Effect of Single High-Dose Vitamin D3 Supplementation on Post-Ultra Mountain Running Heart Damage and Iron Metabolism Changes: A Double-Blind Randomized Controlled Trial.

Exercise-induced inflammation can influence iron metabolism. Conversely, the effects of vitamin D3, which possesses anti-inflammatory properties, on ultramarathon-induced heart damage and changes in iron metabolism have not been investigated. Thirty-five healthy long-distance semi-amateur runners were divided into two groups: one group received 150,000 IU of vitamin D3 24 h prior to a race (n = 16), while the other group received a placebo (n = 19). Serum iron, hepcidin (HPC), ferritin (FER), erythroferrone (ERFE), erythropoietin (EPO), neopterin (NPT), and cardiac troponin T (cTnT) levels were assessed. A considerable effect of ultramarathon running on all examined biochemical markers was observed, with a significant rise in serum levels of ERFE, EPO, HPC, NPT, and cTnT detected immediately post-race, irrespective of the group factor. Vitamin D3 supplementation showed a notable interaction with the UM, specifically in EPO and cTnT, with no other additional changes in the other analysed markers. In addition to the correlation between baseline FER and post-run ERFE, HPC was modified by vitamin D. The ultramarathon significantly influenced the EPO/ERFE/HPC axis; however, a single substantial dose of vitamin D3 had an effect only on EPO, which was associated with the lower heart damage marker cTnT after the run.

Cardiac Findings Following Cerebrovascular Disease.

BACKGROUND: Accumulating evidence suggests that cardiac findings after stroke are an important, yet understudied, manifestation of brain-heart interactions. Our aim was to investigate and compare cardiac findings after different cerebrovascular events (acute ischemic stroke, transient ischemic attack, and hemorrhagic stroke). METHODS AND RESULTS: There were 7113 patients screened who were treated between December 2013 and December 2020 at the University Hospital Zurich for ischemic stroke, transient ischemic attack, and hemorrhagic stroke. Seven hundred twenty-one patients without evidence of previous cardiac disease or presumed cardioembolic origin of their cerebrovascular disease and with at least 1 cardiac checkup were included. Clinical reports from the year following disease onset were screened for new cardiac findings, which were categorized as arrhythmia/electrocardiographic changes, myocardial alterations, valvular abnormalities, and coronary perfusion insufficiency. Differences in proportions of findings among groups were analyzed using the Pearson χ2 test or Fisher exact test. ECG changes were observed in 81.7% (n=474) of patients with ischemic stroke, 71.4% (n=70) of patients with transient ischemic attack, and 55.8% (n=24) of patients with hemorrhagic stroke (P<0.001). Myocardial alterations occurred often in all 3 groups (60.9% ischemic stroke [n=353], 59.2% transient ischemic attack [n=58], 44.2% hemorrhagic stroke [n=19]; P=0.396). CONCLUSIONS: Cardiac findings are frequent in patients with cerebrovascular disease, even without prior cardiac problems or suspected cardiac cause. Similarities, especially between patients with ischemic stroke and transient ischemic attack, were observed. Our data suggest that all patients with acute cerebrovascular events should receive thorough workup searching for cardiac manifestations.

Navigating complex cardiac complications: A case report of alcoholic cardiomyopathy and right atrial thrombosis.

RATIONALE: Alcoholic cardiomyopathy (ACM) is associated with various cardiac complications, but the development of isolated right atrial (RA) thrombus without deep vein thrombosis is rare and presents diagnostic challenges. PATIENT CONCERNS: A 53-year-old Hispanic male presented with shortness of breath, chills, cough, bilateral lower extremity edema, and distended abdomen. DIAGNOSES: The patient was diagnosed with ACM, liver cirrhosis, and a large RA thrombus. Initial transthoracic echocardiography showed severe left ventricular systolic dysfunction but failed to detect the RA mass. Subsequent computed tomography scan and transesophageal echocardiography revealed a large oval mass in the RA, measuring 40 mm × 22 mm × 18 mm. INTERVENTIONS: The patient received guideline-directed medical therapy for heart failure and anticoagulation with enoxaparin. He underwent cardiac catheterization for mechanical thrombectomy, which was minimally successful. OUTCOMES: The patient's condition was managed with the prescribed interventions. Regular follow-up was planned to assess thrombolysis. LESSONS: RA thrombosis is an uncommon complication of ACM. A multimodal imaging approach, with a low threshold for transesophageal echocardiography, is crucial in evaluating patients with ACM who present with cardiac complications. This approach enables accurate diagnosis and management of rare conditions like isolated RA thrombosis.

Atrial thrombus after total anomalous pulmonary venous connection repair.

A 6-year-old boy had previously undergone total anomalous pulmonary venous connection repair and postoperative pulmonary vein stenosis release. Magnetic resonance imaging revealed blood stasis caused by a collision between the inflow from the pulmonary veins and the outflow from the left atrial appendage. A surgical specimen revealed evidence of advanced thrombus attachment. Infra-cardiac total anomalous pulmonary venous connection with an antler appearance may be a risk factor for thrombus formation in the left atrial appendage and for postoperative pulmonary venous stenosis due to blood flow collision in the left atrium after total anomalous pulmonary venous connection repair.

Cardiac Involvement in LAMA2-Related Muscular Dystrophy and SELENON-Related Congenital Myopathy: A Case Series.

Background: LAMA2-related muscular dystrophy (LAMA2-MD) and SELENON-related myopathy (SELENON-RM) are two rare neuromuscular diseases characterized by proximal and axial muscle weakness, scoliosis, spinal rigidity, low bone quality and respiratory impairment. Cardiac involvement has previously been described in retrospective studies and case reports, but large case series and prospective studies in unselected cohorts are lacking. Objective: The objective of this study is to conduct prevalence estimations, perform cardiac phenotyping, and provide recommendations for clinical care. Methods: In this case series including two time points, we conducted comprehensive assessments with electrocardiography (ECG) and transthoracic echocardiography (TTE). ECGs were systematically assessed for a large subset of variables. TTE included left and right ventricular ejection fraction (LVEF/RVEF) and left ventricular global longitudinal strain (GLS), the latter being a more early and sensitive marker of left ventricular dysfunction. Results: 21 LAMA2-MD (M = 5; 20±14 years) and 10 SELENON-RM patients (M = 7; 18±12 years) were included. In most patients, QRS fragmentation and Q waves, markers of heterogeneous ventricular activation, were present both at baseline and at follow-up. GLS was abnormal (age specific in children, > -18% in adults) in 33% of LAMA2-MD and 43% of SELENON-RM patients at baseline. Reduced LVEF (<52% in males, <54% in females and <55% in pediatric population) was observed in three LAMA2-MD patients at baseline and in none of the SELENON-RM patients. GLS and LVEF did not change between baseline and follow-up. RVEF was normal in all patients. Conclusion: ECG abnormalities and abnormal GLS are prevalent in LAMA2-MD and SELENON-RM, yet abnormal LVEF was only seen in LAMA2-MD patients. One LAMA2-MD patient had a clinically relevant deterioration in LVEF during 1.5-year follow-up. We advise routine screening of all patients with LAMA2-MD or SELENON-RM with ECG and echocardiography at diagnosis, minimally every two years from second decade of life and if new cardiac signs arise.

The geriatric nutritional risk index is related to adverse hospitalization outcomes in individuals undergoing cardiac surgery.

Malnutrition is linked to adverse outcomes in post-cardiac surgery patients. This study investigates the correlation between the Geriatric Nutritional Risk Index (GNRI) and adverse hospital outcomes in patients following cardiac surgery. This retrospective study included elderly patients with heart disease who were admitted to the Department of Cardiology, Fujian Medical University Union Hospital from January 2020 to December 2022. Patients were divided into two groups based on the cut-off value (98 g/dL). Data from 407 patients were assessed, with 278 (68.3%) classified as having nutritional risk and 129 (31.7%) as having no nutritional risk. Notable distinctions were observed in body weight, BMI, and left ventricular ejection fraction (P < 0.05). Laboratory indicators indicated lower levels of serum albumin, lymphocytes, red blood cells, hemoglobin, admission blood glucose, and admission triglyceride in the nutritional risk group (P < 0.05). Neutrophils and serum creatinine were higher in the nutritional risk group (P < 0.05). Poor prognosis was prevalent in the nutrition risk group (64.7%), with higher incidences of adverse outcomes (P < 0.05). Univariate and multivariate studies showed that GNRI < 98 g/dL was an independent predictor of postoperative cardiac surgery. Nutritional risk was an important predictor of adverse hospital outcomes after the surgery.

The Potential Mechanisms Behind Adverse Effect of Coronavirus Disease-19 on Heart and Liver Damage: A Review.

Background: Coronaviruses (CoVs) belong to the RNA viruses family. The viruses in this family are known to cause mild respiratory disease in humans. The origin of the novel SARS-COV2 virus that caused the coronavirus-19 disease (COVID-19) is the Wuhan city in China from where it disseminated to cause a global pandemic. Although lungs are the predominant target organ for Coronavirus Disease-19 (COVID-19), since its outbreak, the disease is known to affect heart, blood vessels, kidney, intestine, liver and brain. This review aimed to summarize the catastrophic impacts of Coronavirus disease-19 on heart and liver along with its mechanisms of pathogenesis. Methods: The information used in this review was obtained from relevant articles published on PubMed, Google Scholar, Google, WHO website, CDC and other sources. Key searching statements and phrases related to COVID-19 were used to retrieve information. Original research articles, review papers, research letters and case reports were used as a source of information. Results: Besides causing severe lung injury, COVID-19 has also been reported to affect and cause dysfunction of many other organs. COVID-19 infection can affect people by downregulating membrane-bound active angiotensin-converting enzyme (ACE). People who have deficient ACE2 expression are more vulnerable to COVID-19 infection. The patients' pre-existing co-morbidities are major risk factors that predispose individuals to severe COVID-19. Conclusion: The disease severity and its broad spectrum phenotype is a result of combined direct and indirect pathogenic factors. Therefore, protocols that harmonize many therapeutic preferences should be the best alternatives to de-escalate the disease and obviate deaths caused as a result of multiple organ damage and dysfunction induced by the disease.

Lysozyme 1 Inflamed CCR2+ Macrophages Promote Obesity-Induced Cardiac Dysfunction.

BACKGROUND: Macrophages are key players in obesity-associated cardiovascular diseases, which are marked by inflammatory and immune alterations. However, the pathophysiological mechanisms underlying macrophage's role in obesity-induced cardiac inflammation are incompletely understood. Our study aimed to identify the key macrophage population involved in obesity-induced cardiac dysfunction and investigate the molecular mechanism that contributes to the inflammatory response. METHODS: In this study, we used single-cell RNA-sequencing analysis of Cd45+CD11b+F4/80+ cardiac macrophages to explore the heterogeneity of cardiac macrophages. The CCR2+ (C-C chemokine receptor 2) macrophages were specifically removed by a dual recombinase approach, and the macrophage CCR2 was deleted to investigate their functions. We also performed cleavage under target and tagmentation analysis, chromatin immunoprecipitation-polymerase chain reaction, luciferase assay, and macrophage-specific lentivirus transfection to define the impact of lysozyme C in macrophages on obesity-induced inflammation. RESULTS: We find that the Ccr2 cluster undergoes a functional transition from homeostatic maintenance to proinflammation. Our data highlight specific changes in macrophage behavior during cardiac dysfunction under metabolic challenge. Consistently, inducible ablation of CCR2+CX3CR1+ macrophages or selective deletion of macrophage CCR2 prevents obesity-induced cardiac dysfunction. At the mechanistic level, we demonstrate that the obesity-induced functional shift of CCR2-expressing macrophages is mediated by the CCR2/activating transcription factor 3/lysozyme 1/NF-κB (nuclear factor kappa B) signaling. Finally, we uncover a noncanonical role for lysozyme 1 as a transcription activator, binding to the RelA promoter, driving NF-κB signaling, and strongly promoting inflammation and cardiac dysfunction in obesity. CONCLUSIONS: Our findings suggest that lysozyme 1 may represent a potential target for the diagnosis of obesity-induced inflammation and the treatment of obesity-induced heart disease.

Total extracts from Abelmoschus manihot (L.) alleviate radiation-induced cardiomyocyte ferroptosis via regulating redox imbalances mediated by the NOX4/xCT/GPX4 axis.

ETHNOPHARMACOLOGICAL RELEVANCE: Radiation-induced heart disease (RIHD) is one of the most serious complications in patients receiving chest radiotherapy, partially offsetting its benefits. At present, there is a lack of effective treatments for RIHD. Ferroptosis is a newly discovered type of cell death that results from iron-dependent lipid peroxide accumulation. It was recently shown that irradiation generates severe ferroptosis, providing new insights for the treatment of RIHD. Abelmoschus manihot (L.) possesses excellent pharmacological properties and is widely used in treating various ischemic heart and brain diseases; however, its efficacy and mechanism in treating RIHD are unknown. AIM: This study aimed to investigate the efficacy and mechanism of total extracts from A. manihot (L.) (TEA) in treating RIHD. MATERIALS AND METHODS: C57BL/6 mice and H9C2 cells were exposed to irradiation to induce RIHD in vivo and in vitro, respectively. In vivo, we evaluated the protective effects of TEA (150 and 300 mg/kg) on RIHD. Body and heart weight changes of mice were calculated in each group, and malondialdehyde (MDA) level, glutathione/oxidized glutathione (GSH/GSSH) and nicotinamide adenine dinucleotide phosphate (NADPH/NADP+) ratios, western blot, heart histology, and immunohistochemistry were used to evaluate TEA effectiveness. We identified the potential mechanism of radiation-induced cardiomyocyte injury in H9C2 cells treated with small interfering RNA. We determined the effective dose of TEA (0.6 mg/mL) using a Cell Counting Kit-8 assay. Intracellular Fe2+ and lipid peroxidation levels were detected by Phen Green™ SK diacetate probe, BODIPY 581/591 C11 staining, and MDA, GSH, and NADPH kits, and the level of target protein was evaluated by immunofluorescence and western blot. RESULTS: Radiation inhibited system Xc-cystine (xCT)/glutathione peroxidase 4 (GPX4) expression and activity in cardiomyocytes in a time and dose-dependent manner. After silencing xCT/GPX4, MDA significantly increased and GSH/GSSH and NADPH/NADP+ ratios were reduced. xCT/GPX4 inhibition drove ferroptosis in radiation-induced H9C2 injury. Oxidative stress in H9C2 was significantly enhanced by irradiation, which also significantly increased NADPH oxidase 4 (NOX4) expression and inhibited nuclear factor E2-related factor 2 (Nrf2) expression in vivo and in vitro. Inhibition of xCT/GPX4 drove ferroptosis in radiation-induced H9C2 injury, which was aggravated by inactivation of Nrf2 and alleviated by inhibition of NOX4. Compared with the ionizing radiation-only group, TEA improved body weight loss, MDA levels, and histological changes induced by irradiation in mice hearts, and increased the ratio of GSH/GSSH and NADPH/NADP+in vivo; it also reduced lipid peroxidation and intracellular Fe2+ accumulation, restored MDA levels, and elevated the ratios of GSH/GSSH and NADPH/NADP+ in irradiation-injured H9C2 cells. TEA up-regulated Nrf2, xCT, and GPX4 expression and inhibited NOX4 expression in vivo and in vitro. CONCLUSIONS: Ferroptosis induced by redox imbalance mediated through the NOX4/xCT/GPX4 axis is a potential mechanism behind radiation-induced cardiomyocyte injury, and can be prevented by TEA.

Cardiac disease-induced trauma and stress-related disorders.

OBJECTIVE: This review aims to present an updated overview of cardiac disease-induced trauma and stress-related disorders such as acute stress disorder (ASD), adjustment disorder (AjD), and posttraumatic stress disorder (PTSD). First, the prevalence of these disorders, their diagnostic criteria, and their differences from other trauma-related disorders are described. Special challenges in diagnosis and treatment are identified, with various screening tools being evaluated for symptom assessment. Additionally, the risk factors studied so far for the development of symptoms of cardiac-induced posttraumatic stress disorder and the bidirectional relationship between posttraumatic stress disorder and cardiovascular diseases are summarized. Various therapeutic interventions, including pharmacological approaches, are also discussed. Finally, various areas for future research are outlined. BACKGROUND: Experiencing a cardiovascular disease, particularly a life-threatening cardiac event, can potentially lead to stress-related disorders such as ASD, AjD, and cardiac disease-induced PTSD (CDI-PTSD). If left untreated, these disorders are associated with a worsening cardiac prognosis and higher mortality rates. Approaching treatment through a trauma-focused lens may be beneficial for managing CDI-PTSD and stress-related disorders. CONCLUSION: Future research should explore treatment options for both the patients and the caregivers as well as investigate the long-term effects of trauma-focused interventions on physical and mental health outcomes.

Association between Mobility of Residual Left Atrial Thrombus and Stroke Severity in Patients with Nonvalvular Atrial Fibrillation.

BACKGROUND: The differences in the characteristics of ischemic stroke associated with a mobile versus nonmobile residual left atrial thrombus (LAT) are unclear. We investigated whether the mobility of an LAT detected by transthoracic echocardiography is associated with the clinical features of stroke. METHODS: This study included 20 consecutive patients with nonvalvular atrial fibrillation who were admitted to our hospital for treatment of acute ischemic stroke and then found to have an LAT on transthoracic echocardiography. The patients were divided into two groups: those with a mobile LAT (Group M) and those with a nonmobile LAT (Group N). The clinical, neuroradiological, and echocardiographic variables were assessed. RESULTS: The LAT was mobile in 11 patients (Group M) and nonmobile in nine patients (Group N). The median National Institutes of Health Stroke Scale score on admission was higher in Group M than N (17 vs. 7, respectively; p=0.196). Four patients in Group M and one in Group N developed in-hospital stroke recurrence (36% vs. 11%, respectively; p=0.319). The prevalence of large vessel occlusion (15 events in Group M and 10 events in Group N, including in-hospital recurrent events) was significantly higher in Group M than N (73% vs. 30%, respectively; p=0.049), which seemed to lead to poorer functional outcomes in Group M than N (ratio of modified Rankin scale score of 0-2 at discharge: 18% vs. 44%, respectively; p=0.336). CONCLUSIONS: The mobility of LAT may affect stroke severity in patients with nonvalvular atrial fibrillation.

Cardiac-to-Bronchial Fistula in Hepatocellular Carcinoma: A Case Report.

Hepatocellular carcinoma (HCC) stands as a significant contributor to cancer-related mortality globally. While the acute and often fatal manifestations of locally advanced HCC primarily present within the abdomen, it is crucial to recognize that the respiratory and circulatory systems can also fall victim due to the liver's unique anatomical position within the body. Here, we present the case of a 63-year-old male recently diagnosed with locally advanced HCC with vascular invasion. Shortly after receiving target therapy and focal radiotherapy, the patient developed repeated secondary infections and a persistent diaphragmatic defect. As the necrotic tissue invaded the pleural space, subsequent tumor-to-bronchial and tumor-to-cardiac fistulas emerged, resulting in an abnormal connection between the respiratory and cardiovascular systems, leading to massive air emboli in circulation. This report highlights the risk of supradiaphragmatic complications in HCC patients with post-treatment secondary infections, particularly in patients predisposed to developing diaphragmatic defects.

Cardioembolic Stroke.

Cardioembolism accounts globally for around 25% of ischemic strokes and is more often associated with higher rates of morbidity and mortality. Potential sources of cardioembolism into the intracranial circulation include paradoxic embolism, dysrhythmias, structural heart disease, and valvular heart disease. To identify the etiology of a patient's ischemic stroke, thorough investigation of the intracardiac structures, assessment of dysrhythmias, and consideration of high-risk events such as cardiac surgery are crucial. Treatment after cardioembolic stroke can be personalized based on the underlying cardioembolic source to minimize the risk of recurrent cerebral ischemic events.

Gastropericardial fistula: A successfully operated heart code.

Gastropericardial fistula is a rare, extremely serious and life-threatening condition. Its most common aetiology is secondary to iatrogenic injury following gastric surgery. Clinical manifestations may be non-specific with precordial pain, simulating an acute coronary syndrome, and may be accompanied by electrocardiogram abnormalities. Diagnosis is made by thoracoabdominal computed tomography (CT) with oral and intravenous contrast. Treatment is surgical and consists of repair of the anomalous communication. We present the case of an 81-year-old male patient with gastropericardial fistula who underwent surgery, with the aim of reviewing the diagnosis and the appropriate therapeutic strategy.

Stroke-heart syndrome: current progress and future outlook.

Stroke can lead to cardiac complications such as arrhythmia, myocardial injury, and cardiac dysfunction, collectively termed stroke-heart syndrome (SHS). These cardiac alterations typically peak within 72 h of stroke onset and can have long-term effects on cardiac function. Post-stroke cardiac complications seriously affect prognosis and are the second most frequent cause of death in patients with stroke. Although traditional vascular risk factors contribute to SHS, other potential mechanisms indirectly induced by stroke have also been recognized. Accumulating clinical and experimental evidence has emphasized the role of central autonomic network disorders and inflammation as key pathophysiological mechanisms of SHS. Therefore, an assessment of post-stroke cardiac dysautonomia is necessary. Currently, the development of treatment strategies for SHS is a vital but challenging task. Identifying potential key mediators and signaling pathways of SHS is essential for developing therapeutic targets. Therapies targeting pathophysiological mechanisms may be promising. Remote ischemic conditioning exerts protective effects through humoral, nerve, and immune-inflammatory regulatory mechanisms, potentially preventing the development of SHS. In the future, well-designed trials are required to verify its clinical efficacy. This comprehensive review provides valuable insights for future research.

Physical exercise in hypertensive heart disease: From the differential diagnosis to the complementary role of exercise.

Arterial hypertension (AH) is one of the most common pathologic conditions and uncontrolled AH is a leading risk factor for cardiovascular disease and mortality. AH chronically causes myocardial and arterial remodelling with hemodynamic changes affecting the heart and other organs, with potentially irreversible consequences leading to poor outcomes. Therefore, a proper and early treatment of AH is crucial after the diagnosis. Beyond medical treatment, physical exercise also plays a therapeutic role in reducing blood pressure, given its potential effects on sympathetic tone, renin-angiotensin-aldosterone system, and endothelial function. International scientific societies recommend physical exercise among lifestyle modifications to treat AH in the first stages of the disease. Moreover, some studies have also shown its usefulness in addition to drugs to reduce blood pressure further. Therefore, an accurate, personalized exercise prescription is recommended to optimize the prevention and treatment of hypertension. On the other hand, uncontrolled AH in athletes requires proper risk stratification and careful evaluation to practice competitive sports safely. Moreover, the differential diagnosis between hypertensive heart disease and athlete's heart is sometimes challenging and requires a careful and comprehensive interpretation in order not to misinterpret the clinical findings. The present review aims to discuss the relationship between hypertensive heart disease and physical exercise, from diagnostic tools to prevention and treatment strategies.

Monocyte-Derived Macrophages Aggravate Cardiac Dysfunction After Ischemic Stroke in Mice.

BACKGROUND: Cardiac damage induced by ischemic stroke, such as arrhythmia, cardiac dysfunction, and even cardiac arrest, is referred to as cerebral-cardiac syndrome (CCS). Cardiac macrophages are reported to be closely associated with stroke-induced cardiac damage. However, the role of macrophage subsets in CCS is still unclear due to their heterogeneity. Sympathetic nerves play a significant role in regulating macrophages in cardiovascular disease. However, the role of macrophage subsets and sympathetic nerves in CCS is still unclear. METHODS AND RESULTS: In this study, a middle cerebral artery occlusion mouse model was used to simulate ischemic stroke. ECG and echocardiography were used to assess cardiac function. We used Cx3cr1GFPCcr2RFP mice and NLRP3-deficient mice in combination with Smart-seq2 RNA sequencing to confirm the role of macrophage subsets in CCS. We demonstrated that ischemic stroke-induced cardiac damage is characterized by severe cardiac dysfunction and robust infiltration of monocyte-derived macrophages into the heart. Subsequently, we identified that cardiac monocyte-derived macrophages displayed a proinflammatory profile. We also observed that cardiac dysfunction was rescued in ischemic stroke mice by blocking macrophage infiltration using a CCR2 antagonist and NLRP3-deficient mice. In addition, a cardiac sympathetic nerve retrograde tracer and a sympathectomy method were used to explore the relationship between sympathetic nerves and cardiac macrophages. We found that cardiac sympathetic nerves are significantly activated after ischemic stroke, which contributes to the infiltration of monocyte-derived macrophages and subsequent cardiac dysfunction. CONCLUSIONS: Our findings suggest a potential pathogenesis of CCS involving the cardiac sympathetic nerve-monocyte-derived macrophage axis.