Andrzej Tomasik

Background: Cardiometabolic diseases present a major challenge to contemporary public health. Diabetes mellitus (DM) is widely recognized as a strong cardiovascular risk factor. However, the utility of glycated hemoglobin percentage (HbA1c) for assessing cardiovascular health in individuals without DM remains uncertain. This study examines the association between HbA1c levels and both the presence and severity of subclinical atherosclerosis and arterial stiffness in non-diabetic individuals. Methods: A retrospective analysis was conducted on the data from 59 patients (72.88% female; mean age: 54.82 ± 17.34 years) who exhibited no signs of acute illness or exacerbation of chronic diseases. All patients were hospitalized in the Department of Internal Medicine, Angiology and Physical Medicine at the Medical University of Silesia in Katowice, Poland, between June 2022 and May 2024. HbA1c level determination, central blood pressure measurement with pulse wave analysis (PWA), carotid–femoral pulse wave velocity (cfPWV) measurement, and Doppler ultrasound of the carotid arteries and lower extremity arteries measuring the intima–media thickness (IMT) in the common carotid arteries (cIMT), common femoral arteries (cfIMT), and superficial femoral arteries (sfIMT) were performed. Spearman’s rank correlation test was applied for statistical analysis. Subsequently, a multivariate analysis model was constructed, adjusting for age, sex, body mass index (BMI), and smoking. Results: Among the assessed parameters, the strongest positive correlations were found between HbA1c and parameters such as cIMT (R = 0.532; p < 0.001), cfIMT (R = 0.63; p < 0.001), sfIMT (R = 0.539; p < 0.001), and cfPWV (R = 0.504; p < 0.001). In the multivariate analysis model, a significant relationship was found only between HbA1c and augmentation index normalized to a heart rate of 75 per minute (AIx75) (β = −0.286; 95% CI: −0.566, −0.006; p = 0.045). Conclusions: In summary, although HbA1c correlates with some parameters related to arterial stiffness and subclinical atherosclerosis in non-diabetic patients, most observed relationships are explained by confounding variables.

Sarcopenia is increasingly recognized as a key extracardiac manifestation of heart failure (HF), contributing to functional impairment, reduced quality of life, and adverse clinical outcomes. Characterized by progressive loss of skeletal muscle mass, strength, and physical performance, it affects more than half of hospitalized HF patients. It is independently associated with increased mortality and reduced exercise capacity. The pathophysiology of sarcopenia in HF is multifactorial and closely linked to metabolic and nutritional disturbances. Chronic inflammation, neurohormonal activation, oxidative stress, endothelial dysfunction, and anabolic resistance contribute to muscle catabolism and impaired protein synthesis. These alterations are further exacerbated by inadequate dietary protein intake and micronutrient deficiencies, promoting progressive muscle wasting and functional decline. Sarcopenia may also represent an early and potentially modifiable stage in the continuum toward cardiac cachexia. This narrative review provides a comprehensive synthesis of current evidence on the epidemiology, pathophysiological mechanisms, and management of sarcopenia in HF, with particular emphasis on nutritional and metabolic determinants. Emerging data support a multimodal therapeutic approach integrating exercise training with targeted nutritional strategies, including adequate protein intake, essential amino acid supplementation, and correction of micronutrient deficiencies. However, evidence from large, well-designed trials remains limited. In summary, improved recognition and integrated management of sarcopenia in HF are essential. Future research should focus on the development of effective, nutrition-centered therapeutic strategies.

Sarcopenia is increasingly recognized as a key extracardiac manifestation of heart failure (HF), contributing to functional impairment, reduced quality of life, and adverse clinical outcomes. Characterized by progressive loss of skeletal muscle mass, strength, and physical performance, it affects more than half of hospitalized HF patients and is independently associated with increased mortality and reduced exercise capacity. The pathophysiology of sarcopenia in HF is multifactorial and closely linked to metabolic and nutritional disturbances. Chronic inflammation, neurohormonal activation, oxidative stress, endothelial dysfunction, and anabolic resistance contribute to muscle catabolism and impaired protein synthesis. These alterations are further exacerbated by inadequate dietary protein intake and micronutrient deficiencies, promoting progressive muscle wasting and functional decline. Sarcopenia may also represent an early and potentially modifiable stage in the continuum toward cardiac cachexia. This narrative review provides a comprehensive synthesis of current evidence on epidemiology, pathophysiological mechanisms, and management of sarcopenia in HF, with particular emphasis on nutritional and metabolic determinants. Emerging data support a multimodal therapeutic approach integrating exercise training with targeted nutritional strategies, including adequate protein intake, essential amino acid supplementation, and correction of micronutrient deficiencies. However, evidence from large, well-designed trials remains limited. In summary, improved recognition and integrated management of sarcopenia in HF are essential. Future research should focus on the development of effective, nutrition-centered therapeutic strategies.

Background: There exists some inconsistent evidence on the relationship between altered cardiac morphology, its function, and frailty. Therefore, this study aimed to assess the associations among frailty, lean body mass, central arterial stiffness, and cardiac structure and geometry in older people with a normal ejection fraction. Methods: A total of 205 patients >65 years were enrolled into this ancillary analysis of the FRAPICA study and were assessed for frailty with the Fried phenotype scale. Left ventricular dimensions and geometry were assessed with two-dimensional echocardiography. Fat-free mass was measured using three-site skinfold method. Parametric and non-parametric statistics and analysis of covariance were used for statistical calculations. Results: Frail patients were older and women comprised the majority of the frail group. Frail men and women had comparable weight, height, fat-free mass, blood pressure, central blood pressure, and carotid–femoral pulse wave velocity to their non-frail counterparts. There was a linear correlation between the sum of frailty criteria and left ventricular end-diastolic diameter (Spearman R = −0.17; p < 0.05) and relative wall thickness (Spearman R = 0.23; p < 0.05). In the analysis of covariance, frailty and gender were independently associated with left ventricular mass (gender: β of −0.37 and 95% CI of −0.50–−0.24 at p < 0.001), the left ventricular mass index (gender: β of −0.23 and 95% CI of −0.37–−0.09 at p < 0.001), and relative wall thickness (frailty: β of −0.15 and 95% CI of −0.29–−0.01 at p < 0.05; gender: β of 0.23 and 95% CI of 0.09–0.36 at p < 0.01). Frailty was associated with a shift in heart remodeling toward concentric remodeling/hypertrophy. Conclusions: Frailty is independently associated with thickening of the left ventricular walls and a diminished left ventricular end-diastolic diameter, which are features of concentric remodeling or hypertrophy. This association appears to be more pronounced in women. Such adverse cardiac remodeling may represent another phenotypic feature linked to frailty according to the phenotype frailty criteria.

Background: There exists some inconsistent evidence on the relationship between altered cardiac morphology, its function, and frailty. Therefore, this study aimed to assess the associations among frailty, lean body mass, central arterial stiffness, and cardiac structure and geometry in older people with a normal ejection fraction. Methods: A total of 205 patients >65 years were enrolled into this ancillary analysis of FRAPICA study and were assessed for frailty with Fried phenotype scale. Left ventricular dimensions and geometry were assessed with two-dimensional echocardiography. Fat-free mass was measured using three-site skinfold method. Parametric, non-parametric statistics and analysis of covariance were used for statistical calculations. Results: Frail patients were older and women comprised the majority of the frail group. Frail men and women had comparable weight, height, fat-free mass, blood pressure, central blood pressure, and carotid-femoral pulse wave velocity to their non-frail counterparts. There was a linear correlation between the sum of frailty criteria and left ventricular end diastolic diameter (negative) and relative wall thickness (positive). In the analysis of covariance, frailty and gender were independently associated with left ventricular mass, left ventricular mass indexed, and relative wall thickness. Frailty shifts heart remodeling toward concentric remodeling/hypertrophy. Conclusions: Frailty is independently associated with thickening of the left ventricular walls and a diminished left ventricular end-diastolic diameter, leading to concentric remodeling or hypertrophy. This phenomenon is more pronounced in women. This adverse cardiac remodeling may serve as another phenotype feature of frailty according to the phenotype frailty criteria.

Regular physical activity has a beneficial impact on the cardiovascular system. However, the intense and prolonged exertion typical of professional athletes and amateur marathon runners can lead to adaptive changes in the heart. These changes encompass both structural and functional modifications, which may have positive or negative effects on cardiac function and contribute to the development of so-called “athlete’s heart.” Prolonged exercise induces adaptations at the molecular and cellular levels, including altered gene expression and remodeling of myocardial proteins. It may also cause transient elevations in biomarkers such as N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin. Some athletes experience cardiac arrhythmias, including atrial fibrillation. Morphological changes, such as myocardial hypertrophy or chamber dilation, can be assessed using echocardiography. Studies have reported potentially benign valvular abnormalities, as well as cases of myocardial fibrosis and arrhythmias. Early diagnosis of cardiac conditions in marathon runners is essential for effective prevention and health monitoring. This article reviews the current data on cardiac changes in endurance athletes, based on the literature from the past decade.

Background: Frailty syndrome significantly worsens the prognosis of elderly people. Sarcopenia and malnutrition are integral parts of aging, but there is a lack of knowledge about the overlap of these states, as well as their diagnostic methods and treatments. This study aimed to assess the malnutrition and sarcopenia scale in patients with frailty syndrome and the viability of evaluating the concentrations of the following potential biomarkers: albumin, total protein, and fibrinogen. Methods: A total of 170 patients >65 years were assessed for frailty using the Fried frailty scale. The risk of sarcopenia was measured using the SARC-F scale, and the risk of malnutrition was measured using the Mini Nutritional Assessment (MNA) scale. Serum albumin, protein, and fibrinogen levels were measured. The following fat-free body mass and respiratory parameters were measured: peak expiratory flow (PEF) and forced expiratory volume-one second (FEV1). Results: A total of 53 patients were classified as robust (31%), 96 as prefrail (57%), and 21 as frail (12%) according to Fried frailty criteria. Frail patients had significantly reduced serum albumin and increased fibrinogen compared to the prefrail and robust groups (p < 0.05). A total of 38% of frail patients were at risk of sarcopenia, and 52% were at risk of malnutrition. Frail patients had lower PEF and FEV1 values, with decreases in respiratory parameters correlating with fat-free body mass and muscle strength. Conclusions: Frail patients are at substantial risk of malnutrition and sarcopenia. The MNA and SARC-F scales, combined with routine screening of elderly patients with frailty, may effectively identify patients with the highest risk.

Diabetes-related pathophysiological processes contribute to endothelial dysfunction, arterial stiffening (AS), hypertension, vascular remodeling, and impaired myocardial perfusion. This study aimed to assess the relationship between arterial wall parameters and sST2 concentration as potential risk factors in type 2 diabetes (T2DM) and investigate sex-related differences. To achieve this, we enrolled 100 patients with suspected or exacerbated coronary artery disease (CAD) and divided them into a T2DM group (n = 58) and a control group (n = 42). Endothelial reactivity (lnRHI), ABI, sST2 levels, and carotid–femoral (cfPWV) and carotid–radial pulse wave velocity (crPWV) were assessed. Coronary angiography was performed in every patient, and epicardial flow and myocardial perfusion were evaluated using QuBE and FLASH. Our results showed that the coronary angiographic findings were similar in both groups. However, T2DM patients had a significantly higher central AS (cfPWV 10.8 ± 2 vs. 9.9 ± 2.7 m/s, p < 0.05) and vascular age (70.0 ± 12.3 vs. 61.3 ± 15.4 years, p < 0.05), while peripheral AS, RHI, and ABI showed no differences. CfPWV correlated with renal function; higher HbA1c and sST2 levels were additionally associated with advanced vascular age. Notably, central AS and vascular age were higher in men with T2DM but not in women. These findings indicate that T2DM patients exhibit increased central AS and vascular aging, influenced by sST2 levels, suggesting fibrosis as a target for precision medicine in T2DM.

. Background: Frailty syndrome significantly worsens the prognosis of elderly people. An integral part of aging is sarcopenia and malnutrition. There is a lack of knowledge about the overlap of these states, as well as diagnostic methods and treatment. Methods: 170 patients >65 years were assessed for frailty using the Fried frailty scale. The risk of sarcopenia was measured using the SARC-F scale, and the risk of malnutrition was measured using the Mini Nutritional Assessment (MNA) scale. Serum albumin, protein, and fibrinogen levels were measured. Fat-free body mass and respiratory parameters were measured: peak expiratory flow (PEF) and forced expiratory volume- one second (FEV1). Results: 53 patients were classified as robust (31%), 96 as prefrail (57%), and 21 as frail (12%). Frail patients had significantly reduced serum albumin and increased fibrinogen compared to the pre-frail and robust groups (p<0.05). 38% of frail patients are at risk of sarcopenia, and 52% are at risk of malnutrition. Frail patients have lower PEF and FEV1 values. The decrease in respiratory parameters correlates with fat-free body mass and muscle strength. Conclusions: Patients with frailty are the group at most significant risk of malnutrition and sarcopenia compared to their healthy peers and patients in the prefrail stage. MNA and SARC-F scales combined with routine screening of elderly patients with frailty may allow for effective identification of patients at risk of malnutrition and sarcopenia.

Epigenetic biomarkers offer promising potential for early identification and risk stratification of frail individuals susceptible to adverse cardiovascular outcomes. This scope review aimed to identify and evaluate epigenetic biomarkers concurrently associated with frailty and increased cardiovascular risk, potentially facilitating more precise patient stratification and treatment decisions. A two-stage literature search was performed using PubMed, Scopus, Web of Science, and Embase databases from the year 2000 through 27 December 2024. Stage 1 identified studies reporting epigenetic biomarkers associated with frailty in blood-derived human samples. Stage 2 assessed cardiovascular relevance by screening the frailty biomarkers identified in Stage 1 for their documented association with cardiovascular diseases. Two independent reviewers conducted screening, data extraction, and risk-of-bias assessments, resolving disagreements via a third reviewer. The primary outcomes were the association of biomarkers with frailty severity and cardiovascular risk. Key epigenetic biomarkers identified included microRNAs (particularly miR-21, miR-146a, miR-451, and miR-92a) and DNA methylation markers (LINE-1 methylation, epigenetic clocks like GrimAge and DunedinPACE, and possibly novel, emerging clocks like DNAmCVDscore and the Smoking Index). Due to specificity limitations, these biomarkers are most promising when used collectively as part of multimarker panels rather than individually. Future research should validate multimarker panels, explore novel biomarkers, and assess clinical integration to optimize precision medicine in frail cardiovascular populations.