The aim – to study the clinical characteristics of patients with stable coronary heart disease (CHD) and heart failure (HF) with mid-range left ventricular (LV) ejection fraction (EF) (40–49 %; HFmrEF), undergoing the planned coronary artery bypass grafting (CABG) in the real-life clinical practice settings.
Material and methods. We conducted a cross-sectional one-center study and consecutively enrolled 622 patients with stable CHD (mean age 61±9 yr, 526 (84.6 %) males and 96 (15.4 %) females), undergoing planned CABG. We analyzed demographic, clinical, laboratory, echocardiographic and coronary angiographic data. The population of enrolled patients was stratified into three groups according to the LVEF degree: group 1 (LVEF ≥ 50 %; 350 (56.3 %)); group 2 (LVEF 40–49 %; 11 (18.5 %)); and group 3 (LVEF < 40 %; 157 (25.2 %)).
Results. The set of parameters in group 2, having intermediate values when compared to groups 1 and 3, were: the frequency of baseline aldosterone antagonists administration; the frequency of patients without mitral and tricuspid regurgitation; the frequency of patients with moderate or severe mitral regurgitation; mean systolic pulmonary artery pressure; the frequency of patients with LV aneurysm, detected by coronary ventriculography.
Conclusion. The population of patients with CHD and HFmrEF, undergoing CABG in the real-life clinical practice settings, is associated with clinical heterogeneity. Further studies are warranted, aimed to determine the predictors of favorable and unfavorable dynamics of LVEF in this category of patients in the post-CABG period.
The aim – to evaluate the effect of different regimes of lipid lowering therapy on the effectiveness of urgent myocardial revascularization and the development of cardiac remodeling in patients with acute coronary syndrome with ST segment elevation (STEMI).
Material and methods. The study involved 135 STEMI patients admitted an average of 4.5 hours after symptoms onset and treated with primary percutaneous intervention. Lipid-lowering treatment was prescribed immediately after presentation. Patients were randomly assigned to one of four groups treated by moderate (group I and group II) or high (group III and group IV) intensity lipid-lowering therapy. Group I (26 patients) was assigned to atorvastatin 10 mg / ezetimibe 10 mg combination, group II (24 patients) – to atorvastatin 40 mg, group III (42 patients) – to atorvastatin 40 mg / ezetimibe 10 mg combination, and group IV (43 patients) – to atorvastatin 80 mg. Echocardiography was performed in all the patients during first 24 hours after symptoms onset and 90 days after STEMI development. Left ventricular (LV) dilatation was defined as at least 25 % increase of end-diastolic volume.
Results. Patients from groups III and IV showed a tendency to the reduction of post-MI LV dilatation after 3 month of treatment (Р<0.1). In our study use of high intensity lipid-lowering therapy reduced the risk of LV remodeling by 30 % (p<0.05), that was also associated with significantly higher LDL reduction. Having no initial differences, on the 90th day the average LDL level was 1.63±0.40 in patients with high intensity treatment vs. 2.21±0.30 mmol/l in patient with therapy of moderate intensity (Р<0.01).
Conclusion. The use of high-intensity lipid-lowering therapy with achievement of target LDL levels after STEMI can reduce the incidence of post-MI LV dilatation.
The aim – to estimate the role of geometric parameters of mitral valve deformation and remodeling of the left ventricle (LV) in the formation of mitral insufficiency in patients with systolic dysfunction after myocardial infarction (MI) of different localization.
Material and methods. We assessed 99 patients with left ventricular (LV) systolic dysfiunction after MI with mild to severe mitral insufficiency. We evaluated mitral insufficiency by means of echocardiography through determining EROA (effective regurgitant orifice area), assessed indexes of LV global and local remodeling. mitral insufficiency was moderate and severe in 36 patients with anterior MI (group 1) and in 43 patients with inferior/posterior MI (group 2), the control group consisted of 21 healthy individuals.
Results. In both groups of patients rates of global and local LV remodeling were significantly higher than in the control group (P<0.0001). Sphericity index was significantly higher in group 1, compared to group 2 (P=0.003). The indexes of local remodeling were significantly higher in group 1, especially anterior papillary muscle (PM) tethering distance (Р=0.03), posterior displacement of the anterior PM (Р=0.03), PM height (Р=0.01), interpapillary distance (Р=0.02). Correlation between EROA and sphericity index in group 1 was revealed (Kendall τ 0.46, P<0.0001), in group 2 this correlation was weak (Kendall τ 0.23, Р=0.016). In group 1 correlation of EROA with anterior and posterior PM tethering distance was revealed (Kendall τ 0.41 and 0.52, P<0.0001). In group 2 EROA correlation with posterior PM tethering distance and anteroposterior mitral valve diameter was revealed (Kendall τ 0.36 and 0.48, P<0,0001). Correlation between EROA and inferior apical segment akinesia and WMSI of posterior PM was revealed in group 1 (Kendall τ 0.71 and 0.51, P<0.0001), and relation between mitral insufficiency and obstructive lesion in circumflexus (Cx) and right coronary artery (RCA) (Р=0.0008 та Р=0.002) in this group.
Conclusions. LV spherisation and PM dislocation are more pronounced in ischemic CMP after anterior MI, compared to inferoposterior MI. Apical and posterior PM displacement, akinesia of inferior apical segment, Cx and RCA obstruction are major determinants of ischemic mitral insufficiency after anterior MI, while posterior PM tethering and anteroposterior mitral annular dilatation are determinants of mitral insufficiency after inferoposterior MI. The obtained data might determine surgical approaches in ischemic mitral insufficiency of different mechanisms.
The aim – to evaluate the results of ECG daily monitoring in patients with peripheral arterial disease (PAD) of the lower extremities and to investigate association with clinical and genetic (T(–786)C polymorphism of the eNOs gene promoter parameters.
Material and methods. The study involved 100 men with lower extremities PAD, average age 60.7±0.9 years. We performed Holter monitoring, echocardiography, Doppler ultrasound of the lower extremities and carotid arteries, selective coronary angiography. The study of allelic polymorphism of eNOs gene promoter was performed by polymerase chain reaction.
Results and discussion. The patients were divided into 2 groups: I – 63 (63 %) without ischemic heart disease (IHD), ІІ – 37 (37 %) patients with IHD. Decreased glomerular filtration rate (GFR), which was more often recorded in group II, was related to the ventricular arrhythmias (Р=0.03) and atrial fibrillation (Р=0.02). Supraventricular arrhythmias were found in 42 patients. Patients of the II group, in which supraventricular arrhythmias were registered, more often were carriers of C allele (Р=0.008). Ventricular arrhythmias were detected in 27 patients. Among them, patients with concomitant coronary artery disease were more likely to be carriers of C allele (Р=0.002). There was a relationship between atrial fibrillation and angina (Р=0.045), past myocardial infarction (MI) (Р=0.02, including repeated one, Р=0.0001), decrease in GFR (Р=0.02). Conduction defects were more often recorded in group II (Р=0.01).
Conclusions. Ischemic ECG changes are significantly associated with the younger age (Р=0.045), the earlier onset of PAD (Р=0.02), the presence of the C allele the polymorphism eNOs promoter gene (Р=0.002), symptoms of carotids damage (p=0.004) and suffered acute cerebrovascular disorders (Р=0.007). According to Holter ECG monitoring, arrhythmias and blockades were detected in both clinical groups.
The aim – to determine the most informative diagnostic markers of severity of post-infarct interventricular septal rupture (PIIVSP), as well as the most effective methods of treatment of this complication based on their own experience in treating patients.
Material and methods. During the period from 1991 to 2017, 65 patients with PIIVSP were treated, average age (59.1±6.7) years: 44 (67.7 %) men aged 52–73 years (average 57.4±9.5 years) and 21 (32.3 %) women aged 64–76 years (average 62.2±11.7 years). 41 patients had a posterior localization of the defect, at 24 – anterior localication.
Results. PIIVSP leads to complicated hemodynamic disorders, related to the size of PIIVSP, the amount of blood loss through the gap, the size of the IM zone, the degree of damage to the coronary arteries and the presence of necrosis of the papillary muscles. Congestive heart failure and cardiogenic shock are important factors influencing the results of treatment of PIIVSP. A main factor determining the development of congestive heart failure and cardiogenic shock in patients with PIIVSP in its anterior localization is a left ventricular dysfunction, resulting from widespread myocardial necrosis. A method of surgical geometric reconstruction of left ventricle with one «sandwich» patch was used. The mortality was 13.8 %, mostly because of acute heart failure.
Conclusions. Surgical treatment of PIIVSP is a method of choice, since it is most effective compared to medication and endovascular therapy, providing defect closure and restoration of left ventricle geometry.
The aim – was to investigate the possible association of the aldosterone synthase gene (CYP11B2) polymorphism and the recessive pattern of inheritance with left ventricular diastolic function in patients with coronary heart disease and postinfarction cardiosclerosis (PIC).
Material and methods. One hundred patients (age 57.3±8.9 years) were examined by general clinical methods. The study included patients with a history of myocardial infarction for more than 6 months and up to 2 years from the date of the event. Genetic testing was performed by polymerase chain reaction in real mode. The study material was venous blood of patients with coronary heart disease, PIC. Echocardiography was done for the evaluation of diastolic function in all patients.
Results. The E wave velocity parameters were higher among patients with TT + TC genotype compared to the data of patients with CC genotype. The wave-velocity parameters A were higher, and DT was longer in patients with CC variant of the genotype compared to the TT + TC variant of the aldosterone synthase gene polymorphism, which indicates a greater frequency of LV relaxation disturbance in patients with CC variant of polymorphism compared to TT + TC variant of the genotype. The indices of higher diastolic LV diastolic pressure, an increase in its preload (E/E´, AR) were higher in the group of patients with TT and TC, a variant of aldosterone synthase gene polymorphism. The patients with TT + TC variant of polymorphism more often encountered more severe forms of LV diastolic dysfunction (pseudonormalization, restriction) compared with the data of patients with a variant of polymorphism of the aldosterone synthase gene (P<0.0001), which indicates a more severe course of the disease in these patients.
Conclusion. The risk of developing more severe forms of diastolic LV dysfunction in patients with TT + TC genotype CYP11B2 is higher, compared to the CC genotype in patients with IHD, PIC.
The aim – to evaluate asymmetric dimethylarginine (ADMA) concentration and its possible relationship with clinical features, anamnesis, laboratory parameters, cardiac ultrasound in patients with ST-elevation myocardial infarction after intravenous fibrinolysis.
Material and methods. We examined 40 patients with myocardial infarction after intravenous fibrinolysis. Blood sampling was performed at admission. C-reactive protein (CRP) concentration was accessed. Quantitative determination of ADMA concentration was performed with high-performance liquid chromatography. Cardiac ultrasound was done in all patients. Fibrinolysis efficacy was evaluated according to the ECG criteria.
Results. ADMA concentration in examined patients was 0.1–4.94 mkmol/l. Patients were divided into four groups according to ADMA quartiles (increase of ADMA concentration from group I to group IV). All patients in group IV were smokers, the difference was significant in groups I and II (P=0.04). Time to fibrinolysis was significantly higher in group IV than in groups II (P=0.02) and III (P=0.04). Mean ADMA concentration was significantly higher in patients with anterior compared to patients with inferior infarction (1.79±1.5 and 0.8±0.75 mkmol/l, respectively, Р=0.02). In correlation analysis ADMA level was related to history of smoking, high-sensitive CRP and glycemia level at admission, time to fibrinolysis, heart rate on the second day of infarction, and ultrasonic parameters – end-diastolic volume (EDV), and-systolic volume and ejection fraction. Fibrinolysis was significantly less effective in patients with higher ADMA level.
Conclusion. Significant increase of ADMA level was found in presence of smoking, longer of time to fibrinolysis and in anterior localization of infarction. ADMA level increase was associated with increase of hsCRP level, younger age, EDV and admission glycemia increase, decrease of glomerular filtration rate and body mass index, increase of time to fibrinolysis (regression analysis). Fibrinolysis was significantly less effective in patients with higher ADMA level.
The aim – to evaluate the recovery of the exercise tolerance during first 6 months after acute myocardial infarction (MI) with emergent coronary angiography and stenting through adding cycle ergometer physical trainings (PT) to standard medical care.
Material and methods. 76 patients (men, 52.2±1.2 years old) were prospectively evaluated in dynamics during 1–1.5; 2.5; 4 and 6 months after MI. All of them received standard medical care and everyday dosage walking. They were divided into two groups (gr). The 1st gr (41 pts) in addition to previous treatment had PT at cycle ergometer 3 times per week in individual regimen with 75 % of achieved load (complete program consisted of 30 sessions). After 15 PT sessions the control test was performed and intensity of next training regimen was corrected according to its result. 35 pts (2nd gr) received medical treatment and walking without PT.
Results. The additional sub-analysis was performed according to the 1) time of opening of infarct-related coronary artery (< 2 hours, 2–6 hours and > 6 hours) and 2) complete/incomplete revascularization. The threshold levels of work capacity were quite high in pts of the 1st and 2nd grs with opening of infarct-related coronary artery up to 2 hours at the beginning of the study (87.5±3.2 W in 1st and 91.7±3.2 W in 2nd gr). The increasing load was observed after 15 trainings in the 1st gr up to 116.7±3.6 W (Р<0.01), at the same time in the 2nd gr – up to 100.0±0.0 W, with further increasing of capacity in the 1st gr up to 130.0±3.6 W (Р<0.01). After late revascularization (> 6 hours) in the 1st gr the increase of work capacity from first to second and fourth tests was 88.5±4.6, 113.5±4.6 (Р<0.05) and 128.8±3.6 W (Р<0.01), in 2nd gr – 81.3±4.5, 85.4±3.7 and 90.0± 6.7 W, respectively (Р<0.01). Regardless of the extension of revascularization, the work capacity in the 1st gr increased (125.0±4.3 W at 2.5 th and 133.0±3.3 W at 6th month, Р<0.01), just as up to the 6th month in the 2nd gr. It achieved 104.0±6.5 W in complete revascularization and 85.7±5.0 W in incomplete revascularization.
Conclusions. It was established high effect of PT (30 sessions) at the cycle ergometer in individual regimen in early period after myocardial infarction during the 6-month follow up. Quite good recovery of work capacity in pts without PT was revealed only in subgroup with early revascularization (< 2 hours). Further studies are required to explain equally high effect of PT in pts with complete and incomplete revascularization.
The aim – to estimate the effect of intravenous 5-lipoxygenase inhibitor quercetine for prevention of the acute kidney injury (AKI) due to roentgen contrast media usage during percutaneous coronary interventions in patients with ST-elevation myocardial infarction (STEMI).
Material and methods. The retrospective cohort of 254 STEMI patients was studied. All the patients underwent the percutaneous coronary interventions (angiography alone, or followed by angioplastics/stenting) and had serial serum creatinine data. AKI (determined as rise in serum creatinine ≥ 44 μmol/l or ≥ 25 % rise in creatinine over baseline) was present in 40 cases (15.7 %). Then all cases were brought to the automated case-match-control pairing algorithm. Two matched groups of patients were selected: 24 pts were treated with quercetine 500 mg by intravenous infusion immediately before angiography and next 5 days – 500 mg twice daily intravenous (group 1) and 24 pts were controls (group 2). Cases were matched by 7 clinical criteria, including: age, gender, weight, prescription of drugs, which could affect serum creatinine levels (statins, ACE inhibitors, intestinal adsorbents, trimetazidine). Patients with severe congestive heart failure, nephropathy, anemia and systemic hypotension/shock at baseline were excluded.
Results. Incremental dynamics in serum creatinine level was observed in 37.5 % and 56.5 % of group 1 and group 2, respectively (mean 16.8±2.7 % vs 32.3±6.0 % of increase, respectively, Р<0.05). Rate of AKI incidence was 4.2 % in group 1 and 33.3 % in group 2 (Р<0.05). The cumulative rate of 2-10 day non-hemorrhagic adverse events was 45.8 % in group 1 and 91.7 % in group 2 (Р<0.001).
Conclusion. Our data suggest that infusion of 5-lipoxygenase inhibitor quercetine during acute phase of STEMI may prevent the development of AKI and related worsening of STEMI clinical course. This suggestion requires further investigation with larger number of patients in a prospective trial.
The aim – to determine the prevalence of gene polymorphism of folate metabolism in patients with myocardial infarction (MI) compared to healthy subjects in Ukraine.
Material and methods. The study involved 51 male, age up to 50 years (mean 43.21±2.8 yrs), who survived myocardial infarction in 2011–2014. The control group consisted of 35 male subjects, having no significant differences regarding age, smoking and hereditary history.
Results. The study of gene polymorphism revealed heterozygous type MTHFR 677 CT in 29 (56.9 %) patients with MI and 12 (34.3 %) healthy individuals (P<0.05), heterozygote MTHFR 1298 AS – in 25 (49.0 %) patients and 9 (25.7 %) healthy subjects (P<0.05).
Conclusions. Higher prevalence of gene polymorphism of MTHFR, MTR 2756, MTRR 66 among young survivors of myocardial infarction indicates the possible effect of folate metabolism disorders in the pathogenesis of myocardial infarction at a young age. The presence of genetic susceptibility significantly increases the risk of MI in this group of patients.