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S100A8 and S100A9, which are prominent members of the calcium-binding protein S100 family and recognized as calprotectin, form a robust heterodimer known as S100A8/A9, crucial for the manifestation of their diverse biological effects. Currently, there is a consensus that S100A8/A9 holds promise as a biomarker for cardiovascular diseases (CVDs), exerting an influence on cardiomyocytes or the cardiovascular system through multifaceted mechanisms that contribute to myocardial injury or dysfunction. In particular, the dualistic nature of S100A8/A9, which functions as both an inflammatory mediator and an anti-inflammatory agent, has garnered significantly increasing attention. This comprehensive review explores the intricate mechanisms through which S100A8/A9 operates in cardiovascular diseases, encompassing its bidirectional regulatory role in inflammation, the initiation of mitochondrial dysfunction, the dual modulation of myocardial fibrosis progression, and apoptosis and autophagy. The objective is to provide new information on and strategies for the clinical diagnosis and treatment of cardiovascular diseases in the future.

Abstract Aims Cancer therapy-related cardiac dysfunction (CTRCD) is a dreaded complication of anthracycline therapy. CTRCD most frequently appears in patients with cardiovascular risk factors (CVR) or known cardiovascular disease. However, limited data exist on incidence and course of anthracycline-induced CTRCD in patients without preexisting risk factors. We therefore aimed to longitudinally investigate a cohort of young women on anthracycline treatment due to breast cancer without cardiovascular risk factors or known cardiovascular disease (NCT03940625). Methods and results We enrolled 59 women with primary breast cancer and scheduled anthracycline-based therapy, but without CVR or preexisting cardiovascular disease. We conducted a longitudinal assessment before, immediately and 12 months after cancer therapy with general laboratory, electrocardiograms, echocardiography and cardiovascular magnetic resonance (CMR), including myocardial relaxometry with T1, T2 and extracellular volume mapping. Every single patient experienced a drop in CMR-measured left ventricular ejection fraction (LVEF) of 6 ± 3% immediately after cancer therapy. According to the novel definition 32 patients (54.2%) developed CTRCD after 12 months defined by reduction in LVEF, global longitudinal strain (GLS) and/or biomarkers elevation, two of them were symptomatic. Global myocardial T2 relaxation times as well as myocardial mass increased coincidently with a decline in wall-thickening. While T2 values and myocardial mass normalized after 12 months, LVEF and GLS remained impaired. Conclusion In every single patient anthracyclines induce a decline of myocardial contractility, even among patients without pre-existing risk factors for CTRCD. Our data suggest to thoroughly evaluate whether this may lead to an increased risk of future cardiovascular events. Graphical Abstract Reduced myocardial contractility in low-risk patients receiving anthracycline-based cancer therapy. This study included 59 otherwise healthy women with primary breast cancer undergoing anthracycline-based chemotherapy. CMR was performed at baseline, directly and 12 months after cancer therapy. A decline in left ventricular function was observed in every single patient accompanied by transient edema. More than 50% were diagnosed with cancer therapy related cardiovascular dysfunction. LVEF: left ventricular function, CTRCD: cancer therapy related cardiovascular dysfunction, GLS = Global longitudinal strain, hs-TnT = high sensitive Troponin T, NT-pro BNP = NT-pro brain natriuretic peptide

Myocardial strain is a dimensionless parameter reflecting the degree of deformation of the whole or local myocardium under stress, which can quantitatively detect myocardial injury and guide the early diagnosis, intervention and prognostic assessment of cardiac diseases. Cardiac ultrasound, cardiac CT and cardiac magnetic resonance can all be used for strain imaging and analysis, with two-dimensional speckle-tracking echocardiography being the most widely used means of myocardial strain detection today. However, due to inter-observer variations in manual analysis of myocardial strain and differences in the imaging systems and analysis software, the consistency and reproducibility of measured strain values among vendors are poor, limiting the clinical application of myocardial strain. Artificial intelligence (AI) can overcome the defects of strain measurement to a certain extent through automatic strain calculation and image quality assessment, which has a broad developmental prospect. This review focuses on the progress of AI-assisted measurement of myocardial strain in ultrasound, magnetic resonance, and other imaging modalities, as well as its application to disease diagnosis and patient prognosis assessment. This will improve the efficiency and consistency of strain measurement and promote the routine application of myocardial strain to clinical practice, which will play an incremental role in assessing myocardial injury and cardiac function. However, most of the current studies involve small sample sizes and lack external validation, and the reliability of their results needs to be further verified.

Ischemia-reperfusion (IR) injury remains a pivotal contributor to myocardial damage following acute coronary events and revascularization procedures. Phosphoinositide 3-kinase (PI3K), a key mediator of cell survival signaling, plays a central role in regulating inflammatory responses and cell death mechanisms. Trans-chalcone (Tch), a natural compound known for its anti-inflammatory activities, has shown promise in various disease models. The aim of the current study was to investigate the potential protective effects of Tch against myocardial injury induced by ischemia and reperfusion challenges by targeting the PI3K-inflammasome interaction. Experimental models utilizing male rats subjected to an in vivo model of IR injury and myocardial infarction were employed. Administration of Tch (100 μg/kg, intraperitoneally) significantly reduced myocardial injury, as indicated by limited infarct size and decreased levels of the myocardial enzyme troponin. Mechanistically, Tch upregulated PI3K expression, thereby inhibiting the activity of the NOD-like receptor protein 3 inflammasome followed by the activation of pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. Moreover, it mitigated oxidative stress and suppressed vascular-intercellular adhesion molecules, contributing to its cardioprotective effects. The PI3K/Akt pathway inhibitor LY294002 considerably attenuated the beneficial effects of Tch. These findings highlight the therapeutic potential of Tch in ameliorating myocardial injury associated with IR insults through its modulation of the PI3K/Akt-inflammasome axis. The multifaceted mechanisms underlying its protective effects signify Tch as a promising candidate for further exploration in developing targeted therapies aimed at mitigating ischemic heart injury and improving clinical outcomes in cardiovascular diseases characterized by IR injury.

Abstract Objective Patients with epilepsy have high risk of experiencing uncommon causes of death. This study aimed to evaluate patients who underwent unusual deaths related to epilepsy and identify factors that may contribute to these deaths and may also include sudden unexpected death in epilepsy (SUDEP). Methods We analyzed 5291 cases in which a postmortem imaging (PMI) study was performed using plane CT, because of an unexplained death. A rapid troponin T assay was performed using peripheral blood samples. Clinical information including the cause of death suspected by the attending physician, body position, place of death, medical history, and antiseizure medications was evaluated. Results A total of 132 (2.6%) patients had an obvious history of epilepsy, while 5159 individuals had no history of epilepsy (97.4%). Cerebrovascular disease was the cause of death in 1.6% of patients in the group with epilepsy, and this was significantly lower than that in the non‐epilepsy group. However, drowning was significantly higher (9.1% vs. 4.4%). Unspecified cause of death was significantly more frequent in the epilepsy group (78.0% vs. 57.8%). Furthermore, the proportion of patients who demonstrated elevation of troponin T levels without prior cardiac disease was significantly higher in the epilepsy group (37.9% vs. 31.1%). At discovery of death, prone position was dominant (30.3%), with deaths occurring most commonly in the bedroom (49.2%). No antiseizure medication had been prescribed in 12% of cases, while 29.5% of patients were taking multiple antiseizure medications. Significance The prevalence of epilepsy in individuals experiencing unusual death was higher than in the general population. Despite PMI studies, no definitive cause of death was identified in a significant proportion of cases. The high troponin T levels may be explained by long intervals between death and examination or by higher incidence of myocardial damage at the time of death. Plain Language Summary This study investigated unusual deaths in epilepsy patients, analyzing 5291 postmortem imaging cases. The results showed that 132 cases (2.6%) had a clear history of epilepsy. In these cases, only 22% cases were explained after postmortem examination, which is less than in non‐epilepsy group (42.2%). Cerebrovascular disease was less common in the epilepsy group, while drowning was more common. Elevated troponin T levels, which suggest possibility of myocardial damage or long intervals between death and examination, were also more frequent in the epilepsy group compared to non‐epilepsy group.

Objective To investigate the effect of moxibustion on Neiguan acupoint in preventing myocardial damage caused by anthracycline-based chemotherapy in breast cancer patients, and to explore the feasibility of moxibustion on Neiguan acupoint in reducing cardiotoxicity induced by chemotherapy. Methods A total of 80 breast cancer patients who underwent adjuvant chemotherapy with EC-T (pirarubicin + cyclophosphamide followed by docetaxel) regimen after surgery in the Department of Breast Cancer, Shaanxi Provincial Cancer Hospital from May 2020 to May 2021 were selected and divided into control group (n=40) and experimental group (n=40) randomly. During the first four cycles of chemotherapy, both groups received dexrazoxane on the same day as pirarubicin. The experimental group received moxibustion on Neiguan acupoint for three consecutive days starting one day before chemotherapy. The electrocardiograms, cardiac function, levels of cardiac troponin I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and Karnofsky Performance Status (KPS) score were observed before and after four cycles of chemotherapy. Results After four cycles of chemotherapy, the incidences of arrhythmia ［22.5%(9/40) vs 50.0%(20/40), χ2=6.545, P=0.011］ and QRS wave voltage decrease［27.5%(11/40) vs 55.0%(22/40), χ2=6.241, P=0.012］ in the experimental group were lower than those in the control group. The cardiac function classification in the experimental group was better than that in the control group ( Z=2.388，P＜0.017). After four cycles of chemotherapy, left ventricular ejection fraction (LVEF) decreased and left ventricular end-diastolic diameter (LVEDD) increased in the control group, while LVEF and LVEDD changes were not significant in the experimental group. The cTnI levels, NT-proBNP levels, and KPS scores increased in both groups, and LVEF, LVEDD, cTnI, NT-proBNP levels, and KPS scores were better in the experimental group than those in the control group (P＜0.05). Conclusion Moxibustion on Neiguan acupoint has a significant protective effect on myocardial damage caused by chemotherapy in breast cancer patients, and can further improve myocardial function on the basis of dexrazoxane.

Cardiovascular diseases remain the leading cause of death in the world, and that is why finding an effective and multi-functional treatment alternative to combat these diseases has become more important. Fibrates and thiazolidinediones, peroxisome proliferator-activated receptors alpha and gamma are the pharmacological therapies used to treat dyslipidemia and type 2 diabetes, respectively. New mechanisms of action of these drugs have been found, demonstrating their pleiotropic effects, which contribute to preserving the heart by reducing or even preventing myocardial damage. Here, we review the mechanisms underlying the cardioprotective effects of PPAR agonists and regulating morphological and physiological heart alterations (metabolic flexibility, mitochondrial damage, apoptosis, structural remodeling, and inflammation). Moreover, clinical evidence regarding the cardioprotective effect of PPAR agonists is also addressed.

Heart failure is a continuously developing syndrome of cardiac insufficiency caused by diseases, which becomes a major disease endangering human health as well as one of the main causes of death in patients with cardiovascular diseases. The occurrence of heart failure is related to hemodynamic abnormalities, neuroendocrine hormones, myocardial damage, myocardial remodeling etc, lead to the clinical manifestations including dyspnea, fatigue and fluid retention with complex pathophysiological mechanisms. Currently available drugs such as cardiac glycoside, diuretic, angiotensin-converting enzyme inhibitor, vasodilator and β receptor blocker etc are widely used for the treatment of heart failure. In particular, natural products and related active ingredients have the characteristics of mild efficacy, low toxicity, multi-target comprehensive efficacy, and have obvious advantages in restoring cardiac function, reducing energy disorder and improving quality of life. In this review, we mainly focus on the recent advance including mechanisms and active ingredients of natural products for the treatment of heart failure, which will provide the inspiration for the development of more potent clinical drugs against heart failure.

We aimed to investigate the potential benefits of two doses of ivabradine (IVA)-an If sodium channel blocker against isoproterenol (ISO)-induced myocardial damage in rats.The rats were randomly divided into 4 groups: Control group (n=8); Saline was administered, ISO group (n=12); 150 mg/kg ISO was administered for 2 days, ISO+IVA (1 mg/kg) group (n=12); 1 mg/kg IVA was administered for 4 days in addition to ISO. ISO+IVA (10 mg/kg) group (n=12): 10 mg/kg IVA was administered for 4 days in addition to ISO. Thereafter, hemodynamic, histopathological, and biochemical studies were performed. In the ISO+IVA (1 mg/kg) and ISO+IVA (10 mg/kg) groups, ISO-induced myocardial changes including an increase in density of granulation tissue and degenerated cardiomyocyte were equally decreased. HR was mildly reduced, and arterial blood pressures were slightly increased in the IVA-treated groups versus the ISO group. In the hearts of IVA-treated groups, malondialdehyde (MDA) levels were significantly reduced and glutathione (GSH) level and catalase (CAT) activity were mildly increased compared to the ISO group. Elevation of GSH and CAT activity were more pronounced in the ISO+IVA (10 mg/kg) group. Our results indicate that both 1 mg/kg and 10 mg/kg doses of IVA are effective against heart damage induced by ISO via its negative chronotropic, anti-oxidant (dose-dependent), anti-inflammatory and anti-degenerative properties. [Med-Science 2023; 12(3.000): 667-73]

Myocardial damage significantly impacts the prognosis of patients with cancer; however, the mechanisms of myocardial damage induced by cancer and its treatment remain unknown. We previously reported that medium-chain fatty acids (MCFAs) improve cancer-induced myocardial damage but did not evaluate the differences in effect according to MCFA type. Therefore, this study investigated the role of inflammatory cytokines in cancer-induced myocardial damage and the effects of three types of MCFAs (caprylic acid [C8], capric acid [C10], and lauric acid [C12]). In a mouse model, the C8 diet showed a greater effect on improving myocardial damage compared with C10 and C12 diets. Myocardial tubes differentiated from H9C2 cardiomyoblasts demonstrated increased mitochondrial oxidative stress, decreased membrane potential and mitochondrial volume, and inhibited myocardial tube differentiation following treatment with high-mobility group box-1 (HMGB1) but not interleukin-6 and tumor necrosis factor-α cytokines. However, HMGB1 treatment combined with C8 improved HMGB1-induced mitochondrial damage, enhanced autophagy, and increased mitochondrial biogenesis and maturation. However, these effects were only partial when combined with beta-hydroxybutyrate, a C8 metabolite. Thus, HMGB1 may play an important role in cancer-related myocardial damage. C8 counteracts HMGB1’s effects and improves cancer-related myocardial damage. Further clinical studies are required to investigate the effects of C8.

Antioxidant protection is one of the key reactions of cardiomyocytes (CMCs) in response to myocardial damage of various origins. The thioredoxin interacting protein (TXNIP) is an inhibitor of thioredoxin (TXN). Over the recent few years, TXNIP has received significant attention due to its wide range of functions in energy metabolism. In the present work, we studied the features of the redox-thiol systems, in particular, the amount of TXNIP and glutathione synthetase (GS) as markers of oxidative damage to CMCs and antioxidant protection, respectively. This study was carried out on 38-week-old Wistar-Kyoto rats with insulin-dependent diabetes mellitus (DM) induced by streptozotocin, on 38- and 57-week-old hypertensive SHR rats and on a model of combined hypertension and DM (38-week-old SHR rats with DM). It was found that the amount of TXNIP increased in 57-week-old SHR rats, in diabetic rats and in SHR rats with DM. In 38-week-old SHR rats, the expression of TXNIP significantly decreased. The expression of GS was significantly higher compared with the controls in 57-week-old SHR rats, in DM rats and in the case of the combination of hypertension and DM. The obtained data show that myocardial damage caused by DM and hypertension are accompanied by the activation of oxidative stress and antioxidant protection.

Introduction: Significant attention has been paid to myocardial damage mediated by the single-stranded RNA virus. Qingfei Paidu decoction (QFPDD) has been proved to protect the damage caused by the influenza virus A/PR/8/1934 (PR8), but its specific mechanism is unclear.Methods: Molecular biological methods, together with network pharmacology, were used to analyze the effects and underlying mechanism of QFPDD treatment on PR8-induced myocardial damage to obtain insights into the treatment of COVID-19-mediated myocardial damage.Results: Increased apoptosis and subcellular damage were observed in myocardial cells of mice infected by PR8. QFPDD treatment significantly inhibited the apoptosis and subcellular damage induced by the PR8 virus. The inflammatory factors IFN-β, TNF-α, and IL-18 were statistically increased in the myocardia of the mice infected by PR8, and the increase in inflammatory factors was prevented by QFPDD treatment. Furthermore, the expression levels or phosphorylation of necroptosis-related proteins RIPK1, RIPK3, and MLKL were abnormally elevated in the group of infected mice, while QFPDD restored the levels or phosphorylation of these proteins. Our study demonstrated that HIF-1α is a key target of QFPDD in the treatment of influenza virus-mediated injury. The HIF-α level was significantly increased by PR8 infection. Both the knockdown of HIF-1α and treatment of the myocardial cell with QFPDD significantly reversed the increased inflammatory factors during infection. Overexpression of HIF-1α reversed the inhibition effects of QFPDD on cytokine expression. Meanwhile, seven compounds from QFPDD may target HIF-1α.Conclusion: QFPDD can ameliorate influenza virus-mediated myocardial damage by reducing the degree of cell necroptosis and apoptosis, inhibiting inflammatory response and the expression of HIF-1α. Thus, our results provide new insights into the treatment of respiratory virus-mediated myocardial damage.

Abstract Background Diabetic cardiomyopathy results in cardiac structural and functional abnormalities. Previous studies have demonstrated that inhibiting the RhoA/ROCK signalling pathway increases the injury resistance of cardiomyocytes. The early detection of cardiac structural and functional alterations may facilitate an improved understanding of the pathophysiologic progress and guide therapy. This study aimed to identify the optimal diagnostic measures for the subtle early alterations of cardiac dysfunction in type 2 diabetes mellitus (T2DM) rats. Methods Twenty-four rat models were divided into four groups and received treatments for 4 weeks: the CON group (control rats), the DM group (T2DM rats), the DMF group (T2DM rats receiving fasudil) and the CONF group (control rats receiving fasudil) group. Left ventricular (LV) structure was quantified by histological staining and transmission electron microscopy. LV function and myocardial deformation were assessed by high-frequency echocardiography. Results Treatment with fasudil, a ROCK inhibitor, significantly protected against diabetes-induced myocardial hypertrophy, fibrosis and mitochondrial dysfunction. Impaired LV performance was found in T2DM rats, as evidenced by significant reductions in the ejection fraction (EF), fractional shortening (FS) and the mitral valve (MV) E/A ratio (which decreased 26%, 34% and 20%, respectively). Fasudil failed to improve the conventional ultrasonic parameters in T2DM rats, but the myocardial deformation measured by speckle-tracking echocardiography (STE) were significantly improved (global circumferential strain, GCS: P = 0.003; GCS rate, GCSR: P = 0.021). When receiver operating characteristic (ROC) curves were used in combination with linear regression analysis, STE parameters were found to be characterized by both optimal prediction of cardiac damage [AUC (95% CI): fractional area change, FAC: 0.927 (0.744, 0.993); GCS: 0.819 (0.610, 0.945); GCSR: 0.899 (0.707, 0.984)] and stronger correlations with cardiac fibrosis (FAC: r = -0.825; GCS: r = 0.772; GCSR: r = 0.829) than conventional parameters. Conclusion The results suggest that STE parameters are more sensitive and specific than conventional parameters in predicting the subtle cardiac functional changes that occur in the early stage, providing new insight into the management of diabetic cardiomyopathy.

IntroductionExtracorporeal cardiopulmonary resuscitation (ECPR) is an emerging strategy in highly selected patients with refractory cardiac arrest (CA). Animal models can help to identify new therapeutic strategies to improve neurological outcome and cardiac function after global ischemia in CA. Aim of the study was to establish a reproducible ECPR rat model of ventricular fibrillation CA (VFCA) that leads to consistent neuronal damage with acceptable long-term survival rates, which can be used for future research.Materials and methodsMale Sprague Dawley rats were resuscitated with ECPR from 6 min (n = 15) and 8 min (n = 16) VFCA. Animals surviving for 14 days after return of spontaneous resuscitation (ROSC) were compared with sham operated animals (n = 10); neurological outcome was assessed daily until day 14. In the hippocampal cornu ammonis 1 region viable neurons were counted. Microglia and astrocyte reaction was assessed by Iba1 and GFAP immunohistochemistry, and collagen fibers in the myocardium were detected in Azan staining. QuPath was applied for quantification.ResultsOf the 15 rats included in the 6 min CA group, all achieved ROSC (100%) and 10 (67%) survived to 14 days; in the 8 min CA group, 15 (94%) achieved ROSC and 5 (31%) reached the endpoint. All sham animals (n = 10) survived 2 weeks. The quantity of viable neurons was significantly decreased, while the area displaying Iba1 and GFAP positive pixels was significantly increased in the hippocampus across both groups that experienced CA. Interestingly, there was no difference between the two CA groups regarding these changes. The myocardium in the 8 min CA group exhibited significantly more collagen fibers compared to the sham animals, without differences between 6- and 8-min CA groups. However, this significant increase was not observed in the 6 min CA group.ConclusionOur findings indicate a uniform occurrence of neuronal damage in the hippocampus across both CA groups. However, there was a decrease in survival following an 8-min CA. Consequently, a 6-min duration of CA resulted in predictable neurological damage without significant cardiac damage and ensured adequate survival rates up to 14 days. This appears to offer a reliable model for investigating neuroprotective therapies.

For today the exact mechanisms of myocardial infarction and ischemia/reperfusion injury are still not fully understood. ER stress and integrated stress response pathways are thought to play an essential role in myocardial damage. This includes activation of endoplasmic reticulum kinase (PERK), induction of activating transcription factor 4 (ATF4), expression of pro-apoptotic transcription factor (CHOP) and P53 up-regulated modulator of apoptosis (PUMA) involved in apoptosis control. We used a rat model of isoproterenol-induced myocardial damage to elucidate the possible cardioprotective effect of Ginger through the influence on ER stress-induced apoptotic pathway. We also compared its effect with Captopril, inhibitor of angiotensin-converting enzyme. Male albino Wistar rats received 1.0 or 2.0 ml of Zingiber officinale (Ginger) powder suspension (200 mg/ml) daily by intra-gastric intubation for 28 days. Isoproterenol at a dose of 85 mg/kg was IP injected on the 27th and 28th days. Serum aspartate transaminase (AST) level was measured using kinetic kit. Heart tissue was used for RNA extraction, evaluation of gene expression by Q-RT-PCR, immuno-histochemical determination of caspase-3 expression and histopathological studies. Our results showed that Isoproterenol administration increased CHOP-mRNA expression 4 folds in cardiac muscle tissue compared to normal control. Ginger pretreatment significantly decreased both CHOP and ATF4, and PUMA mRNA expression compared to Isoproterenol-treated groups. A significant reduction in ATF4 mRNA expression in a group pretreated with Captopril and Ginger compared to normal control group was observed. The results showed that Ginger reduced AST serum levels which correlated with results of histopathological studies of heart tissue. Our findings suggest that the protective effects of Ginger against myocardium damage induced by Isoproterenol may be mediated by reducing­ the endoplasmic reticulum stress by affecting the ATF4-CHOP-PUMA pathway.

Cardiorenal interaction in acute heart failure (AHF) is becoming an increasingly recognized factor to consider in the management of cardiac surgical patients. Achieving adequate control of water balance and simultaneously preserving kidney function is the goal of the optimal management strategy for patients with AHF. The majority of preoperative hospitalizations to intensive care units in patients with infective endocarditis (IE) are associated with the development of AHF. The term “cardiorenal syndrome” (CRS) is used to define kidney dysfunction on the background of AHF. Due to the lack of clear clinical manifestations of CRS in IE, the diagnosis and treatment of this pathology may be delayed and contribute to the increase in the number of postoperative complications. Recent data, both in basic science and in clinical research, have changed our understanding of CRS. To date, several types of impaired interaction between the kidneys and the heart have been identified. The aim. To study the peculiarities of CRS in patients with IE complicated by AHF. Materials and methods. The basis of this study was the clinical data of 41 patients with active IE who were treated at the National Amosov Institute of Cardiovascular Surgery of the National Academy of Medical Sciences of Ukraine from 1/1/2020 to 8/31/2020. In order to study the features of clinical manifestation and the course of CRS, a comparative analysis was conducted based on the history and results of laboratory and instrumental research for the group of patients with IE complicated by preoperative AHF, and patients without clinical manifestations of AHF at the time of hospitalization. For an in-depth study of myocardial damage in heart failure, troponin, NT-proBNP, lactate levels were analyzed; dysfunction of the urinary system was assessed by the level of urea and serum creatinine, the volume of diuresis. Results. A reliable relationship between the levels of NT-proBNP and serum creatinine at the preoperative stage was revealed (p˂0.001), as an indicator of the presence of CRS in patients with IE. In the early postoperative period, signs of CRS persisted in patients with IE complicated by preoperative AHF (serum creatinine 157.0±8.5 μmol/l [p

Chloroacetyl chloride is a potent acylation agent that decomposes violently in water to produce chloroacetic acid and irritant hydrogen chloride. It and its decomposition products are corrosive to the eyes, skin, and respiratory system and can cause multiple organ failure. Herein, we report cases of poisoning by chloroacetyl chloride and its decomposition products in the skin and respiratory system. After exposure, one patient developed vomiting, irritability, coma, hypoxemia, hypotension, acidosis, and hypokalemia. Another patient developed bronchiolitis, pneumonia, and decreased vision. One patient died and two recovered. Chloroacetyl chloride and its decomposition products are corrosive and can damage multiple organs after absorption through the skin and respiratory tract, leading to severe heart failure. Cardiogenic shock may be the primary cause of early mortality.

Sepsis is defined as “a life-threatening organ dysfunction caused by a dysregulated host response to infection”. Although the treatment of sepsis has evolved rapidly in the last few years, the morbidity and mortality of sepsis in clinical treatment are still climbing. Sirtuins (SIRTs) are a highly conserved family of histone deacetylation involved in energy metabolism. There are many mechanisms of sepsis-induced myocardial damage, and more and more evidence show that SIRTs play a vital role in the occurrence and development of sepsis-induced myocardial damage, including the regulation of sepsis inflammation, oxidative stress and metabolic signals. This review describes our understanding of the molecular mechanisms and pathophysiology of sepsis-induced myocardial damage, with a focus on disrupted SIRTs regulation. In addition, this review also describes the research status of related therapeutic drugs, so as to provide reference for the treatment of sepsis.

Pneumonia is a common clinical disease in the neonatal period and poses a serious risk to infant health. Therefore, the understanding of molecular mechanisms is of great importance for the development of methods for the rapid and accurate identification, classification and staging, and even disease diagnosis and therapy of pneumonia. In this study, a nontargeted metabonomic method was developed and applied for the analysis of serum samples collected from 20 cases in the pneumonia control group (PN) and 20 and 10 cases of pneumonia patients with metabolic acidosis (MA) and myocardial damage (MD), respectively, with the help of ultrahigh-performance liquid chromatography–high-resolution mass spectrometry (UPLC–HRMS). The results showed that compared with the pneumonia group, 23 and 21 differential metabolites were identified in pneumonia with two complications. They showed high sensitivity and specificity, with the area under the curve (ROC) of the receiver operating characteristic curve (ROC) larger than 0.7 for each differential molecule. There were 14 metabolites and three metabolic pathways of sphingolipid metabolism, porphyrin and chlorophyll metabolism, and glycerophospholipid metabolism existing in both groups of PN and MA, and PN and MD, all involving significant changes in pathways closely related to amino acid metabolism disorders, abnormal cell apoptosis, and inflammatory responses. These findings of molecular mechanisms should help a lot to fully understand and even treat the complications of pneumonia in infants.

Background: To investigate the effect of cholesterol accumulation in cells on the inflammatory process of acute myocardial infarction and cardiomyocytes and its mechanism. Methods: Blood samples of 15 patients with myocardial infarction were clinically collected to detect enzyme levels of cholesterol and related myocardial parameters in the serum. Correlation analysis was carried out. At the cellular level, simulation of cholesterol entry and exit from cells was conducted by a liposome-loaded cholesterol model in this study, and BNP and inflammatory factors were detected with enzyme-linked immunosorbent assay. Moreover, to investigate the molecular mechanism of myocardial damage caused by cholesterol, Gramd1b and Prkaca of HL-1 were knocked down with small interference RNA technique. Then, inhibitor C3 was used to weaken RhoA activity to explore the level of cardiac muscle cell BNP in order to identify key protein target sites that may be involved in the process of cholesterol damage to cardiac muscle cells. Results: Serum cholesterol concentration showed a significantly positive correlation with the levels of AST, CK, and LD in serum of patients with myocardial infarction. Cholesterol accumulation in cardiac muscle cells significantly increased the levels of BNP, inflammatory factors (IL-1β, IL-6, TNF-α, and CCL-2) in cardiac muscle cells, which exacerbated cardiomyocyte damage. Conversely, cholesterol excretion caused significant downregulation of BNP and inflammatory factors. Moreover, after knocking down Gramd1b, the accumulation of cholesterol in myocardial cells decreased, the levels of BNP and inflammatory factors significantly reduced, and the degree of myocardial cell damage was weakened. Knockdown of Prkaca inhibited RhoA activity and reversed cholesterol-induced elevation of BNP and inflammatory factors. Conclusion: ASTER B-mediated intracellular accumulation of cholesterol in cardiac muscle cells may cause cardiomyocyte damage and inflammatory factor infiltration through PKA-Ca2+-RhoA pathways.

Abstract Background Stable coronary artery disease (CAD) patients with myocardial damage have a poor prognosis compared to those without myocardial damage. Recently, malnutrition has been reported to affect the prognosis of cardiovascular diseases. However, the effects of malnutrition on prognosis of CAD patients with myocardial damage remains uncertain. We investigated the effects of malnutrition on prognosis of CAD patients with myocardial damage who received percutaneous coronary intervention (PCI). Methods Subjects comprised 241 stable CAD patients with myocardial damage due to myocardial ischemia or infraction. Patients underwent successful revascularization for the culprit lesion by PCI using second-generation drug-eluting stents and intravascular ultrasound. The geriatric nutritional risk index (GNRI), which is widely used as a simple method for screening nutritional status using body mass index and serum albumin, was used to assess nutritional status. Associations between major cardiovascular and cerebrovascular events (MACCE) and patient characteristics were assessed. Results Mean GNRI was 100 ± 13, and there were 55 malnourished patients (23%; GNRI

Background. In addition to infecting the respiratory system, COVID-19 also has a negative impact on the cardiovascular system. COVID-19 causes acute myocardial damage as well as chronic damage to the cardiovascular system. According to the studied literature, we found that among all cardiac arrhythmias among elderly and senile patients during and after a new coronovirus infection, supraventricular arrhythmias are most often recorded according to HM-ECG and ECG. There is no doubt that the syndrome of senile asthenia, supraventricular arrhythmias and the new coronavirus infection are inextricably linked and aggravate each other's condition. Therefore, we set a purpose to study the prevalence and clinical course of supraventricular arrhythmias among elderly and senile patients with SA syndrome against the background of a new coronovirus infection (COVID-19). Materials and methods. The study included 57 patients who were hospitalized in the covid hospital in Penza. In the course of the study, laboratory and instrumental indicators were analyzed. All patients were assessed for the syndrome of senile asthenia and preasthenia using the “Age is not a hindrance” questionnaire. Results. A total of 57 patients took part in the study. The age of the patients varied from 65 to 94 years, with an average of 74 ± 6 years. Women – 32 (56.1 %), men – 25 (43.9 %). During the study, the following arrhythmias were registered among patients according to 12-lead ECG and HM-ECG data: sinus tachycardia was detected among 13 people (22.8 %); sinus bradycardia – 10 people (17.5 %); AV nodal tachycardias were registered in only 2 patients (3.5 %); atrial fibrillation among 24 patients (42.1 %); atrial flutter – 3 cases (5.3 %); supraventricular extrasystoles were detected in 5 patients (8.8 %). Conclusions. In the course of the study, we found that among elderly and senile patients against the background of a new coronovirus infection (CJVID-19), of all supraventricular arrhythmias, the most common is atrial fibrillation (42.1 % of cases), followed by sinus tachycardia (22.8 % ), and having a protracted long non-stopping character and sinus bradycardia (17.5 % of cases). Among the study group of patients, according to the questionnaire "Age is not a hindrance", senile asthenia syndrome was recorded among 34 patients (59.6 %). According to the XM-ECG data, paroxysmal atrial fibrillation (45.9 %) was predominantly registered in this group of patients. According to ECHO-KG data, the majority of patients with atrial fibrillation had an enlarged left atrium (Arithmetic mean (M): 41.15, Median (Me): 42), which indicates an increased risk of arrhythmia complications.

BackgroundPatients with muscular dystrophy have mutations in the gene that can lead to severe muscle wasting, respiratory issues or heart failure between ages 30 and 40. Currently, there is no effective treatment for DMD-induced heart failure.Case presentationWe report a patient with recurrent unexplained fever and muscle soreness was definitely diagnosed with DMD. An analysis of the patient's genetics revealed a nonsense mutation (C.1207G > T). His DMD was treated with hormones. Also, the patient's fever is under control because of hormone therapy. However, as the disease progresses, the heart structure and function gradually change, and eventually malignant arrhythmias occur.ConclusionWe report a rare case of DMD involving the heart causing heart failure and malignant arrhythmia. Currently, no complete treatment is available for these patients, but our treatment regimen may benefit our patient and improve his outcomes.

Extracellular vesicles (EVs) obtain properties of immunomodulation and tissue repair from their parental mesenchymal stem cells (MSCs), and upon delivery may be associated with fewer adverse events. EVs derived from adipose-tissue MSCs restored kidney function by attenuating kidney inflammation in a swine model of metabolic syndrome (MetS) and renal artery stenosis via anti-inflammatory pathways. EVs also ameliorated myocardial injury in renovascular hypertension (RVH) secondary to inflammation in cardiorenal disease, but the mechanisms regulating this effect are unknown. We hypothesize that the anti-inflammatory cytokine interleukin (IL)-10 mediates the reparative effects of EVs on cardiovascular complications in a preclinical swine model with coexisting MetS and RVH. Twenty-three pigs established as Lean controls or RVH models were observed for 16 weeks. At 12 weeks RVH subgroups received an intrarenal delivery of 1011 either wildtype (WT) EVs or EVs after IL-10 knockdown (KD) (RVH+WT-EVs or RVH+IL-10-KD-EVs, respectively). Cardiac and renal function were studied in-vivo and myocardial tissue injury in-vitro 4 weeks later. RVH pigs showed myocardial inflammation, fibrosis, and left ventricular diastolic dysfunction. WT-EVs attenuated these impairments, increased capillary density, and decreased myocardial inflammation in-vivo. In-vitro, co-incubation with IL-10-containing WT-EVs decreased activated T-cells proliferation and endothelial cells inflammation and promoted their migration. Contrarily, these cardioprotective effects were largely blunted using IL-10-KD-EVs. Thus, the anti-inflammatory and pro-angiogenic effects of EVs in RVH may be partly attributed to their cargo of anti-inflammatory IL-10. Early intervention of IL-10-containing EVs may be helpful to prevent cardiovascular complications of MetS concurrent with RVH.

The adult human heart poorly regenerate after injury due to the low self-renewal capability retained by adult cardiomyocytes. In the last two decades, several clinical studies have reported the ability of stem cells to induce cardiac regeneration. However, low cell integration and survival into the tissue has limited stem-cell-based clinical approaches. More recently, the release of paracrine mediators including extracellular vesicles (EV) has been recognized as the most relevant mechanism driving benefits upon cell-based therapy. In particular, EV have emerged as key mediators of cardiac repair after damage, in terms of reduction of apoptosis, resolution of inflammation and new blood vessel formation. Herein, mechanisms involved in cardiac damage and regeneration, and current applications of EV and their small non-coding RNAs (miRNAs) in regenerative medicine are discussed.

Background: Yunpi-Huoxue-Sanjie (YP-SJ) formula is a Chinese herbal formula with unique advantages for the treatment of diabetic cardiovascular complications, such as Diabetic cardiomyopathy (DCM). However, potential targets and molecular mechanisms remain unclear. Therefore, our research was designed to evaluate rat myocardial morphology, fat metabolism and oxidative stress to verify myocardial protective effect of YP-SJ formula in vivo. And then to explore and validate its probable mechanism through network pharmacology and experiments in vitro and in vivo.Methods: In this study, DCM rats were randomly divided into five groups: control group, model group, and three YP-SJ formula groups (low-dose, middle-dose, and high-dose groups). Experimental rats were treated with 6 g/kg/d, 12 g/kg/d and 24 g/kg/d YP-SJ formula by gavage for 10 weeks, respectively. Cardiac function of rats was measured by high-resolution small-animal imaging system. The cells were divided into control group, high glucose group, high glucose + control serum group, high glucose + dosed serum group, high glucose + NC-siRNA group, high glucose + siRNA-FoxO1 group. The extent of autophagy was measured by flow cytometry, immunofluorescence, and western blotting.Results: It was found that YP-SJ formula could effectively improve cardiac systolic function in DCM rats. We identified 46 major candidate YP-SJ formula targets that are closely related to the progression of DCM. Enrichment analysis revealed key targets of YP-SJ formula related to environmental information processing, organic systems, and the metabolic occurrence of reactive oxygen species. Meanwhile, we verified that YP-SJ formula can increase the expression of forkhead box protein O1 (FoxO1), autophagy-related protein 7 (Atg7), Beclin 1, and light chain 3 (LC3), and decrease the expression of phosphorylated FoxO1 in vitro and in vivo. The results showed that YP-SJ formula could activate the FoxO1 signaling pathway associated with DCM rats. Further experiments showed that YP-SJ formula could improve cardiac function by regulating autophagy.Conclusion: YP-SJ formula treats DCM by modulating targets that play a key role in autophagy, improving myocardial function through a multi-component, multi-level, multi-target, multi-pathway, and multi-mechanism approach.

Abstract Introduction Myocardial damage is a mostly incurable complication of multiple myeloma (MM) that seriously affects the treatment outcome and quality of life of patients. Exosomal circular RNAs (exo-circRNAs) play an important role in tumor occurrence and development and are considered key factors in MM pathogenesis. However, the role and mechanism of action of exo-circRNAs in MM-related myocardial damage are still unclear. This study aimed to investigate correlations between exo-circRNAs and MM and to preliminarily explore the role of exo-circRNAs in MM-related myocardial damage. Methods Six MM patients and five healthy controls (HCs) were included in the study. High-throughput sequencing and qRT-PCR verification were used to obtain a profile of abnormally expressed exo-circRNAs. GO, KEGG, miRanda, TargetScan and Metascape were used for bioinformatics analyses. H9C2 cells treated with exosomes from U266 cells were used in cell experiments. CCK-8, PCR, immunofluorescence and western blotting assays were used to detect cell proliferation and expression of autophagy-related indicators. Electron microscopy was used to observe the number of autophagic vesicles. Results Bioinformatics analysis showed that circRNAs with upregulated expression had the potential to promote MM-related myocardial damage. In addition, PCR results confirmed that circ-G042080 was abundantly expressed in the serum exosomes of 20 MM patients. Correlation analysis showed that the expression level of circ-G042080 was positively correlated with the clinical level of MM and MM-related myocardial damage and that circ-G042080 might interfere with MM-related myocardial damage through a downstream miRNA/TLR4 axis. Cell experiments demonstrated that the circ-G042080/hsa-miR-4268/TLR4 axis might exist in H9C2 cells incubated with exosomes and cause abnormal autophagy. Conclusion Abnormal expression of serum exo-circRNAs was found to be associated with MM-related myocardial damage, suggesting that exo-circRNAs might become a new diagnostic marker of MM-related myocardial damage and a therapeutic target.

Background. Senile asthenia is characterized by a decrease in the function and reserve of the physiological systems of the body, including the cardiovascular system. Senile asthenia is considered as a process of accelerated aging with a cumulative manifestation of age-related disorders in many physiological systems that predispose to adverse outcomes. Cardiovascular pathology is one of the main comorbidities observed in COVID-19. The aim of the study is to assess the prevalence of cardiovascular diseases in patients with senile asthenia syndrome against the background of a new coronavirus infection. Materials and methods. The study included 54 patients who were hospitalized at the covid hospital in Penza. In the course of the study, laboratory and instrumental indicators were analyzed. All patients underwent assessment of SA using the index of senile asthenia. Results. When analyzing the data obtained when calculating the index of senile asthenia, 61.1% (n=33) of patients suffered from SA. Among concomitant comorbid conditions, arterial hypertension was detected in 78.8%, dyslipidemia was 54.5%, diabetes mellitus in 21.2%, atrial fibrillation in 12.1% of patients. Heart failure with reduced ejection fraction (LV EF 50%) determined in 13 patients (56.5%). Ischemic heart disease in this category of patients occurred in 10.4% of cases. Conclusions. Major cardiovascular and metabolic comorbidities such as hypertension, coronary heart disease, atrial fibrillation, and diabetes mellitus contribute to a poor prognosis in patients with frailty due to COVID-19. All patients require careful hemodynamic and electrocardiographic monitoring.

Paraneoplastic pemphigus (PNP) is a rare mucocutaneous autoimmune disease. It has multiple clinical accompanied symptoms by affecting various types of epithelia, including the gastrointestinal and respiratory tract. However, an extensive review of the literature found no cases of PNP associated with myocardial damage. Here, we present a 56-year-old male patient with clinically and histopathologically typical paraneoplastic pemphigus (PNP), who had sustained myocardial injury due to non-cardiac disease involvement. Therefore, we suppose that, when persistent cardiac necrosis markers are elevated in patients with paraneoplastic pemphigus (PNP), the possibility of concomitant myocardial damage should get more attention from clinicians to obtain quick diagnosis and treatment.

Having the issue of coronavirus disease 2019 (COVID-19) in mind, there is always a dilemma surrounding elective and non-urgent neurosurgical operations. The unanswered question is regarding whether there is any post-COVID-19 complications that hinder a patient from becoming a candidate for a neurosurgical operation. If that is the case, what should we do? In the present article, we report our single-center experience with an unusual bleeding during the operation of a huge cerebellar tumor in a girl previously infected with COVID-19. In the end, we recommend our experience to our colleagues. Abstract There are still some conditions that pediatric neurosurgeons may face in the context of coronavirus disease 2019 (COVID-19) which have not been fully addressed so far. Authors have postulated an ongoing inflammatory myocardial status in a significant proportion of patients who have recovered from COVID-19. We report our experience with a 10-month-old girl who had recovered form COVID-19 and had a case of fourth-ventricle mass in the midline of the posterior fossa. She was scheduled for microneurosurgical resection of the mass following the insertion of a ventriculoperitoneal shunt. There were no significant issues regarding the induction of anesthesia. A midline suboccipital approach was chosen, and the patient was fully prepared and draped. Suboccipital soft tissues and muscles were dissected layer by layer through the midline avascular line. A marked gush of blood off the midline was observed during the opening in Y of the dura mater. Then, we started to approach the occipital sinus. However, there was an unusual loss of ∼ 200 mL of blood lost from this area. Despite the proper packed-cell transfusion, the patient developed bradycardia and a sudden rhythm of asystole. The cardiopulmonary cerebral resuscitation (CPCR) was initiated immediately. Despite the maximal effort, the heart rate did not change and remained asystole. We recommend that pediatric neurosurgeons postpone the procedures to be performed in patients who have recovered from COVID-19 for more than one month after a thorough preoperative cardiac evaluation has been performed.

The COVID-19 pandemic caused by SARS-CoV-2 is the greatest medical problem of our time. The presence of concomitant cardiovascular pathology (CVD) in a patient predisposes to a severe course and the formation of adverse outcomes of COVID-19. It is currently known that SARS-CoV-2 infection leads, on the one hand, to exacerbation and decompensation of the patient's CVD, and, on the other hand, it is the origin of acute CVD. Understanding the impact of COVID-19 on the cardiovascular system is essential to provide comprehensive care for critically ill patients. In this review, we summarize the rapidly changing data on cardiovascular damage associated with COVID-19.

Abstract Background Del Nido cardioplegia (DNC) has been proven safe and effective in pediatric patients. However, the use of DNC in adult undergoing cardiovascular surgery lacks support with substantial evidence. This study aimed to evaluate the efficacy of DNC as a cardioplegia of prophylaxis to ventricular arrhythmias associated to cardiovascular surgery in adult patients. Methods This study recruited nine hundred fifty-four patients who underwent cardiopulmonary bypass surgeries in Nanjing Hospital affiliated to Nanjing Medical University between January 2019 and December 2019. Among 954 patients, 324 patients were treated with DNC (DNC group), and 630 patients were treated with St. Thomas cardioplegia (STH group). The incidence of postoperative arrhythmia as well as other cardiovascular events relavant to the surgery were investigated in both groups. Results In DNC group, the incidence of postoperative ventricular arrhythmias was lower (12.4% vs. 17.4%, P = 0.040), and the length of ICU stay was shorter (1.97 ± 1.49 vs. 2.26 ± 1.46, P = 0.004). Multivariate logistic regression demonstrated that the use of DNC helped to reduce the incidence of postoperative ventricular arrhythmias (adjusted odds ratio 0.475, 95% CI 0.266–0.825, P = 0.010). The propensity score-based analysis and subgroup analysis indicated that DNC has the same protecting effects towards myocardial in all kinds of cardiopulmonary bypass surgeries. Conclusions Del Nido cardioplegia may potentially reduce the incidence of postoperative ventricular arrhythmias, shorten the length of ICU stay and improve the overall outcome of the patients undergoing cardiovascular surgery.

The novel coronavirus infection COVID-19 in most cases manifests with respiratory symptoms and fever, however, some patients may have cardiovascular and gastroenterological manifestations. A feature of the clinical syndrome of COVID-19 is the development of pronounced immunopathological reactions and disorders of hemostasis, leading to the development of a wide range of cardiovascular complications. The course of COVID-19 may be complicated by the development of acute myocardial infarction, venous and arterial thrombosis and thromboembolism in various vascular pools, the development of acute myocardial damage and myocarditis. Among the gastroenterological manifestations, diarrhea, nausea or vomiting, as well as abdominal pain, are most often detected. These symptoms may precede the appearance of respiratory signs of the disease, and in some cases come to the fore in the clinical picture of the disease. In addition, in some patients there are laboratory signs of liver injury (increased serum transaminases). The exact pathogenesis of the above disorders continues to be studied.

The objective: based on publications to provide up-to-date information on the frequency, basic variants and predictive significance of cardiovascular complications of the coronavirus infection caused by SARS-CoV-2.Results: the article identifies variants of cardiovascular disorders in COVID-19 caused by various comorbidities in particular hypertension, specific virus-associated myocardial damage, and side effects of medications. It analyzes the role of angiotensin-converting enzyme 2 type II receptors during infection with the coronavirus and potential changes in the renin–angiotensin–aldosterone system including in patients receiving angiotensin-converting enzyme inhibitors or blockers of angiotensin receptors. The data on the frequency and prognostic role of arrhythmias, virus-associated myocardial damage and heart failure, the risk of ischemia, and myocardial infarction are presented. The adverse cardiovascular events of drugs of different groups prescribed for treatment of COVID-19 and possible drug interactions are described. The current recommendations for cardiotonic and cardioprotective therapy in patients with cardiovascular complications are analyzed.Conclusion. The SARS-Cov-2 virus has a pronounced cardiac tropic effect which requires maximum cardiac alertness in the treatment of patients in this category, timely use of electrocardiography, echocardiography, control of biomarkers of myocardial damage and tension, as well as a reasonable use of cardiotonic and cardioprotective drugs.

The progress of space science and technology has ushered in a new era for humanity’s exploration of outer space. Recent studies have indicated that the aerospace special environment including microgravity and space radiation poses a significant risk to the health of astronauts, which involves multiple pathophysiological effects on the human body as well on tissues and organs. It has been an important research topic to study the molecular mechanism of body damage and further explore countermeasures against the physiological and pathological changes caused by the space environment. In this study, we used the rat model to study the biological effects of the tissue damage and related molecular pathway under either simulated microgravity or heavy ion radiation or combined stimulation. Our study disclosed that ureaplasma-sensitive amino oxidase (SSAO) upregulation is closely related to the systematic inflammatory response (IL-6, TNF-α) in rats under a simulated aerospace environment. In particular, the space environment leads to significant changes in the level of inflammatory genes in heart tissues, thus altering the expression and activity of SSAO and causing inflammatory responses. The detailed molecular mechanisms have been further validated in the genetic engineering cell line model. Overall, this work clearly shows the biological implication of SSAO upregulation in microgravity and radiation-mediated inflammatory response, providing a scientific basis or potential target for further in-depth investigation of the pathological damage and protection strategy under a space environment.

Wearable cardioverter defibrillator (WCD) is a life saving, wearable, noninvasive therapeutic device that prevents fatal ventricular arrhythmic propagation that leads to sudden cardiac death (SCD). WCD are frequently prescribed to patients deemed to be at high arrhythmic risk but the underlying pathology is potentially reversible or to those who are awaiting an implantable cardioverter-defibrillator. WCD is programmed to detect appropriate arrhythmic events and generate high energy shock capable of depolarizing the myocardium and thus re-initiating the sinus rhythm. WCD guidelines dictate very high reliability and accuracy to deliver timely and optimal therapy. Computational model-based process validation can verify device performance and benchmark the device setting to suit personalized requirements. In this article, we present a computational pipeline for WCD validation, both in terms of shock classification and shock optimization. For classification, we propose a convolutional neural network-“Long Short Term Memory network (LSTM) full form” (Convolutional neural network- Long short term memory network (CNN-LSTM)) based deep neural architecture for classifying shockable rhythms like Ventricular Fibrillation (VF), Ventricular Tachycardia (VT) vs. other kinds of non-shockable rhythms. The proposed architecture has been evaluated on two open access ECG databases and the classification accuracy achieved is in adherence to American Heart Association standards for WCD. The computational model developed to study optimal electrotherapy response is an in-silico cardiac model integrating cardiac hemodynamics functionality and a 3D volume conductor model encompassing biophysical simulation to compute the effect of shock voltage on myocardial potential distribution. Defibrillation efficacy is simulated for different shocking electrode configurations to assess the best defibrillator outcome with minimal myocardial damage. While the biophysical simulation provides the field distribution through Finite Element Modeling during defibrillation, the hemodynamic module captures the changes in left ventricle functionality during an arrhythmic event. The developed computational model, apart from acting as a device validation test-bed, can also be used for the design and development of personalized WCD vests depending on subject-specific anatomy and pathology.

The most common manifestations of the 2019 novel coronavirus disease (COVID-19) include fever, cough, dyspnea. Nevertheless, many atypical forms of presentation might be present, delaying a correct diagnosis.Acute kidney injury (AKI) is one of the important complications of COVID-19, occurring in 0.5–7% of cases and in 2.9–23% of ICU patients. The exact mechanisms by which COVID-19 induces AKI in different clinical settings is still a matter of debate.We present the case of a 53-year old woman, without any prior renal pathology, admitted to a Cardiology Department for atypical thoracic pain and oligo-anuria, without respiratory symptoms, who was diagnosed with SARS-CoV-2 infection. The patient had a significant rise in high-sensitivity cardiac troponin (from 304 ng/L to 889 ng/L in one hour) and mild systolic dysfunction (LVEF 45%), which led to the initial misdiagnosis of an acute myocardial infarction. Blood tests confirmed the diagnosis of acute kidney injury (creatinine 8.8 mg/dL in two different samples). She received hydro-electrolytic rebalancing treatment, with good clinical and biological evolution. To our knowledge this is one of the first reports, that highlights the existence of myocardial injury secondary to acute kidney injury caused by SARS-CoV-2 infection, in a patient without respiratory symptoms.

Endurance exercise induces an increase in the expression of exercise-induced peptides that participate in the repair and regeneration of skeletal muscles. The present study aimed to evaluate the time course and role of exercise-induced cytokines in muscle damage and repair after a marathon race. Fifty-seven Brazilian male amateur marathon finishers, aged 30–55 years, participated in this study. The blood samples were collected 24 h before, immediately after, and 24 and 72 h after the São Paulo International Marathon. The leukogram and muscle damage markers were analyzed using routine automated methodology in the clinical laboratory. The plasma levels of the exercise-induced cytokines were determined using the Human Magnetic Bead Panel or enzyme-linked immunosorbent assays [decorin and growth differentiation factor 15 (GDF-15)]. A muscle damage was characterized by an increase in plasma myocellular proteins and immune changes (leukocytosis and neutrophilia). Running the marathon increased interleukin (IL)-6 (4-fold), IL-8 (1.5-fold), monocyte chemoattractant protein-1 (2.4-fold), tumor necrosis factor alpha (TNF-α) (1.5-fold), IL-10 (11-fold), decorin (1.9-fold), GDF-15 (1.8-fold), brain-derived neurotrophic factor (BDNF) (2.7-fold), follistatin (2-fold), and fibroblast growth factor (FGF-21) (3.4-fold) plasma levels. We also observed a reduction in musclin, myostatin, IL-15, and apelin levels immediately after the race (by 22–36%), 24 h (by 26–52%), and 72 h after the race (by 25–53%). The changes in BDNF levels were negatively correlated with the variations in troponin levels (r = −0.36). The variations in IL-6 concentrations were correlated with the changes in follistatin (r = 0.33) and FGF-21 (r = 0.31) levels after the race and with myostatin and irisin levels 72 h after the race. The changes in IL-8 and IL-10 levels had positive correlation with variation in musclin (p < 0.05). Regeneration of exercise-induced muscle damage involves the participation of classical inflammatory mediators, as well as GDF-15, BDNF, follistatin, decorin, and FGF-21, whose functions include myogenesis, mytophagia, satellite cell activation, and downregulation of protein degradation. The skeletal muscle damage markers were not associated to myokines response. However, BDNF had a negative correlation with a myocardial damage marker. The classical anti-inflammatory mediators (IL-10, IL-8, and IL-6) induced by exercise are associated to myokines response immediately after the race and in the recovery period and may affect the dynamics of muscle tissue repair.

In the course of human history, we encountered several devastating waves of pandemics, affecting millions of lives globally and now the rapid and progressive spread of the novel SARS-CoV-2, causing Coronavirus disease (COVID-19) has created a worldwide wave of crisis. Profoundly straining national health care systems, it also significantly impacted the global economic stability. With the introduction of COVID-19 measures, mainly driven by immunization drives, casualties due to the virus were reported to decrease considerably. But then comes into play the post-Covid morbidities, along with their short and long-term effects on the elderly and the co-morbid population. Moreover, the pediatric population and the otherwise healthy cohort of the young athletes were also reported being largely affected by the varying amount of post-recovery virus-induced Cardiac manifestations, in the subsequent waves of the pandemic. Therefore, here we thrived to find answers to the seemingly unending series of questions that popped up with the advent of the disease, nevertheless, there still lies a blind spot in understanding the impacts of the disease on the Cardiovascular Health of an individual, even after the clinical recovery. Thus, along with the current data related to the diverse cardiovascular complications due to SARS-COV-2 infection, we suggest long-term ‘Cardiac surveillance' for the COVID-19 recovered individuals.

Several studies performed in humans have demonstrated that the onset of systemic inflammatory response syndrome (SIRS) represents a high risk condition to develop myocardial damage and arrhythmias. Therefore, we also hypothesized cardiac involment for dogs affected by SIRS. To assess this hypothesis, 24 dogs with a diagnosis of SIRS (13 entire males, 7 entire females, and 4 spayed females) with an age ranging from 4 to 11 years (mean 5.6 years) and an average weight of 24 kg (range from 5 to 47 kg) were enrolled. The dogs were divided into two groups according to their prognosis: Survivors (G1) and not survivors (G2), composed by 13 and 11 dogs, respectively. Moreover, healthy dogs were included as the control group (CTR). All the dogs with a history of cardiac or renal disease were excluded. At the inclusion, each patient underwent a physical examination and a complete cell count, and a biochemistry panel (including electrolyte profile) was performed; moreover, the blood cardiac Troponin I (cTnI) was measured. For each clinical variable indicative of SIRS, a score between 0 (absence) and 1 (presence) was applied. Furthermore, an electrocardiographic examination was recorded. Seventeen out of 24 (70.8%) dogs with SIRS showed arrhythmias, of which n. 6 belonged to the G1, while n. 11 belonged to the G2. Most represented findings were sinus tachycardia (7/17; 41.1%), followed by monomorphic premature ventricular beats (6/17; 35.3%), less common were first-degree atrioventricular block (2/17; 11.7%) and sinus bradycardia 1/17; 5.8%). Notably, in G1 dogs, only sinus tachycardia and premature ventricular beats were observed. G2 dogs presented a number of total and banded leukocytes significantly higher than those of G1 (p = 0.002 and 0.049), in the same manner, the clinical score suggestive of SIRS (3 vs. 2.1) was significantly higher in G2 than in G1 dogs (p = 0.01). Moreover, a significantly higher value of cTnI was observed in the G2 group compared to the G1 group (p = 0.006). Data presented here suggested a cardiac involvement in dogs with SIRS, analogously to humans, that may significantly influence the patient’s prognosis.

Combretastatin A4-phosphate (CA4P) is a vascular disrupting agent that was recently described for the treatment of solid canine tumors. Conventional echocardiography and pulsed wave tissue Doppler imaging did not reveal cardiotoxicity in dogs, however, the gold standard for assessing myocardial damage in humans receiving cardiotoxic chemotherapeutics is two-dimensional speckle-tracking echocardiography. The current study evaluated the cardiotoxic effect of a single dose of CA4P in dogs using peak systolic strain measurements and the variability of these measurements. Echocardiographic examinations of seven healthy beagles and five canine cancer patients that received CA4P were retrospectively reviewed. Peak systolic regional longitudinal strain (LSt), peak systolic regional circumferential strain (CSt), and peak systolic regional radial strain (RSt) were measured before and 24 h after administration of CA4P. Peak systolic strain measurements were compared to serum cardiac troponin I (cTnI). To quantify intra- and inter-observer measurement variability, seven echocardiographic examinations were selected and each strain parameter was measured by three observers on three consecutive days. After CA4P administration, the median LSt and CSt values decreased by 21.8% (p = 0.0005) and 12.3% (p = 0.002), respectively, whereas the median RSt values were not significantly different (p = 0.70). The decrease in LSt was correlated with increased serum cTnI values (Spearman rho = −0.64, p = 0.02). The intra-observer coefficients of variation (CV) were 9%, 4%, and 13% for LSt, CSt, and RSt, respectively, while the corresponding interobserver CVs were 11%, 12%, and 20%. Our results suggest that regional peak systolic strain measurements may be useful for the early detection of cardiotoxicity that is caused by vascular disrupting agents and that LSt may be promising for the follow-up of canine cancer patients.

Resumen: La intoxicación por monóxido de carbono es una urgencia médica que, si no se diagnostica a tiempo y se trata adecuadamente, puede provocar secuelas neurológicas importantes o incluso la muerte. El cuadro clínico dependerá de la intensidad de la exposición a dicho gas y varía según el grado de afectación de los órganos involucrados. En este caso, nos encontramos a un paciente de 63 años, que sufre una intoxicación prolongada de monóxido de carbono por mala combustión de una caldera y precisa tratamiento urgente con oxígeno hiperbárico justificado por una fracción de carboxihemoglobina elevada, añadida a cardiopatía severa de base. Finalmente se consigue estabilizar al paciente, sufriendo como secuela un infarto no Q a consecuencia de la hipoxia ocasionada. Abstract: Carbon monoxide poisoning is a medical emergency that, if it isńt diagnosed in time and treated properly, can cause significant neurological sequelae or even death. The symptomatology will depend on the intensity of the exposure and varies according to the degree of involvement of the organs involved. In this case, we have a 63-year-old patient who suffers from prolonged carbon monoxide poisoning due to poor boiler combustion and requires urgent treatment with hyperbaric oxygen justified by an elevated carboxyhemoglobin fraction, added to severe underlying heart disease. Finally, the patient was stabilized, suffering as a consequence a non-Q infarct as a consequence of the hypoxia caused.

The purpose of this paper is to provide scientific and practical information on assessment of the risk of myocardical damage development after noncardiac operations (NOMD): ischemia or myocardial infarction (MI), and/or heart failure (HF) and their prevention in adult patients. This overview of literature consists of two parts. The first part analyzes epidemiology, etiopathogeneis, and POCC risk prediction methods; the second part describes the possibilities of adjuvant pharmacological cardioprotection and approaches to optimizing anesthesiological support of operative interventions in high cardiac risk patients.The problem of perioperative cardiac complications in noncardiac surgey is one of relevant complex issues of contemporary medicine. In line with contemporary views, NOMD is now regarded as a separate variant of a pathological process in the heart muscle. According to extensive studies, about 40% of mortality of adult patients during non-cardial operative inverventions are caused by various NOMD and/or HF. The problem under discussion is particularly relevant when medical assistance is rendered to elderly patients.

Tangeretin is a polymethoxylated favone isolated from the peel of citrus fruits that possesses a broad spectrum of pharmacological functions. However, there has been limited information regarding tangeretin’s potential protective impact on the myocardium. As the myocardium is widely recognized as a potential target of oxidative stress induced by physical fatigue, this study aimed to assess tangeretin’s potential protective effects related to myocardial oxidative stress in fatigued mice. Using an intervention/control protocol on 5 groups of mice (N = 50; 1 control; 4 intervention; 4 week duration) with exhaustive swimming as the measured outcome, we found that tangeretin enhanced the activity of antioxidant enzymes, reduced the level of oxidative stress and injury, and protected myocardial morphology and ultrastructure. It was also found that tangeretin activated the Keap1/Nrf2 signaling axis to up-regulate the expression of phase II antioxidant and detoxifying enzymes. These findings suggest that tangeretin may impart beneficial effects by reducing physical fatigue-associated myocardial injury.

Notch signaling pathway is a universal regulator of cell fate in embryogenesis and in maintaining the cell homeostasis of adult tissue. Through local cell-cell interactions, he controls neighboring cells behavior and determines their capacity for self-renewal, growth, survival, differentiation, and apoptosis. Recent studies have shown that the control of regenerative processes in the heart is also carried out with the participation of Notch system. At the heart of Notch regulates migration bone marrow progenitors and stimulates the proliferation of cardiomyocytes, cardiac progenitor cell activity, limits cardiomyocyte hypertrophy and fibrosis progression and stimulates angiogenesis. Notch signaling pathway may be regarded as a very promising target for the development of drugs for the stimulation of regeneration in the myocardium.

Background Steroid use after cardiac arrest has been reported to improve survival and neurological outcome in cardiac arrest survivors. The study aimed to evaluate the effect of post‐arrest hydrocortisone use on myocardial damage and cardiac mitochondrial injury in a rat model of ventricular fibrillation cardiac arrest. Methods and Results Ventricular fibrillation cardiac arrest was induced and left untreated for 5 minutes in adult male Wistar rats. Cardiopulmonary resuscitation and electric shocks were then applied to achieve return of spontaneous circulation (ROSC). Successfully resuscitated animals were randomized into 3 groups: control, low‐dose hydrocortisone (2 mg/kg), and high‐dose hydrocortisone (8 mg/kg). The low‐dose hydrocortisone and high‐dose hydrocortisone (treatment) groups received intravenous hydrocortisone immediately after ROSC and the control group received saline as placebo. Each group consisted of 15 animals. Within 4 hours of ROSC, both treatment groups showed a higher cardiac output than the control group. At the fourth hour following ROSC, histological examination and transmission electron microscopy demonstrated less myocardial damage and mitochondrial injury in the animals treated with hydrocortisone. In the treatment groups, hydrocortisone mitigated the acceleration of Ca2+‐induced mitochondrial swelling and suppression of complex activity observed in the control group. At the 72nd hour after ROSC, a significantly higher proportion of animals treated with hydrocortisone survived and had good neurological recovery compared with those given a placebo. Conclusions Hydrocortisone use after cardiac arrest may mitigate myocardial injury and cardiac mitochondrial damage and thus improve survival, neurological and histological outcomes in a rat model of ventricular fibrillation cardiac arrest.

Background: In December 2019, a novel communicable disease, novel coronavirus infected pneumonia (NCIP) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) broke out. We aimed to analyze the characteristics and severity of patients with myocardial damage in NCIP. Methods: We enrolled 215 adult patients with NCIP from January 2020 to February 2020. Outcomes were followed up until March 1st, 2020. Results: 28.37% of the total patients showed increased level of TnI (>0.040 ng/ml). Patients were older and had more cardiovascular complications in increased TnI group. Higher CRP, NT-proBNP, lower immune CD3, CD4 and CD8 cell account and more involved lobes detected by CT scan in the lung were observed in increased TnI group. Patients with elevated TnI had higher CURB-65 scores and were more likely given glucocorticoid therapy and mechanical ventilation than patients in normal TnI group. Conclusions: Markers of cardiomyocyte injury were elevated not least in elderly males with pre-existing cardiovascular disease. Patients with elevated TnI presented more severe situation, leading to multiple organ dysfunctions, which appeared as a pivotal feature of patients with NCIP that requires attention by clinicians in order to provide necessary treatment as soon as possible and improve patients' outcomes.

Aim. To study the effectiveness of using the anatomically optimized distal renal denervation (RDN) in comparison with the standard approach for reducing myocardial damage and left ventricular (LV) hypertrophy in patients with resistant hypertension (HTN).Material and methods. The randomized double-blind study of the efficacy and safety of distal RDN compared to conventional main renal artery intervention (ClinicalTrials.gov NCT02667912) for the treatment of resistant HTN included 26 patients. All patients were divided into two groups: group 1 (n=16) — distal RDN, group 2 (n=10) — conventional RDN. In addition to 24-hour blood pressure (BP) monitoring, initially and 12 months after the intervention, contrast- enhanced cardiac magnetic resonance imaging was performed to determine the left ventricular mass and non-coronary myocardial damage area. All patients signed informed consent. Twenty-four patients completed the present study.Results. After 12 months, the mean 24-hour BP significantly decreased after both distal RDN (from 167,2±28,5/93,2±19,3 to 147,0±13,7/81,5±9,3 mm Hg (p

BACKGROUND The novel severe acute respiratory syndrome coronavirus 2 threatens human health, and the mortality rate is higher in patients who develop myocardial damage. However, the possible risk factors for myocardial damage in patients with coronavirus disease 2019 (COVID‐19) are not fully known. METHODS AND RESULTS Critical type patients were selected randomly from 204 confirmed COVID‐19 cases occurring in Renmin Hospital of Wuhan University from February 1, 2020 to February 24, 2020. Univariate analyses were used to compare the 2 groups: the myocardial damage group and the non–myocardial damage group. A total of 82 critical patients with COVID‐19 were recruited: 34 with myocardial damage and 48 without myocardial damage. A total of 30 patients died in the myocardial damage group, and 20 died in the non–myocardial damage group. In univariate analysis, the proportion of elderly patients (>70 years old, 70.59% versus 37.50%; P=0.003) and patients with cardiovascular disease (41.18% versus 12.50%; P=0.003) was higher among myocardial damage patients than among non–myocardial damage patients. Multivariate analysis showed that age >70 years old (hazard ratio [HR], 2.44; 95% CI, 1.01–5.40), CRP (C‐reactive protein) >100 mg/L (HR, 1.92; 95% CI, 0.94–3.92), lactate dehydrogenase >300 U/L (HR, 2.67; 95% CI, 1.03–6.90), and lactic acid >3 mmol/L (HR, 3.25; 95% CI, 1.57–6.75) were independent risk factors for myocardial damage in patients with COVID‐19. CONCLUSIONS Old age (>70 years old), CRP >100 mg/L, lactate dehydrogenase >300 U/L, and lactic acid >3 mmol/L are high‐risk factors related to myocardial damage in critical patients with COVID‐19.