Chapter 1 INTRODUCTION Alcohol drinking has been practiced in the majority of human society since early times. Alcohol (ethyl alcohol) is a drug which acts principally as a depressant on central nervous system. Its effects on behavior are well known and regular use gives rise to an increased tolerance, so that the drinker needs to take gradually increasing amounts to obtain the same effect. Chronic excessive alcohol consumption leads to life threatening hazards (Best, 1999). Alcohol related diseases are rising rapidly in Western countries as well as in Asia. According to the World Health Organization (2008), there are about 2 billion people worldwide who consume alcoholic beverages and 76.3 million with diagnosable alcohol related disorders. Alcohol consumption is the leading risk factor for disease burden in developed countries and the third largest risk factor in developing countries (WHO, 2008). Excessive alcohol intake has detrimental effects on the cardiovascular system leading to cardiomyopathy, coronary heart diseases, hypertension and hemorrhagic stroke (Klatsky, Armstrong and Friedman, 1990). As Schuckit (2008) described, alcohol can also damage the liver, pancreas, stomach, intestine and central nervous system. The effects of alcohol on central nervous system are generally proportional to blood ethanol concentration. However, individuals who are habituated to alcohol may have few symptoms, despite massive blood ethanol concentration. Young people who are not accustomed to alcohol may become comatose at more modest blood ethanol concentration (Johnson and Robinson, 1988). Peripheral neuropathy is a common finding in chronic alcoholics. There also is a population having autonomic neuropathy in chronic alcoholics (Duncan et al., 1980). Johnson and Robinson (1988) reported that vagal neuropathy in chronic alcoholics is associated with significantly higher mortality than in general population. They also suggested that the major cause of death in chronic alcoholic is due to cardiovascular diseases. 2
Experience with diabetic population suggests that sudden and unexpected deaths can be expected more frequently in those with autonomic neuropathy (Ewing and Clarke, 1982). Barter and Tanner (1987) stated that autonomic neuropathy in alcoholic population might have similar prognostic significance. Cardiac arrhythmias, silent myocardial infarct, respiratory complications, and unexpected cardiovascular arrest are all known to cause death amongst diabetics with autonomic neuropathy (Niakan et al., 1986). Such complications might also be a significant cause of mortality amongst alcoholics with cardiovascular autonomic neuropathy (CAN) (Villalta et al., 1989). Yu Htwe (1997) studied autonomic neuropathy in patients with alcohol dependence syndrome (ADS). He reported that overall prevalence of autonomic neuropathy was 24% out of 50 patients with ADS and reported that most of the patients with autonomic neuropathy were asymptomatic. Published figures on the frequency of CAN amongst alcoholics vary between 15% and 77% (Weise et al., 1985). Some groups found a CAN in alcoholics with central and /or peripheral neurological diseases secondary to alcoholism (Duncan et al., 1980; Monforte et al., 1995). However, there is documented evidence that even in alcoholics without peripheral neuropathy, there is subclinical disorders in neurocardiac function (Matikainen, Juntunen and Salmi, 1986). Diverging views exist concerning association between the presence of CAN and the patients’ nutritional status or their duration of alcohol consumption (Villalta et al., 1989). Using standardized bedside tests, disruptions in cardiovagal regulation could frequently be shown in chronic alcoholics (Matikainen, Juntunen and Salmi, 1985). However, in some studies, disruptions in sympathetic regulation have also been reported (Chida et al., 1994; Miralles et al., 1995). Agelink et al. (1998) stated that there is dissociated appearance of parasympathetic...
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