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Background: Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease; it is characterized by left ventricular (LV) hypertrophy that cannot be explained by hemodynamic causes. It is believed that sarcomere dysfunction underlies the pathogenesis of this disease, however, only half of patients with the HCM phenotype have mutations in sarcomere-encoding genes. HCM is distinguished by both high genetic and clinical heterogeneity and therefore more studies are seeking to investigate a regulation of gene expression in HCM and how the abnormalities in this process can affect disease phenotype. One of the levels of regulation of gene expression - a post-transcriptional level - is mediated by short non-coding microRNAs that inhibit protein synthesis., Aim: To identify the correlations between levels of circulating microRNAs, previously shown to be associated with HCM, and clinical parameters of HCM patients., Materials and Methods: Correlation analysis of miR-499a-5p, miR-454 and miR-339-5p plasma levels and clinical parameters of 33 HCM patients, examined from 2019 to 2021, has been performed., Results: Variants in HCM-associated genes were found in 49% of patients. There were no clinical differences between genotype-positive and genotype-negative patients. MiR-499a-5p level correlated with LV ejection fraction, miR-454 level - with LV diastolic function parameters and miR-339-5p level - with left atrium dimension., Conclusion: Levels of certain circulating microRNAs correlate with echocardiographic parameters in HCM patients.

Aim      To determine specific clinical characteristics caused by a combination of the rs397516037 pathogenic variant in the myosin-binding protein C (MTBPC3) and the rs749628307 polymorphic variant in the vinculin (VCL) gene in a Russian family of carriers and to evaluate the contribution of the rs749628307 polymorphic variant in the VCL gene to the development of hypertrophic cardiomyopathy (HCMP).Material and methods  The family under study included one healthy person and 3 patients with HCMP. A targeted analysis of proband's exome was performed. A structural alignment for both forms of the VCL protein, the canonical form and the form with p.Arg230His substitution, was performed.Results The pathogenic rs397516037 variant and the potentially pathogenic rs749628307 variant were detected in the proband and several family members. A possibly damaging variant rs749628307 was detected in the proband and several family members evaluated in this study. The structural alignment confirmed that the rs749628307 variant did not alter the protein structure significantly and could not cause an impairment or loss of the protein function.Conclusion      This study demonstrated that apparently the rs749628307 variant in the VCL gene does not affect the protein structure in a pathogenetically significant way, neither does it affect the severity and form of the clinical manifestations of HCMP; therefore, it cannot be considered as pathogenic.

Objective: To analyze the incidence and causes of mitral valve replacement in patients with obstructive hypertrophic cardiomyopathy (HCM)., Material and Methods: There were 172 patients (98 women and 74 men) with obstructive HCM and severe mitral valve insufficiency between November 2017 and May 2023. All patients complained of chronic heart failure NYHA class III. Surgical correction of left ventricular outflow tract (LVOT) obstruction and mitral valve repair with elimination of systolic anterior motion were technically successful in 160 (93.0%) patients., Results: The need for mitral valve replacement was noted in 12 (7.0%) patients. Mean cardiopulmonary bypass time was 83.5±19.2 min (94; 127), aortic cross-clamping - 62.8±14.3 min (70; 102). In 5 cases, primary mitral valve replacement was scheduled due to obvious organic lesion of the mitral valve (tearing of chords, rheumatic lesion with leaflet restriction). In 7 patients, valve replacement was forced after ineffective primary septal myectomy (LVOT pressure gradient, severe mitral insufficiency)., Conclusion: Mitral valve replacement is an involuntary strategy after ineffective myectomy with severe mitral insufficiency and high LVOT pressure gradient.

This article presents a case of diagnosis and treatment of a rare form of left ventricular (LV) hypertrophic cardiomyopathy (HCMP), asymmetric topical HCMP without obstruction of the LV outflow tract, and raises the issue of diagnosis and treatment of rare forms of this disease. In the Federal Center for Cardiovascular Surgery in 2019-2020, 5 cases of asymmetric hypertrophic apical cardiomyopathy were observed and documented with echocardiography (EchoCG), cardiac magnetic resonance imaging (MRI), and Holter ECG monitoring. A 60-year-old female patient underwent a comprehensive evaluation, including physical examination, EchoCG, MRI, Holter ECG monitoring, and coronary angiography. Apical HCMP was detected. The clinical picture was explainable from the perspective of functional and structural alterations in the LV myocardium, where full obstruction of the cardiac apex develops during systole. The small LV cavity is unable to provide effective hemodynamics. Changed small coronary arteries also contribute to this disorder, which, in results, affects myocardial oxygen supply. The administered therapy included antiplatelets, beta-blockers, angiotensin II receptor blockers, diuretics, and ranolazine. The effect of therapy was assessed as positive. Risk of sudden death, according to European Guidelines, 2014 was 0.86 %.

Myocardial bridging is often detected during diagnostic coronary angiography in patients with congenital and acquired heart defects. In most cases, muscle bridging does not require surgical treatment. Myocardial bridging and tunnels causing compression of one or more major coronary arteries is a potential cause of myocardial ischemia in patients with hypertrophic cardiomyopathy. The authors report surgical treatment of a patient with obstructive hypertrophic cardiomyopathy and myocardial bridging of the left anterior descending artery.

Aim      To evaluate the structural and functional condition of the vasculature using fingertip photoplethysmography and computerized videocapillaroscopy in patients with hypertrophic cardiomyopathy (HCMP).Material and methods  The study included patients with HCMP (n=48; 28 (57 %) men; age, 54.3±13.6 years) and healthy volunteers (control group, n=33, 15 (45 %) men; age, 58.2±8.8 years). Standard laboratory and instrumental examination (blood count and biochemistry, electrocardiography, echocardiography, Holter electrocardiogram monitoring) were performed for all HCMP patients. The condition of vascular wall at various levels of the vasculature was evaluated by fingertip photoplethysmography (apparatus Angioscan-01) and computerized nail-fold videocapillaroscopy (apparatus Capillaroscan-01). The photoplethysmography study analyzed structural parameters, including the arterial wall stiffness index (aSI) of large blood vessels and the resistance index (RI) of small muscular arteries. Endothelial dysfunction was evaluated by the occlusion index (OI) and phase shift (PS). The capillaroscopy study assessed structural parameters, including the resting capillary density (rCD) and the capillary density following venous occlusion (voCD), and functional parameters, including the percentage of perfused capillaries (PPC), the percentage of restored capillaries (PRC), and the capillary density after the reactive hyperemia test (rhCD).Results The study showed increases in aSI (8.8 [6.8; 12.2] and RI (32.5 [17.4; 47.9] in the HCMP group. The OI was significantly lower in the HCMP group (1.3 [1.1; 1.5]) than in the control group (1.8 [1.5; 2.7], р<0.001). Also, PS values were significantly decreased in the HCMP group (4.4 [2.3; 8.6]) compared to the control group (8.4 [5.1; 12.1]. p=0.018). Disorders of structural and functional capillary indexes were observed in HCMP patients compared to the control group; rCD and voCD were decreased in the HCMP group (60 [52.6; 68] and 88 [75; 90], respectively) compared to the control group (75.8 [60; 87] and 90 [73; 101]), however, no intergroup difference reached a statistical significance. The rhCD, PPC, and PRC values were decreased in the HCMP group (66.3 [55; 72], 86.7 [70.9; 104.2] and 1.7 [-6.95; 20.3], respectively) compared to the control group (86 [68.6; 100], 103 [96; 114] and 18.4 [8.1; 27.4], respectively); PPC and PRC values were significantly different (р<0.005 and p<0.004, respectively).Conclusion      In patients with HCMP, fingertip photoplethysmography and computerized videocapillaroscopy showed increased wall stiffness in both large blood vessels and microvasculature, pronounced endothelial dysfunction, and decreases in capillary density and percentage of restored capillaries following respective tests.

The authors report the diagnosis and surgical treatment of 5 patients with dilated phase of hypertrophic cardiomyopathy (HCM). Features of these patients are progressive heart failure, double-level blood flow obstruction and the risk of apical aneurysms. Reconstructive remodeling surgery is a reasonable alternative to heart transplantation despite the existing risk.

Hypertrophic cardiomyopathy (HCM) is a hereditary myocardial disease characterized by ventricular wall and interventricular septum thickening not associated with heart valve disease or any other external cause. Considering different localization of left ventricular obstruction, surgeons should be aware of various surgical approaches to various segments of interventricular septum. A personalized approach to each patient is essential to achieve favorable postoperative effect with minimal incidence of complications. This review is devoted to various surgical approaches to interventricular septum for different phenotypic variants of HCM.

Aim      To evaluate results of myomectomy by intraventricular pressure gradients (IVPG) and blood flows in patients with obstructive hypertrophic cardiomyopathy (OHCMP).Material and methods  The study included a total of 76 subjects, 42 patients with OHCMP (mean age, 39±7 years) and 34 healthy volunteers (mean age, 41±3 years). Prior to and after myomectomy, transthoracic echocardiography was performed and followed by digital image processing and calculation of IVPG and left ventricular (LV) vortex flows. Vector analysis was used to estimate the myocardial displacement rate (V), vortex flows, and LV apex-to-base pressure gradients.Results The study showed a dynamic decrease in the LV apex-to-outflow IVPG by more than 50% and recovery of myocardial contraction velocity in the septal area (р<0.001). The decrease in LV cavity pressure gradient serves as an index for evaluating the effectiveness of OHCMP correction. Myomectomy reduces the load on the myocardium and abolishes mitral valve regurgitation with improvement of LV blood flows as also evidenced by the dynamics of long axis velocity change during the cardiac cycle (dL / dt) and the myocardial contraction velocity (V).Conclusion      Effectiveness of the surgical correction of OHCMP is based on the dynamics of myocardial contraction velocities, vortex blood flows, and a decrease in LV apex-to-base IVPG.

Hypertrophic cardiomyopathy is the most common inherited heart disorder with high clinical heterogeneity. Every fifth patient is older than 60 years at first diagnosis. This review discusses the possible causes for the late onset of hypertrophic cardiomyopathy, the diagnostic and treatment approaches in the elderly.

Authors present is comprehensive clinical and instrumental evaluation of patients with HCM with myocardial ischemia. 104 patients (38.4% of men) with HCM were examined, mean age 58.2±14.7. The examination included risk factors assessment for CAD, ECG, Echo, stress ECG test, 24-hour ECG monitoring. In the presence of myocardial ischemia, CAG (n=66) and MSCT of the coronary arteries (CA) (n=4) were performed. All patients were split up on 2 groups: I - 70 HCM patients with myocardial ischemia, 67.3%, and II (the control group) - 34 HCM patients without myocardial ischemia, 32.7%. The group I was divided on 2 subgroups: 1 - 29 patients with coronary atherosclerosis (41.4%), 2 - 41 patient without coronary atherosclerosis (58.6%). Age (p=0.046), family history (p=0.037), higher systolic and diastolic arterial pressure, long-term arterial hypertension (p<0.05) were determined as significant risk factors for CAD. Smaller diameter of LAD (p=0.008), higher LV mass index, greater LV diastolic function disorder (p<0.05) were detected in group 2 compared to group II. The decrease in myocardial perfusion (MBG scale) was associated with high LV mass index and cardiac arrhythmias. The frequency of concomitant coronary atherosclerosis among HCM patients with myocardial ischemia was determined as 41.4%. Analysis of traditional risk factors for CAD in patients with HCM revealed the strong relation to age, aggravated by a family history of CAD, blood pressure level and duration of hypertension. Smaller diameter of LAD, higher LV mass index, greater LV diastolic function disorder were observed in HCM patients with myocardial ischemia without CAD.

Aim: to determine the diameter and length of cardiomyocytes (CMC) in the ventricular septum (VS) of patients with hypertrophic cardiomyopathy (HCM) and to analyze correlations of a change in CMC sizes with the anatomical features of the heart in the patients., Material and Methods: Longitudinal sections of intraoperative myocardial biopsy specimens taken from 23 patients aged 15-59 years with HCM were treated using immunohistochemical detection of connexin 43; the sizes of 50 CMCs were measured; a 4-point scale was used to assess the degree of myofibril loss (MFL) in these cells. The change in the diameter and length of the cells during their rearrangement as MFL gradually increased, as well as the correlations of CMC sizes with the anatomical parameters of the heart were analyzed., Results: VS CMCs from the patients with HCM were hypertrophic and were in the early stages of rearrangement accompanied by MFL. During this rearrangement, CMCs in some patients grew in length and, less frequently, diameter. The average diameter of CMCs was directly correlated with VS thickness. The average length of the cells in the CMC population with a considerable degree of MFL also directly correlated with VS thickness., Conclusion: The findings could suggest that the factor raising VS thickness in HCM may be an increase in not only diameter of CMCs, but also in length of CMCs, which had impaired orientation in the VS - which are oriented perpendicular to their normal tangential position. The presence of such CMCs in the VS myocardium in patients with HCM can be discussed due to the typical large number of myocardial areas with the impaired parallel arrangement of CMCs.

This review presents modern data about a hereditary disease of myocardium - hypertrophic cardiomyopathy. The main features of its epidemiology, pathophysiological changes in intracardiac hemodynamics, formation of main clinical symptoms of the disease and variants of its clinical course are considered in terms of modern concepts. Much attention is given to characteristics of the variants of the disease and understanding of the formation of its clinical picture of each of them for the choice of the strategy for the management of these patients.

Prognosis of patients with hypertrophic cardiomyopathy (HCMP) to a great extent is determined by clinical variant of the disease. As the system of matrix metalloproteinases (MMPs) plays an important role in development and progression of the processes of fibroformation and tissue remodeling polymorphisms of modifier genes regulating its components can influence clinical course of HCMP. Among possible markers of prognostication of the course of cardiovascular diseases the role of MMPs and their tissue inhibitors has been discussed. With the aim of studying effects of MMPs on the course of HCMP we conducted this investigation in which we included 58 patients and a group of healthy volunteers (control group) with comparable sex and age. In all participants (n=112) we determined polymorphism of MMP-3 - rs3025058 and markers of fibroformation (MMP-3, TIMP-1, TIMP-2, and collagen IV). We found that unfavorable allele variant MMP-3 1171 was associated with hypertrophy of interventricular septum. We also established that levels of TIMP-1 in the group of patients with HCMP were significantly lowered in comparison with those in control group. Concentration of marker MMP-3 was elevated in the group of patients with variant "atrial fibrillation" compared with groups of stable course and progressing course. We revealed medium degree reverse correlation between MMP-3 marker and thickness of left ventricular posterior wall and direct correlation of this parameter with coefficient of asymmetry. Polymorphism MMP-3 - 1171 produced an impact on the level of TIMP-1 marker. The data obtained by us confirm effect of the system of MMPs on formation of hypertrophic remodeling of the heart in HCMP.

The problem of the study of hypertrophic cardiomyopathy (HCM) has preserved its actuality because of high prevalence (1:500), risk of sudden cardiac death (SCD) in individuals of young able-bodied age. Subject of great interest appear problems of search for additional clinical, instrumental and genetic markers, environmental factors which are capable to influence formation of a clinical variant of HCM course, risk of SCD, and prognosis of HCM. Important problem requiring further study appears to be molecular genetic characteristic of the disease. Integrated nomenclature of various forms and variants of course of HCM is essential for elaboration of tactics of management of patients and assessment of results of multicenter trials.

Aim: to study microvolt T-wave alternans (mTWA) and heart rate turbulence (HRT) in patients with hypertrophic cardiomyopathy (HCMP)., Material and Methods: We examined 50 patients with HCMP: 15 (28%) with obstructive form, 23 (46%) with major risk factors of sudden cardiac death (SCD), 7 (14%) with left ventricular thickness more or equal 3 cm, 6 (12%) with family history of SCD, 16 (32%) with attacks of nonsustained ventricular tachycardia (NVT), 5 (10%) with episodes of syncope. Control group comparable by age and gender composition comprised 50 persons without cardiovascular diseases. All patients were subjected to 24-hour ECG monitoring with registration of parameters of variability and HRT (turbulence onset [TO], turbulence slope), maximal mTWA values, mTWA at heart rate 100 bpm, mTWA at 05.00 AM (mTWA05:00)., Results: Patients with HCMP compared to controls were characterized by significantly higher values of mTWA05:00 (19 [13;30] and 9 [4;15] mcV, respectively, p<0.001). There was tendency to greater prevalence of pathological HRT values in patients with HCMP compared with healthy subjects (p=0.083). Prevalence of pathological TO values among patients (16%) was significantly higher than among controls (2%), (p<0.05)., Conclusions: Compared to healthy subjects patients with HCMP were characterized by higher mTWA05:00 and higher prevalence of pathological values of TO. mTWA was directly related to numbers of ventricular extrasystoles and NVT attacks. Patients with attacks of NVT compared with those without had lower SDNN pNN50.

Subject of great interest of contemporary scientific community is a search for additional genetic and environmental factors which are capable to influence formation of a clinical variant of the course of hypertrophic cardiomyopathy (HCMP). It has been shown by many works that besides mutations in genes of sarcomere proteins clinical course of HCMP is also affected by modifier genes of the cardiovascular system such as association of polymorphisms RAAS, sympathoadrenal system, NO-synthase, endothelin system, and system of blood coagulation. Attempts have been made to study effects of these polymorphisms on formation of clinical variant of HCMP course and to search for associations with development of unfavorable variants.

We examined 86 patients with various forms and variants of hypertrophic cardiomyopathy (HCM). Examination of 69 patients with nonobstructive form of the disease included echocardiography. The state of left atrium (LA) was studied by measurement of its systolic and diastolic longitudinal and transversal dimensions with calculation of main parameters of contractility. In 60% of patients with HCM including those with nonobstuctive form we found spherical remodeling of LA with lowering of its contractility. Coefficient of remodeling was suggested as ratio of transversal and longitudinal dimensions of its cavity.

"Athletes Heart" (AH) is a complex of structural, electrophysiological, and functional changes - a consequence of physiological adaptation to regular physical exercise. AH is characterized by biventricular hypertrophy of ventricular myocardium at the background of unchanged parameters of systolic and diastolic function and depends on the type of exercise, body dimensions, sex, and genotype. Although degree of hypertrophy in AH in most cases does not exceed generally accepted limits problems of differential diagnostics of AH and other cardiovascular diseases manifesting by myocardial hypertrophy appear to be most actual. Contemporary possibilities of molecular genetic methods for detection of cause of myocardial hypertrophy are described.

Understanding the molecular basis and cell mechanisms, clinical course, and treatment of hypertrophic cardiomyopathy (HCMP) has progressed substantially in the last decade. The majority of genetic mutations associated with HCMP occur in genes encoding sarcomeric proteins, which are expressed only in cardiomyocytes. The spectrum of morphological features of HCMP includes: hypertrophy of myocardium, myocardial disarray, interstitial fibrosis, mitral valve abnormalities, and microvascular remodeling, is indicative of the involvement of other cell lineages. The link between sarcomeric gene defects and these HCM phenotypes remains elusive. Based on novel insights provided by cardiac developmental biology we can create new effective methods of treatment of this complex disease.

Aim of the study was analysis of dependence of clinical picture and degree of severity of left ventricular hypertrophy (LVH) on polymorphism A/C of ATR1 gene in patients with hypertrophic cardiomyopathy (HCMP) and hypertensive disease (HD). With the method of polymerase chain reaction genotyping for polymorphic markers of A/C of ATR1 gene was carried out in 35 patients with HCMP and 33 patients with LVH developed at the background of long lasting HB. In the work we used clinico-instrumental methods of investigation (electrocardiography - ECG, echocardiography). It was revealed as result of the study that in HCMP type AA in comparison with type AC of ATR1 gene was associated with addition of arterial hypertension, presence of left ventricular outflow tract obstruction, greater severity of heart failure. In case of combination of HD with LVH type AA in comparison with types AC and CC of ATR1 gene is associated with more pronounced LVH.

The data concerning the role of the immune and inflammatory reactions activation in formation of dilatational and hypertrophic cardiomyopathy were presented. The dependence of the humoral-inflammatory disbalance progressing on the processes of the apoptosis and inflammatory cytokins level regulation, determining the immune answer disorder degree in relation with cardiomyopathy form, was established.

Aim: To examine correlation between platelet aggregation and the degree of left ventricular hypertrophy (LVH) in patients with hypertrophic cardiomyopathy (HC)., Material and Methods: Routine clinical examination, ECG, echo-CG, measurement of platelet aggregation, routine biochemical blood tests were made in 45 HC males and 15 healthy controls., Results: HC patients were characterized with high induced and spontaneous platelet aggregation which increased with left ventricular myocardial mass. In LVH, platelets were especially sensitive to the aggregation inductor U-46619, thromboxane A2 analogue., Conclusion: It is demonstrated that there is a positive correlation between platelet aggregation and the degree of LVH in HC patients.

Long-term results (up to 3 years) of operative treatment of first patients with complex obstruction of the left ventricle outflow tract (hypertrophic cardiomyopathy--10 patients, congenital subaortic tunnel stenosis--1 patient) with the help of apico-aortic valved conduit are presented. There was no intrahospital lethality. Two patients died in late terms after operation who had been operated upon for the III degree of circulation insufficiency. Complications associated with using the valved conduit were not noted. All the patients operated upon did not need medicamentous therapy (indirect anticoagulants excluded), seven of them had the 1st functional class NYHA by the moment of examination, two had the 2nd functional class. Continuous observations have revealed a marked tendency to normalization of the hemo- and cardiodynamic parameters.

Cine-magnetic resonance (CMR) tomography was assessed for ability to determine cardiac function and structure in patients with hypertrophic cardiomyopathy (HTCM). CMR tomography findings were compared to those of two-dimension and doppler-echocardiography, cardiac catheterization. The trial entered 16 patients with obstructive, 22 patients with nonobstructive HTCM and 14 healthy controls. CMR tomography was performed on a superconducting tomograph (1.5 T) in synchronism with ECG. CMR tomography helped detect obstruction for the blood outflowing from the left ventricle. This was impossible with the use of spin-echo. It also defined area and volume of low-intensity regions. CMR tomography proved sensitive in bringing out mitral regurgitation, the results being close to those of doppler-echocardiography. Opportunities of MRT in HTCM gets expanded in cine-regimen as it provides additional information on cardiac function and intracardiac hemodynamics.

A total of 55 patients with hypertropic cardiomyopathy (HCMP) with and without circulatory insufficiency were examined at rest and in the restorative period (up to 24 hours) after graded exercise. The serum levels of lactate were measured and the activity of lysosomal enzymes: acid phosphatase, beta-glucosidase and beta-galactosidase were assayed. Healthy untrained donors (n = 21) and athletes (n = 12) with moderately working myocardial hypertrophy, as evidenced by echocardiography served as controls. The patients with HCMP had higher lactate levels and enhanced activity of lysosomal enzymes both at rest and during exercise than the controls. Highest hyperenzymia was found in HCMP patients with circulatory insufficiency and in those without the latter who showed progressive disease even with signs of circulatory insufficiency during 6-9 month follow-ups. In these groups, the patients had the lowest capacity to restore after exercise. It is concluded that the high activity of blood lysosomal enzymes in HCMP patients is a poor predictor.

Cardiodynamics and myocardial contractile reserve were studied in 60 patients with hypertrophic cardiomyopathy by using radionuclide ventriculography at rest and during graded exercise test. All findings that characterize cardiodynamics (normal or higher overall ejection fraction and stroke volume or lower end-systolic volume, higher maximum ejection rate) show the contractility of the left ventricle in patients with hypertrophic cardiomyopathy which can be regarded to be more severe. During graded exercise test, in patients with hypertrophic cardiomyopathy three types of reactions were identified: (1) positive inotropic effect; (2) negative inotropic effect; (3) intermediate (deviation of major cardiodynamic parameters was no more than 20-25% of the baseline levels). Identification of the above types allows one to assess the presence and conditions of myocardial contractile reserve implementation in these patients and to objectivize the choice of corrective drugs.

Region-specific characteristics of hypertrophic cardiomyopathy (HC) and dilated cardiomyopathy (DC) were compared for 108 relevant patients living in Dubai (United Arab Emirates) and Moscow (Russia). Out of 49 citizens of Dubai 17 had HC, 32 DC, and 59 Moscow patients had HC in 23, DC in 36 cases. It was found that HC in Dubai tends to run a silent latent course, involving mainly basal septum and right ventricle. Apical lesions were more typical for Moscow citizens who also display more severe myocardial impairment. DC in Dubai produces weaker cardiac insufficiency and arrhythmia. Incidence of idiopathic and periportal DC proved higher in Dubai, while alcohol and virus infection underlie DC more frequently in Moscow.

The frequency correlation electrocardiogram (FCECG) was recorded in 27 patients with arterial hypertension (AH) and left ventricular hypertrophy (LVH), 8 patients with hypertrophic cardiomyopathy, 22 patients with coronary heart disease (CHD) and in 10 practically healthy volunteers. V4, V5 and V6 ECG leads were used as channel X, whereas lead II was used as channel Y. Application of V6 lead as channel X turned out most informative. The patients with AH and CHD had pathological indices in channel coherence. The patients with LVH manifested deviations in the spectrum of the amplitudes of lead II. The patients with associated LVH and relative coronary insufficiency demonstrated the unchanged FCECG like the practically healthy persons. In the given case, however, the unchanged FCECG in the above patients reflected the impairment of stimulation spreading in the left ventricular myocardium rather than the lack of its hypertrophy.

An algorithm was proposed to make a differential diagnosis of hypertrophic cardiomyopathy by precordial ECG mapping in 35 leads (PECG-35) of 82 patients with hypertrophic cardiomyopathy and 339 matched patients: those with isolated left and right ventricular hypertrophy, concurrent ventricular hypertrophy, those with coronary heart disease having scars of various sites and having no cicatricial myocardial changes, including those in the presence of left ventricular hypertrophy, as well as 98 healthy individuals. Computer-aided analysis of their mapping was used to calculate the area of Q, R, S, T waves and ST segment and the prolongation of QRS complex. ECG parameters were analyzed by using cluster and dispersion analyses and the kNN method. The cluster analysis of PECG-35 made it possible to divide all the data on hypertrophic cardiomyopathy into 2 groups. For each the complexes of PECG-35 parameters were identified, in whose range the kNN method differentiated hypertrophic cardiomyopathy with a broad spectrum of abnormalities at a high sensitivity of 67-75% and a specificity of 86-90%.

Superficial cardiac ECG mapping was performed to examine 16 patients with acute myocardial infarction and 13 with hypertrophic cardiomyopathy who had electrocardiographic signs of focal myocardial changes (QS complex and/or abnormal Q wave). Deviation of instantaneous ventricular depolarization vectors in the direction opposite the malfunctioning myocardial portion that had partially or completely lost its electric activity was found to underlie the formation of QS complex in patients with acute myocardial infarction. In some patients with hypertrophic cardiomyopathy, an abnormal QS complex is attributed to sharp changes in central and end instantaneous depolarization vector orientation in the direction of the most hypertrophic septal portions, the location of a QS areas corresponding to variants of asymmetric septal hypertrophy.

The author demonstrates a possibility of diagnosing hypertrophic cardiomyopathy (HCMP) at the diagnostic center where the main facilities required for examining cardiological patients are available. Provides the results of examining 23 patients with HCMP (according to sex, age, symptoms, clinical course, localization of myocardial hypertrophy, the presence of obstructive and nonobstructive forms, cases of familial diseases). Describes patients seen for HCMP during 6-10 years, in whom idiopathic hypertrophic subaortic stenosis (IHSS) transformed to symmetric HCMP with hypertrophy of the interventricular septum and free walls of the left and right ventricles associated with changes in the clinical picture of the disease. It is assumed that in some cases, IHSS may be a stage in the development of symmetric HCMP. In the course of the disease, the localization of myocardial hypertrophy, the presence of obstruction and the clinical picture are variable rather than permanent characteristics.