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AIM: A detailed description of immune status abnormalities of adult patients with heart arrhythmia either idiopathic or in combination with primary heart disease such as chronic myocarditis and dilated cardiomyopathy (DCMP). MATERIAL AND METHODS: Eighty two consecutive patients aged 16-57 years admitted to the L.A. Myasnikov Institute of Clinical Cardiology (Moscow) for heart arrhythmia were studied. Among them 35 patients had idiopathic heart arrhythmia (IHA, group 1) with no evidence of any primary heart disease, while other 47 patients (group 2) had heart arrhythmia combined with primary heart disease (chronic myocarditis or DCMP). In group 1 ventricular arrhythmia was recorded in 27 patients (12 cases with ventricular tachyarrhrythmia ?VTA, 15 cases with ventricular extrasystolia- VE). Supraventricular heart arrhythmia was found in 6 patients (3 cases of constantly recurring supraventriccular tachycardia, 2 cases of paroxysmal and 1 with constant atrial fibrillation). The intermittent atrioventricular block of the second-third degree was recorded in 2 patients. The patients of group 2 were divided into subgroups 2a, 2b and 2c. In subgroup 2a (patients with DCMP without signs of heart failure) ventricular arrhythmia was found in 7 patients (VT ? 5, VE ? 2). Supraventricular arrhythmia was recorded in 7 patients 5 of which had constantly recurring supraventricular tachycardia, 1 ? paroxysmal and 1 constant atrial fibrillation. In subgroup 2b (DCMP patients with obvious signs of heart failure) ventricular arrhythmia was recorded in 12 patients, among them 6 had VT and 6 ? VE, 2 ? constant atrial fibrillation). In subgroup 2c (patients with chronic myocarditis) ventricular arrhythmia was in 7 patients (VT ? 5, VE ? 2), constant atrial fibrillation ? in 2, heart conduction abnormalities ? in 3 patients, atrioventricular block of the first or second degree ? in 2, sick sinus syndrome ? in 1. To verify the diagnosis, all the patients have undergone physical examination, blood cell counts and biochemical tests, urine clinical analysis, ECG and ultrasound heart examination as well as 24h ECG monitoring. On demand, bicycle exercise test or treadmill test, coronaroangiography, endomyocardial biopsy and invasive electrophysiological examination were made. RESULTS: Immune status abnormalities found in patients with heart arrhythmia both idiopathic and combined with primary heart diseases such as chronic myocarditis and DCMO correspond to immune defense response during chronic infection. Activation of different anti-infection defense mechanisms was recorded in patients with idiopathic heart rhythm and conductivity abnormalities. Immune deficiency was found in arrhythmia and conductivity abnormalities combined with primary heart diseases (chronic myocarditis or DCMP). A positive correlation exists between the degree of immune defense failure and reduction of myocardial contractility. CONCLUSION: There exists a characteristic pattern of immune status abnormalities in patients with arrhythmia, both idiopathic or combined with primary heart disease (myocarditis, DCMP). The abnormalities depend on severity of arrhythmia, intensity of inflammatory processes in the myocardium and on the degree of left ventricular contractility dysfunction in patients with primary heart diseases.

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In order to assess concentration of C-reactive protein (CRP) and prevalence of autoantibodies against beta(1)-adrenoreceptors (abeta(1)-AR) in patients with cardiac supraventricular arrhythmias we studied 53 patients with arrhythmias and 20 healthy control subjects. Patients with idiopathic arrhythmias (atrial fibrillation or flutter and atrial tachycardia, n=35) comprised group I. Group II was formed of 15 patients with supraventricular arrhythmias and dilated cardiomyopathy (DCM) or chronic myocarditis. Patients of group III (n=23) had supraventricular arrhythmias and arterial hypertension (AH). CRP concentration was determined by recently developed well standardized high sensitivity method. abeta(1)-AR were detected in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of abeta(1)-AR second loop was used as antigen. Patients with supraventricular arrhythmias and DCM or chronic myocarditis had higher median CRP (8.0 mg/1) than patients with idiopathic arrhythmias (0.78 mg/l), with supraventricular arrhythmias and AH (1.57 mg/l), or control group (0.6 mg/l). Groups I, II and III showed similar prevalence of ab1-AR (51.4, 40.0, 52.2%, respectively), that was significantly higher than in control subjects (10%) (p<0.005). These results provide evidence of the possible presence of autoimmune and/or inflammatory processes that may be involved in the genesis of supraventricular arrhythmias.

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The aim of this study was to determine the state of sympathetic innervation in patients with ventricular arrhythmias (VA) using 123I-metaiodobenzylguanidine 123I -MIBG) scintigraphy. Fifty six patients (26 men and 30 women, mean age 37.4+/-11,6) underwent single-photon emission computed tomography (SPECT) imaging and planner scintigraphy after injection of 123I-MIBG (activity 148 MBq). They form three groups. Thirty patients with idiopathic VA (IVA) were included in group I: 14 patients with ventricular extrasystoles (VE) and 16 - with ventricular tachycardias (VT). Group II was formed by 17 patients (with dilated cardiomyopathy, n=7 and chronic myocarditis, n=10), 6 of them had VE and 11 - VT. The control group III was formed by 9 healthy subjects with structurally normal heart without VA. We analyzed early (30 minutes) and delayed (4 hours) images after 123I-MIBG administration. The global sympathetic activity (SA) was assessed by heart/mediastinum ratio and washout rate. Regional SA was assessed by extent and severity of defect. In group I 25 of 30 patients (83.3%) had regional SA abnormalities significantly different from controls (p<0.001). At the same time global uptake of 123I-MIBG in this group was not affected. In group II regional SA abnormalities were revealed in all patients (100%) and global reduction of 123I-MIBG uptake - in 14 patients (82.4%). Regional and global SA abnormalities in group II were different from controls (p<0.0001) and patients with IVA (p<0.001). There was no difference in SA abnormalities between patients with VE and VT. Our results suggest that patients with different VA have abnormalities of sympathetic innervation, including patients with structurally normal heart.

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In order to assess parameters of heart rate variability (HRV) and prevalence of autoantibodies against the beta(1)-adrenoreceptors in patients with cardiac arrhythmias we studied 42 patients with arrhythmias and 20 healthy control subjects. Thirty one patients with idiopathic arrhythmias were included in group I: with paroxysmal atrial fibrillation or flutter (n=13), paroxysmal atrial tachycardia (n=2) and paroxysmal ventricular tachycardia (n=16). Group II was formed of 11 patients with paroxysmal ventricular tachycardia and dilated cardiomyopathy or chronic myocarditis. ab1-AR were determined in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of ab1-AR second loop was used as antigen. Groups I (54.8%) and II (63.6%) showed similar prevalence of ab1-AR, which was significantly higher than in control subjects (10%) (p<0.005). HRV parameters in I group were lower in ab1-AR-positive compared with ab1-AR-negative patients. At the same time HRV parameters in ab1-AR-positive patients were significantly different from those in controls (p<0.05). In group II HRV parameters of ab1-AR-positive and ab1-AR-negative patients were significantly lower than in control subjects (p<0.05). We suppose, that ab1-AR could participate in dysfunction of chronotropic heart regulation and contribute to development of arrhythmias in patients with structurally normal hearts.

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AIM: To assess prevalence of autoantibodies against beta(1)-adrenoreceptors (beta(1)-AR) in patients with arrhythmias of various etiology. MATERIAL: Patients with arrhythmias (n=110, including 59 patients with primary [idiopathic] electrical abnormalities, 33 - with chronic myocarditis and dilated cardiomyopathy [DCM]; 18 - with ischemic heart disease [IHD]) and healthy control subjects (n=20). METHODS: Antibodies against beta(1)-AR were measured in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of beta(1)-AR second loop was used as antigen. RESULTS: Patients with primary electrical abnormalities and chronic myocarditis/DCM had similar prevalence of beta(1)-AR (49.1% and 54.5%, respectively), what was significantly higher than in controls (10%) and in patients with IHD (16.6%). These results provided evidence for the possible presence of an autoimmune process in the genesis of idiopathic arrhythmias. Among patients with idiopathic arrhythmias beta(1)-AR were found in 40% (10 of 25) of patients with ventricular tachycardia (VT), 63.6% (14 of 22) of patients with ventricular extrasystoles (VE), 41.6% (5 of 12) of patients with atrial fibrillation (AF). Among patients with chronic myocarditis and DCM beta(1)-AR were found in 72.2% (13 of 18) of patients with VT, 28.5% (2 of 7) of patients with VE, 37.5% (3 of 8) of patients with AF. Among patients with idiopathic arrhythmias female sex and frequent respiratory viral diseases were more common in beta(1)-AR-positive compared with beta(1)-AR-negative patients. VT and left ventricular ejection fraction <40% were more common in beta(1)-AR-positive than beta(1)-AR-negative patients among those with chronic myocarditis and DCM.

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