Aim      To evaluate the concentration of the WNT signaling cascade proteins (WNT1, -3a, -4, -5a) and the state of the vasculature by photoplethysmography (PPG) in patients with different phenotypes of stable ischemic heart disease (IHD), with obstructive and non-obstructive coronary artery disease (CAD).

Material and methods  This cross-sectional observational study included 80 patients (45-75 years old) with a verified diagnosis of stable IHD. Based on the results of coronary angiography or multislice spiral computed tomography coronary angiography, the patients were divided into two equal groups (n=40), with obstructive IHD (oIHD), and ischemia with no obstructive CAD or angina with no obstructive CAD (INOCA/ANOCA). In the oIHD group, men prevailed (67.5%) while in the INOCA/ANOCA group, women prevailed (57.5%). Noninvasive PPG evaluation of the vasculature was performed, and WNT1, -3a, -4, and -5a concentrations were measured by ELISA in all patients.

Results Higher concentrations of the WNT1 and WNT3a proteins were found in patients with oIHD (p<0.001) while the INOCA/ANOCA group had a significantly higher concentration of WNT5a (p=0.001). According to the PPG data, the arterial stiffness index (aSI) significantly differed between the INOCA/ANOCA (7.6 m/s [6.6; 9.35]) and oIHD (9.25 m/s [7.88; 10.33]) groups, p=0.048). The correlation analysis revealed a relationship between WNT1 and the reflectance index RI (ρ=0.359; p=0.014) in IHD patients (oIHD+INOCA/ANOCA). According to the ROC analysis, the curve for WNT3a turned out to be diagnostically significant (sensitivity and specificity of the model were 85.7 and 87.0%, respectively). The cut-off value of WNT3a was 0.183 pg/ml.

Conclusion      The results of the study showed that the activation of the canonical WNT cascade (WNT1 and WNT3a) was observed in patients with oIHD, while the non-canonical cascade (WNT5a) was activated in patients with INOCA/ANOCA. The obstructive IHD phenotype can be predicted with a WNT3a value ≥0.183 pg/ml.

Aim      To study the role of early blood tests using the polymerase chain reaction (PCR) (before or at initial stages of antibacterial therapy, within the first 24-48 hours after diagnosis) for the diagnosis of infective endocarditis (IE) and improvement of the etiological algorithm.

Material and methods  The study included 154 patients with confirmed IE (DUKE, 2015) who underwent standard microbiological (culture) blood tests with a simultaneous molecular biological test (PCR study/sequencing) on the same type of biological material at the stage of primary diagnosis.

Results In 117 (76.0%) examined patients, the etiologic agent was determined in blood samples by any of the methods used. Concordant results were obtained in 43 (36.8%) patients and discordant in 4 (3.4%) patients. In 29 (24.8%) patients, the causative agent of IE was determined only by the microbiological (cultural) examination of blood samples, and in 25 (21.4%) patients, only by the PCR study, including 3 cases of Bartonella spр. 23 patients had results of the microbiological (culture) blood tests that required clarification (70% CoNS, 26% gram-negative bacteria, one case of Enterococcus faecalis); 16 (69.6%) of 23 were not confirmed by the molecular biological method and were interpreted as contamination. In 1/3 of patients, the PCR blood study allowed increasing the accuracy of determining the causative agent of IE. Based on the integrated approach to the etiological diagnosis of IE, criteria for determining the causative pathogen were developed. This allowed reclassifying 9 (5.9%) diagnoses into the category of confirmed IE and to de-escalate the antibacterial therapy in every third examined patient. The microbiological and PCR studies of blood demonstrated comparable indexes of sensitivity, specificity and diagnostic accuracy [79.0, 86.0, 81.0% and 67.0, 93.0, 74.0%, respectively]. The PCR study of blood at the early stages of IE diagnosis (before or during the initial antibacterial therapy, within the first 24-48 hours after the IE diagnosis) is proposed as a control for Streptococcus spp., Staphylococcus aureus, CoNS, Enterococcus spр., and at the later stages of laboratory examination, especially in IE with an unspecified pathogen, as a priority method.

Conclusion      The PCR study of blood samples is a highly informative method for the etiological diagnosis of IE that allows increasing the accuracy of the pathogen identification in every third patient and, thus, prescribing an effective antibacterial therapy.

Enhanced cancer treatment efficacy has resulted in a significant increase in the number of cancer survivors after the cure of malignant tumors. However, cardiovascular morbidity, including chronic heart failure, has become the leading cause of death and decreased life expectancy among cancer survivors. This is due, in particular, to the cardiotoxic effects of anticancer drugs and associated factors. Cardioprotective approaches aim to reduce the incidence and severity of cardiotoxicity through the use of cardioprotective agents (e.g., dexrazoxane), liposomal drug delivery systems (e.g., liposomal doxorubicin), and optimization of drug administration schedules. Reducing the cardiotoxicity of cancer treatments is a clinically important goal. Phosphocreatine-based therapy represents a potentially valuable new strategy in this area. In this regard, the study "Multicenter prospective observational study to investigate the experience of using phosphocreatine in combination therapy for heart failure caused by cancer treatment" was initiated. This publication presents the protocol of the observational non-interventional NEOCARD study.

Aim    To compare the effects of two combined antihypertensive therapies on indices of the structural and functional state of the left ventricular (LV) myocardium and intrarenal vascular resistance in patients with arterial hypertension (AH) and prediabetes.
Material and methods    The study included 80 patients with poorly controlled AH and prediabetes who were randomized into two groups: patients in group 1 (n=40) received perindopril at a starting dose of 5 mg/day, sustained-release indapamide 1.5 mg/day, and metformin 1000 mg/day; patients in group 2 (n=40) received perindopril 5 mg/day, moxonidine at a starting dose of 0.2 mg/day, and metformin 1000 mg/day. Subsequently, if necessary, the doses of perindopril and moxonidine were titrated to the maximum permissible ones. Prediabetes was diagnosed based on the results of an oral glucose tolerance test. Ultrasound examination of the heart and renal arteries was performed with a SIEMENS ACUSON X 300 ultrasound apparatus (Korea). Statistical analysis was performed using the Statistica 12.0 software (StatSoft Inc., USA).
Results    In both groups after 24 weeks of pharmacotherapy, patients who achieved the target blood pressure had statistically significant and comparable improvements in all studied parameters of the structural and functional state of the LV myocardium and intrarenal vascular resistance. In a comparable number of patients in both groups, the treatment was associated with normalization of the LV myocardial geometry and diastolic function. The combination including moxonidine was associated with a significant decrease in fasting plasma insulin that was more pronounced than with the diuretic treatment.
Conclusion    In patients with AH and prediabetes, the combination therapy including perindopril, metformin and moxonidine provided a significant improvement in the structural and functional state of the LV myocardium and intrarenal vascular resistance comparable to the improvement produced by a combination of perindopril, metformin and sustained-release indapamide. The combination of an ACE inhibitor, biguanide and moxonidine may in some cases be a preferred pharmacotherapy option for patients with AH and early carbohydrate metabolism disorders due to the observed significant metabolic benefits.

Ischemic heart disease, including previous myocardial infarction (MI), is one of the main causes for the development and progression of heart failure (HF). The presence of HF before MI or the development of HF in the setting of acute coronary catastrophe is an extremely unfavorable prognostic factor leading to a multiple increase in the risk of death and rehospitalization due to HF in the post-infarction period. In 2024, the results of two randomized clinical trials (RCTs) (DAPA-MI and EMPACT-MI) were published, which assessed the effect of sodium-glucose co-transporter type 2 inhibitors (SGLT2i) on clinical outcomes in patients with acute MI. In both studies, the predetermined primary composite endpoint was not achieved. At the same time, it was shown that SGLT2i significantly reduced the risk of hospitalization for HF (empagliflozin) and contributed to the improvement of metabolic outcomes (dapagliflozin). Also, the safety of early initiation of SGLT2i in the acute period of MI was demonstrated. Based on the available results of randomized and observational clinical studies, the working group has substantiated the need for implementing these RCT results into clinical practice and proposed an algorithm for administering SGLT2 to patients with acute MI. Thus, in the presence of compelling anamnestic criteria for the diagnosis or previously diagnosed type 2 diabetes mellitus, and/or chronic kidney disease, and/or HF, continuation or timely initiation of SGLT2i during the hospitalization for index MI is recommended to improve cardiovascular and renal outcomes. Based on the results of RCTs in patients with acute MI and taking into account individual risk factors for the development of HF, the initiation of SGLT2i before discharge may be considered in order to reduce the risk of hospitalization for HF.

Abstracts of the National Congress with international participation "Heart Failure 2024". Moscow, 07.12.2024 - 09.12.2024