Interaction of chronic cigarette and ethanol use on myocardium

Abstract

Summary:Chronic cigarette use is common in persons who habitually use other cardioactive agents that have been causally associated with heart disease. This study was undertaken to determine if cigarette use intensifies the abnormalities of myocardial function and composition observed in experimental alcoholism over an 18-month period. Young adult male beagles with tracheostomy were divided into four groups. There were 10 controls (group 1); 9 smoked seven cigarettes per day (group 2); 7 were fed ethanol as 20% of calories (group 3), and 6 received both ethanol and cigarettes (group 4). After a period of 18 months, left ventricular function was assessed under anesthesia. Heart rate, left ventricular end-diastolic pressures, and volumes (indicator dilution) did not differ in the four groups. An index of contractility derived by normalizing peak dP/dt for pre-and afterload was reduced significantly below the level of 2.41 f0.7 cm/s in controls to 1.41f0.35 in group 2, 1.19f0.38 in group 3, and 1.28f0.17 in the ethanol cigarette group (each p < 0.002). Arterial pressures were moderately elevated above group 1 in all three experimental groups without evidence of left ventricular hypertrophy. In contrast to smoking, which elicited no abnormalities of myocardial cation composition, ethanol reduced myocardial potassium and sodium in group 3 without a gain of water content. In group 4, no further decline of tissue cations was observed. Thus, cigarette use when combined with ethanol over a relatively long period produced no greater myocardial abnormalities than ethanol alone and may not be essential to the genesis of cardiomyopathy in alcoholics.

Testing Genetic Susceptibility Loci for Alcoholic Heart Muscle Disease

“…Differences in the duration and quantity of drinking may be important but are far from the sole explanation (Kino et al, 1981;Kupari et al, 1991). Poor nutrition, smoking, concomitant infections, and alcohol additives have been raised as possible cofactors, but there is little proof of their role except for the known toxicity of cobalt and arsenic added to beer (Ahmed et al, 1985;Klatsky, 1998;Kupari et al, 1991;Regan, 1984).…”

Testing Genetic Susceptibility Loci for Alcoholic Heart Muscle Disease

“…Differences in the duration and quantity of drinking may be important but are far from the sole explanation (Kino et al, 1981;Kupari et al, 1991). Poor nutrition, smoking, concomitant infections, and alcohol additives have been raised as possible cofactors, but there is little proof of their role except for the known toxicity of cobalt and arsenic added to beer (Ahmed et al, 1985;Klatsky, 1998;Kupari et al, 1991;Regan, 1984).…”