ALCOHOL INDUCED ELECTROCARDIOGRAPHIC CHANGES

Abstract

Statistically significant increased incidence of electrocardiographic abnormalities were noted in 70 male patients with alcohol dependence compared to equal number of age and sex matched controls.

Introduction

Despite the evidence that alcohol may protect against ischemic heart disease, death due to cardiovascular disease remains the most important cause of mortality in alcoholics. Alcohol may produce demonstrable cardiac dysfunction even when ingested by normal individuals in quantities consumed in social drinking [1]. Alcoholics without any evidence of heart disease are often seen developing palpitations, chest discomfort and syncope, typically following an alcoholic binge. This is dubbed as the ‘holiday heart syndrome’ [2].

Heart disease related to alcohol may have an arrhythmia as the initial manifestation. Cardiac arrhythmias developing in these circumstances are often considered idiopathic in origin since little or no clinical evidence of heart disease may remain after resolution of the arrhythmia. Electrocardiographic abnormalities are common in alcoholics and are frequently the only indicator of alcoholic heart disease during the asymptomatic phase [3, 4, 5, 6, 7, 8].

There is a paucity of Indian work in this field which prompted us to study the electrocardiographic changes in male patients with alcohol dependence.

Material and Methods

Seventy consecutive male inpatients admitted to the psychiatric centre of a base hospital during Oct 91 to Oct 92 and meeting the DSM III R criteria for alcohol dependence [9] were included in the study with their informed consent. A symptomatic analysis pertinent to the cardiovascular system was carried out. Patients were subjected to an ECG evaluation within first six hours of admission, prior to the administration of any medication. Patients with known cardiorespiratory disease, diabetes and those having clinical, radiological, or echocardiographic evidence of cardiomegaly were excluded from the study. Patients with clinical evidence of jaundice, hepatocellular failure, portal hypertension, dehydration, and obvious malnutrition were also excluded from the study. An equal number of age and sex matched subjects without any physical or psychiatric illness formed the control group and were also subjected to an ECG evaluation. In addition all the patients and control subjects underwent routine hematological and metabolic investigations including serum electrolytes.

All the ECGs were subjected to blind evaluation by one of the authors (PB). The corrected QT (QTc) interval was estimated by Bazett's formula:

$$\text{QTc in}\hspace{0.17em}\text{seconds}=\frac{\text{Q}-\text{T interval in seconds}}{\sqrt{R-R}\text{interval in seconds}}$$

Statistical analyses were carried out using the Chi Square test with Yates correction

Results

The mean age of the patients was 35.6 years with a range of 24 to 54 years. An equal number of age and sex matched controls were also selected. Eighty percent of patients and controls were in the age range of 30–50 years. There was no significant difference with regard to socio-demographic variables in these two groups. Although many of the control subjects consumed alcohol, they were neither problem drinkers nor could be labelled as alcohol dependent.

Electrocardiographic abnormalities (excluding prolonged QTc) were noted in 55 patients and 7 control subjects, the difference being highly statistically significant (X² = 61.07; df = 1; p < 0.01). Analysis of the electrocardiographic abnormalities (Table) showed that the commonest abnormalities were sinus bradycardia and tachycardia which were seen in 9 patients each. However, only sinus tachycardia was observed to occur significantly more often in patients compared to the normal controls. Sinus arrhythmia and atrial premature beats were seen in 2 and 3 patients respectively. Ventricular premature beats (Lown's grading < 3) [10] were noted in 4 patients. Intraventricular conduction disturbances were observed in 8 patients of whom 4 had incomplete bundle branch block with RBB morphology (significantly more than in controls).

TABLE.

Electrocardiographic abnormalities in alcoholics (n=70) and normal controls (n=70).

ECG abnormalities	Alcoholics		Controls		Chi square Value	p value	Significance
	n	%	n	%
Sinus bradycardia	9	12.9	5	7.1	0.71	>0.30	NS
Sinus tachycardia	9	12.9	—	—	9.60	<0.01	S
Sinus arrhythmia	2	2.9	1	1.4	0.00	>0.95	NS
Atrial premature beats	3	4.3	—	—	1.36	>0.24	NS
Ventricular premature beats	4	5.7	—	—	2.32	>0.10	NS
Atrial fibrillation	2	2.9	—	—	0.24	>0.48	NS
Intraventricular conduction defects	8	11.4	1	1.4	4.27	< 0.05	S
ST depression	3	4.3	—	—	1.36	>0.24	NS
T wave inversion	7	10.0	—	—	5.41	<0.05	S
Tall T waves	8	11.4	—	—	6.50	<0.01	S
QTc prolongation
> 0.420 sec	15	21.4	2	2.9	9.64	<0.01	S
> 0.390	40	57.1	21	30.0	9.41	<0.01	S

NS = Not significant, S = Significant

ST-T abnormalities were documented only when they were seen in two or more standard or precordial leads. The ST-T abnormalities that were noticed included depression of ST segment with slow upstroke in 3 patients, T wave inversion in 7 patients and tall T waves seen in 8 patients.

The QTc interval was abnormal in 15 patients and in 2 control subjects keeping a normal upper limit of 0.420 sec. This rose to an alarming 40 patients and 21 control subjects when the limit was reduced to 0.390 sec. At both levels the incidence of QTc prolongation was significantly higher in alcoholic group (Table).

Discussion

The high incidence of ECG abnormalities in alcoholics in the present study is in agreement with earlier studies [2, 3, 4] which reported that conduction defects and rhythm disturbances are frequently seen in chronic alcohol consumers. However, in the present study only intraventricular conduction defects and ST-T abnormalities were significantly high in alcoholics as compared to the normal controls which is in agreement with some of the earlier studies [11, 12]. An interesting observation in this study was the presence of tall T waves in 11.4% of the cases. These have been described as an incidental finding in psychotic patients [13].

Prolongation of QTc in chronic alcoholics has been reported in earlier studies [2, 6, 7, 8], but most of these studies were uncontrolled while two studies [6, 7] included patients with clinically overt cardiomyopathy. These drawbacks were avoided in the present study by including a demographically well matched control group and excluding patients with overt cardiac disease. Prolongation of QTc was noted in 21.4% alcoholics and 2.9% of the control subjects when the upper limit of normal QTc was taken to be 0.420 sec as recommended by Chung [14] but rose to 57% in alcoholics and 30% of controls when the Fisch criteria [15] of 0.390 sec was taken. The finding of QTc prolongation in alcoholics may have important clinical implications. Epidemiological studies have shown an increased incidence of sudden deaths in alcoholics with and without liver disease [16, 17]. A recent study has suggested that the mechanisms of sudden death may be related to a polymorphic ventricular tachycardia [18]. QT prolongation in both congenital and acquired conditions is associated with ventricular tachycardia and sudden death. Mechanisms of arrhythmogenesis have been elucidated, which involve the triggering of arrhythmias by critically timed ventricular premature beats. These mechanisms are based on the hypothesis that QT prolongation reflects increased dispersion of ventricular repolarisation time and provides the substrate for re-entry arrhythmias [19]. An alternative mechanism of arrhythmogenesis associated with QT prolongation is suggested by recent evidence that prolonged repolarisation may support triggered automaticity from early after-depolarisation [20].

Sudden death is an important cause of mortality associated with alcoholism. A recent study [8] established that QT prolongation may predict the risk of sudden death in chronic alcoholics. QT prolongation is a known risk factor for lethal arrhythmias in other circumstances, and may reflect myocardial alterations capable of supporting either re-entry and/or triggered automaticity. Whether QT prolongation can be reversed by abstaining from alcohol, or whether other interventions can reduce risk, is unknown. However, beta-blockers, which favourbly influence prognosis in other congenital and acquired long QT conditions, have been associated with improved survival when given to patients with alcoholic liver disease and portal hypertension. This effect was attributed solely to their ability to reduce portal pressure but an anti-arrhythmic action might also be operative [8].

We conclude from this study that patients with alcohol dependence have significantly higher incidence of electrocardiographic abnormalities even in the absence of cardiomegaly or heart disease. Further studies are needed to determine the significance of these electrocardiographic changes.