Search Results (448)

Tuberculosis (TB) is an ancient and re-emerging granulomatous infectious disease that continues to challenge public health. Early diagnosis and prompt effective treatment are crucial for preventing disease progression and reducing both morbidity and mortality. These steps play a vital role in infection control and in lowering death rates at both individual and population levels. Although diagnostic methods have improved sufficiently in recent decades, TB can still present with ambiguous laboratory and imaging features. This ambiguity can lead to diagnostic pitfalls and potentially disastrous outcomes due to delayed diagnosis. In this article, we present a case of TB that was difficult to diagnose. The disease had invaded the mediastinum, right atrium, right coronary artery, and inferior vena cava (IVC), resulting in Budd–Chiari syndrome. This rare presentation created clinical, laboratory, and radiological confusion, resulting in a diagnostic dilemma that ultimately led to open cardiac surgery. The patient initially presented with progressive shortness of breath on exertion and fatigue, which suggested possible heart disease. This suspicion was reinforced by computed tomography (CT) imaging, which showed infiltrative mass lesions predominantly in the right side of the heart, invading the right coronary artery and IVC, with imaging features mimicking angiosarcoma. Although laboratory findings revealed an exudative effusion with lymphocyte predominance and elevated adenosine deaminase (ADA), the Gram stain was negative for bacteria, and an acid-fast bacilli (AFB) smear was also negative. These findings contributed to diagnostic uncertainty and delayed the confirmation of TB. Open surgery with excisional biopsy and histopathological analysis ultimately confirmed TB. We conclude that TB should not be ruled out solely based on negative Mycobacterium bacteria in pericardial effusion or AFB smear. TB can mimic aggressive tumors such as angiosarcoma or lymphoma with invasion of the surrounding tissues and blood vessels. Awareness of the clinical presentation, imaging findings, and potential diagnostic pitfalls of TB is essential, especially in endemic regions. Full article

Background: Cardiac tumors are rare neoplasms with a wide spectrum of clinical presentations, ranging from asymptomatic cases to fatal outcomes. According to the 2021 thoracic tumor classification of the World Health Organization (WHO), papillary fibroelastoma (PFE) is the most common primary cardiac tumor. This study aimed to aggregate and examine data regarding the prevalence, clinical characteristics, and histological results of cardiac tumors. Methods: This multicenter retrospective study was conducted across seven tertiary care institutions and included 274 patients diagnosed with histopathologically confirmed cardiac tumors between January 2013 and December 2024. Results: This study included 274 patients, with an average age of 52.6 ± 16.6 years. Of the study participants, 120 (43.8%) were male and 154 (56.2%) were female. The most prevalent clinical manifestations were dyspnea (43.7%), thoracic pain (22.5%), and cardiac palpitations (21.1%). Echocardiography was the principal diagnostic method, revealing an average tumor size of 3 cm. The most commonly observed mass was cardiac myxoma (CM) in 192 patients (70.1%). The second most frequently detected mass was PFE (28 cases, 10.2%). The third most common cardiac mass was a metastatic tumor (6.9%). Surgical resection was performed in all patients, with infection being the most prevalent consequence, followed by effusion. Conclusions: Cardiac tumors, albeit uncommon, provide considerable diagnostic and treatment difficulties. Our research is founded on an extensive case series that has been histopathologically validated and sourced from various national tertiary centers. This comprehensive dataset offers epidemiological and clinical insights regarding heart tumors in Turkey. Another key finding of our study is that, even though the 5th edition of the 2021 WHO Classification of Thoracic Tumors lists PFE as the most common primary cardiac tumor, myxoma is actually the most common primary cardiac tumor in our study and in many other studies. This finding demonstrates a significant discrepancy between the current international classification and real-world data and suggests that tumor distribution may be related to regional and demographic differences. Full article

Hibiscus syriacus L. (HS), native to Eastern and Southern Asia, has been traditionally used in Asian herbal medicine for its anticancer, antimicrobial, and anti-inflammatory properties. Despite these recognized bioactivities, its potential cardioprotective effects, particularly in the setting of heart failure (HF), remain largely unexplored. This study aimed to investigate the effects of HS extracts and its bioactive constituents on angiotensin II (Ang II)-induced cardiac injury using an in vitro model with H9c2 rat cardiomyocytes. Cells exposed to Ang II were pretreated with HS extracts, and assays were performed to assess cell viability, reactive oxygen species (ROS) generation, protein synthesis, and secretion of inflammatory mediators, including tumor necrosis factor-alpha, interleukin 1β (IL-1β), and interleukin 6 (IL-6), as well as chemokine (CCL20) and HF-related biomarkers, such as brain natriuretic peptide (BNP) and endothelin-1. The results demonstrated that HS extracts significantly and dose-dependently attenuated Ang II-induced ROS accumulation and suppressed the secretion of pro-inflammatory cytokines, chemokines, BNP, and endothelin-1. Additionally, HS and its purified components inhibited Ang II-induced protein synthesis, indicating anti-hypertrophic effects. Collectively, these findings highlight the antioxidative, anti-inflammatory, and antihypertrophic properties of HS in the context of Ang II-induced cardiac injury, suggesting that HS may represent a promising adjunctive therapeutic candidate for HF management. Further in vivo studies and mechanistic investigations are warranted to validate its clinical potential. Full article

Valvular hemangiomas are uncommon vascular anomalies that appear on the surface of heart valves. They can cause an array of non-specific symptoms and are consequently rarely diagnosed, with only 31 such cases (including the present one) reported to date in the literature; the present case is the first report of an arteriovenous hemangioma with a tricuspid localization. During the preoperative echocardiographic examination for a ventricular septal defect, a mass was incidentally discovered on the tricuspid valve of a 9-month-old infant. The involved leaflet was surgically removed and sent to the pathology department for analysis and subsequently diagnosed as an arteriovenous hemangioma. The patient recovered well, with no local tumor recurrence or other complications. The microscopic examination showed multiple blood vessels which stained positive for the endothelial markers CD31 and CD34 and which did not express D2-40, normally found in lymphatic endothelia. Surprisingly, endothelial cells lining the vessels also showed positivity for SMA, a mesenchymal cell marker, indicating a possible involvement of endothelial-to-mesenchymal transition and its opposite process, mesenchymal-to-endothelial transition, in the pathogenesis of these vascular anomalies. Full article

Transmembrane protein 43 (TMEM43 or LUMA) encodes a highly conserved protein found in the nuclear and endoplasmic reticulum membranes of many cell types and the intercalated discs and adherens junctions of cardiac myocytes. TMEM43 is involved in facilitating intra/extracellular signal transduction to the nucleus via the linker of the nucleoskeleton and cytoskeleton complex. Genetic mutations may result in reduced TMEM43 expression and altered TMEM43 protein cellular localization, resulting in impaired cell polarization, intracellular force transmission, and cell–cell connections. The p.S358L mutation causes arrhythmogenic right ventricular cardiomyopathy type-5 and is associated with increased absorption of lipids, fatty acids, and cholesterol in the mouse small intestine, which may promote fibro-fatty replacement of cardiac myocytes. Mutations (p.E85K and p.I91V) have been identified in patients with Emery–Dreifuss Muscular Dystrophy-related myopathies. Other mutations also lead to auditory neuropathy spectrum disorder-associated hearing loss and have a negative association with cancer progression and tumor cell survival. This review explores the pathogenesis of TMEM43 mutation-associated diseases in humans, highlighting animal and in vitro studies that describe the molecular details of disease processes and clinical, histologic, and molecular manifestations. Additionally, we discuss TMEM43 expression-related conditions and how each disease may progress to severe and life-threatening states. Full article

Myocardial injury following polytrauma is a significant yet often underdiagnosed condition that contributes to acute cardiac dysfunction and long-term cardiovascular complications. This review examines the role of systemic inflammation, oxidative stress, neuro-hormonal activation, and immune dysregulation in trauma-induced myocardial damage. Key immunological markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and adhesion molecules (ICAM-1, VCAM-1), are implicated in endothelial dysfunction, myocardial apoptosis, and ventricular remodeling. The interplay between these factors potentially exacerbates cardiac injury, increasing the risk of heart failure. Biomarker-guided approaches for early detection, combined with advanced imaging techniques such as speckle-tracking echocardiography and cardiac MRI, offer promising avenues for risk stratification and targeted interventions. Anti-inflammatory and oxidative stress-modulating therapies may mitigate myocardial damage and improve outcomes. This article highlights the clinical relevance of integrating immunological markers into diagnostic and therapeutic strategies to enhance the management of trauma-related cardiac dysfunction and reduce long-term morbidity. Full article

Cardiac tumors in dogs, although rare in the past, have shown an increasing incidence due to advances in veterinary imaging, especially echocardiography, CT, and MRI with contrast agents. Right atrial hemangiosarcoma is the most common form of tumor associated with pericardial effusion and cardiac tamponade, followed by chemodectoma, which is more common in brachycephalic breeds. The diagnosis is based on echocardiographic examination, supplemented by advanced methods and possibly biopsy. Clinical signs are often non-specific, requiring an integrated approach. Treatment includes pericardiocentesis, chemotherapy, and, in some cases, surgery, but the prognosis remains reserved. Full article

Apoptosis is a highly regulated process of programmed cell death and plays a crucial pathogenic role in a variety of conditions including cardiovascular diseases. There are two pathways leading to apoptosis, the intrinsic and extrinsic pathways. In the intrinsic pathway, also known as the mitochondria-mediated pathway, the cell kills itself because it senses cell stress. Mitochondria account for 30% of cardiomyocyte volume, and therefore, the heart is vulnerable to apoptosis. The extrinsic pathway, also known as the death receptor-mediated pathway, is initiated by death receptors, members of the tumor necrosis factor receptor gene superfamily. Excessive apoptosis is involved in cardiac dysfunction in different cardiac conditions, including heart failure, ischemic heart disease, and cirrhotic cardiomyopathy. The last entity is a serious cardiac complication of patients with cirrhosis. To date, there is no effective treatment for cirrhotic cardiomyopathy. The conventional treatments for non-cirrhotic heart failure such as vasodilators are not applicable due to the generalized peripheral vasodilatation in cirrhotic patients. Exploring new approaches for the treatment of cirrhotic cardiomyopathy is therefore of utmost importance. Since apoptosis plays an essential role in the pathogenesis and progression of cardiovascular conditions, anti-apoptotic treatment could potentially prevent/attenuate the development and progression of cardiac diseases. Anti-apoptotic treatment may also apply to cirrhotic cardiomyopathy. The present review summarizes apoptotic mechanisms in different cardiac diseases, including cirrhotic cardiomyopathy, and potential therapies to regulate apoptosis in these conditions. Full article

In chronic kidney disease (CKD), various disorders occur that worsen with the progression of CKD. These include increased levels of hormones such as adiponectin, leptin, and prolactin, changes in feedback loops and metabolism, and decreased renal clearance, contributing to significant morbidity and mortality. We conducted a cross-sectional observational study on 157 randomly selected patients with various stages of chronic kidney disease, 29% of whom had diabetes. We recorded clinical and usual laboratory data. We determined muscle mass and adipose tissue mass using bioimpedance. In addition, we measured serum prolactin levels, tumor necrosis factor-alpha (TNF-α), Interleukin 6 (IL-6), and Interleukin-1 beta (IL-1β). N-terminal pro-B-type natriuretic peptide (NT-proBNP) was evaluated as a marker of cardiac function. We evaluated the relation between prolactin, TNF-α, IL-6, IL-1β, and NT-proBNP by bivariate and multivariate analysis. In bivariate analysis, we recorded associations of prolactin with inflammatory markers: TNF-α (r = 0.65, p < 0.001), IL-6 (r = 0.66, p < 0.001), and IL-1β (r = 0.25, p = 0.002). In multivariate analysis we observed that serum prolactin values are associated with IL-1β [median (25th–75th percentile): [−0.001 (−0.001; −0.00003), p = 0.037], muscle mass [−0.03 (−0.04; −0.01), p = 0.003], and NT-proBNP [0.0001 (0.0001; 0.0001)] p < 0.001 In conclusion, in chronic kidney disease, prolactin is associated with inflammatory markers (IL-1β, TNF-α, IL-6), and nutritional status. Additionally, prolactin has been linked to NT-ProBNP, a marker of cardiac function. Full article

Proton therapy is increasingly used to treat pediatric and adult brain tumors, but there is still uncertainty surrounding the biological effects of protons on the heart. Also, the molecular and functional responses to proton irradiation are still unknown. This study investigates the effect of protons on cardiac disease by comparing their effects on the hearts of rats exposed to hypergravity. A total of 20 Sprague Dawley rats were tested, including a group that was irradiated with 0.1 Gy of protons to the heart, a group exposed to hypergravity, a group exposed to both protons and hypergravity, and a control group. Changes in AQP4, calcium homeostasis, and fibrosis-related markers were investigated using Western blotting, immunohistochemistry, etc. The proton-irradiated group showed no changes compared to the control group. In rats exposed to hypergravity, the cardiac fibrosis markers TGF-ꞵ1, MMP9, and MMP2 were increased. On the other hand, the group exposed to hypergravity followed by proton irradiation tended to display a significant decrease in these markers. Along with reduced fibrosis-related markers, the consistent tendency was also confirmed in the cardiac calcium homeostasis-related proteins and AQP4 through Western blotting. In summary, our findings indicate that rats subjected to hypergravity experienced both cardiac hypertrophy and fibrosis, while proton therapy appeared to mitigate the effects of cardiac disease. These results suggest that proton therapy prevents heart disease triggered by hypergravity, providing insights for protecting astronauts’ cardiovascular health. Full article

Background: The use of photon-counting detector computed tomography (PCD-CT) has improved image quality in cardiac, pulmonary, and musculoskeletal imaging. Abdominal imaging research, especially about the use of PCD-CT in hepatocellular carcinoma (HCC), is sparse. Objectives: We aimed to compare the image quality of tumors, the liver parenchyma, and the vasculature in patients with HCC using PCD-CT reconstructions at different slice thicknesses and kernels to identify the most appropriate settings for the clinical routine. Methods: CT exams from twenty adult patients with HCC performed with a clinically approved, first-generation PCD-CT scanner (Naeotom Alpha^®, Siemens Healthineers), were retrospectively reviewed. For each patient, images were reconstructed at four different sharp kernels, designed for abdominal imaging (Br40; Br44; Br48; Br56) and at three slice thicknesses (0.4 mm; 1 mm; 3 mm). The reconstruction with the Br40 kernel at 3 mm (Br40_{3 mm}) was used as a clinical reference. Three readers independently assessed the image quality of different anatomical abdominal structures and hypervascular HCC lesions using a five-point Likert scale. In addition, image sharpness was assessed using line-density profiles. Results: Compared with the clinical reference, the Br44_{1 mm} and Br48_{1 mm} reconstructions were rated superior for the assessment of the hepatic vasculature (median difference +0.67 [+0.33 to +1.33], p < 0.001 and +1.00 [+0.67 to +1.67], p < 0.001). Reconstructions for Br40_{1 mm} (+0.33 [−0.67 to +1.00], p < 0.001), and Br44_{3 mm} (+0.0 [0.0 to +1.00], p = 0.030) were scored superior for overall image quality. The noise demonstrated a continuous increase when using sharper kernels and thinner slices than Br40_{3 mm} (p < 0.001), leading to a decrease in contrast-to-noise ratio. Although there was a trend toward increased image sharpness using the slope analysis with higher kernels, this was not significantly different compared with the reference standard. Conclusion: PCD-CT reconstruction Br40_{1 mm} was the most suitable setting for overall image quality, while reconstructions with sharper kernels (Br44_{1 mm} and Br48_{1 mm}) can be considered for the assessment of the hepatic vasculature in patients with HCC. Full article

Cardiac dysfunction is a severe complication of sepsis that significantly increases mortality in affected patients. Previous studies have shown better myocardial responses with preserved cardiac function in female animals compared to males following lipopolysaccharide (LPS)-induced sepsis. Our published findings have revealed that females exhibited less cardiac dysfunction than males when exposed to equivalent doses of tumor necrosis factor (TNF)α, which is markedly elevated in both heart tissue and serum following LPS. These raise the question of whether the observed sex differences in LPS-induced myocardial dysfunction are a direct effect of LPS or a secondary consequence mediated by inflammatory cytokines, like TNFα. In this study, we aimed to uncover sex differences in LPS-caused direct effects on cardiac function. To do so, isolated hearts from aged-matched adult male and female mice were subjected to LPS infusion using a Langendorff method. Left ventricular developed pressure (LVDP) was continuously recorded. The female estrous cycle was determined via vaginal smear. The oxidative phosphorylation (OXPHOS) pathway and estrogen receptors (ERs) were determined in heart tissue using Western blot. We found that males exhibited worse LV function than females following the infusion of LPS at 5.0 mg/kg body weight. However, no significant differences in cardiac function and expression of ERs were observed between female groups at different estrous stages. Interestingly, LV function returned to baseline after the initial depression of LVDP during the rapid response to LPS and then depressed again following the 50 min LPS infusion. Protein levels of OXPHOS were altered differently between male and female hearts after 50 min LPS infusion. Our data demonstrate that male hearts exhibit higher sensitivity to LPS-induced rapid cardiac dysfunction compared to females, although estrogen may have a minimal influence on LPS-induced rapid functional depression. Sex differences may exist in myocardial mitochondrial responses to direct LPS insult via the OXPHOS pathway. Full article

Muscle loss unresponsive to nutritional supplementation affects up to 80% of cancer patients and severely reduces survival and treatment response. Exercise may help preserve muscle mass and function, yet the translatability of preclinical methods remains questionable. This study aimed to assess how voluntary wheel running, a clinically relevant physical activity, protects skeletal and cardiac muscle against cancer-mediated dysfunction and identify underlying molecular mechanisms. Methods: BALB/c mice were assigned to sedentary nontumor-bearing (SED+NT), sedentary tumor-bearing (SED+T), wheel run nontumor-bearing (WR+NT), and wheel run tumor-bearing (WR+T). Tumor-bearing groups received 5 × 10⁵ C26 cells; WR mice had wheel access for 4 weeks. Muscle function and tissue were analyzed for protective mechanisms. Results: SED+T mice exhibited significant fat and lean mass loss, indicating cachexia, which was prevented in WR+T mice. SED+T also showed 15% reduced grip strength and cardiac dysfunction, while WR+T preserved function. WR+T mice had lower expression of muscle wasting markers (Atrogin1, MuRF1, GDF15, GDF8/11). Physical activity also reduced tumor mass by 57% and volume by 37%. Conclusion: Voluntary wheel running confers tumor-suppressive, myoprotective, and cardioprotective effects. These findings support physical activity as a non-pharmacological strategy to combat cancer-related muscle wasting and dysfunction. Full article

Background/Objectives: Metabolic syndrome is one of the leading causes of mortality worldwide, with high-fat diet (HFD) intake being a significant driving force. Despite long-term research, new interventions are still being sought to improve cardiovascular disorders associated with metabolic syndrome. Methods: To explore the therapeutic potential of a slow-releasing H₂S donor, we evaluated the effects of 3 weeks of treatment with GYY-4137 on systolic blood pressure (sBP), cardiac parameters, adiposity, selected plasma markers, and the vascular function of the thoracic aortas (TAs) and mesenteric arteries (MAs) isolated from male spontaneously hypertensive rats (SHRs) fed an HFD for 8 weeks. Results: HFD administration induced cardiac remodeling, increased adiposity, and decreased adrenergic contractility in both TAs and MAs. Moreover, although high-fat intake improved TAs relaxation, it decreased aortic protein expression of endothelial NO synthase and the involvement of NO in vasoactive responses of both TAs and MAs. In addition, protein expression of inducible NOS and tumor necrosis factor alpha (TNFα) in aortas was increased, as were plasma levels of chemerin, which has been proposed as a possible link among metabolic and vascular disorders and inflammation. Treatment with GYY-4137 reduced sBP, improved relaxation of the MAs, partially restored the contractility of the TAs, generally restored NO signaling, and decreased the protein expression of the inducible NOS and TNFα, as well as plasma chemerin levels. Conclusions: A slow H₂S-releasing donor could partially ameliorate the metabolic changes induced by increased fat intake during essential hypertension and trigger beneficial vasoactive effects associated with the NO signaling restoration and suppression of inflammation. Full article

Cardiovascular injury caused by fine particulate matter (PM2.5) exposure is an escalating public health concern due to its role in triggering systemic inflammation and oxidative stress. This study elucidates the sirtuin 1 (SIRT1)-mediated epigenetic mechanisms underlying the protective effects of phytosome-encapsulated Zea mays L. var. ceratina tassel extract (PZT) in a rat model of PM2.5-induced cardiovascular inflammation. Male Wistar rats were pretreated with PZT (100, 200, and 400 mg/kg body weight) for 21 days before and throughout a 27-day PM2.5 exposure period. SIRT1 expression and associated inflammatory and oxidative stress markers were evaluated in cardiac and vascular tissues. The findings revealed that PZT significantly upregulated SIRT1 expression, a key epigenetic regulator known to modulate inflammatory and antioxidant pathways. The activation of SIRT1 inhibited the nuclear factor-kappa B (NF-κB) signaling pathway, leading to a reduction in pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) within cardiac tissue. In vascular tissue, treatment with PZT reduced the levels of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β), thereby mitigating inflammatory and fibrotic responses. Furthermore, SIRT1 activation by PZT enhanced the antioxidant defense system by upregulating superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), which was associated with a decrease in malondialdehyde (MDA), a marker of lipid peroxidation. Collectively, these results demonstrate that PZT confers cardiovascular protection through SIRT1-dependent epigenetic modulation, mitigating PM2.5-induced inflammation, oxidative stress, and tissue remodeling. The dual anti-inflammatory and antioxidant actions of PZT via SIRT1 activation highlight its potential as a functional food-based preventative agent for reducing cardiovascular risk in polluted environments. Full article