Michał Maksymilian Wilk

Introduction: Takayasu arteritis (TA) is a rare large-vessel vasculitis that in selected patients can lead to severe cardiovascular complications, including advanced heart failure (HF), requiring heart transplantation (HTx). Marked pre-transplant high levels of anti-HLA antibodies and notable sensitization substantially complicate donor selection and may prolong time spent on transplant waitlists. In highly sensitized recipients, HTx may therefore require individualized perioperative desensitization strategies to reduce the risk of antibody-mediated graft injury. Case Summary: We present the case of a 46-year-old woman with TA and advanced HF who underwent HTx after individualized perioperative desensitization in the setting of significant pre-transplant sensitization (PRA > 60%). Her postoperative course required intensive clinical and immunological monitoring and treatment. The early PT course was complicated by severe clinical deterioration, including a life-threatening episode of asystole that occurred in temporal association with peak anti-HLA class I and II antibody levels. Discussion: The case highlights the complexity of alloimmune management in a patient with TA and marked pre-transplant sensitization. Also, the temporal relationship between peak antibody levels and clinical instability suggests the need for close immune surveillance, tailored desensitization and individualized immunosuppressive treatment strategies in this high-risk group. Conclusions: This case describes the clinical course of a highly sensitized patient with TA who underwent HTx following an individualized perioperative desensitization strategy based on a modified Hannover protocol. Although transplantation was followed by substantial postoperative complications, the patient remained clinically stable during follow-up. The efficacy of the modified desensitization strategy cannot be established from a single case.

Introduction: Heart transplantation (HTx) remains the definitive treatment for selected patients with advanced heart failure. The early post-transplant period is characterized by substantial morbidity and requires intensive surveillance. The aim of this study was to describe the clinical course of the first 100 heart transplant recipients treated at our newly established center, with particular emphasis on in-hospital outcomes and the 12-month follow-up. Methods: We retrospectively analyzed 100 consecutive patients who underwent orthotopic HTx between February 2021 and May 2023 at our center. Demographic, clinical, hemodynamic, laboratory, treatment, and post-transplant follow-up data were collected. The follow-up assessment included survival, rejection, infectious complications, renal replacement therapy (RRT), heart failure decompensation, hospitalizations, outpatient visits, and changes in pharmacotherapy. Cox proportional hazards regression and Receiver Operating Characteristic (ROC) analyses were also performed to assess factors associated with 12-month mortality. Results: The study population comprised 82 (82%) men and 18 (18%) women with a median age of 54 years (IQR, 45–64). The in-hospital course was characterized by substantial early morbidity: 17 patients (17%) died during the index hospitalization, with a median time to death of 17 days (IQR, 3–78). RRT was required in 44% of patients. Among hospital survivors, the median length of hospital stay was 43 days and the median ICU stay was 7 days. During the 12-month follow-up, clinically significant cellular graft rejection (grade ≥ 3) occurred at least once in 51% of patients, infectious complications in 45%, and one patient underwent retransplantation. The twelve-month all-cause mortality was 23%. Patients had a mean of 8 planned hospitalizations, 0.4 unplanned admissions, and 1.3 outpatient visits per patient. Exploratory analyses identified possible associations between selected pre-transplant variables and 12-month mortality. Conclusions: The first 100 HTx recipients treated at the newly established center experienced a clinically demanding in-hospital course, with a 17% in-hospital mortality. After discharge, the first year remained characterized by frequent cellular rejection incidence, and infectious complications. The twelve-month survival was 77%. These findings provide a comprehensive description of the early in-hospital and 12-month clinical course of a newly established Htx program.

Introduction: Adipose tissue (AT) is increasingly recognized as an active endocrine and immunological organ involved in the pathophysiology of heart failure with preserved ejection fraction (HFpEF). Dysfunctional AT, particularly visceral, promotes chronic low-grade inflammation, endothelial dysfunction, and microvascular damage. At the same time, higher body mass is associated with paradoxically lower natriuretic peptide (NP) levels, which may impact diagnostic accuracy in HFpEF. Methods: This narrative review summarizes the current evidence on the interplay between adipose tissue, NPs, and HFpEF, focusing on pathophysiological mechanisms, AT distribution, and clinical implications. Results: Adipokine-mediated inflammation contributes to the myocardial stiffness, fibrosis, and cardiac remodeling characteristic of HFpEF. Visceral adipose tissue, including epicardial fat, exhibits a more proinflammatory profile than subcutaneous fat. Obesity is associated with decreased NP levels due to increased clearance and decreased production. Consequently, lower NP levels may lead to underdiagnosis or misclassification of HFpEF, particularly in diagnostic algorithms such as HFA-PEFF and H₂FPEF. Patients with low BMI or cachexia exhibit elevated NP levels, reflecting advanced disease and catabolic states. Conclusions: The obesity-natriuretic paradox poses a key diagnostic challenge in HFpEF. Interpretation of natriuretic peptide levels should take body composition into account, and refinement of biomarker cutoff values may improve diagnostic accuracy.

Heart failure (HF) remains a major challenge in cardiovascular medicine, contributing to high global rates of hospitalization and mortality. Recent research (2022–2025) has emphasized its heterogeneity, highlighting distinct phenotypes—HFpEF, HFmrEF, and HFrEF—driven by mechanisms such as chronic inflammation, myocardial fibrosis, and neurohormonal imbalance. Advances in therapy, particularly with sodium–glucose cotransporter-2 inhibitors (SGLT2i), angiotensin receptor–neprilysin inhibitors (ARNI), and iron supplementation, have reshaped treatment strategies. Moreover, the growing recognition of overlaps between HF and cardiomyopathies such as hypertrophic, Takotsubo, and amyloidosis underscores the need for integrated care. This review summarizes recent findings from leading journals, mapping the evolving understanding of HF pathophysiology and management, and outlining emerging directions for research and clinical practice.

In recent years, significant advancements in the understanding of the processes underlying heart failure (HF) have been made, particularly regarding the role of chronic low-intensity inflammation or smoldering inflammation (SI). This review consolidates findings from the available literature and illustrates the relationships between inflammation, neurohormonal activation, metabolic derangements, and comorbidities in HF, with a focus on heart failure with preserved ejection fraction (HFpEF).A comprehensive literature search was conducted using PubMed®, Wiley Online Library, Scopus, and Web of Science (limited to 2025). The search terms included "heart failure", "HFpEF", "inflammation", "smoldering inflammation", "biomarkers", "cytokines", "fibrosis", and "comorbidities". Peer-reviewed articles, reviews, as well as clinical and observational studies describing the mechanistic, prognostic and therapeutic aspects of SI in HF were included. Studies limited to acute coronary syndrome (ACS) were excluded.Structural changes leading to hemodynamic perturbations in HFpEF are correlated with processes mediated by SI. Several biomarkers measure inflammation and provide diagnostic and prognostic value, including C-reactive protein (CRP), interleukin-6 (IL-6), soluble suppression of tumorigenicity 2 (sST2), galectin-3 (Gal-3), and iron homeostasis. Clinical trials demonstrate the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide 1 (GLP-1) receptor agonists, and other targeted interventions in the modulation of SI.Smoldering inflammation is a key mechanism in the pathogenesis of HFpEF and the progression of comorbidities. Understanding SI may improve risk stratification and management strategies. Both established and emerging anti-inflammatory therapies, when administered alone or in combination, may target SI in order to enhance HF management.

Heart failure (HF) is a challenging syndrome, affecting 64 million people worldwide, and is associated with high mortality rates. There are several potential biomarkers that help us diagnose the disease as well as help us assess the prognosis. Cardiac troponins I and T are effective tools for predicting poor outcomes in HF. Cardiac troponins are intracellular proteins responsible for regulating and conducting muscle contractions. They indicate cardiomyocyte injury caused by ischemia, toxins, inflammation, wall stress, and other factors. Some of these injuries may be reversible. The blood level of troponins is influenced by various factors, both physiological—such as sex, age, and weight—and pathological, including microbiological organisms, autoantibody complexes, and conditions like pulmonary embolism, stroke, sepsis, or kidney disease. Numerous studies demonstrate the effectiveness of troponin measurement in prognostication for patients with acute and chronic HF. However, it has been found that many patients with chronic heart failure have undetectable serum levels of cardiac troponins, leading to the adoption of high-sensitivity cardiac troponins (hs-cTn). Expanding this knowledge is crucial for enabling more intensive stratification and early identification of patients with poorer prognoses.

This narrative review explores the multifaceted role of lactate in heart failure (HF), focusing on its diagnostic and prognostic significance in both acute and chronic HF. Lactate functions not only as a marker of hypoperfusion and anaerobic metabolism but also as an active metabolic substrate. In acute HF, elevated lactate levels often signal circulatory insufficiency and predict adverse outcomes. In chronic HF, especially HFpEF, lactate dynamics during exercise reflect metabolic inefficiency and correlate with functional impairment. This review emphasizes the dual nature of lactate and discusses its potential utility in risk stratification and therapeutic guidance.

Heart failure (HF) is a complex clinical syndrome characterized by the heart’s inability to maintain sufficient circulation, leading to inadequate organ perfusion and fluid buildup. A thorough understanding of the molecular, biochemical, and hemodynamic interactions that underlie this condition is essential for improving its management and enhancing patient outcomes. Recent advancements in cardiovascular research have emphasized the critical role of microRNAs (miRNAs) as post-transcriptional regulators of gene expression, playing an important part in the development and progression of HF. This review aims to explore the contributions of miRNAs, systemic congestion markers, and traditional biomarkers to the pathophysiology of heart failure, with the objective of clarifying their prognostic value and potential clinical applications. Among the miRNAs studied, miR-30d, miR-126-3p, and miR-483-3p have been identified as key players in processes such as left ventricular remodeling, regulation of pulmonary artery pressure, and adaptation of the right ventricle. These findings underscore the importance of miRNAs in modulating the structural and functional changes seen in HF. Beyond the heart, HF affects multiple organ systems, including the kidneys and liver, with markers of dysfunction in these organs—such as worsening renal function and liver stiffness—being closely linked to increased morbidity and mortality. This highlights the interdependence of the heart and other organs, where systemic congestion, indicated by elevated venous pressures, exacerbates organ dysfunction. In this context, traditional biomarkers like natriuretic peptides and cardiac troponins remain vital tools in the diagnosis and management of HF. Natriuretic peptides reflect ventricular strain, while troponins are indicators of myocardial injury, both of which are critical for risk stratification and monitoring disease progression. Emerging diagnostic techniques, such as lung ultrasonography and advanced echocardiographic methods, offer new ways to assess hemodynamic status, further aiding therapeutic decision-making. These techniques, alongside established biomarkers, provide a more comprehensive approach to understanding the complexities of heart failure and managing its impact on patients. In conclusion, miRNAs, systemic congestion markers, and traditional biomarkers are indispensable for understanding HF pathophysiology and determining patient prognosis. The integration of novel diagnostic tools with existing biomarkers holds the promise of improved strategies for the management of heart failure. However, further research is needed to validate their prognostic value and refine their role in optimizing treatment outcomes.