Excessive, long-term alcohol consumption leads to functional and structural changes in the myocardium. These changes include myocyte death, intracellular dysfunction and the deterioration of mitochondrial structure and sarcoplasmatic reticulum [10]. Also, it has been shown that the cardiac myofibril shortening, the composition of contractile proteins and calcium homeostasis were disturbed by chronic alcohol use [11]. These pathological changes may lead to alcoholic cardiomyopathy.
The main purpose of the study was to demonstrate early systolic abnormalities of the left and the right ventricle among the chronic alcoholic patients.
It was already shown that despite the normal LVEF, the subclinical systolic LV dysfunction measured by 2DSTE can occur among the alcoholics [4]. Chronic alcohol abuse leads also to the deterioration of the RV function [12].
Abstaining from alcohol can lead to the improvement of myocyte function and the increase in ejection fraction of the left ventricle [6,13]. 2DSTE can show subtle subclinical cardiac changes despite preserved ejection fraction [14,15,16,17,18,19]. In the presented study global longitudinal strain of left ventricle was also significantly lower comparing to the control group and reference values despite normal ejection fraction of the LV.
In several studies the correlation between alcohol consumption and LV function was analysed, but the results were conflicting and inconsistent [4,20].
In previously published observations it was shown that consuming more than 90 g of alcohol/day for more than 5 years can cause detectable changes in the cardiac structure [21,22,23]. It has been supposed that the duration of alcohol consumption is more important than the quantity of the daily alcohol consumption in developing heart failure [24,25].
A small study showed no difference in the LV size and function in two alcoholic groups: drinking more and less than 125 mL/day [26]. Kupari and al. published that diastolic dysfunction is an early abnormality in asymptomatic alcoholics with median 11 years duration of alcohol abuse, but found no relation between quantity and duration of the alcohol consumption and echocardiographic parameters describing the LV function [27]. Likewise, Silberbauer et al. found no correlation between the LV diastolic dysfunction and the duration and amount of chronic alcohol intake [16]. Cerqueira et al. showed no differences in the LV diastolic dysfunction and chronic alcohol abuse, but in another study Fernandez-Sola et al. found a strong correlation between alcohol consumption and the decrease of the E/A index in dose-dependent manner [18,28]. In the presented study no significant correlation was found between diastolic dysfunction and amount and time of alcohol abuse.
Lazarevic et al. compared three group of alcoholics based on the duration of alcohol abuse and found that asymptomatic alcoholics had slightly dilated ventricles with a normal LVEF, but the duration of alcohol dependency was not correlated with the LV diameters, volume or function [29]. Urban et al. proved that the total lifetime dose of alcohol (20 kg/body weight) was correlated with increased LV mass and a decreased LVEF [30]. Kalayci et al. found in a small study that lower GLS correlates with the total lifetime of alcohol intake [31].
In our study we found that LV GLS was significantly lower in the study group than in the control group. Reduction of LV GLS was correlated with amount of used alcohol in dose-dependent manner, patients drinking more than 5 drinks daily had significantly lower LV GLS than patients using less than 5 drinks daily. It was also showed, that heavy alcohol abuse (duration of drinking binges more than 5 years) leads to greater impairment of LV GLS than moderate drinking (duration of drinking binges from 1 to 5 years).
Chronic alcohol consumption can lead not only to deterioration of the LV function, but also it can cause functional abnormalities of the RV; significant reduction of the RV global longitudinal strain was observed among chronic asymptomatic alcoholics. In the presented study we observed, that RV GLS was significantly lower in the heavy drinkers comparing to moderate drinkers. Lower RV GLS value was reduced in dose dependent manner, in patients drinking more than 5 drinks daily RV dysfunction was more marked than in moderate drinkers (1-5 drinks daily).
Light to moderate chronic alcohol consumption can cause subtle LA functional abnormalities comparing to nondrinkers and may predispose to incident AF [32]. There is no published data concerning the RA dysfunction in chronic alcoholic patients so far. In the study global strain of the left atrium and the right atrium were significantly decreased in the active group comparing to the controls. Likewise LV and RV GLS, global longitudinal strain of both atria was correlated with amount of alcohol used daily and time of alcohol binges.