Kardiologiya最新文献

It is known that the advances in cancer treatment leading to increased survival in malignant neoplasms, entail a variety of adverse cardiovascular toxic effects that can be quite serious and even potentially fatal. An important component that influences the degree of cardiotoxicity risk is the patient's clinical and functional state and the cardiovascular history at the time of cancer diagnosis. This information can be used in practice for the cardiovascular screening and clinical and functional evaluation of a patient with a neoplasm before the start of antitumor therapy. After completion of the cardiotoxic therapy, as well as during subsequent follow-up, it is advisable to re-evaluate the risk of long-term cardiotoxicity to determine the frequency and intensity of cardiovascular monitoring. For convenience of calculating the risk of cardiotoxicity in cancer patients undergoing the antitumor treatment, the authors of this article have developed two computer programs that can be used as PC applications (https://disk.yandex.ru/d/NuhzYnicWo9FSw) and on mobile devices (https://disk.yandex.ru/d/uXAriKZ6qhkULA.). These programs facilitate the selection of the correct strategy for the management of cancer patients that is aimed at reducing the likelihood of cardiotoxic complications of the antitumor treatment.

Background: Traditional right ventricular pacing (RVP) can lead to asynchronous cardiac mechanical contractions and increase the risk of adverse cardiac events. This study aimed to compare the clinical complications between left bundle branch area pacing (LBBAP), which is both novel and physiological, and RVP in a cohort requiring ventricular pacing.

Material and methods: A retrospective study was conducted on patients with initial implantation of a dual-chamber, permanent pacemaker and with ventricular pacing proportion more than 20 % from January 2019 to December 2020. Patients were divided into the LBBAP or RVP group and follow-up was conducted routinely. The primary outcome was ventricular lead complications, including an increase in the ventricular lead threshold or a decrease in R-wave amplitude. Overall complications were defined as ventricular lead complications, ventricular lead dislocation, ventricular lead perforation, adverse cardiovascular events and cardiovascular death.

Results: A total of 248 patients were included in the analysis (LBBAP, n=98; RVP, n=150). The pacing QRS duration in LBBAP patients was significantly shorter than in RVP patients (110.3±22.7 vs 140.0±29.3 ms, p<0.01). For a mean follow-up duration of 13 mos, the risk of ventricular lead complications was higher in the LBBAP group than in the RVP group (62.0 % vs. 36.5 %, p=0.03). LBBAP was comparable to RVP within one year follow-up when considering overall complications. At the one year follow-up ultrasound examinations, the LA in LBBAP group was decreased (p=0.04). Considering the larger initial left ventricular end-diastolic diameter (LVEDD) in the LBBAP group, the similarity of LVEDD values in both groups at follow-up suggested that LVEDD was reduced in patients treated with LBBAP. There was no difference in left ventricular ejection fraction (LBBAP LVEF, baseline = 61.2±8.6 %) between the two groups at baseline or follow-up.

Conclusions: LBBAP patients were more prone to ventricular lead threshold increase and amplitude decrease than RVP patients. The risk of overall complications in the two pacing modalities were equal in one year follow-up duration. LBBAP is safe and effective in patients with VP>20 % and without seriously depressed LVEF.

The review addresses principal approaches to intensifying therapy in patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). The position of Russian experts on the strategy of switching within one class of PAH-specific therapy is presented. Particular attention is paid to the strategy of therapy optimization in the form of replacing phosphodiesterase type 5 inhibitors with a stimulator of soluble guanylate cyclase (riociguat) in patients with PAH and inoperable/residual CTEPH who cannot not achieve treatment goals on phosphodiesterase type 5 inhibitors. The authors analyzed and identified the criteria justifying the choice of a specific therapy strategy in favor of switching from a phosphodiesterase type 5 inhibitor to riociguat.

Background: The primary objective was to investigate the relationship between and obesity and epicardial fat volume (EFV) in individuals diagnosed with coronary artery disease (CAD), with the aim of determining whether a consistent linear relationship exists among these factors.

Material and methods: This cross-sectional study involved a total of 510 participants. To explore the relationship between EFV and obesity in CAD patients, we controlled for potential confounding variables, including age, sex, diabetes mellitus, smoking history, arterial hypertension, hypercholesterolemia, hypertriglyceridemia, statin use, vasculopathy, and prior acute myocardial infarction.

Results: After adjusting for confounding factors, a non-linear relationship was observed between obesity and EFV, with an inflection point identified at 200 ml. The effect sizes and their respective confidence intervals were 1.02 (CI: 1.02-1.03) and 0.99 (CI: 0.98-1.00) on either side of this inflection point. Below a EFV of 200 ml, a positive correlation between obesity and EFV was apparent.

Conclusion: The relationship between obesity and EFV in CAD patients is non-linear, and this should be considered when developing prognostic models for CAD. The findings suggest that the relationship between EFV and obesity is more complex than previously thought and warrants further investigation to better understand its implications for both CAD and obesity risk assessment and management.

Background: Heart failure (HF) is a global health issue, and its complication with acute kidney failure (AKF) increases the risk of mortality. This study aimed to investigate the predictive value of fluid balance for mortality in patients with HF complicated by AKF. A retrospective analysis was performed using the MIMIC-IV database to evaluate the relationship between fluid balance and mortality in patients with HF complicated by AKF.

Material and methods: Adult patients with HF and AKF and who were listed in the MIMIC-IV database between 2008 and 2019 were included. The patients were divided into survival and non-survival groups. The primary outcome measure was fluid intake and output in the first three days in the intensive care unit (ICU). The main outcome being in-ICU mortality and the secondary outcome being 28‑day mortality after ICU admission. A multivariable Cox proportional hazards model was used to assess the relationship between fluid balance and the risk of death, after adjusting for potential confounding factors.

Results: A total of 1433 eligible patients were included. The study found that compared to the death group, patients in the survival group maintained lower positive balance on day 1 (453.51 ml vs 1813.66 ml), negative balance on day 2 (-246.75 ml vs 646.00 ml), and negative balance on day 3 (-350.21 ml vs 312.92 ml). Additionally, fluid balance on the first day predicted ICU mortality rate (AUC 0.658, p<0.01), on the second day it predicted ICU mortality rate (AUC 0.654, p<0.01), and on the third day it also predicted ICU mortality rate (AUC 0.634, p<0.01).

Conclusion: Positive fluid balance in patients with HF and AKF is independently associated with higher in-hospital mortality. Monitoring and managing fluid balance may provide clinicians with an important tool to improve patient outcomes.

The article addresses the diagnostic criteria based on magnetic resonance imaging (MRI) in transient constrictive pericarditis (TCP), a rare form of constrictive pericarditis characterized by temporary signs of constriction. Constrictive pericarditis evident as myocardial thickening and fibrosis results in impaired diastolic filling and can manifest itself with symptoms similar to those of other pathologies, such as restrictive cardiomyopathy. The article presents two clinical cases of TCP, where the role of MRI in the diagnosis and monitoring of patients is highlighted. For diagnostics, echocardiography and MRI were used along with laboratory tests, including the tests for inflammation markers and troponin. MRI allows not only to visualize changes in the pericardial structure but also to monitor changes in the condition, which is important for choosing the treatment tactics. In both cases, symptoms were successfully resolved, and the patients' condition was normalized with drug therapy. The results highlight the importance of early diagnosis and proper management tactics to prevent irreversible changes in the pericardium and heart failure.

Aim: To determine the characteristics of atherosclerotic plaques (ASP) remaining after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS), that are significantly associated with cardiovascular events (CVE), according to computed tomography angiography (CTA) data.

Material and methods: CTA was performed in 249 ACS patients on days 3-7 of the disease (in 41 patients, on a 64-slice CT scanner, and in the rest, on a 320-slice CT scanner). CTA data of all patients were analyzed on a Vitrea workstation. Patients with at least one noncalcified atherosclerotic plaque were included.

Results: During 39.1 [18.0; 57.4] months of follow-up (from 7 days to 128 months), 71 of 249 (28.5%) ACS patients had the primary endpoint (PEP), which included non-fatal myocardial infarction, unstable angina, cardiac death, PCI, and ischemic stroke. According to the univariate Cox analysis, 14 of 30 CTA characteristics of ASP turned out to be significant predictors of achieving the PEP: the number of involved arteries (HR=1.314, CI: 1.06-1.628, p=0.013, C=0.59); the total length of ASPs (HR=1.013, CI: 1.005-1.022, p=0.002, C=0.62); the number of ASPs with obstructive stenosis (HR=1.286, CI: 1.095-1.509, p=0.002, C=0.61); the minimum density (HR=0.968, CI: 0.949-0.987, p=0.001, C=0.64); a minimum density <30 HU (HR=2.695, CI: 1.495-4.869, p=0.0009, C=0.62); the number of ASPs with a minimum density <30 HU (HR=1.391, CI: 1.186-1.633, p=0.00005, C=0.64); the number of ASPs with a minimum density ≤46 HU (HR=1.211, CI: 1.043-1.407, p=0.012, C=0.58); the presence of a low-density area <30 HU (HR=2.387, CI: 1.389-4.101, p=0.001, C=0.57); the number of atherosclerotic plaques with a low-density area <30 HU (OR=1.912, CI: 1.317-2.775, p=0.001, C=0.57); the number of atherosclerotic plaques with spotty calcifications (HR=1.384, CI: 1.134-1.688, p=0.001, C=0.59); the maximum length (HR=1.014, CI: 1.001-1.028, p=0.041, C=0.61); the maximum stenosis (HR=1.018, CI: 1.002-1.033, p=0.025, C=0.61); the presence of a low-density area ≤46 HU (HR=2.049, CI: 1.24-3.386, p=0.005, C=0.57); the number of ASPs with a low-density area ≤46 HU (HR=1.643, CI: 1.191-2.265, p=0.002, C=0.58). [HR, hazard ratio; CI, 95% confidence interval; C, Harrell's C statistics]. According to the multivariate analysis, the first 10 of the listed CTA characteristics retained their prognostic significance, while the predictive significance was found for the "total plaque burden", a conditional characteristic we first proposed, which is the sum of the areas (burden) of all plaques identified by CTA in the patient.

Conclusion: 14 CTA characteristics of ASPs in patients with ACS are significant predictors of future CVE, and 11 of them are independent of known risk factors.

During the development of chronic heart failure (CHF), the lungs and the external respiratory system (ERS) as a whole undergo significant remodeling. These changes are most clearly manifested during physical exercise (PE), when the requirement for ventilation increases, and the ERS works under stress. Patients with CHF during exercise are characterized by the so-called pattern of frequent shallow breathing, when minute ventilation increases mainly due to an increase in the respiratory rate, and the depth of breathing increases to a much lesser extent than in individuals without CHF. The pattern of frequent shallow breathing is an adaptive response that prevents rapid exhaustion of the respiratory muscles (RM) due to the decreased compliance of the lung tissue and airways, and, accordingly, increased work of breathing typical of patients with CHF. In such conditions, tachypnea becomes the only available mechanism for maintaining the required ventilation volume. As the exercise load increases, the inability to adequately increase the depth of breathing contributes to the growth of physiological dead space, and the ventilation efficiency drops. The progressive decrease in the ventilation efficiency is evident as a paradoxically low level of carbon dioxide released relative to the ventilated volume. Such "working conditions" lead to hyperactivation of the inspiratory metaboreflex, which causes a whole pathogenetic cascade, including sympathicotonia, deterioration of the blood supply to the motor muscles and hyperactivation of their metaboreflex, which leads to further limitation of exercise tolerance. Sympathicotonia characteristic of CHF enhances the activation of carotid chemoreceptors. Along with hypocapnia, this can lead to the development of periodic breathing and central sleep apnea to further worsen the prognosis. Progressive sympathicotonia, hypoxia, endothelial dysfunction, and chronic inflammation result in aggravation of skeletal muscle myopathy. Thus, the condition of RM is at least an important, if not the leading factor in the pathogenesis of impaired exercise tolerance, which requires continuous therapeutic treatment. Such treatment cannot be of a "rehabilitation" nature, i.e., be used for a limited time, but must be performed on a permanent basis. The search for optimal methods of the respiratory and skeletal muscle training in order to weaken the mutually reinforcing connection between the carotid chemoreflex and muscle metaboreflex, as well as the search for such forms of their implementation, in which they will become a permanent part of the treatment, is extremely important for successful management of CHF patients.

Advances in modern drug and surgical treatment of patients with hypertrophic cardiomyopathy (HCM) have resulted in a significant increase in the life expectancy of these extremely severe patients. Therefore, in addition to the genetic markers, major neurohumoral systems and morpho-functional parameters of intracardiac hemodynamics, the course and prognosis of the disease are influenced by concomitant pathology. In infancy and early childhood, HCM is associated with tumors of chromaffin tissue of various localizations; however, the older the patient, the greater the likelihood of developing metabolic syndrome, secondary atherosclerosis and ischemic heart disease (IHD), and hypertension, which significantly complicates the verification of the HCM diagnosis. We have previously described cases of IHD secondary to HCM, which significantly affected the course and prognosis of both diseases. However, in old age, other comorbidities may also occur in addition to the diseases described above. Based on long-term observation of a large cohort of patients, this article analyzes a wide range of HCM combinations with pathology of other organs and systems, including malignant neoplasms, which makes significant adjustments to the treatment of both the underlying disease and cancer. The material is presented in the form of a brief review of literature on this topic and our own clinical observations and studies.

Aim: To study the plasma proteome of patients with type 1 acute myocardial infarction (AMI) to identify potential markers for long-term prognosis of the risk for developing cardiovascular complications.

Material and methods: The study included 64 patients with type 1 AMI with and without ST segment elevation who underwent primary percutaneous coronary intervention upon admission. The following information on cardiovascular events was collected for 36 months after admission: death from cardiovascular pathology, recurrent AMI, stroke, repeat myocardial revascularization and/or endarterectomy. Peripheral blood sampling followed by a plasma proteome analysis using chromatography-mass spectrometry was performed in all patients before hospitalization.

Results: During 36 months after hospitalization, cardiovascular complications were detected in 23 (36%) patients. These patients were included in the group with an unfavorable prognosis, while the remaining patients made up the group with a positive prognosis. A mass spectrometric analysis of the plasma proteome and comparison of the groups identified seven differentially represented proteins. Also, a multivariate regression analysis, ROC curves, and Kaplan-Meier models showed that four proteins (apolipoprotein C1, complement factor H, di-N-acetylchitobiase, and ficolin-2) were predictors of the risk for developing cardiovascular complications in the long term. An integrated parameter was developed that took into account the plasma concentrations of all four above proteins. This parameter was used to construct a model for assessing the risks of unfavorable long-term prognosis in AMI patients with a sensitivity of 87% and a specificity of 78%.

Conclusion: The study results demonstrated that plasma concentrations of apolipoprotein C1, complement factor H, di-N-acetylchitobiase, and ficolin-2 are reliable prognostic markers for assessing the risks of cardiovascular events in patients with AMI in the long term.