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18CARDIAC ARRHYTHMIAS AND CARDIOHEMODYNAMIC DISORDERS IN PATIENTS VIRAL CIRRHOSIS OF THE LIVER
Munira Alisherovna Khusainova Suvon Totliboyevich Yarmatov
Samarkand State Medical Institute
ABSTRACT
Cirrhosis of the liver (CP) is one of the most pressing medical problems of the last decade [1-6]. This is due to a large increase in viral liver diseases, especially those caused by hepatitis B and C viruses [2]. Cirrhosis of the liver is characterized by hyperdynamic blood circulation, which manifests itself in the form of visceral vasodilation and increased cardiac output [1, 2, 5]. These disorders of systemic circulation, combined with high intrahepatic resistance, contribute to the development and progression of portal hypertension and often represent the main complications of cirrhosis in the form of varicose bleeding and ascites [2, 5]. The possibility of associated specific disorders in the myocardium in cirrhosis of the liver has been recognized relatively recently [1, 2, 4-7]. These disorders include enlargement of the left ventricular cavity associated with its diastolic dysfunction and systolic incompetence during exercise [2, 4-8]. The combination of such disorders is characteristic of the so-called cirrhotic cardiomyopathy [2, 6].
Keywords: Cirrhosis of the liver, portal hypertension, cirrhotic cardiomyopathy, 24-hour ECG
INTRODUCTION
Meanwhile, the syndrome of cirrhotic cardiomyopathy has not yet been definitively classified and many mechanisms of the development of myocardial dysfunction in patients with CP are unknown [2-6]. The absence of these data indicates a lack of awareness of practitioners about changes in the cardiovascular system in patients with cirrhosis of the liver. Early diagnosis and clinical intervention may possibly improve the survival of these patients.
To assess the function of the heart, much attention is currently being paid to the study of myocardial viability as a quantitative measure of the contractility of the heart muscle (mainly local) [6]. Tissue Doppler echocardography is a method that allows us to quantify the rate of convergence of various segments of the myocardium and cardiac structures [9]. It is possible that the use of this more sensitive diagnostic method will make it possible to predict the severity of myocardial dysfunction in patients with viral CP.
To date, a large amount of data has been collected indicating a close relationship between the state of autonomic regulation of heart rhythm and the risk of developing
life-threatening ventricular arrhythmias [10]. It is believed that increased sympathetic activity predisposes to the development of ventricular arrhythmias, while an increase in parasympathetic tone has protective action [10]. A decrease in heart rate variability is associated with sympathetic activation, myocardial hypertrophy, remodeling of the heart cavities, myocardial dysfunction, the occurrence of ventricular arrhythmias, and the development and progression of heart failure [8]. Meanwhile, the information available in the literature about such disorders in patients with CP is contradictory. In this regard, the aim of our study was to study the frequency and nature of cardiac arrhythmias and some cardiohemodynamic parameters in patients with viral cirrhosis of the liver.
MATERIALS AND METHODS
The paper analyzes the results of a survey of 45 patients (51% men, 49% women) with viral cirrhosis of the liver of class A, B, C according to the Child-Pugh criteria, who were treated in the city infectious diseases hospital of Chita. The average age of the patients was 40.2 (34; 44) years, the duration of the disease was 3.7 (2.6; 6.7) years. The diagnosis of CP was confirmed morphologically (laparoscopy with targeted biopsy) in 4 patients, in the remaining patients it was made on the basis of clinical, laboratory and instrumental data. The viral genesis of liver damage was confirmed by the presence of markers of viral hepatitis B in the blood serum (HBsAg, antibodies of classes M and G to HbcorAg, HBV DNA, C (Antibodies of classes M and G to HCV, HCV RNA). Depending on the presence of ascites, patients were divided into 2 groups: 23 (52%) patients had no ascites (group 1), 22 (48%) patients were diagnosed with ascites of varying severity (group 2), the control group consisted of 11 healthy volunteers of the appropriate age without signs of liver pathology. The study did not include: patients older than 52 years with essential and symptomatic arterial hypertension, heart and lung diseases, chronic alcoholism and severe concomitant pathology. There were no pronounced signs of heart failure in the groups of examined patients.
Standard and tissue myocardial Doppler echocardiography was performed according to the standard method with the determination of a complex of generally accepted morphofunctional parameters in the patient's position on the left side. Tissue Doppler echocardiography was performed from apical access at the level of two or four chambers, and the Doppler spectrum was recorded from the fibrous ring of the mitral, tricuspid valves and ventricular segments, calculated systolic and diastolic indices according to six dimensions: the maximum speed of the first positive peak (Sm1), reflecting isovolumetric systolic strain, the second peak (Sm2) actually systolic contraction of the myocardium, the maximum speed of the first negative peak is Eaten, the maximum speed of the second negative peak Am, attitudes Eat/Am, the time before the reduction in myocardial Ivs, relaxation time Ivr. Holter ECG monitoring was performed using the Astrocard complex. HRV was studied on the basis of statistical
analysis obtained during Holter monitoring of a 24-hour ECG recording with the calculation of the following indicators: 1) time □ the average heart rate in 1 min, the standard deviation from the average duration of the sinus intervals RR (SDNN), the average standard deviation RR of all 5-minute fragments of the recording (SDANN), the average standard deviation RR deviations from the mean values of the duration of the RR intervals in all 5-minute segments of ECG (SDNN index), average quadratic deviation of the average of the sum of squared differences between the duration of adjacent RR intervals (RMSSD), percentage of successive RR intervals differing more than 50 MS (pNN50); 2) in the spectrum obtained by fast Fourier transform, the power spectrum of HRV in the high frequency range (0,15-0,40 Hz) □ HF spectral power of HRV in the low frequency range (0.04 to 0.15 Hz) □ LF, relationships LF/HF.
The variance of the QT interval was calculated as the difference between the mean maximum and minimum value of the QT interval in six precordial ECG leads. To correct the variance of the QT interval depending on the heart rate (variance of the corrected QTc interval), a modified H. Bazett formula was used: where dQTc is the variance of the corrected QT interval; dQT is the variance of the QT interval; RR is the duration of the cardiac cycle. The coefficient of variation of the QT interval (QTvar) was calculated using the formula: QTvar = (QTc) / (QT cp) x 100%, where QTsp is the average value of the QT interval.
Statistical data processing was carried out using the statistical software package Statistica 6.0. The distribution of almost all variation series did not comply with the criteria of normality, so the analysis used methods of non-parametric statistics. The nonparametric Mann-Whitney test was used to assess the difference between the groups. The correlation analysis was performed using Spearman's rank correlation coefficient.
RESULTS
According to the XM ECG data, ventricular extrasystoles of various grades □ from I to IV B class according to the Laun-Wolf classification-were detected in 5 (22%) patients of group 1 and 7 (32%) patients of group 2. When comparing the corrected QT interval in patients with viral cirrhosis of the liver, its lengthening was noted: for example, this indicator in patients of the 1st group was 457.9[441;468], in the 2nd group-478[433;501], in the control group-427.9[405;438], p<0.001. Supraventricular arrhythmias were represented by supraventricular extrasystoles in 9 (39.1%) patients of group 1 and in 11 (50%)-group 2; paroxysmal atrial fibrillation □ in 1 (4.3%) patients and in 4 (18.1%), respectively. Given that the size of the left atrium plays an important role in the etiology of rhythm disturbances [10], we analyzed the anatomical characteristics of the left atrium (LP), taking into account the values of the body surface (LP/PT, cm/m2). It
was found that the maximum volume of LP was greater in patients with cirrhosis of the liver compared to the control, and in patients with ascites this
violation is more pronounced, (p<0.001). A number of researchers point to the contribution of the left atrium to the diastolic filling of the LV, which is necessary to maintain normal cardiac output [6, 10]. In this study, a decrease in early diastolic flow (Em) of the medial segment of the lateral wall of the left ventricle and the posterior part of the interventricular septum was found in patients of groups 1 and 2 compared to the control (p<0.001). Accordingly, it decreased and passive LP emptying, while active LP emptying increased, and we observed a decrease in the Em/Am ratio of the posterior interventricular septum and an increase in the segmental time of isovolumetric relaxation of the lateral LV wall in patients of both groups compared to healthy individuals, with the presence of ascites was accompanied by more pronounced changes in left ventricular diastolic function (p<0.001).
The established changes suggest a violation of the □ sucking " action of the left ventricle and a decrease in the function of the left atrium, which increases in the presence of ascites, which probably occurs as a result of chronic pressure overload of the myocardium.
In addition, the peak systolic velocity (Sm) of the lateral wall (segments 3, 9) decreased in patients with ascites: it was lower by 23% and 25%, respectively, compared to group 1, p<0.001. It is likely that the global longitudinal systolic function of the LV in patients with ascites, in contrast to patients without ascites, was reduced. The index of myocardial performance of the Tem at the level of the tricuspid ring also increased in patients with ascites, which characterizes a decrease in the global function of the pancreas in comparison with the control and patients without ascites, (p<0,001). Taking into account the fact that an important pathogenetic mechanism in the development of rhythm disorders in various diseases of the cardiovascular system is a powerful activation of the sympathoadrenal system and taking into account fluctuations in the average daily heart rate in patients with viral cirrhosis complicated by ascites (84.3 [81.7;90]) and patients without ascites (73 [65;85]), we studied the main spectral, temporal and geometric indicators of heart rate variability in patients with viral cirrhosis. The SDNN parameters, which reflect the overall tone of the autonomic nervous system in patients with and without ascites, were lower by 45% and 52%, respectively, in comparison with the control. Similar patterns were observed for the SDNN index, and in the 2nd group it was lower by 8% than in the 1st. The SDANN indicator, which characterizes slow changes in HRV, was significantly reduced in both groups compared to healthy individuals. The spectral parameter HF (in groups 1 and 2 by 22% and 29%, respectively), reflecting the effect on the heart function of the vagus nerve, the time index RMSSD (by 66% and 66%, respectively) and PNN50 (by 78% and 81%, respectively), decreased. The LF/HF ratio, which characterizes the balance of influence on the heart of the parasympathetic and sympathetic divisions, was 62% and 10% higher in individuals of the 1st and 2nd groups compared to the control (p<0.001).
Thus, in patients with cirrhosis of the liver, a decrease in heart rate variability with a predominance of sympathetic tone was found, which, ultimately, can lead to electrical instability of the myocardium.
DISCUSSION
The study confirms the data on the presence of myocardial dysfunction in patients with viral cirrhosis of the liver, and the presence of ascites is accompanied by more pronounced disorders of cardiohemodynamics [1-7]. There is a remodeling of the left atrium with the formation of rhythm disturbances, prolongation of the QT interval, violation of LV diastolic function, and a decrease in heart rate variability. In patients with viral cirrhosis of the liver, complicated by ascites, the contractility of the ventricular myocardium decreases. The occurrence of arrhythmias in viral cirrhosis of the liver is probably facilitated by collateral blood circulation, leading to hypervolemia of the small circle with the development of dystrophic changes in the myocardium, leading to the formation of ectopic activity [3].
During the correlation analysis, a significant positive correlation was established between the peak systolic velocity (Sm) of the LV lateral wall, which characterizes the contractility of the LV myocardium, and the studied HRV indicators (r=0.45-0.72; p<0.001), while a significant negative relationship was established with HR (r=-0.52; p<0.001). Consequently, the decrease in global longitudinal LV systolic function was probably accompanied by a decrease in HRV and an increase in heart rate. Significant correlations were found between the final diastolic size of the left atrium, LV CSR, and heart rate variability. Consequently, HRV indicators naturally decreased with an increase in the systolic volume of the left ventricle and the diastolic size of the left atrium.
CONCLUSION
Thus, in patients with liver cirrhosis of viral etiology installed cardiohemodynamics disorders: increased left atrium, arrhythmias, impaired segmental diastolic left ventricular function, and these changes are more pronounced in patients with ascites. The presence of ascites contributes to a decrease in the global longitudinal systolic function of the ventricles.
In patients with viral cirrhosis of the liver, ventricular extrasystoles and supraventricular heart rhythm disorders were detected, which were more often recorded in patients with ascites.
The revealed cardiological disorders and cardiac arrhythmias may contribute to the deterioration of the clinical condition of patients with viral cirrhosis of the liver.
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