This review presents the modern evidence on the association between sleep apnoea syndrome and cardiovascular disease. Among other aspects, the recently discovered mechanisms linking sleep apnoea and the development of atherosclerosis, coronary heart disease, and cardiac arrhythmias, are discussed. The authors focus on the sleep apnoea syndrome impact on quality of life.

Aim. To investigate the association between single-nucleotide polymorphisms (SNPs) rs10757278 and rs1333049 of the 9p21.3 locus and family history of coronary heart disease (CHD) in myocardial infarction (MI) patients. Material and methods. The MI group (n=243) and the control group (n=280) were comparable by such parameters as age, gender, arterial hypertension, diabetes mellitus, hypercholesterolemia, overweight and obesity, abdominal obesity, and smoking history. However, the groups were significantly different in terms of family history of CHD (p=0,004). Genome DNA was extracted from venous blood using the phenol-chloroform extraction method. The SNPs rs10757278 (9p21.3) and rs1333049 (9Sр21.3) were tested using real-time polymerase chain reaction (PCR) and the AB 7900HT device, according to the producer’s protocol (TaqMan probes, Applied Biosystems, USA). Results. A statistically significant association between MI and the CC rs1333049 genotype or the GG rs10757278 genotype was observed in the whole study sample and separately in men and women. The MI odds ratio (OR) for carriers of the CC rs1333049 genotype was 2,02 (95% confidence interval, CI, 1,32–3,08) in the whole sample, 1,91 (1,11–2,95) in men, and 2,91 (1,22–6,91) in women. For carriers of the GG rs10757278 genotype, respective OR values were 1,98 (1,30– 3,02), 1,77 (1,08–2,87), and 2,94 (1,26–6,87). Among participants without CHD in family history, OR for the CC rs1333049 genotype (1,92, 95% CI 1,16–3,16) and the GG rs10757278 genotype (1,82, 95% CI 1,10–3,00) were comparable for those among MI patients with CHD in family history (respective OR 2,19 (1,28–3,75) and 2,23 (1,31–3,81)). Conclusion. For the first time in Russia, the association between MI-related polymorphisms of the 9p21.3 chromosome and family history of CHD was analysed. Two SNPs (rs1333049 and rs10757278) of the 9p21.3 locus predicted MI risk independently from either conventional risk factors or CHD in family history.

Aim. To assess the impact of insertion-deletion polymorphism of apolipoprotein A gene on the development of dyslipidemia among adolescents with essential arterial hypertension (EAH), in regard to the ethnic group: non-indigenous Slavic vs. indigenous Buryat. Material and methods. In total, 399 adolescents were examined: 226 patients with the verified EAH diagnosis and 173 controls. Among EAH patients, 144 adolescents (63,7%) were from the non-indigenous ethnic group, while 82 (36,3%) were from the indigenous one; among controls, the respective figures were 94 (53,4%) and 79 (45,7%). Dyslipidemia was diagnosed using the unified criteria. For genetic analyses, total DNA was extracted from venous blood samples, using a non-enzymatic method. DNA fragments were amplified in the polymerase chain reaction (PCR), using the reagent kit “SNP express” according to the producer’s protocol (Litech, Moscow). Results. The deletion allele prevalence in adolescents from the indigenous ethnic group was 8,2% among controls and 8,0% among EAH patients (p=1,000). In the non-indigenous ethnic group, the respective figures were 7,9% and 9,8% (p=0,493). According to the multivariate analysis results, lipid levels in non-indigenous carriers of various insertion-deletion ApoA1 genotypes could be predicted as follows: triglyceride (TG) levels = 1,552 + (-0,653 ApoA1 (II); model F=7,174, p=0,009;  R²=9,4%; very low-density lipoprotein cholesterol (VLD-CH) levels = 0,613 + (-0,189 ApoA1 (II)); model F=4,738, p=0,033; R²=6,3%. Among indigenous patients – carriers of various insertion/deletion ApoA1 genotypes, this polymorphism did not appear to have a significant impact on lipid metabolism parameters. Conclusion. The genome impact on clinical and biochemical phenotype is variable and differs across ethnic groups. Multivariate analyses have demonstrated that TG and VLD-CH levels are associated with the insertion/deletion ApoA1 gene polymorphism. Therefore, this genetic marker could be regarded as a “modifier” gene which determines biochemical polymorphism in non-indigenous patients. In adolescents from the indigenous ethnic group, this molecular and genetic marker appeared irrelevant.

 

 

Aim. To assess the impact of climacteric disturbances in menopause on the dynamics of endothelial function among women with arterial hypertension (AH). Material and methods. The study included 129 women: 101 with elevated blood pressure (BP) levels and 28 without AH. All participants underwent echocardiography, 24-hour BP monitoring (BPM), brachial artery (BA) Doppler ultrasound, and reactive hyperemia test with nitroglycerine. The parameters of 24-hour BPM, left ventricular myocardial mass index, diastolic function, and endothelial function were analysed by age and the time of the climacteric disturbance development. Results. According to the 24-hour BPM results, examined women had Stage I–II AH. AH duration increased with age and reached 4,67±0,45 years for pre-menopausal women, 6,47±0,57 years for women in early menopause, and 12,48±0,94 years for women in late menopause. Left ventricular diastolic dysfunction was registered in all three groups; among women in late menopause, it was significantly more pronounced than among pre-menopausal women (p<0,05). Mean values of BA diameter were 3,88±0,07, 4,11±0,08, and 4,08±0,08 mm among women in pre-menopause, early menopause, and late menopause, respectively (p<0,05). The reactive hyperemia test demonstrated inadequate BA dilatation in 36,1%, 46,9%, and 60,6%, respectively.>< 0,05). The reactive hyperemia test demonstrated inadequate BA dilatation in 36,1%, 46,9%, and 60,6%, respectively. Conclusion. Endothelial dysfunction was more pronounced among women in late menopause, which supports the presence of the association between more severe vascular disturbances and menopause among hypertensive women, as well as suggests a post-menopausal increase in cardiovascular risk levels.

 

 

Aim. To assess arterial structure and function in men with arterial hypertension (AH) combined with dyslipidemia and obesity, in comparison to men with AH and normal body weight.Material and methods. The study included 205 men with the combination of AH, dyslipidemia, and obesity, as well as 42 men with AH and normal body weight. All participants (age 20–71 years) underwent ultrasound examination and oscillometry. Results. Men with disturbed lipid metabolism demonstrated a tendency towards the increase in intima-media thickness (IMT) of common carotid artery (CCA), starting from the age of 45 years. Endothelial dysfunction, manifested as reduced endothelium-dependent vasodilatation, manifested from the age of 35–38 years. These changes occurred, on average, 15 years earlier than in AH patients without dyslipidemia and obesity. Among men with AH and disturbed lipid metabolism, CCA IMT values strongly correlated with age, body mass index, waist circumference, peak systolic blood flow velocity, cholesterol levels, and pulse wave velocity.Conclusion. Obesity and dyslipidemia are not only strong predictors of cardiovascular risk, but also aetiological factors of vascular pathology.

 

 

Aim. To identify the most important risk factors of recurrent atrial fibrillation (AF) and their prognostic value in patients with arterial hypertension (AH). Material and methods. In total, the study included 60 patients with Stage 1–3 AH (Grade I–III, cardiovascular risk 2–4): 20 with the first episode of AF (33%) and 40 with recurrent AF (67%). In all patients, sinus rhythm was restored with pharmacological or electric impulse therapy. At baseline and 6 months after restoring sinus rhythm, the assessment of medical history, antihypertensive and antiarrhythmic therapy, echocardiography, and Doppler ultrasound were performed. To identify silent cardiac arrhythmias and conductivity disorders, Holter electrocardiography monitoring was performed; coronary heart disease was verified with the bicycle stress test. Statistical analyses were performed using the Statistica 6.0 software. Results. The early recurrence of AF was associated with Stage 3 AH, AF in anamnesis, and left atrium dilatation. Conclusion. The combination of Stage 3 AH, AF in anamnesis, and left atrium dilatation was associated with a higher risk of recurrent AF, compared to each of these factors in isolation.

 

 

Aim. To assess cardio-renal interactions and the functional status of heart and kidneys in patients with acute myocardial infarction (AMI) who underwent the post-AMI coronary revascularisation. Material and methods. In total, 100 men, aged 45–60 years, were examined, including 50 AMI patients who underwent the revascularisation surgery. Cardiac structure and function, as well as excretory, glomerular, and tubular renal functions, were assessed. Results. Patients who underwent revascularisation demonstrated lower creatinine levels. In this group, the prevalence of the serum creatinine concentration >115 μmol/l and glomerular filtration rate (GFR) < 60 ml/min was significantly lower than in the patients treated conservatively. Urine levels of β2-microglobulin, reflecting the tubular renal function, were significantly lower in AMI patients after revascularisation. In addition, the revascularisation group demonstrated an improvement in cardio-renal interactions, compared to the conservative treatment group. Conclusion. Among AMI patients who underwent coronary revascularisation, in comparison to the patients treated conservatively, there was an improvement in cardio-renal interactions and a positive dynamics in both cardiac structure and function and renal functional status. In the revascularisation group, renal function parameters were significantly associated with the parameters of cardiac structure and function, which confirmed the existence of cardio-renal interactions.

 

 

 

Aim. To assess the impact of renal and local coronary risk factors (RFs) on cardiovascular survival in patients with coronary heart disease (CHD) before and after myocardial revascularisation. Material and methods. The study included 90 CHD patients with indications for myocardial revascularisation. In all participants, the presence of renal RFs (microalbuminuria (MAU) and increased levels of β₂ -microglobulin (β₂ -MG)) was assessed at different intervention stages. In addition, the number of coronary arteries (CA) affected by atherosclerosis, as well as CA atherosclerosis severity, was assessed. Results. Among the majority of CHD patients with myocardial revascularisation indications, MAU was observed at all intervention stages. The endpoint incidence was associated with MAU, β₂ -MG levels, the number of CA affected by atherosclerosis and CA with hemodynamically non-significant stenosis. The levels of β₂ -MG significantly correlated with atherosclerotic plaque growth rate. Conclusion. The increased risk of coronary events was associated with elevated levels of MAU and β₂ -MG and the increased number of CA affected by atherosclerosis and CA with hemodynamically non-significant stenosis. Elevated CV risk was linked to β₂ -MG levels of ≥0,1 ng/ml. The levels of β₂ -MG increased in parallel with the CHD progression.

Body surface potential mapping (BSPM) is a non-invasive and effective method for diagnosing coronary heart disease (CHD) and acute myocardial infarction (AMI). However, most existing systems of BSPM are unable to create standard diagnostic criteria. Aim. To develop the neural network model (NNM) for diagnosing Q-wave AMI and to assess the model effectiveness. Material and methods. The BSPM method in 90 leads was used in 96 controls, 35 patients with anterior Q-wave AMI, 43 with posterior Q-wave AMI, 14 with inferior Q-wave AMI, and 21 with lateral Q-wave AMI. The input NNM layer was decomposed into five subsets corresponding to horizontal levels of registered signals, using amplitudes of Q, R, S, and T waves and the ST segment. The output layer produced the probability of the norm (controls) and different AMI locations. Results. Exploring the NNM performance in controls and AMI patients, sensitivity of 100% and specificity of 97,4% was observed. Sensitivity reached 100% for anterior Q-wave AMI, 94,4% for posterior Q-wave AMI, 85,7% for inferior Q-wave AMI, and 83,3% for lateral Q-wave AMI. Conclusion. Our data have demonstrated the effectiveness of NNM in AMI diagnostics.

 

 

 

Aim. To compare the parameters of lipid profile and calcium and phosphate metabolism in patients with coronary heart disease (CHD) or CHD combined with aortic stenosis (AS). Material and methods. The study included 147 CHD patients, aged over 60, with stable angina pectoris, (functional Class (FC) I–IV) and degenerative calcific AS. The comparison group included 41 CHD patients without calcification or stenosis of aortal valve. In all participants, the parameters of lipid profile and calcium and phosphate metabolism were assessed. Results. Dyslipidemia was more prevalent in CHD patients without AS (85,4% vs. 68%). AS was linked to lower levels of total cholesterol and triglycerides. However, the combination of AS and mitral calcification was characterised by higher levels of low-density and non-high-density lipoprotein cholesterol (LDL–CH and non-HDL–CH). More severe AS was associated with decreased levels of non-HDL–CH and elevated levels of parathyroid hormone, ionized calcium, and alkaline phosphatase. There was a direct correlation between the levels of parathyroid hormone and the presence of calcific AS (r=0,532; p=0,013). Conclusion. The results obtained confirm the disturbance of lipid and calcium metabolism among patients with calcific AS, which suggests that this cardiac valve pathology could be regarded as a manifestation of ectopic calcinosis.

 

 

Aim. In patients with chronic heart failure (CHF) of ischemic aetiology, to assess the dynamics of heart rate variability (HRV) and ventricular ectopic activity during the complex, ivabradine-including therapy. Material and methods. In total, 90 patients with CHF and stable angina pectoris were examined. All participants were randomised into three equally sized groups: Group 1, receiving perindopril and ivabradine, as a part of the complex treatment; Group 2, receiving perindopril, bisoprolol, and ivabradine; and Group 3, receiving perindopril and bisoprolol. The therapy duration was 6 months. At baseline and in the end of the treatment phase, the following parameters were assessed: HRV measures (mean 24-hour hear rate (HR), SDNN, triangular index (HRVti), and mean weighted variation of rhythmogram (MWVR)); mean 24-hour QT, QTc, QTc dispersion (QTcd), and ventricular extrasystolia (VE). Results. The treatment was associated with a significantly greater reduction of mean 24-hour HR in Groups 1 and 2 vs. Group 3 (p<0,001). In Group 3, the SDNN increase was significantly lower than in Groups 1 and 2 (p><0,001), where SDNN values were similar (p=0,091). Group 3 also demonstrated a significantly ><0,001). In Group 3, the SDNN increase was significantly lower than in Groups 1 and 2 (p<0,001), where SDNN values were similar (p=0,091). Group 3 also demonstrated a significantly ><0,001), where SDNN values were similar (p=0,091). Group 3 also demonstrated a significantly lower increase in MWVR, compared to Groups 1 and 2 (p<0,001). This parameter was similar in Groups 1 and 2 (p=0,065). The increase in HRVti was more pronounced in Group 2 than in Groups 1 and 3 (p><0,001). The reduction in the total 24-hour VE number was significantly more pronounced in Group 2 than in Groups 1 and 3 (p><0,001). The dynamics of 24-hour QTc and QTcd was similar across three groups.><0,001). This parameter was similar in Groups 1 and 2 (p=0,065). The increase in HRVti was more pronounced in Group 2 than in Groups 1 and 3 (p<0,001). The reduction in the total 24-hour VE number was significantly more pronounced in Group 2 than in Groups 1 and 3 (p<0,001). The dynamics of 24-hour QTc and QTcd was similar across three groups. Conclusion. Including ivabradine in the complex therapy of patients with CHF and stable angina pectoris was associated with improved HRV, no marked QTc or QTcd changes, and a moderate preventive effect on VE.

 

 

 

 

 

 

Aim. To assess the effects of the combination therapy with atenolol and amlodipine on the synchronisation of 0,1-Hz rhythms of heart rate variability (HRV) and distal vessel filling (DVF). Material and methods. The study included 25 patients with Stage 1–2 arterial hypertension (AH), aged 58±8 years. The registration of 0,1-Hz oscillations in HRV and DVF was performed during the passive tilt test with spontaneous breathing; each test stage lasted for 10 minutes. Synchronisation was assessed by the phase difference between 0.1 Hz-rhythms in HRV and DVF. Frequency values of the HRV spectrum in LF and HF-ranges were also assessed. The duration of combination therapy was 8 weeks. Results. In patients with AH and a markedly manifested autonomic dysfunction, the therapy with atenolol and amlodipine was associated with some improvement in the functional interaction between HRV and DVF 0,1-Hz rhythms. In the rest of AH patients, the treatment was linked to stable levels of cardiac 0,1-Hz regulation and slightly decreased synchronisation levels. All participants demonstrated an increase in the influence of respiratory parasympathetic effects. Conclusion. The combination therapy with atenolol and amlodipine effectively corrected autonomic cardiovascular dysfunction in patients with Stage 1–2 AH.

 

 

Aim. To investigate the effects of various antihypertensive combinations on metabolic parameters in patients with arterial hypertension (AH). Material and methods. The study included 144 AH patients and 7 groups of combination therapy: Group 1 (n=30) – trandolapril/verapamil SR; Group 2 (n=19) – perindopril/indapamide; Group 3 (n=15) – felodipine/metoprolol; Group 4 (n=20) – amlodipine/atenolol; Group 5 (n=20) – ACE inhibitor/hydrochlorothiazide (HCT); Group 6 (n=22) – telmisartan/lacidipine; and Group 7 (n=18) – metoprolol/HCT. In all participants, the parameters of lipid, carbohydrate, and purine metabolism were assessed. The effects of antihypertensive combinations on the risk of metabolic disturbances were studied using the factor regression analysis of quantitative and qualitative parameters (factors) as weighted ordered functions. Results. The negative effects on the levels of cholesterol (CH), triglycerides (TG), and glucose were most pronounced for the combination of metoprolol and HCT, while the combination of amlodipine and atenolol demonstrated the weakest negative effects on CH and glucose levels. The levels of CH, TG, and uric acid were affected to the least extent by the combination therapy with ACE inhibitor and HCT, which was also associated with a reduction in glucose levels. The combination of trandolapril and verapamil SR had the largest positive effect on the levels of CH, TG, and uric acid, together with a beneficial effect on glucose levels. The combination therapy with perindopril and indapamide was the most beneficial for the levels of CH and TG, while the felodipine/metoprolol combination had the most pronounced positive effects on TC and glucose levels. The combination of lacidipine and telmisartan was the most beneficial for glucose levels, but negatively affected the levels of uric acid. The perindopril/indapamide combination demonstrated negative effects on glucose levels. The full doses of diuretics and β-blockers negatively affected the levels of TC and glucose, while the full doses of ACE inhibitors benefited these metabolic parameters. Conclusion. The combination of a β-blocker and HCT was the least desirable, in terms of metabolic safety, for the treatment of AH patients. Including ACE inhibitors in the combination therapy demonstrated beneficial metabolic effects. To minimise the pre-existing metabolic disturbances and prevent the negative metabolic effects of diuretics, full doses of ACE inhibitors are required.

 

 

Aim. To compare total disease costs by the treatment regimen and blood pressure (BP) control levels among patients with arterial hypertension (AH). Material and methods. Pharmacoeconomic analyses of total disease costs were performed for two treatment regimens and 4115 patients participating in the open, multi-centre observational programme “PRORYV”: a retrospective cost analysis for the 12 pre-inclusion weeks and a prospective cost analysis for the 12 weeks of the programme participation. Results. The treatment with a fixed-dose combination of perindopril and amlodipine (Prestance) was more expensive for the patients than the pre-inclusion treatment (955,15±849,96 vs. 566,78±432,70 RUB per person per month). However, total direct costs for the Prestance-treated patients were 2,6 times lower (3164,07 vs. 8245,33 RUB per person for 12 weeks). Total treatment costs were also lower: 3463,47 vs. 14226,03 RUB per person for 12 weeks, respectively. Switching to a more effective treatment regimen (Prestance) modifies the distribution of the therapy costs, due to decreased incidence and duration of hospitalisation episodes and reduced number of medical visits and ambulance calls. Conclusion. The reduction in the AH treatment costs and modification of their distribution provides an opportunity for a wider use of more effective medications. Switching one patient from ineffective treatment to Prestance covers the costs of additional treatment of 310% patients (n=12757) for 12 weeks.

 

 

The review discusses the clinical impact of salt consumption on the cardiovascular system status. The therapeutic potential of reduced salt intake, in order to facilitate regression of cardiovascular disturbances, is also discussed. Daily consumption of standard or increased amounts of salt results in the complex multilevel changes of cardiac chambers, arterial and venous vessels, and microcirculation in individuals with normal and elevated blood pressure (BP). The underlying mechanisms, both hemodynamic and non-hemodynamic, are present even in normotensive people. Reduced salt consumption is associated with the regression of structural cardiovascular disturbances.

The paper focuses on various aspects of restenosis and in-stent thrombosis, as complications of percutaneous coronary intervention. The complex assessment of this problem is warranted, as it remains far from being resolved, despite the recent technical and therapeutic advances.