Background: Left bundle branch pacing (LBBP) has emerged as a physiological pacing strategy designed to preserve native ventricular activation and reduce the adverse effects of conventional right ventricular pacing. The introduction of stylet-driven leads for conduction system pacing has expanded accessibility, particularly in regions where lumenless systems are not readily available. Aim: To evaluate and summarize current evidence on the long-term effects of LBBP using stylet-driven leads on left ventricular systolic function, with emphasis on echocardiographic parameters such as mitral annular plane systolic excursion (MAPSE) and mitral annular peak systolic velocity (S’). Materials and Methods: A narrative literature review was conducted using PubMed, Scopus, and Web of Science databases to identify studies published between 2018 and 2025. Relevant original research articles, systematic reviews, and consensus statements addressing LBBP, stylet-driven lead implantation, and echocardiographic outcomes were included. Results: Recent evidence demonstrates that left bundle branch pacing (LBBP) preserves or improves left ventricular systolic function compared with conventional right ventricular pacing. Improvements in MAPSE and S’ suggest better ventricular synchrony and contractile efficiency. From a safety perspective, the MELOS-RELOADED Registry reported similar procedure-related complication rates between left bundle branch area pacing (LBBAP) and right ventricular pacing (RVP), with stable capture thresholds and sensing parameters during follow-up. These findings support the safety of LBBAP when performed by experienced operators. Conclusion: LBBP using stylet-driven leads is a feasible and effective physiological pacing modality that maintains left ventricular systolic function and broadens access to conduction system pacing. Long-term multicenter studies are needed to establish its durability, optimize device performance, and evaluate impacts on clinical outcomes such as heart failure progression and mortality.
Introduction. Pulmonary hypertension associated with congenital heart disease (PH–CHD) is characterized by reduced exercise tolerance and impaired functional capacity due to chronic pulmonary vascular disease and right ventricular pressure overload. Although supervised exercise training is recommended for stable pulmonary arterial hypertension, evidence in adults with PH–CHD remains limited. Aim. This study aimed to evaluate the effects of a short-term supervised aerobic exercise program on functional capacity and quality of life in adults with pulmonary hypertension associated with congenital heart disease. Materials and Methods. A quasi-experimental, single-group pre–post study was conducted in adults aged 18-50 years with PH–CHD, functional class I–III, and stable pharmacological therapy. Participants underwent a supervised, moderate-intensity aerobic exercise program (40-60 % of heart rate reserve), 30 minutes per session, twice weekly for six weeks. Functional capacity was assessed using the 6-minute walk test (6MWT). Secondary outcomes included estimated maximal oxygen consumption (VO₂ max), metabolic equivalents (METs), and quality of life assessed by the EMPHASIS-10 questionnaire. Results and Discussion. Thirteen participants completed the intervention. The mean 6-minute walk distance (6MWD) increased significantly from 331.62±38.46 m to 384.31±57.31 m (mean difference: 52.69 m; p<0.001). Estimated VO₂ max and METs also improved significantly (both p<0.001). Although EMPHASIS-10 scores showed a numerical reduction, the change was not statistically significant (p=0.445). No cardiovascular adverse events were observed. Conclusions. A 6-week supervised aerobic exercise program is safe and results in clinically meaningful improvements in functional capacity in adults with pulmonary hypertension associated with congenital heart disease; however, short-term training may be insufficient to significantly improve quality of life.
Introduction. In cardiac surgery patients, lower gastrointestinal bleeding (LGIB) can be a problem because of the antithrombotic therapy. Aim. To provide a comprehensive review of recent literature addressing lower gastrointestinal bleeding in patients with cardiovascular disease who are receiving antithrombotic therapy, with an emphasis on identifying sources of hemorrhage, strategies for prevention, and current treatment approaches. Materials and methods. English-language publications, obtained from the databases PubMed, Embase, and the Cochrane Library from January 2010 to March 2026, were analyzed. Results. The most common causes of LGIB are diverticular disease, angiodysplasia, inflammatory bowel disease, neoplasia, and anorectal pathology. Colonic diverticulosis is the cause of 25-66 % of LGIB. Direct oral anticoagulants (DOACs) are more likely to cause bleeding than warfarin. The source of bleeding can be detected by colonoscopy, CT angiography, selective angiography, digital rectal examination, anoscopy, and sigmoidoscopy. Endoscopic hemostasis is 85-95 % effective. Angiographic embolization is successful in 70-90 % of cases. Discussion and recommendations. Circulatory disorders, numerous comorbidities, duration of surgical operations, artificial circulation, and intensive anticoagulant therapy can make a source of bleeding that is not serious for the general cohort dangerous. Conclusions. LGIB in cardiac surgery patients is a critical complication. Anticoagulation requires a balance between the risks of bleeding and thrombosis. In patients at risk, potential sources of LGIB should be identified before heart surgery. Priority is given to minimally invasive methods of treating colorectal pathology. Apixaban has the lowest risk of bleeding profile. A cardiac surgery clinic should have a full arsenal of endoscopic and angiographic methods of hemostasis.
Background. High-risk percutaneous coronary intervention (HR-PCI) is increasingly performed in patients with complex coronary anatomy and severe left ventricular (LV) dysfunction. Mechanical circulatory support (MCS), including veno-arterial extracorporeal membrane oxygenation (V-A ECMO), is used to enhance procedural safety; however, its impact on long-term outcomes remains uncertain. Aim. To evaluate one-year clinical outcomes, safety, and prognostic determinants of prophylactic V-A ECMO use in patients undergoing HR-PCI. Materials and Methods. This prospective single-center observational study included 43 consecutive patients undergoing HR-PCI with planned V-A ECMO support between 2019 and 2025. The primary endpoint was all-cause mortality at 12 months. Secondary endpoints included major adverse cardiovascular and cerebrovascular events (MACCE), defined as a composite of death, myocardial infarction, stroke, and repeat revascularization. Left ventricular ejection fraction (LVEF) dynamics were also assessed. Results. Procedural success was achieved in 90.7 % of patients, with successful ECMO weaning in 88.4%. Major bleeding events classified as BARC 3-5 were observed in 20.9 % of patients, while vascular complications occurred in 11.6 %. Despite favorable periprocedural outcomes, all-cause mortality at 12 months was 25.6 %, and the incidence of MACCE was 46.5 %. Nonfatal myocardial infarction and stroke occurred in 4.7 % of patients each, while repeat revascularization was performed in 11.6 % of patients. Patients with baseline LVEF <30 % had significantly higher mortality (38.9 % vs. 16.0 %; p=0.048) and a higher incidence of MACCE (61.1 % vs. 36.0 %; p=0.048). Survival analysis demonstrated significantly lower one-year survival in this group (61 % vs. 84 %; log-rank p=0.048). A modest but statistically significant improvement in LVEF was observed at 6 and 12 months. Conclusions. Prophylactic V-A ECMO in HR-PCI provides high procedural success and effective hemodynamic stabilization; however, long-term outcomes remain primarily determined by baseline myocardial function. Severe left ventricular systolic dysfunction was a key predictor of adverse one-year outcomes, suggesting that V-A ECMO may improve procedural safety but does not necessarily translate into a significant long-term prognostic benefit.
Background. Heart rate variability (HRV) is a reliable indicator of neurohumoral regulation and adaptive capacity. Alterations in HRV reflect cardiovascular dysfunction, especially under excessive catecholamine exposure. High doses of epinephrine are known to induce myocardial ischemic injury, leading to cardiomyopathy accompanied by autonomic imbalance. Recent studies highlight the reparative potential of organ-specific peptide complexes derived from cryopreserved tissues, including xenogenic heart extracts. Aim. The study aimed to evaluate the effects of cryopreserved porcine heart extract (CPHE) on HRV dynamics in rats with experimentally induced epinephrine cardiomyopathy. Materials and methods. The experiments were performed on 73 adult white rats (250-350 g, 12 months old), divided into four groups: intact control, epinephrine only, epinephrine + amiodarone, and epinephrine + CPHE. Myocardial damage was induced by subcutaneous injection of epinephrine hydrotartrate (0.5 mg/100 g). CPHE was administered intraperitoneally (50 µg/100 g) daily for 4 weeks; amiodarone served as a reference drug (10 mg/kg, i.m.). HRV spectral indices (VLF, LF, HF, TP) were recorded using the “Poly-Spectrum/8B” system, and data were statistically processed using the Kruskal–Wallis test. Results. One day after epinephrine administration, total HRV power decreased 2.5-3.5-fold compared with normal values. Treatment with CPHE or amiodarone resulted in a transient increase in HF power and a significant reduction in the LF/HF ratio versus untreated animals (1.0-1.4 vs 2.2, p<0.05), indicating enhanced parasympathetic influence. By day 7, spectral power remained reduced in all groups. On day 14, total power increased by 37 % in the amiodarone group, while long-term administration (28 days) of both agents failed to restore HRV indices to normal values. Conclusions. CPHE administration in rats with epinephrine-induced cardiomyopathy temporarily enhances parasympathetic modulation at the early stages of treatment, reflecting a compensatory neurohumoral response. However, neither CPHE nor amiodarone restored HRV spectral power after one month, suggesting that toxic doses of epinephrine cause profound and prolonged autonomic dysfunction. These findings support the cardioprotective potential of xenogenic heart extracts while emphasising the severity of catecholamine-induced myocardial injury.
