patient-
identified 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,
office-based substance abuse assessments often lack suffi-
cient detail to identify alcohol problems and rely on an
individual’s willingness to disclose use [11]. In fact, when
comparing assessment methodologies used by admitting
physicians and house officers at a tertiary care hospital and
psychiatrists at our own institution, we found that admis-
sion screening assessment for alcohol use in the tertiary
care hospital was very often limited to the general question,
‘‘Do you drink?’’
52 Heart Fail Rev (2009) 14:51–55
123
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 atten-
tion to the importance of abstinence. The clinical course of
ACM can be altered significantly with proper interventions,
especially when alcohol abuse or use is ongoing.
The clinical vignettes that follow are intended to illus-
trate ‘‘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 mod-
erate to marked left ventricular enlargement, mild right
ventricular enlargement, severe global hypokinesis, and a
calculated left ventricular ejection fraction of approxi-
mately 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 office, 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.
Case 2. Do you drink? ‘‘socially.’’
A 56-year-old male was admitted with complaints of
increasing shortness of breath, bilateral lower extremity
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 defibrillator was placed at that time.
On admission, the patient was classified 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’’ alcohol—up to ‘‘a fifth’’ 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 1–2 times
per week ‘‘depending on the social situation.’’
‘‘Exactly how much do you drink when you are drink-
ing?’’ Yielded that he consumed of two double shots of
scotch (about 54 g) per event.
Clarification 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 other-
wise 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 dila-
ted 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 esti-
mated left ventricular ejection fraction of 15–20%.
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 3–4
beers per month. Diagnosis of prior alcohol abuse and
ongoing use allowed for a re-conceptualization of under-
lying cardiomyopathy and referral for alcohol treatment.
Heart Fail Rev (2009) 14:51–55 53
123
Case 4. Do you drink? ‘‘no.’’ the hidden alcohol history
A 70-year-old male with a history of a prior distant myo-
cardial infarction (20 years ago), hypertension, and
hypercholesterolemia was admitted with complaints of
worsening shortness of breath. For the past 6 months, the
patient’s condition required readmission every 2–4 weeks
for acute shortness of breath caused by flash 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 defibrillator.
The current cardiac catherization showed the proximal
left anterior descending artery had 100% stenosis, proximal
circumflex had 50% stenosis, and the distal right coronary
artery had 80% stenosis and an ejection fraction of
approximately 20%. Echocardiogram demonstrated four-
chamber dilatation with significantly decreased left ven-
tricular systolic function, severe global hypokinesis, left
atrial enlargement, and moderate mitral regurgitation.
Office 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.
Practical considerations: approaches to improved
history taking
It is significant that in all of these clinical cases the alcohol
abuse history was hidden despite definite, albeit superficial,
assessment by the clinician. The CAGE questionnaire a 4-
item interview-based assessment of alcohol use has been
demonstrated to have a sensitivity of 93% and a specificity
of 76% for the identification 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 awak-
ening for the day. While cited as a standard assessment, the
above vignettes demonstrate how the CAGE can be inef-
fective as acknowledgement of alcohol consumption is
required. Recognition of the reluctance of many to affirm
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
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 alco-
hol?’’ 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 identified, 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 find 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 compli-
ance, 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 significantly 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 inter-
ventions for the patient with ACM. While no studies have
54 Heart Fail Rev (2009) 14:51–55
123
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 prepara-
tion. Funded by NHLBI contract # HC 25197.
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