Alcohol, Chemistry and
In order to understand how alcohol may help or hinder the functioning of the cardiovascular systems, one needs to think about the components of the system and how they work. Simply the heart, a big muscle, is connected to a series of tubes, the arteries and the veins, which carry blood to the various parts of the body. Arteries carry the blood away from the heart, while veins bring blood back to the heart. The arteries are connected to the veins via very small vessels called capillaries. Electrical and chemical signals to the heart cause it to pump the blood into the arteries. Further, a number factors can cause the blood vessels to expand (dilate) or contract. In doing so they can increase or decrease the amount of effort the heart needs to put forth to deliver the blood. With these ideas in mind, then it is clear that substances such as ethanol and other factors can either make the system work better or hinder its function. As examples, factors, which make the heart work harder such as restricted or clogged arteries, veins, or capillaries, can eventually cause damage to the heart. Also, the influence of alcohol on chemical and electrical signals with regulate heart function, can modify the efficacy and efficiency of heart action. In both cases, if blood flow is restricted then other organs can also be damaged due to lack of nutrients or oxygen.
How does ethanol help or hinder cardiovascular function? One possible mechanism by which ethanol may modify cardiovascular function is by the modulation of blood concentrations of high density (HDL) and low density (LDL) lipoproteins (complexes of fat molecules and proteins). Of the various types of lipoproteins circulating in the body, two seem most relevant with respect to the development of arterial plaque deposits (fatty deposits on the artery walls, atherogenesis). The plaque deposits in turn led to degenerative changes in the walls and hardening of the arteries (atherosclerosis). The current belief is that high levels of HDL and low levels of LDL are desirable. A ratio of LDL to HDL of 2.5:1 to 4.5:1 is best. Low or moderate consumption of ethanol helps to maintain the optimal concentrations of these lipoproteins, thus diminishing the chances of arterial plaque formation and coronary artery disease (CAD).
A second possible mechanism for ethanols effects involves modulation of cellular signaling with the inner lining (endothelium) of blood vessels. Cells in the endothelium send out chemical signals in response to fatty deposits in the arteries. These chemical signals trigger an inflammatory response. Through a sequence of events a blood clot may form at the site of the inflammatory response. The blood clot is potentially dangerous for two reasons. First, it restricts blood flow and second, it can come loose and lodge elsewhere in the circulatory system. An interruption of the blood supply could produce a heart attack (i.e. myocardial infarction). Impairing of the blood supply to the brain could cause a stroke. Therefore, any factor that can reduce this sequence of events has the potential to diminish the deleterious effects. Moderate alcohol consumption seems to serve this function by reducing plaque formation, inhibiting clot formation, and promoting blood clot dissolution.
The cardiovascular consequences of heavy ethanol consumption are several. If ethanol exposure occurs prenatally at a period when the heart of the infant is developing, then structural damage is observed and manifests as diminished capacity of the heart to function properly. If the cardiovascular system is exposed to excessive ethanol later in life, then a variety of problems can manifest, most prominently are cardiomyopathy, hypertension, stroke and cardiac arrhythmias.
Cardiomyopathy refers to a dysfunction of the heart muscle. Heavy ethanol consumption leads to dilated cardiomyopathy, which refers to low cardiac output and enlargement of the heart and its chambers.
. This condition (alcoholic cardiomyopathy) eventually leads to congestive heart failure and accounts for 20 to 50% of all cases of cardiomyopathy in the Western countries. Interestingly, although this condition is more prominent in men than in women, women are actually more susceptible to alcohol-induced cardomyopathy than men (Urbano-Marquez et al, 1995).
There appear to be several mechanisms by which ethanol can lead to cardiomyopathy. These include the following:
The relationship between hypertension (increased blood pressure) and chronic alcohol consumption appears solid and to be independent of the usual factors of obesity and smoking (Beilin and Puddey, 1992; Klatsky, 1995; and Camagro and Rimm, 1996). This association has been observed in white, black, and Asian men and women (Klatsky, 1995) suggesting that it is not unique to a specific group. Again women may be different than men in their susceptibility.
Several mechanisms have been suggested to account for the relationship of heavy ethanol consumption and hypertension. A general mechanism that proposed is that ethanol activates the sympathetic nervous system which among other things constricts blood vessels and increases the contractile force of the heart (Russ et al, 1991). In addition, other hypotheses center around the impact of ethanol on several chemicals e.g. the catecholamines, epinephrine and norepinephrine, and magnesium and calcium ions, which play an important role in cardiac function and vascular tone, respectively. Finally, it has been suggested that the baroreceptors in the walls of the arteries may be reduced in sensitivity due to ethanol consumption, thus diminishing their role in the regulation of arterial contraction and relaxation (El-Mas and Abdel-Rahman, 1993).
The relationship of ethanol consumption and stroke is like a two edged sword. On the one hand it seems as mentioned above that a moderate amount of ethanol consumption may reduce plaque and clot formation as well as dissolve the clots, both of which are good. However, clots that become loose due to drinking can lodge elsewhere to restrict blood flow to the brain (ischemic stroke). Ethanols relationship to ischemic stroke can involve CAD, hypertension, heart rhythm disturbances, and cardiomyopathy. In addition to ischemic strokes, clots may fail to form after chronic and/or heavy ethanol consumption and result in hemorrhagic stroke (interruption of blood flow due to bleeding). Thus, it appears that ethanol consumption can be both good and bad, particularly with respect to stroke. It cautions one to err on the side of moderation in ethanol consumption.
Cardiac arrhythmias refer to an alteration in the rhythm of the heartbeat. Such alterations lead to fluctuations in the supply of blood to the body and brain, thus potentially affecting the function of these organs. Cardiac arrhythmias have been observed after both acute intake of large amounts of ethanol and after chronic alcohol consumption. For example, ethanol intake over a long weekend may result in electrophysiological anomalies referred to as "holiday heart syndrome", whereas sudden cardiac death has been associated with alcoholism (Zakhari, 1997). A number of hypotheses have been advanced to explain the disturbances in cardiac rhythms. These include scaring of the heart muscle, alterations in the chemicals, which influence heart function such as electrolytes and catecholamines, and alterations in the amount of oxygen coming to the heart.
In summary, ethanol consumption can be both beneficial and harmful. The precise outcome for any one individual is hard to predict, nevertheless as a general guide one can use the information in the Table below.
TABLE: EFFECTS OF MODERATE AND HEAVY DRINKING
Beilin, L.J. and Puddey, I.B. (1992) Alcohol and hypertension. Clinical and Experimental Hypertension Theory and Practice A14 (1&2:119 138.
Camargo, C.A. Jr. and Rimm, E.B. (1996) Epidemiological research on moderate alcohol consumption and blood pressure. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 31. NIH Pub. No. 96-4133, Bethesda, MD. National Institutes of Health. PP. 25 62.
El-Mas, M.M. and Abdel-Rahman, A.A. (1993) Direct evidence for selective involvement of aortic baroreceptors in ethanol-induced impairment of baroreflex control of heart rate. Journal of Pharmacology and Experimental Therapeutics 264(3):1198 1205.
Klatsky, A. B. (1995) Blood pressure and alcohol intake. In: Laragh, J.H. and Brenner, B.M. eds. Hypertension: Pathophysiology, Diagnosis, and Management, 2nd ed. New York: Raven Press, pp. 2649 2667.
Paice, A.G., Hesketh, J.E., Richardson, P.J., and Preedy, V.R. (1996) The effect of starvation and ethanol on c-myc messenger RNA expression in the heart. Biochemical Society Transactions 24(2):212S.
Preedy, V.R., Paice, A.G., Patel, V.P., Why, H., and Richardson, P.J. (1996) Alcohol and heart proteins. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 31. NIH Pub. No. 96-4133, Bethesda, MD. National Institutes of Health. pp. 341 355.
Russ, R. Abdel-Rahman, A. -R.A., and Wooles, W.R. (1991) Role of the sympathetic nervous system in ethanol-induced hypertension in rats. Alcohol 8(4):301-307.
Thomas, A.P., Rozanski, D.J., Nocolas, J.M., and Renard-Rooney, D.C. (1996) Alcohol and myocardial contractility. In: Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 31. NIH Pub. No. 96-4133, Bethesda, MD. National Institutes of Health. pp. 317 340.
Urbano-Marquez, A. , Estruch, R. , Fernandez-Sola, J., Nicolas, J.M., Pare, J.C., and Rubin, E. (1995) The greater risk of alcoholic cardiomyopathy and myopathy in women compared with men. Journal of the American Medical Association, 274(2):149 154.
Zakhari, S., and Wassef, M., eds. Alcohol and the Cardiovascular System. National Institute on Alcohol Abuse and Alcoholism Research Monograph No. 31. NIH Pub. No. 96-4133, Bethesda, MD. National Institutes of Health, 1996.