Kardiologiya最新文献

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.

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.

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.

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.

The extensive use of therapeutic doses of heparin to prevent thrombosis in critically ill patients with COVID-19 during the pandemic has led to an increased incidence of bleeding and heparin-induced thrombocytopenia (HIT). In addition, the introduction of the AstraZeneca and Johnson&Johnson vaccines against COVID-19 into clinical practice was associated with the development of a rare but very severe, adverse thrombotic complication, vaccine-induced immune thrombotic thrombocytopenia (VITT). Thrombotic complications of VITT turned out to be similar to HIT both clinically and pathophysiologically. HIT is a potentially fatal immune-mediated adverse drug response that results in emergence of antibodies that activate platelets in the presence of heparin. HIT is characterized by a high incidence of venous and arterial thromboses, often with fatal outcomes. Currently, there are clearly defined international guidelines for the diagnosis, treatment and prevention of HIT. In case of thrombotic complications, non-heparin anticoagulants should be used.

Aim: Assessment of WNT1, WNT3a, and LRP6 concentrations in patients with ischemic heart disease (IHD) and obstructive and non-obstructive coronary artery (CA) disease.

Material and methods: This cross-sectional observational study included 50 IHD patients (verified by coronary angiography, CAG), of which 25 (50%) were men, mean age 64.9±8.1 years; 20 patients had non-obstructive CA disease (stenosis <50%), and 30 patients had hemodynamically significant stenosis. Concentrations of WNT1, WNT3a and LRP6 were measured in all patients.

Results: The concentrations of WNT1 and WNT3a proteins were significantly higher in patients with IHD and obstructive CA disease (p < 0.001), while the concentration of LRP6 was higher in the group with non-obstructive CA disease (p = 0.016). Data analysis of the group with obstructive CA disease showed a moderate correlation between WNT1 and LRP6 (ρ=0.374; p=0.042). Correlation analysis of all groups of patients with CA disease revealed a moderate association between the concentrations of WNT1 and uric acid (ρ=0.416; p=0.007). Regression analysis showed that risk factors for the development of IHD, such as increased body mass index, age, smoking, dyslipidemia, and hypertension, did not significantly influence the type of CA disease in IHD patients. According to ROC analysis, the obstructive form of IHD was predicted by a WNT3a concentration higher than 0.155 ng/ml and a LRP6 concentration lower than 12.94 ng/ml.

Conclusion: IHD patients with non-obstructive CA disease had the greatest increase in LRP6, while patients with obstructive CA disease had significantly higher concentrations of the canonical WNT cascade proteins, WNT1 and WNT3a. According to the ROC analysis, a WNT3a concentration >0.155 ng/ml can serve as a predictor for the presence of hemodynamically significant CA stenosis in IHD patients (sensitivity 96.7%; specificity 70%), whereas a LRP6 concentration >12.94 ng/ml can predict the development of non-obstructive CA disease (sensitivity 76.7%; specificity 65%).

Significant advances in timely diagnosis and modern antitumor therapy have led to a considerable increase in the survival rate of cancer patients. On the other hand, the incidence of cardiovascular (CV) diseases and their complications is increasingly growing, including due to side effects of anticancer drugs. CV complications are the most common cause of non-oncological death of cancer patients. The development of polychemotherapy-induced arterial hypertension (AH) is closely associated with the use of certain groups of drugs, for example, inhibitors of vascular endothelial growth factor (iVEGF). Such AH is generally dose-dependent and reversible after interruption or termination of treatment. However, systemic AH, regardless of its genesis, is one of the key risk factors for many CV events (myocardial infarction, stroke, heart failure, arrhythmias) and kidney disease. Therefore, thorough blood pressure monitoring and its timely and adequate correction if needed are indicated when using certain groups of chemotherapy drugs. This article describes a clinical follow-up of a patient with induced AH associated with the iVEGF antitumor therapy for advanced uterine cancer with a rapid development of left ventricular myocardial dysfunction.