Document Sample
					                                                 Journal of Community Medicine, Jan-June, 2010, Vol. 6 (1)


                                          Manoj Kumar Bansal
                                           Consultant Cardiologist,
                                             Ahmadabad, India

         Epidemiologists, physicians and the public, all have been interested in the effects of alcohol on the
cardiovascular system since long. The relation between alcohol consumption and cardiovascular disease is of
great interest also because social drinking is a potentially modifiable behavior. Evidence from large
epidemiologic studies leads to the conclusion that moderate alcohol intake reduces risk of non- fatal and fatal
coronary heart disease although the literature is not unanimous and that detrimental effects of alcohol on
cardiac function are linked to heavy consumption.

Epidemiological Studies
        Many large population prospective studies have examined the relationship between alcohol
consumption and the incidence of coronary heart disease and stroke. The results of these studies are not
unanimous on the shape of relationship between risk of fatal and non-fatal coronary heart disease and alcohol
consumption. These differences are attributed to the fact that the risk factor profiles and the classification of
alcohol intake as moderate or severe, varied amongst these studies. The Framingham Heart Study1, the
Yugoslavia Cardiovascular Disease Study and the Physicians Health Study found an inverse relationship
between alcohol intake and the incidence of coronary heart disease. The Nurses’ Health Study and the British
Regional Health Study did not find a clear dose-response relationship between alcohol intake and the incidence
of coronary heart disease.

         The post trial follow-up of the Multiple Risk Factor Intervention Trial found an inverse dose response
relationship between alcohol intake and coronary heart disease death rate, while an increased age adjusted
coronary heart disease mortality was associated with an increased alcohol intake in the five year follow-up
study of 4,532 middle aged Finnish men. The Framingham Heart Study and the Nurses’ health study found an
L-shaped pattern of relationship between alcohol intake and mortality from coronary heart disease, with
mortality decreasing with increasing consumption up to a point and then remaining the same. The Lipid
Research Clinics follow-up study reported a U-shaped relationship suggesting that there was an initial
decrease in coronary heart disease death rate followed by an increase in deaths at higher levels of alcohol

Effects of Alcohol on Cardiac Myocyte
         There are several ways through which alcohol causes damage to the cardiac myocyte. Alcohol causes
hindrance in excitation contraction coupling and in the sarcoplasmic reticulum it causes reduced calcium
sequestration and inhibits the sarcolemmal ATP-dependent Na+/K+ pump. It damages the mitochondrial
oxidative phosphorylation and causes a reduction in the mitochondrial respiratory ratio. Increased extra cellular
and interstitial protein synthesis occur resulting in myofibrillar degeneration and replacement fibrosis.
Substances such as cobalt or lead when added to alcoholic beverages are cardiotoxic and cobalt was
responsible for the mysterious fulminant cardiomyopathy that killed persons in Belgium, Quebec, Omaha and
Minneapolis between 1964 and 1966. This cardiomyopathy disappeared upon removal of the cobalt from the
alcoholic drinks. Illegally produced alcoholic beverages often contain lead as a contaminant.

Alcoholic Cardiomyopathy
         Although initially believed to be due to nutritional deficiencies and insufficient thiamine consumption, it
has now been shown by a number of studies that alcoholic cardiomyopathy is caused by the direct toxicity of
alcohol and its metabolites, acetaldehyde and acetate to the heart. A dose related toxic effect of alcohol on the
heart has also been shown and a direct correlation exists between alcohol consumption and abnormal LV
function, with both the mean daily alcohol intake and the duration affecting the risk of developing
cardiomyopathy. Generally the patients who develop alcoholic cardiomyopathy have been drinking 80 g of
alcohol per day for at least 10 years. These patients generally present with increased fatigue, dyspnea on
exertion, orthopnea, paroxysmal nocturnal dyspnea or arrhythmias. Cessation of alcohol intake is the mainstay
of treatment and has a significant effect on the disease manifestation and progression.

         Hypertension develops twice more commonly as compared to age and gender matched controls in
individuals who drink more than two drinks daily3. This dose related effect gets even more prominent when the
intake of alcohol exceeds thirty grams per day. Even when consumed as a part of social consumption, alcohol
is associated with a modest rise in systolic arterial pressure, while considerable increase may occur with heavy
drinking. Alcohol consumption has been shown to increase the plasma levels of renin and aldosterone and this
has also been proposed as a potential mechanism by which alcohol can cause hypertension. Moderation of
alcohol consumption to no more than two drinks per day in men and to no more than one drink per day in
women causes an approximate reduction of 2-4 mm Hg in systolic blood pressure.

Arrhythmias and Sudden Cardiac Death
         A number of arrhythmias both atrial and ventricular are caused by alcohol consumption. The most
common arrhythmia associated with alcohol intake is atrial fibrillation and accounts for a significant proportion
of patients aged less than 65 years who develop atrial fibrillation.

         Holiday heart syndrome is a term that refers to the episodes of atrial fibrillation occurring after binge
drinking, usually on weekends or holidays. The other arrhythmias that occur in persons who consume alcohol
include atrial and ventricular premature beats, atrial flutter, supraventricular tachycardias, ventricular
tachycardia and ventricular fibrillation. There is an increase in the incidence of sudden cardiac death with heavy
alcohol consumption.

Hemorrhagic Stroke
          Alcohol consumption has been shown to increase the risk of both intracerebral hemorrhage and
subarachnoid hemorrhage. When the intake of alcohol is more than 150 grams per week, the risk of
subarachnoid hemorrhage is significantly increased. Binge drinking is a more significant risk factor for
subarachnoid hemorrhage. The transiently increased blood pressure levels while consuming alcohol and during
the withdrawal period has been proposed to be an important mechanism for intracerebral hemorrhage, acting in
conjunction with the cerebral arteriolar vasoconstriction caused by alcohol. The increased risk of subarachnoid
hemorrhage associated with alcohol is due to mechanisms other than chronic hypertension.
Alcohol has also been shown to increase the risk of intracerebral hemorrhage. This increase occurs in a dose
dependent manner and is independent of chronic hypertension. Recent heavy drinking significantly increases
the risk of intracerebral hemorrhage.

Coronary Artery Disease
         There is a decreased risk of cardiovascular morbidity and mortality in men and women consuming mild
to moderate amounts of alcohol. Several prospective studies have confirmed this risk reduction of coronary
artery disease in persons consuming up to moderate amounts of alcohol. The French have a lesser incidence
of coronary artery disease when compared to residents of other countries with similar dietary habits, and this
was termed French paradox. This decreased incidence was thought to be due to the antithrombotic activity and
antioxidants in red wine but later it was reported that when consumed in mild to moderate amounts other
alcoholic beverages also confer protection from coronary artery disease 4. However, many other studies have
suggested that the cardio-protective effects of wine are more as compared to other alcoholic beverages.
Consumption of moderate amounts of alcohol increases the serum concentrations of HDL cholesterol and
apolipoprotein A-I and inhibits aggregation of platelets apart from causing an improved fibrinolysis.
         Consumption of alcohol in moderate amounts also decreases the incidence of sudden cardiac death.
In the Physicians Health Study, the persons who consumed two to four or five to six drinks per week had a
significantly reduced risk of sudden death as compared to those who rarely or never drank. Subsequent
mortality is reduced in survivors of myocardial infarction, who consume moderate amounts of alcohol5.

         An increased incidence of atherosclerotic coronary artery disease has been reported in persons
consuming heavy amounts of alcohol. There is also an increase in cardiovascular morbidity and mortality with
heavy alcohol use. Consumption of such heavy amounts of alcohol causes systemic arterial hypertension and

Moderate Drinking- What is that amount?
        No precise definition of moderate drinking exists and the criteria used in various prospective and
retrospective studies vary. Moderate drinking has been defined by the US Dietary Guidelines Advisory
Committee on the Dietary Guidelines for Americans as no more than two drinks per day for men and no more
than one drink per day for women. The Royal College of Physicians, Psychiatrists, and General Practitioners
advised a sensible limit of alcohol intake of 21 units per week for men and 14 units for women.

         Several large prospective and retrospective studies have examined the effects of alcohol on the
cardiovascular system. Consumption of moderate amounts of alcohol protects from coronary artery disease
while consumption of heavy amounts increases the incidence. Alcohol consumption causes hypertension and
also increases the incidence of hemorrhagic stroke independent of the effect of hypertension. Long term
alcohol use is associated with the development of alcoholic cardiomyopathy.

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3.     Klatsky AL: Alcohol and cardiovascular disease - more than one paradox to consider. Alcohol and
       hypertension: Does it matter? Yes. J Cardiovasc Risk 10:21,2003.
4.     Mukamal KJ, Conigrave KM, Mittleman MA: Roles of drinking pattern and type of alcohol consumed in
       coronary artery disease in men. N Eng J Med 348:109, 2003.
5.     Mukamal KJ, Maclure M, Muller JE. Prior alcohol consumption and mortality following acute myovardial
       infarction. JAMA 285:1965, 2001