3 articles
Patients with heart failure frequently present with varying degrees of skeletal muscle dysfunction, from early fatigue to sarcopenia and cachexia. Sarcopenia, defined as the loss of muscle mass and/or function, contributes to the physical dimension of frailty. Both conditions are associated with adverse outcomes in heart failure. Although sarcopenia and frailty often coexist, they are distinct syndromes with a bidirectional relationship with heart failure. According to European data, the prevalence of sarcopenia ranges from 20-50% in heart failure with reduced ejection fraction and approximately 18% in heart failure with preserved ejection fraction. This study aimed to evaluate sarcopenia among frail patients with chronic heart failure and to identify associated risk and protective factors.
A cross-sectional observational study was conducted on 44 frail patients with chronic heart failure. Data collection included clinical, functional, and anthropometric parameters, using the SARC-Calf questionnaire, gait speed and the Timed Up and Go test. Patients were stratified into three study groups according to frailty severity assessed by the Edmonton Frail Scale: Study Group 1 – mild frailty, Study Group 2 – moderate frailty, and Study Group 3 – severe frailty. Statistical analysis included Chi-square and Fisher’s exact tests. Odds Ratios with 95% Confidence Intervals were calculated. A p < 0.05 was considered statistically significant.
Of the 44 patients included, 32 (72.7%) were women and 12 (27.3%) men, with a mean age of 67.3 ± 8.9 years. Sarcopenia risk (SARC-Calf ≥4) was identified in 56.8%, and severe sarcopenia in 15.9%, exclusively among women. Functional impairment was present in 88.9% of Study Group 1, 91.7% of Group 2, and 100% of Group 3. Arterial hypertension (71.4%), diabetes mellitus (57.1%), and obesity (42.8%) were more prevalent among sarcopenic patients. C-reactive protein levels >6 mg/L and elevated NT-proBNP were associated with sarcopenia risk (p = 0.039). Metformin use was linked to absence of sarcopenia (p = 0.008), while low physical activity, statin use, and inflammation were more frequent in sarcopenic patients.
Sarcopenia was highly prevalent in frail heart failure patients, particularly among women. Cardiac dysfunction, inflammation, and metabolic comorbidities are key contributors, highlighting the need for early screening and tailored interventions.
Refractory heart failure with a poor prognosis is a key feature of dilated cardiomyopathy. Inflammatory cardiomyopathy, often diagnosed via in vivo subendomyocardial biopsy, is considered a potential precursor to dilated cardiomyopathy. The Dallas criteria, applied to morphometric and electron microscopic studies of biopsy samples, are essential for differentiating the features of various inflammatory stages. Building upon these established diagnostic principles, our study integrates immunohistological analysis with measurements of intramyocardial indices and intracardiac hemodynamics. This comprehensive approach aims to characterize the natural course of inflammatory cardiomyopathy, seeking to improve the understanding of the clinical trajectories and tissue structures that define both inflammatory cardiomyopathy and its progression to dilated cardiomyopathy.
The study included 75 patients with inflammatory cardiomyopathies and 75 patients with dilated cardiomyopathies. The following procedures were performed: coronary angioventriculography, repeated subendomyocardial biopsy, immunohistologic analysis, and assessment of intracardiac and intramyocardial hemodynamics.
Morphohistologic analysis of inflammatory cardiomyopathies at different stages revealed a maximum of 10-12 lymphocytes, which decreased to only isolated lymphocytes in late stages. In biopsies from early-stage inflammatory dilated cardiomyopathies, the morphologic appearance showed lymphocytic infiltration of the myocardial stroma, vasculitis of intramural arteries and arterioles. The biopsies performed after 36 months showed dystrophic structures, microfocal and diffuse replacement fibrosis, predominantly perivascular, which are indistinguishable from the features of dilated cardiomyopathy. Intracardiac hemodynamic indices in patients with dilated and inflammatory cardiomyopathies did not differ. Similarly, left ventricular regional contractility, as verified by radiopaque ventriculography, was not significantly different. The degree of radiotracer detection on thallium-201 scintigraphy was statistically insignificant between the two conditions. Immune complexes and immunoglobulins G, M, and A in the blood were elevated in both groups, likely as a consequence of heart failure.
Morphostructural analysis of biopsies taken from patients with inflammatory dilated cardiomyopathies, at different stages of its natural course reveals the progressive development of dilated cardiomyopathies. These structural changes correlate closely with findings from intracavitary and hemodynamic assessments and measures of regional contractility, supporting a direct link between dilated and inflammatory cardiomyopathies.
Diagnosing community-acquired pneumonia in patients with chronic heart failure can be challenging. Oxidative stress and inflammatory response play an important role in the development and diagnosis of community-acquired pneumonia and are also involved in many cardiovascular diseases, including chronic heart failure.
A total of 210 patients were enrolled and divided into two groups: group 1 (n = 105) – patients with community-acquired pneumonia associated with chronic heart failure, and group 2 (n = 105) – patients with community-acquired pneumonia without chronic heart failure. Several biomarkers were measured. For oxidative stress, we assessed prooxidant markers (ischemic modified albumin, advanced glycation end-products, advanced oxidation protein products, malonic dialdehyde) and antioxidant markers (total antioxidant activity with CUPRAC and ABTS methods, superoxide dismutase and catalase). Inflammatory status was assessed by determining leukocyte count, erythrocyte sedimentation rate, lactate dehydrogenase, fibrinogen and C-reactive protein. In all patients, N-terminal pro b-type natriuretic peptide values were determined.
The age of patients in the study group ranged from 50 to 92 years, with an overall mean of 70.6 ± 8.89 years (95% CI [68.8-72.3]), (F = 18.109; p = 0.205). Ischemic modified albumin values were higher in patients in Group 1 compared to Group 2: 236.60 ± 57.23 µM/L and 229.77 ± 64.35 µM/L, respectively (F = 0.660; p = 0.045). Serum lactate dehydrogenase had higher values in Group 1, compared to the control group: 232.65 ± 109.80 units/L and 192.40 ± 44.98 units/L, respectively (p = 0.001). The mean fibrinogen values were also higher in Group 1 (5.24 ± 1.60 g/L), compared to Group 2 (4.51 ± 1.78 g/L), p = 0.002. Total antioxidant activity by CUPRAC method, had higher values in Group 1 (6.70 ± 4.62) versus Group 2 (4.99 ± 2.29), p = 0.006.
The coexistence of community-acquired pneumonia and chronic heart failure resulted in a higher inflammatory response and greater accumulation of pro-oxidative reaction products. This condition was characterized by increased serum lactate dehydrogenase, erythrocyte sedimentation rate and fibrinogen levels. Furthermore, the state of heightened oxidative stress was marked by increased ischemic modified albumin and total antioxidant activity detected with CUPRAC method.