[Left ventricular global function index as a predictor of adverse cardiovascular events in patients with acute coronary syndrome].

Aim      To evaluate the prognostic significance of the left ventricular global function index (LV GFI) in patients with acute coronary syndrome (ACS) using echocardiography (EchoCG).Material and methods             The LV GFI is an index that integrates LV cavity volumes, stroke volume, and myocardial volume. This study included 2169 patients with ACS (1340 (61.8%) men) aged 64.1±12.6 years from two observational multicenter studies, ORACLE I and ORACLE II. 1800 (83 %) cases were associated with increased concentrations of myocardial injury markers, including 826 (38.1 %) cases of ST segment elevation myocardial infarction (MI). The observation was started on the 10th day of clinical condition stabilization and lasted for one year. EchoCG was performed with evaluation of LV GFI, which was calculated as a ratio of LV stroke volume to LV global volume. The LV global volume was calculated as a sum of mean LV cavity volume (LV end-diastolic volume + LV end-systolic volume / 2) and LV myocardial volume.Results The main outcome of the study was all-cause death (n=193); recurrent coronary complications (n=253) were analyzed separately. The only EchoCG parameter indicating an adverse outcome during the one-year follow-up was a LV GFI decrease to below 22.6 % with a sensitivity of 72 % and a specificity of 60% (area under the curve, AUC=0.63). A LV GFI <22.6 % was an independent predictor of all-cause death (p=0.019) along with age (p=0.0001), history of MI (p=0.034), and presence of heart failure (HF) (p=0.044), diabetes mellitus (p=0.012), and peripheral atherosclerosis (p=0.001). The LV GFI <22.6 %, (p=0.044), heart rate upon discharge from the hospital (p=0.050), history of MI (p=0.006), presence of HF (p=0.014), and peripheral atherosclerosis (p=0.001) were also independent predictors for recurrent coronary complications. Decreased LV GFI was associated with the risk of fatal outcomes independent of the LV ejection fraction at baseline.Conclusion      In patients with ACS, the left ventricular global function index is an independent predictor for all-cause death and recurrent coronary complications and may be used for risk stratification.

[The Risk of Developing Ischemic Stroke in Patients After Exacerbation of Ischemic Heart Disease].

Aim      To develop a model for evaluating the risk of stroke in patients after exacerbation of ischemic heart disease who were admitted to the hospitals included into a vascular program.Materials and methods This study included 1803 patients with acute coronary syndrome (ACS) from four institutions of Moscow, Kazan, Astrakhan, and Krasnodar where the vascular program was established. Mean age of patients was 64.9±12.78 years, 62,1 % of them were men. The patients were followed up for one year after the discharge from the hospital. External validation of the developed prognostic model was performed on a cohort of patients with ACS included into the RECORD-3 study.Results During the follow-up period, 42 cases of ischemic stroke were observed. The risk of ischemic stroke was associated with the presence of atrial fibrillation (odd ratio (OR) 2.640; р=0.037), diabetes mellitus (OR 2.718; р=0.041), and chronic heart failure (OR 7.049; р=0.011). Protective factors were high-density lipoprotein cholesterol >1 mmol/l (OR 0.629; р=0.041), percutaneous coronary intervention during an index hospitalization (OR 0.412; р=0.042), anticoagulant treatment (OR 0.670; р=0.049), and achieving the blood pressure goal (OR 0.604; р=0.023). The prognostic model developed on the basis of regression analysis showed a good predictive value (area under the ROC curve, 0.780), sensitivity of 80 %, and specificity of 64.6 %. The diagnostic value of other scales for risk assessment was somewhat lower. The area under the ROC curve was 0.692±0.0245 for the GRACE scale and 0.708±0.0334 for CHA2DS2­VASc. In the external validation of the scale based on data of the RECORD-3 study, the diagnostic value was lower although satisfactory as well (area under the ROC curve, 0.651); sensitivity was 78.9 %, and specificity was 52.3 %.Conclusion      The study resulted in development of a simple clinical scale, which will probably allow identifying groups at risk of stroke more precisely than with standard scales.

[Changes in the management of patients with acute coronary syndrome - have the disease outcomes changed?]

Aim        To analyze results of changing the management tactics in patients with acute coronary syndrome (ACS) in clinical practice from 2004 through 2018 expressed as improvement in prognosis.Material and methods        Results of two observational studies were analyzed: ORACLE I (2004-2007), which included 1193 patients with ACS (mean age, 61.1±11.69 years; men, 63.3 %) and ORACLE II (2014-2017), which included 1652 patients from 4 vascular centers (mean age, 64.61±12.67 years; men, 62.3 %).Results   Patients included into the ORACLE II study in 2014 were significantly older and the proportion of patients with diabetes mellitus was greater than in the ORACLE I study (14.7 and 22.6 %, respectively). After matching the groups by major clinical characteristics, it was found that introducing the invasive management tactics for ACS patients was associated with a reduced rate of all-cause death (from 8.2 to 6.1 % for one year), a tendency towards decreased number of coronary death cases (from 5.6 to 4.0 %), and a decrease in risk of recurrent coronary complications (from 17.4  to 7.7 %).Conclusion            Implementing the vascular program statistically significantly decreased the total death rate for at least one-year observation in comparable patient groups.

[External validation of the ORACLE bleeding risk score using the database of the RECORD 3 registry].

AIM: To validate a domestic scale for assessment risk of bleeding ORACUL (ОРАКУЛ) based on an independent sample of patients with acute coronary syndrome (ACS). MATERIALS AND METHODS: External validation of the ORACUL score was carried out using database of an independent observational study RECORD-3 which comprised data from all patients hospitalized for 1 month (march-april 2015) in 47 centers of 37 cities in 21 regions of Russia. Total number of included patients was 2370, mean age 64.2±11.96 years, 821 patients (34.6%) had ST-elevation, other patients - non-ST elevation ACS. RESULTS: The following bleeding events were registered in RECORD-3: bleedings during hospitalization (n=34, 1.43%), inhospital bleedings requiring withdrawal of antithrombotic treatment (n=16, 0.68%), inhospital bleedings, which required drug or surgical treatment or hemotransfusion (n=16, 0.68%). Forty eight hemorrhagic complications were registered during 6 months of observation after hospital discharge. Diagnostic value of the ORACUL score for estimation of risk of bleedings during index hospitalization was good (C-criterion 0.691±0.050; р<0.001), sensitivity of the model was 58.1%, specificity 79.9%. Earlier on the cohort of patients of the ORACUL study diagnostic value of the score for inhospital bleedings was found to be 0.777±0.046. Difference of diagnostic values was inessential. For estimation of the bleeding risk during 6 months of post discharge observation area under the ROC curve (C-criterion) was 0.628±0.045 (р=0.003), sensitivity and specificity of the model were 53.9 and 73.7%, respectively. On the ORACUL study cohort AUC 0.748±0.048 (р=0.071). CONCLUSION: External validation confirmed that statistical power of the OCACUL score is sufficient for prediction of bleedings during both periods of hospitalization and after hospital discharge.

[Risk of Stroke After Exacerbation of Ischemic Heart Disease: Data of 3­Years Follow-up].

PURPOSE: to analyze possible associations of clinical and genetic factors with development of ischemic stroke after exacerbation of ischemic heart disease (IHD). MATERIALS AND METHODS: The Russian multicenter study aimed at assessment of risk of unfavorable outcomes after exacerbation of IHD "Exacerbation of IHD: logical probabilistic ways to course prognostication for optimization of treatment" (meaning of Cyrillic acronym - oracle) was conducted in 16 centers of 7 cities in Russia. We included into the study 1 208 patients with unstable angina and ST-elevation or non-ST-elevation myocardial infarction (MI). Data on outcomes were known for 1 193 patients, 15 patients were lost for follow-up. RESULTS: Mean duration of follow-up was 644±14.45 (4-1 995) days. Shortest, longest, and mean time before development of stroke was 22, 1433 and 389±56.6 days after inclusion. Patients with strokes were older, more often had history of IHD prior to index hospitalization, arterial blood pressure level compatible with stage 3 arterial hypertension, less often were smokers, and more often had MI recurrences or repetitive episodes of severe ischemia during the index hospitalization. Patients also more often had documented atrial fibrillation during hospitalization, and lower level of glomerular filtration rate. Of studied genetic markers carriage of A allele of polymorphic marker G (-1082) A of interleukin-10 gene was significantly associated with risk of stroke development. Using linear regression analysis, we constructed a model of estimation of the stroke development risk. Comparison of diagnostic value of different scales for stroke risk assessment showed that area under the curve was 0.656, 0.686, and 0.756 for the GRACE, CHA2DS2­VASc, and ORACLE scores, respectively.

[Family History of Cardiovascular Disease in Patients With Early Development of Acute Coronary Syndrome].

The aim of the study was to analyze clinical features of patients with premature acute coronary syndrome (ACS) in relation to family history of cardiovascular disease (CVD) and familial hypercholesterolemia (FH). MATERIALS AND METHODS: Of 2832 patients included in ORACUL 1 and ORACUL 2 multicenter observational trials 512 pts who developed premature ACS (≤55 years for men, ≤60 years for women) and had known family history and LDL level were selected for this study. Of these patients 297 had positive family history (51 with FH, 246 no FH), 215 had negative family history. RESULTS: Among patients with positive family history there were more women (31 vs 20.9 %), while among patients with negative family history there were more men (79.1 vs 69 %). The fact of regular alcohol consumption was significantly more frequently observed among patients with positive family history but without FH, compared to patients with positive family history with FH (69.6 vs 47.1 %). Women with positive family history smoked more frequently than females with negative family history (51.1 vs 31.1 %). Among patients with negative family history compared with patients with positive family history there were more people who at admission had hyperglycemia exceeding 11.1 mmol / l (10.3 vs 4.4 %). Multiple vessel disease and coronary calcinosis were present in 73.2 and 24.7 %, respectively, of patients with positive family history, and in 56.9 and 9.8 %, respectively, of those with negative family history. Among patients with positive family history multivessel disease was more frequent in the subgroup with FH, while coronary calcinosis was more frequent in the subgroup without FH. CONCLUSION: Thus, premature development of ACS might be associated not only with genetic factors but also with family history ("inheritance") of adverse habits. Herewith coronary calcinosis is more prevalent in patients with FH.

[Association of parameters of heart rate variability with severity of bronchial obstruction and presence of pulmonary hypertension in patients with chronic obstructive pulmonary disease].

With the aim of assessing parameters of heart rate variability (HRV) and heart rhythm turbulence (HRT) in patients with chronic obstructive pulmonary disease (COPD) in dependence on severity of the course of this disease and presence of pulmonary hypertension (PH) we examined 73 patients (28 with COPD and 45 healthy subjects). Invasive measurement of central hemodynamics was conducted. Compared with the control group in patients with COPD we revealed lowering of temporal as well as frequency HRV parameters. No significant changes of HRV parameters depended on severity of COPD course. However a tendency to maximal lowering of HRV parameters was noted in the group of patients with COPD with first sec forced expiratory volume <50%. Comparison of patients with and without PH with controls revealed tendency to maximal lowering of HRV parameters in the PH group. Thus measurement of HRV can be used for supplementary assessment of severity of the disease and detection of PH.

[Genetic predisposition to development of atrial fibrillation in patients with hypertensive disease].

We studied associations of genes of adrenoreceptor types 1, 2 and 3 (ADRB1, ADRB2, ADRB3), connexin (CX40) and voltage gated potassium channel type 2 (KCNH2) with development of atrial fibrillation (AF) in patients with hypertensive disease. We examined 102 patients with hypertensive disease which in 51 was complicated with AF. The groups were comparable by sex, age, Ketle index, presence of concomitant diseases. We determined alleles and genotypes of polymorphic markers G(-44)A and A71G of CX40 gene, Lys897Thr of KCNH2 gene, Ser49Gly of ADRB1 gene, Trp64Arg of ADRB3 gene with the help of PCR. Left atrial volume turned out to be significantly higher in patients with AF (88.7 +/- 4.13 ml and 65.4 +/- 3.96 ml, respectively, p = 0.001). No associations of genotypes of polymorphic markers Ser49Glu of ADRB1 gene, G(-44)A and A 71G of CX40 gene, Lys897Thr of KCNH2 gene, with emergence of AF in patients with arterial hypertension were revealed. For polymorphic marker Trp64Arg of ADRB3 gene frequency of Trp allele turned out to be significantly higher (OR 2.20, p = 0.0176), while frequency of Arg allele significantly lower (OR 0.43, p = 0.0176) in the group of patients with AF. In patients with AF frequency of Arg/ Arg genotype turned out to be significantly lower (OR 0.24, p = 0.0257).

[Myocardial hypertrophy in patients with hypertensive disease: the role of genetic polymorphism of beta-adrenoreactive structures].

Aim of the study was investigation of association of polymorphic markers Gly389Arg and Ser49Gly of ADRB1 gene, Gly1l6Arg and Glu27Gln of ADRB2 gene, Trp64Arg of ADRB3 gene, and 825 of GNB3 gene with structural and functional peculiarities of the left ventricular (LV) myocardium in patients with hypertensive disease. We examined 177 patients - 83 (46.9%) men and 94 (53.1%) women. Mean age was 60.6 +/- 0.76 years. In the studied group there were 19 patients (10.9%) with I degree arterial hypertension (AH), 57 patients (32.8%) with II degree AH, and 101 patients (56.3%) with III degree AH. Structural peculiarities of LV myocardium were investigated with the help of echocardiography. There turned out to be 40 patients without signs of LV hypertrophy and 137 patients with increase of LV myocardial mass index. patients with LV hypertrophy had higher frequency of genotype Arg/Arg of polymorphic maker Gly398Arg of ADRB1 gene (=0.008. OR 2.32 [CI 1.34 - 4.11]). In patients with concentric and eccentric hypertrophy significantly higher frequency of Arg/Arg genotype compared with patients with normal LV geometry and concentric LV remodeling was also noted. At conduction of multifactorial analysis independently connected with increase of LV myocardial mass turned out age of patients, level of systolic arterial pressure, presence of excessive body mass and carriage of Arg/Arg genotype of polymorphic marker Gly389Arg of ADRB1 gene.

[Association of genetic factors with clinical peculiarities of hypertensive disease in patients with burdened familial anamnesis].

With the aim to investigate association of polymorphisms of candidate genes with clinical peculiarities of hypertensive disease in patients having burdened familial anamnesis we examined 413 (229 men and 184 women, mean age 60.3 +/- 0.59 years) patients with essential arterial hypertension (AH). Determination of alleles and genotypes of polymorphic markers of ACE, AGT, AT2R1, CYP11B2, NOS3, ENDl, GNB3, PPARA, PPARG2, MTHFR, CAT, SOD2, PON1, PON2 sigma APOB, APOE, LPL genes was carried out with the use of polymerase chain reaction. Patient with AH having hereditary load were younger (58.9 +/- 0.75 and 61.3 +/- 0.89 years, respectively, p=0.017) and had significantly lower age of debut of the disease (44.4 +/- 0.84 and 47.5 +/- 1.03 years, respectively; p=0.013), higher values of systolic (204.8 +/- 7.66 and 187.0 +/- 2.04 mm Hg; p=0.032) and diastolic (111.2 +/- 1.05 and 107.3 +/- 1.17 mm Hg, respectively; p=0.025) arterial pressure (AP) compared with patients with AH without hereditary loaded anamnesis. Portion of patients with 3 degree of severity of AH was higher among patients with "familial" AH (53.6 and 44.1%, respectively, p=0.018). Early debut (in the age younger than 45 years in men and 55 years in women) was associated with carriage of genotype TT of polymorphic marker C825 of GNB3 gene (OR 2.65 95CI [1.27-5.54], p=0.005) and genotype AA of polymorphic marker A(A153)G of AT2R1 gene (OR 1.67 95% CI [1.03-2.77], p=0.024). Higher AP level corresponding to 3-rd degree AH in the group of patients with burdened familial anamnesis was associated with carriage of Asn allele of polymorphic marker Lysl98Asn of EDN1 gene (OR 2.24 95% CI [1.20-4.18], p=0.008), 4a allele of polymorphic marker 4a/4b of NOS3 gene (OR 2.23 C/[1.29-3.83], p=0.002), genotype ArgArg of polymorphic marker Glnl92Arg of PON1 gene (OR 6.14 C7[1.46-25.67], p=0.01), T allele of polymorphic marker of C825T gene GNB3 (OR 1.75 C/[1.11-2.76], p=0.01) and genotype AA of polymorphic marker A(A153)G of AT2R1 gene (OR 2.61 C/11.29-5.34], p=0.005). In patients without burdened familial anamnesis 3-rd degree AH was associated with higher frequency of allele Ala of polymorphic marker Pro12A1a of PPARG2 gene.

[Genetic aspects of development of microalbuminuria in patients with hypertensive disease].

Aim of the study was to investigate association of gene candidate polymorphisms encoding elements of the renin-angiotensin system and participating in regulation of vascular tone with development of microalbuminuria in patients with hypertensive disease. We examined 93 patients (52 women, 41 men, mean age 58.3+/-1.12 years, mean duration of hypertension 15.6+/-1.16 years) with hypertensive disease. Two patients had arterial hypertension (AG) with I, 22 with II, 63 with III degree of blood pressure (BP) elevation. Thirty four patients smoked, 2 had stroke in anamnesis, 33 had ischemic heart disease, in 58 heredity burdened with cardiovascular diseases was noted. In 38 patients hypertrophy of left ventricular myocardium was revealed. As gene-candidates we considered AGT, ACE, AT2R1, CYP11B2, MTHFR, PPARA, PPARG2, NOS3. Patients with microalbuminuria had significantly higher systolic and diastolic BP levels. Groups did not differ significantly according sex, age, disease duration, glucose level. There were no significant differences in involvement of other target organs - hypertrophy of left ventricular myocardium and atherosclerosis of carotid arteries. Patients with microalbuminuria had significantly higher level of blood cholesterol. Patients with and without microalbuminuria differed only in frequencies of genotypes of polymorphic marker A(-153)G of AT2R1 gene. Genotype AA predisposed to development of nephropathy--odds ratio (OR) 4.71 (95CI 1.78-12.97), while genotype AG was protective (OR 0.20 95%CI 0.07 to 0.56, p=0.031). According to results of multifactorial analysis independent factors affecting increase of risk of development of nephropathy in the studied group were level of systolic BP and carriage of genotype AA of polymorphic marker A(-153)G of AT2R1 gene.

[Antihypertensive and organ-protective action of a 36-week monotherapy with telmisartan in hypertensive patients].

AIM: To study hypotensive effectiveness and organ-protective properties of telmisartan in patients with essential hypertension (EH). MATERIAL AND METHODS: The trial enrolled 33 patients with EH of stage II, blood pressure (BP) elevation of the first and second degree, with ultrasound-diagnosed left ventricular (LV) hypertrophy and/or increased thickness of intima-media complex (IMC) of the muscular-elastic vessels. The patients received 40-80 mg/day telmisartan monotherapy for 36 weeks. Hypotensive efficacy of the drug was assessed at 24-hr BP monitoring, a protective effect--at echocardiography and ultrasound duplex scanning of the vessels. RESULTS: A 36-week telmisartan monotherapy significantly improved all the analysed parameters of 24-hr BP monitoring. LV myocardial mass reduced by 12.7%, index of this mass--by 12.9%. Overall thickness of intima-media of the muscular-elastic vessels (common carotid and femoral arteries) lowered by 11.9%. CONCLUSION: Long-term telmisartan monotherapy improves parameters of 24-hr BP monitoring, protects the heart and the vessels against remodeling, promotes reduction of LV hypertrophy and intimamedia thickness of muscular-elastic arteries.

[Atherosclerosis/calcinosis of the carotid and peripheral arteries in patients with initial and terminal stages of chronic renal failure].

AIM: To perform ultrasound dopplerography (UD) investigation of severity and prevalence of atherosclerosis/calcinosis of the central and peripheral arteries in patients with chronic renal failure (CRF); to estimate correlation between the vascular lesions and cardiovascular risk factors. MATERIAL AND METHODS: UD of major arteries and echocardiography were made in 46 patients with CRF: 10 patients with initial CRF (creatinine 1.4-2.2 mg/dl) and 36 patients with terminal CRF on hemodialysis. RESULTS: Calcinates and atherosclerotic plaques were registered in the carotid and femoral arteries of all the patients. Atherosclerotic lesion was more frequent than calcinosis in the carotid arteries. Calcinosis was more frequent in the femoral arteries. The popliteal and tibial arteries were affected only by calcinosis which occurred in 20% patients with initial and 44.4% patients with terminal CRF. Calcinosis severity increased with progression of CRF while atherosclerosis severity depended more on the patients' age than on severity of CRF. The pulse wave speed in the carotid and femoral arteries was higher in marked left ventricular hypertrophy, seven (19.4%) of these patients had reduced ejection fraction of the left ventricle < 40%. CONCLUSION: Compound atherosclerotic/calcinosis lesion of the vessels is registered at early stages of CRF and progress with progression of renal failure.

[Genetic predictors of left ventricular hypertrophy: do polymorphisms of peroxisome proliferator activated nuclear receptor genes play any role?]. / Geneticheskie prediktory gipertrofii levogo zheludochka: igraet li rol' polimorfizm genov iadernykh retseptorov, aktiviruemykh proliferatorom peroksisom?

AIM: To assess possible associations of polymorphic markers of PPARA and PPARG2 genes with presence of left ventricular hypertrophy (LVH) in patients with hypertension. MATERIAL: Patients with hypertension (n=163, mean age 60.93+/-0.82 years) with (n=110) and without (n=53) LVH. METHODS: Echocardiography was used for evaluation of left ventricular mass and mass index and polymerase chain reaction - for identification of alleles and genotypes of polymorphic markers of ACE, NOS3, PPARA, PPARG2 genes. RESULTS AND CONCLUSION: There was no association between presence of LVH and polymorphic marker Pro12AIa. Carriers of 4a allele of a polymorphic marker ecNOS4a/4b of NOS3 gene, A allale of a polymorphic marker G7831A of ACE gene, and C allele of PPARA gene had significantly greater left ventricular myocardial mass index. Monofactorial regression analysis showed that degree of LVH was significantly related to age, duration of hypertension, maximal systolic blood pressure. No relationship was found between left ventricular mass index and smoking, maximal diastolic blood pressure, habitual systolic and diastolic blood pressure, duration of hypertension, presence of ischemic heart disease, diabetes. According to results of multifactorial analysis A allele of a polymorphic marker G7831A of ACE gene, age and maximal systolic blood pressure were while C allele of PPARA gene was not independently related to the presence of LVH.

[Polymorphic markers I/D and G7831A of angiotensin-I-converting enzyme gene and left ventricular hypertrophy in patients with essential hypertension]. / Polimorfnye markery I/D i G7831A gena fermenta, prevrashchaiushchego angiotenzin I, i gipertrofiia miokarda u bol'nykh arterial'noi gipertoniei.

AIM: To elucidate possible association of angiotensin-I-converting enzyme (ACE) gene polymorphic markers I/D and G7831A with left ventricular hypertrophy (LVH) in patients with essential hypertension. MATERIAL: Patients with essential hypertension (n=123, 37 with and 86 without LVH, mean age 59.15+/-1.19 years). METHODS: Left ventricular (LV) mass was determined echocardiographically by Devereux method. Alleles and genotypes of ACE gene polymorphic markers were identified by polymerase chain reaction. RESULTS AND CONCLUSION: There was no association between I/D marker of ACE gene and LVH. Carriers of A allele compared with carriers of G allele of G7831A marker had significantly higher LV mass (284.1+/-10.20 g, and 248.5+/-14.42 g, respectively, p=0.033) and LV mass index (151.7+/-5.23 g/m2 and 131.0+/-6.74 g/m2, respectively; p=0.02). Among patients with LVH frequency of A allele was significantly higher than among patients without LVH (0.401 and 0.230, respectively; p=0.0065, OR=2.116 [1.197-3.7481]). Using binary logistic regression model we have found that presence of LVH was linked with age, sex and maximal systolic blood pressure (BP). Such factors as smoking, maximal diastolic BP, ordinary systolic and diastolic BP, duration of hypertension, coronary artery disease and diabetes were not related to LV mass index. Using multifactorial logistic regression model we have found that the presence of A allele of G7831A polymorphic marker of ACE gene, age and maximal systolic BP could be considered as independent risk factors of LVH.

[Hereditary factors and left ventricular hypertrophy]. / Nasledstvennye faktory i gipertrofiia levogo zheludochka.

Left ventricular hypertrophy (LVH) is an independent risk factor for morbidity and mortality from cardiovascular disease in men and women with hypertension and in asymptomatic subjects with normal blood pressure. In hypertensive patients it is a stronger coronary risk factor than casual blood pressure readings. Correlation between levels of high blood pressure, duration of hypertension and left ventricular mass is poor. Epidemiological studies suggest that left ventricular hypertrophy may be influenced by genetic factors. In our review we present study groups of genes contributing to the development of left ventricular hypertrophy: 1) genes that encode components of hormonal pathways, 2) genes of key sympathetic and parasympathetic receptors, 3) genes that modify intracellular ion homeostasis, 4) genes that modify energy metabolism, 5) genes that modify motor unit composition and regulation. Angiotensinogen gene, angiotensin-converting enzyme gene, angiotensin receptor type 1 gene, aldosterone synthase gene, nitric oxide synthase gene, type A natriuretic peptide receptor gene, beta(2)-adrenergic receptor gene, G-protein beta(3) subunit gene are associated with left ventricular hypertrophy.