Vol 28, No 1 (2026): Cardiology and nephrology

Constrictive pericarditis (CP) is a relatively rare disease characterized by impaired ventricular diastolic filling resulting from thickening, fibrosis, and reduced elasticity of the pericardial layers, leading to the development of chronic heart failure (HF). The etiology of CP is heterogeneous and includes infectious, autoimmune, iatrogenic, and other causes. Traumatic etiology of this condition is extremely rare and may be associated with delayed onset of clinical manifestations, which significantly complicates timely diagnosis. This article presents a clinical case of post-traumatic CP in a 47-year-old patient that developed four months after combined blunt chest trauma. Initially, the disease manifested as exudative pericarditis; however, despite anti-inflammatory therapy, signs and symptoms of HF persisted and progressed. The diagnosis was established based on comprehensive instrumental evaluation, including echocardiography, cardiac magnetic resonance imaging, and computed tomography. Characteristic features of CP were identified, such as a D-shaped left ventricle, increased respiratory variation of transmitral flow, thickening of the pericardial layers, the presence of fibrous adhesions, and signs of restricted ventricular diastolic filling. Conservative therapy, including anti-inflammatory and glucocorticosteroid agents, proved to be insufficiently effective. Due to persistent pericardial constriction and ongoing clinical manifestations of HF, pericardiectomy was performed. Surgical treatment resulted in marked clinical improvement, normalization of hemodynamic parameters, and regression of echocardiographic signs of constriction. Histological examination of the excised pericardium confirmed pronounced sclerotic and inflammatory changes. Clinical case highlights the necessity of long-term follow-up of patients after chest trauma and emphasizes the importance of multimodal imaging for early diagnosis of post-traumatic pericardial involvement. In addition, the case illustrates the complexity of differential diagnosis of HF in atypical disease courses and underscores the importance of a multidisciplinary approach involving cardiologists, functional diagnostics specialists, and cardiovascular surgeons at all stages of the diagnostic and therapeutic process.

Background. Despite numerous studies on COVID-19, the cardiac complications of this infection in people with valvular heart disease, in particular, with aortic insufficiency (AI), are poorly understood. Echocardiographic analysis of signs of subclinical myocardial dysfunction in people with AI after coronavirus infection with COVID-19 may be promising for the prevention of heart failure and adverse cardiac events.

Aim. To study echocardiographic markers of myocardial dysfunction in people with AI after coronavirus infection with COVID-19.

Materials and methods. The results of echocardiography of 59 patients with AI were analyzed 1 and 6 months after recovering from COVID-19 infection of varying severity. The criteria for non-inclusion in the study were patients with hemodynamically significant valvular heart disease requiring surgical treatment, patients with cancer (receiving chemotherapy), patients with severe concomitant pathology, patients with signs of acute inflammation, with unsatisfactory visualization of the heart, as well as patients who refused to participate in the study. Echocardiography was performed using an ultrasound system Vivid E95 with an assessment of standard parameters, as well as global longitudinal strain of the left ventricle (GLS LV) and 3D left ventricular ejection fraction.

Results. In patients with AI, 1 month after severe COVID-19, compared with the control, a decrease in global longitudinal strain with normal LVEF values, an increase in the right ventricle, a decrease in systolic excursion of the tricuspid annular plane systolic excursion (TAPSE) and tricuspid annulus systolic velocity and there is also an increase in the estimated systolic pressure of the pulmonary artery. These changes in individuals with AI persisted 6 months after severe COVID-19. At the same time, there was a more pronounced increase of the right ventricle.

Conclusion. Our results may indicate the presence of subclinical LV dysfunction with preserved LVEF, structural and functional changes in the right ventricle, and pulmonary hypertension in patients with AI from 1 to 6 months after severe COVID-19. Dynamic echocardiographic monitoring is recommended for patients with AI after severe COVID-19 infection, including assessment of global longitudinal strain of the left ventricle, size and contractility of the right ventricle, and the estimated systolic pressure of the pulmonary artery.

Coronary artery disease (CAD) remains a leading cause of mortality, and its frequent coexistence with atrial fibrillation (AF) significantly worsens prognosis, presenting physicians with a complex choice between stroke prevention, protection from coronary events, and minimization of bleeding risk. Even in patients with stable CAD, a high residual risk of thrombotic complications persists, driven by ongoing activation of the coagulation cascade, which traditional antiplatelet monotherapy cannot fully control. The strategy of dual pathway inhibition of thrombus formation has improved treatment outcomes: adding rivaroxaban at a "vascular" dose of 2.5 mg twice daily to acetylsalicylic acid provides a significant reduction in the risk of cardiovascular death and ischemic events with an acceptable safety profile. This approach is justified in patients at high ischemic risk, particularly those with a history of myocardial infarction or multivessel CAD. In the presence of AF, the principles of antithrombotic protection fundamentally change, mandating the inclusion of full-dose anticoagulation. The key strategy to address this challenge is treatment de-escalation: from the shortest possible courses of triple therapy (anticoagulant plus two antiplatelet agents) in the acute phase after percutaneous coronary intervention to dual therapy (anticoagulant plus clopidogrel) during the first year of follow-up. In the long term, stable patients benefit from a transition to anticoagulant monotherapy, which is non-inferior to combination therapy in preventing thrombotic events and significantly superior in terms of safety, as confirmed by large clinical trials and meta-analyses. Thus, rivaroxaban possesses the most comprehensive evidence base among direct oral anticoagulants, covering the entire spectrum of clinical scenarios, from secondary prevention in isolated CAD to the management of patients with concomitant AF. This enables a truly individualized approach, carefully balancing ischemic and bleeding risks in real-world clinical practice.

Background. Rapid ventricular pacing is routinely used during balloon aortic valvuloplasty and transcatheter aortic valve implantation (TAVI). Temporary right ventricular (RV) pacing via a temporary transvenous pacing lead is the standard approach. Direct left ventricular (LV) pacing using a 0.035-inch guidewire during transcatheter aortic valve procedures may represent a promising alternative and warrants further investigation.

Aim. To compare outcomes of LV rapid pacing via a 0.035-inch guidewire with conventional RV rapid pacing using a temporary transvenous pacing lead during TAVI.

Materials and methods. From 2015 to 2025, data from 217 patients who underwent TAVI at the Moscow City Center of Interventional Cardioangiology of Sechenov First Moscow State Medical University (Sechenov University), were retrospectively analyzed. The present analysis included two comparable cohorts: 53 patients who underwent conventional transvenous RV pacing and 57 patients who received LV pacing via a guidewire. Primary endpoints were in-hospital (7-day) and 30-day mortality. Secondary endpoints included successful pacing with the required hemodynamic effect, procedure duration, fluoroscopy time, contrast volume and permanent pacemaker implantation, and intra- and perioperative complications.

Results. No differences were observed in primary endpoints; in-hospital and 30-day mortality were 0% in both groups. In the guidewire-based LV pacing group, rapid pacing was successful in all cases, and no crossover to conventional transvenous pacing was required. Guidewire-based pacing was associated with a reduction in fluoroscopy time (median 21.2 vs 26.0 min; p=0.016) and radiation exposure (median 1.7 vs 3.0 mSv; p=0.036). Two cases of cardiac tamponade occurred in the conventional RV pacing group due to RV perforation by the temporary pacing lead. No myocardial perforation occurred in the guidewire pacing group.

Conclusion. LV rapid pacing via a 0.035-inch guidewire during TAVI is a safe and effective technique providing reliable pacing with a low complication rate and may reduce fluoroscopy time and radiation exposure.

Cardiovascular diseases (CVD) represent a leading cause of mortality in most industrialized countries. Community-acquired pneumonia significantly worsens the clinical course of CVD and increases the risk of cardiovascular death. Streptococcus pneumoniae (pneumococcus) is one of the most common etiological pathogens of community-acquired bacterial pneumonia. It may cause direct myocardial injury through hematogenous dissemination, as well as exert indirect deleterious effects on the cardiovascular system via the induced inflammatory response and the action of bacterial toxins, the most important of which is pneumolysin. Myocardial and vascular wall injury, along with platelet activation, may substantially contribute to the decompensation of heart failure, as well as to the development of myocardial infarction, stroke, and cardiac arrhythmias in patients with pneumonia. Most cardiovascular complications (CVC) occur during the early acute phase of pneumonia; however, some may also develop in the delayed period, creating conditions for the long-term persistence of an increased risk of cardiovascular death for several years after the infection. The risk of CVC in patients with pneumonia may be reduced by the use of aspirin and statins, as well as effective antibiotic therapy; however, these approaches do not completely eliminate the risk. Vaccination against pneumococcal infection is the most effective method for the prevention of CVC associated with S. pneumoniae. Currently, several types of pneumococcal vaccines are available, with conjugate vaccines being the most advanced, providing sustained immunity against the most prevalent pneumococcal serotypes after a single administration. Vaccination against S. pneumoniae is recommended across a wide spectrum of CVD, including pulmonary hypertension, chronic heart failure, myocarditis, and dilated cardiomyopathy. Broad implementation of pneumococcal vaccination in patients at high cardiovascular risk may significantly reduce both the incidence of cardiovascular complications and overall mortality in this population.