Kardiologiya最新文献

Aim: To study the clinical status and data of laboratory and instrumental examination of patients with non-obstructive ischemic heart disease (IHD) and multifocal atherosclerosis (MFA) included in the KAMMA registry.

Material and methods: The subanalysis included 1,893 IHD patients who underwent coronary angiography (CAG) and ultrasonic examination of peripheral arteries. Based on the CAG data, patients were divided into two groups: group 1, patients with obstructive coronary atherosclerosis (CA) (maximum stenosis ≥50% and/or history of percutaneous coronary intervention/coronary artery bypass grafting, n=1728; 91.3%) and group 2, patients with non-obstructive CA (maximum stenosis <50%, n = 165; 8.7%).

Results: A comparative analysis based on the degree of coronary obstruction in patients with verified IHD who were included in the KAMMA registry showed that 8.7% of them had coronary artery stenosis of less than 50%. The overwhelming majority of patients with non-obstructive CA had MFA affecting the brachiocephalic arteries in 94.3% and the lower extremity arteries in 40.2%. Among patients with non-obstructive IHD, women predominated; risk factors such as smoking and type 2 diabetes mellitus were less frequent in this group than in the obstructive IHD group. Patients with non-obstructive CA more frequently had a history of dyslipidemia; they had higher total cholesterol and non-high-density lipoprotein cholesterol; and they more frequently received moderate-intensity statin therapy than patients with obstructive CA (55.8% vs. 34.5%). Characteristic features of patients with non-obstructive CA were less severe IHD and less frequent history of acute coronary syndrome. However, the incidence of stroke, peripheral arterial thrombosis, and chronic arterial insufficiency of the lower extremities did not differ in groups 1 and 2, whereas the incidence of paroxysmal atrial fibrillation was higher in the non-obstructive IHD group.

Conclusion: IHD patients without coronary obstruction also require assessment of the peripheral arterial status, as they may have advanced MFA, which should be taken into account when choosing the "aggressiveness" of therapy.

Aim: Atrial fibrillation (AF) is a rhythm disorder characterized by very rapid and disorganized atrial-derived electrical activations with uncoordinated atrial contractions. Very short periods of AF-like activity (micro-AF) may be precursors of undetected, silent episodes of atrial fibrillation. Here, we examined the relationship between natriuretic peptide concentrations and echocardiography findings in patients with micro-AF.

Material and methods: The electrocardiograms (ECGs) of patients complaining of palpitations were recorded with a 24‑hour Holter monitor, and the patients were consecutively included in the study. Micro-AF was defined as sudden, irregular atrial tachycardia lasting less than 30 sec with episodes of ≥5 consecutive supraventricular depolarizations with the absolute absence of p-waves. After a G-power test, patients were consecutively included in the study: 45 patients in the micro-AF group and 45 patients in the control group. Laboratory parameters, ECG and echocardiographic findings of the two groups were compared.

Results: N-terminal pro B-type natriuretic peptide (Pro-BNP) and serum troponin T concentrations were higher in the micro-AF group, (375.5±63.6 pg / ml vs. 63.1±56.8 pg / ml, p<0.001; 13±11.4 ng / dl vs. 4.4±2.4 ng / dl, p<0.001 respectively.) Each 1 pg / ml increase in serum Pro-BNP increased the risk of micro-AF by 1.8 %. In the ROC analysis, the cut-off value of Pro-BNP for the diagnosis of micro-AF was 63.4 pg / ml, with a sensitivity of 91.1 % and a specificity of 73.3 %. Atrial electro-mechanical delay durations were significantly higher in the micro-AF group. To predict micro-AF, the inter-annulus plane electromechanical delay time (inter-annulus plane AEMD) had a cut-off value of 18.5 sec, with a sensitivity of 93.3 % and a specificity of 91.1 %. Left intra-annulus plane electro-mechanical delay time (intra-annulus AEMD LEFT) had a cut-off value of 11.5 sec with a 95.6 % sensitivity and 75.6 % specificity. In the ECG evaluation, maximum P wave duration (Pmax) (113±10.2 ms vs. 98±10.4 ms; p<0.001), minimum P wave duration (Pmin) (73.8±5.5 ms vs.70±6.3 ms; p<0.001) and P wave dispersion (PWD) (39.1±7.9 ms vs.28±7.6 ms; p<0.001) were longer in the micro-AF group.

Conclusions: Micro-AF in patients may be predicted by evaluating ECG, echocardiographic, and serum natriuretic peptide data.

Aim: To evaluate the efficacy and safety of azilsartan medoxomil for preoperative preparation and improving the long-term prognosis of elective percutaneous coronary intervention (PCI) in patients with ischemic heart disease (IHD), arterial hypertension (AH), and type 2 diabetes mellitus (DM).

Material and methods: The study sample included patients with type 2 DM referred for elective PCI who had poor blood pressure (BP) control according to 24-hour BP monitoring (24-BPM) (mean daily systolic BP ≥130 mmHg, mean daily diastolic BP ≥80 mmHg). The data were collected from 2018 through 2020. A total of 75 patients was included and distributed by simple randomization into two groups: group 1 (main, n=37) received azilsartan medoxomil as an antihypertensive drug at a dose of 40 mg/day (previously prescribed angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ARB) were discontinued); group 2 (control, n=38) continued on their previous antihypertensive therapy. The follow-up period was 6 months. During each of 5 consecutive follow-up visits, the patient was examined, 24-BPM was recorded, and urinary markers of renal dysfunction (glomerular filtration rate, GFR; neutrophil gelatinase-associated lipocalin, NGAL; urine albumin-creatinine ratio, UACR; kidney injury molecule, KIM-1; and interleukin-18, IL-18) were measured.

Results: During the azilsartan treatment, GFR decreased by 7.4%, while in the control group, it decreased by 18.9% (p<0.001). For 6 months of follow-up, no changes in the NGAL concentration were found in the main group, while the NGAL concentration in the control group increased by 12.9%. With azilsartan, there was a decrease in the urinary concentration of IL-18 (16.9%), while in patients of the control group, IL-18 increased (7.14%). Proteinuria progressed in both groups, which was expectable given the presence of DM; however, in patients receiving azilsartan, the UACR value increased by 37.5%, while in patients of the control group, it increased by 96.15%. These differences were statistically significant. No statistically significant differences were found in the concentrations of cystatin C and KIM-1.

Conclusion: This study demonstrated two important facts: the possibility for diagnosing contrast-induced acute kidney injury (CI-AKI) using new, more sensitive markers of kidney damage, which is important for assessing the effectiveness of prevention, and the possibility of using ARBs, in particular azilsartan, for the prevention of CI-AKI in patients with IHD in combination with AH and DM.

Aim: To evaluate the efficacy of cardiac resynchronization therapy (CRT) in patients with chronic heart failure (CHF) associated with cardiac dyssynchrony and to identify the factors that influence the CRT efficacy.

Material and methods: This retrospective study included 155 patients after implantation of CRT devices. The CRT devices with a built-in cardioverter-defibrillator (CRT-D) and without it (CRT-P) were implanted in 139 (89.7%) and 16 (10.3%) patients, respectively. The follow-up period was 52.37±35.94 months. Based on the study results, two groups of patients were formed depending on the presence of a clinical response to CRT, responders and non-responders. The factors that influenced the clinical response to CRT were studied. The effect of the baseline state of patients on the effect of therapy was assessed. The need for CRT optimization and a possibility of using electrocardiographic criteria for that purpose were studied. Modern devices and leads for CRT, their functional capabilities and their influence on the CRT efficacy were characterized. Statistical analysis was performed with an IBM SPSS Statistics 21.0 (Chicago, USA) package.

Results: CRT implantation with the left ventricular lead placement according to the traditional technique, through the coronary sinus, was successful in 130 (87.9%) patients. Difficulties with the left ventricular lead placement were noted in 13 (8.3%) patients when other techniques were used. After 6 months, a hemodynamic and clinical response was observed in 112 (72.2%) patients, and no positive response in 43 (27.8%). The increase in left ventricular ejection fraction in the responder group was more than 21.8±3.7%, which was associated with an improvement of the 6-minute walk test results. Th clinical response was significantly influenced by the possibility of stimulation from the basal parts of the heart; the use of more modern devices for CRT and quadripolar left ventricular leads; timely CRT optimization; and persistent dyssynchrony in non-responders. During the follow-up period, 34 (21.9%) patients died. The death rate in the non-responder group was significantly higher than in the responder group, 18 (41.3%) vs. 16 (14.3%), p=0.001. The main cause of death in the group of non-responders was CHF. Heart transplantation was performed in 3 (1.9%) patients.

Conclusion: CRT increases the life span and improves the quality of life in patients with CHF and cardiac dyssynchrony. There was a group of patients with no benefit from CRT in this study. Modern devices allow increasing the number of patients who benefit from CRT. Periodic optimization of CRT is necessary. When optimizing CRT, it is possible to use electrocardiographic criteria of effectiveness: duration of the QRS complex and changes in the position of the electrical axis of the heart.

Aim: To study clinical and demographic characteristics, treatment options, and clinical outcomes in patients with myocardial infarction with non-obstructive coronary arteries (MINOCA) compared with patients with myocardial infarction with obstructive coronary arteries (MIOCA).

Material and methods: This single-center prospective observational study included 712 successive patients diagnosed with acute myocardial infarction (MI), who routinely underwent direct coronary angiography. Based on the presence of stenosing coronary atherosclerosis, the patients were divided into two groups: MIOCA (coronary stenosis ≥50%) and MINOCA (coronary stenosis <50% without other, alternative causes). Clinical outcomes included in-hospital and long-term overall mortality, and cardiovascular rehospitalization. The median follow-up was 1.5 years.

Results: MINOCA was diagnosed in 73 (10.3%) patients, 37 (50%) of whom were women. The median age of patients with MINOCA was 61 years and in the MIOCA group 65 years. No significant differences in cardiovascular risk factors were found between patients with MINOCA and MIOCA. In 53.4% of cases, the cause of MINOCA was a discrepancy between the myocardial oxygen demand and supply, and in 35.6% of cases, the cause was hypertensive crisis and pulmonary edema. The factors associated with MINOCA included an age ≤58 years, female gender, absence of the ST-segment elevation, absence of areas of impaired local contractility, and presence of aortic stenosis and bronchopulmonary infection. Patients with MINOCA were less likely to be prescribed acetylsalicylic acid, P2Y12 inhibitors, dual antiplatelet therapy, beta-blockers, and statins (p<0.05). Data on long-term outcomes were available for 87.5% of patients (n=623). The prognosis of patients with MIOCA was comparable for in-hospital mortality (1.5% vs. 6.2%; p=0.161) and long-term overall mortality (6.1% vs. 14.7%; p=0.059). Cardiovascular rehospitalizations were more frequent in the MINOCA group (33.3% vs. 21.5%; p=0.042).

Conclusion: The prevalence of MINOCA in our study was 10.3% among all patients with acute MI. MINOCA patients had comparable generally recognized cardiovascular risk factors with MIOCA patients. MINOCA patients had a comparable prognosis for in-hospital and long-term mortality and more often required cardiovascular rehospitalization.

Assessing the functional capacity and exercise tolerance is an important and widely used research tool in patients with heart failure. It is used not only in cardiac rehabilitation and physical therapy, but also for inclusion criteria and outcome measures in studies of drug interventions. This document outlines the scope, guidelines for the implementation and interpretation, and limitations of the methods for assessing the functional capacity and exercise tolerance in clinical trials in patients with heart failure.

Aim: To evaluate the accuracy of a rapid test for semi-quantitative determination of NT-proBNP levels in the diagnosis of CHF in comparison with quantitative assessment; to study the strength of the association of the results of this NT-proBNP test with indicators of the CHF severity.

Material and methods: The concentration of NT-proBNP was determined in 44 patients at bedside both semi-quantitatively using an express test (BioTest, Novosibirsk) and quantitatively in a laboratory. In 11 patients, the severity of CHF was assessed with the CHF Clinical Status Scale (CSS). Echocardiography was performed in all patients.

Results: The sensitivity of the quantitative and semi-quantitative tests coincided and was 95%. The specificity of the quantitative test was 100% in our study, whereas the semi-quantitative test showed a specificity of 92%. The negative predictive value of either test was 96%. The diagnostic accuracy was 98% and 93%, respectively. In patients with significantly high NT-proBNP concentrations, the semi-quantitative test demonstrated a reduced ability to verify values above 1800 pg/ml; in patients with threshold concentrations, the semi-quantitative test showed an increased subthreshold sensitivity. Increases in the NT-proBNP concentration correlated with the severity of CHF according to the stage of the disease.

Conclusion: Due to the sufficiently high sensitivity, specificity, ease of use, and speed of obtaining results, the rapid test for semi-quantitative measuring NT-proBNP is promising for outpatient screening bedside diagnosis of CHF and in the emergency room to confirm or exclude CHF. When determining the dynamics of NT-proBNP during the treatment of CHF, the use of the semi-quantitative rapid test with visual assessment of the results may produce an error compared to the quantitative assessment, which will probably not allow tracking the effect of therapy or predicting exacerbation of the disease.

Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) or gliflozins, are a new class of cardiovascular drugs with a proven clinical efficacy and a beneficial effect on prognosis in patients with heart failure with preserved ejection fraction (HFpEF). Impaired left ventricular (LV) diastolic function (DF) is an important element in the pathogenesis of HFpEF. Experimental studies have found intracellular mechanisms for the so-called diastolic effects in gliflozins. Studies using laboratory models of experimental HFpEF have demonstrated a positive effect of dapagliflozin and empagliflozin on the elastic properties of cardiomyocyte myofilaments, the dynamics of myocardial fibrosis, and intracellular sodium and calcium homeostasis. The significance of anti-inflammatory, antioxidant properties of gliflozins in improving the cardiomyocyte DF has been experimentally established. The effect of SGLT2 inhibitors on LV DF in patients at high risk for cardiovascular diseases and their complications, that has been demonstrated in relatively small clinical studies, is due to primary cardiac and secondary effects. Results of individual studies confirmed the protective (in relation to myocardial relaxation) properties of gliflozins in the conditions of a diastolic stress test. The regression of LV diastolic dysfunction associated with the SGLT2 inhibitor treatment found in small observational studies is important in the context of the significant beneficial effect of empagliflozin and dapagliflozin on the prognosis of cardiovascular diseases that has been demonstrated in large randomized clinical trials in patients with HFpEF.

Aim: To verify the relationship between gene polymorphisms of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) with inflammation markers and codependent metabolic variables in patients with type 2 diabetes mellitus and chronic heart failure (CHF).

Material and methods: This study included 154 patients (mean age, 69.1±3.2 years). The control group consisted of 47 patients with metabolic syndrome (MS) without CHF; the 2nd group included 56 patients with CHF with preserved ejection fraction (CHFpEF); and the 3rd group consisted of 51 patients with CHF with reduced ejection fraction (CHFrEF). The rs1800629 polymorphism of the TNF-α gene (TNF-α: G308A) was studied in real time by the polymerase chain reaction (PCR) method and the rs1800795 polymorphism of the IL-6 gene (IL-6: 174 G>C) was studied by PCR with the electrophoretic detection. The frequencies of polymorphic alleles were compared with the clinical blood test results, plasma concentrations of C-reactive protein (CRP), TNF-α, leptin, and fibrinogen. Differences between the groups were determined using the F test. Relationships between individual studied parameters were identified using the regression analysis.

Results: In most patients, the occurrence of gene polymorphisms was eident as increased plasma concentrations of biomarkers. An association was found between the TNF-α gene polymorphism (G308A) and an increase in plasma TNF-α and between the IL-6 gene polymorphism (174 C>G) and an increase in plasma CRP. In the CHFpEF group, the rs1800629 gene polymorphism was observed in 55% of patients, among whom 93% had increased TNF-α. The rs1800795 gene polymorphism was observed in 82% of CHFpEF patients, among whom 21% had increased CRP. In the CHFrEF group, the G308A transition in the TNF-α gene was observed in 53% of patients; an increase in the respective cytokine was noted in 67% of patients; the IL-6 gene polymorphism 174 C>G was found in 78%, however, only 14% of patients with this polymorphism had also increased CRP. In the control group, the TNF-α G308A gene polymorphism was found in 30% of patients, while an increase in free TNF-α was associated with this polymorphism in 50% of patients; the IL-6 174 C>G gene polymorphism was detected in 78%, while no increase in the CRP level was observed in this group. This demonstrates a high probability of the TNF-α G308A gene polymorphism occurrence in patients with CHF.

Conclusion: Inflammatory markers are important predictors of CHF. The most significant predictor was the TNF-α G308A gene polymorphism, which was observed in more than 50% of patients, the majority of whom had an increase in plasma TNF-α.

The prognosis after heart transplantation continues to improve. Therefore, the prevention of chronic post-transplant sequelae, such as chronic kidney disease, allograft vasculopathy, and malignancies is becoming increasingly important. Everolimus, an inhibitor of the mammalian target of rapamycin (mTOR), is increasingly used for immunosuppression after heart transplantation. However, everolimus may cause a characteristic complex of adverse effects, including dyslipidemia. Currently there are no guidelines for the long-term screening and treatment of dyslipidemia in heart transplant recipients treated with everolimus. This article presents a clinical case of hypercholesterolemia that developed after the start of the everolimus treatment in a heart recipient. The patient was a 39-year-old man who underwent orthotopic heart transplantation for ischemic cardiomyopathy in 2012 (at the age of 27). In 2019, the patient's immunosuppressive therapy was converted from mycophenolate mofetil to everolimus due to the development of cardiac allograft vasculopathy. The change in the immunosuppressive therapy was associated with increases in total cholesterol and low-density lipoprotein cholesterol, which were not reversed with a combined lipid-lowering therapy (maximum doses of rosuvastatin, ezetimibe, fenofibrate). A decrease in lipid levels was achieved with a blocker of hepatic proprotein convertase subtilisin/kexin type 9 synthesis at the level of microribonucleic acid (inclisiran). This case demonstrates the difficulties in correcting dyslipidemia in patients with cardiac allograft, since the treatment with the immunosuppressant everolimus worsens existing dyslipidemia. However, the combination lipid-lowering therapy, that affects various elements of the pathogenesis (specifically, the combined inhibition of hydroxymethylglutaryl-CoA reductase with a statin, cholesterol absorption from the small intestine with ezetimibe, and PCSK9 messenger RNA with inclisiran), provides an effective control of blood lipids and minimizing the adverse effects of immunosuppressive therapy, such as cardiac allograft vasculopathy.