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Myocardial injury and cardiovascular dysfunction are the most common complications of sepsis, and effective therapeutic candidate is still lacking. This study aims to investigate the protective effect of oxycodone in myocardial injury of lipopolysaccharide‐induced sepsis and its related signalling pathways. Wild‐type and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐knockout mice, as well as H9c2 cardiomyocytes cultures treated with lipopolysaccharide (LPS) were used as models of septic myocardial injury. H9c2 cardiomyocytes culture showed that oxycodone protected cells from pyroptosis induced by LPS. Mice model confirmed that oxycodone pretreatment significantly attenuated myocardial pathological damage and improved cardiac function demonstrated by increased ejection fraction (EF) and fractional shortening (FS), as well as decreased cardiac troponin I (cTnI) and creatine kinase isoenzymes MB (CK‐MB). Oxycodone also reduced the levels of inflammatory factors and oxidative stress damage induced by LPS, which involves pyroptosis‐related proteins including: Nod‐like receptor protein 3 (NLRP3), Caspase 1, Apoptosis‐associated speck‐like protein contain a CARD (ASC), and Gasdermin D (GSDMD). These changes were mediated by Nrf2 and heme oxygenase‐1 (HO‐1) because Nrf2‐knockout mice or Nrf2 knockdown in H9c2 cells significantly reversed the beneficial effect of oxycodone on oxidative stress, inflammatory responses and NLRP3‐mediated pyroptosis. Our findings yielded that oxycodone therapy reduces LPS‐induced myocardial injury by suppressing NLRP3‐mediated pyroptosis via the Nrf2/HO‐1 signalling pathway in vivo and in vitro. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Numerous microRNAs (miRs) are abnormally expressed in response to hypoxia‐induced myocardial damage. Herein, miR‐34c‐5p as a potential pharmaco‐target was investigated in a mouse model of chronic intermittent hypoxia (CIH)‐induced myocardial damage. A mouse model of myocardial damage was established using CIH with 7% or 21% O2 alternating 60 s for 12 h/day, 21% O2 for 12 h/day. AntagomiR‐34c‐5p (20 nM/0.1 ml; once a week for 12 weeks) was used as a miR‐34c‐5p inhibitor in a mouse model with tail‐vein injection. In another experiment, mice were administrated with Sirt1 activator SRT1720 (50 mg/kg/day) by intraperitoneal injection. Gene Expression Omnibus database showed a significant upregulation of miR‐34c‐5p expression in the ischemic myocardium of male mice. In CIH‐stimulated mice, miR‐34c‐5p expression was also significantly increased compared with normal mice. Treatment of antagomiR‐34c‐5p significantly restrained CIH‐triggered myocardial apoptosis. After administration of antagomiR‐34c‐5p or Sirt1 activator SRT1720, cardiac hypertrophy and oxidative stress were attenuated in CIH‐stimulated mice. We also found sirtuin 1 (Sirt1) as a direct target of miR‐34c‐5p, which was able to mediate Sirt1 protein expression in cardiomyocytes. AntagomiR‐34c‐5p injection markedly elevated Sirt1 protein expression in CIH‐stimulated mice. AntagomiR‐34c‐5p or Sirt1 activator SRT1720 administration exhibited the antioxidative activity and cardioprotective roles in CIH‐stimulated mice. [ABSTRACT FROM AUTHOR]

Our experiments have previously demonstrated that rutin (RUT) can improve myocardial damage caused by pirarubicin (THP). However, the underlying molecular mechanisms remain uncertain. In this study, we developed an microRNA (miRNA) chip by replicating the rat model of THP‐induced myocardial injury and identified miR‐22‐5p and the RAP1‐member of RAS oncogene family/extracellular regulated protein kinases (RAP1/ERK) signaling pathway as an object of study. Also, in vivo experiments demonstrated that THP caused abnormal changes in the electrocardiogram, cardiac function, and histomorphology in rats (P <.01). THP also reduces the expression of miR‐22‐5p (P <.01) and increases the levels of RAP1/ERK signaling pathway‐related proteins (P <.01, P <.05). RUT significantly improved THP‐induced myocardial damage (P <.01), increased the expression of miR‐22‐5p (P <.01), and decreased the levels of RAP1/ERK signaling pathway‐related proteins (P <.01, P <.05). In vitro studies confirmed that Rap1a is one of the target genes of miR‐22‐5p. miR‐22‐5p overexpression in cardiomyocytes can affect the RAP1/ERK pathway and reduce reactive oxygen species production and cardiomyocyte apoptosis caused by THP (P <.01), which is consistent with the effect of RUT. Our results indicate that RUT treats THP‐induced myocardial damage, which may be achieved by upregulating miR‐22‐5p, causing changes in its target gene Rap1a and the RAP1/ERK pathway. [ABSTRACT FROM AUTHOR]

Uric acid crystal is known to activate the NLRP3 inflammasome and to cause tissue damages, which can result in many diseases, such as gout, chronic renal injury and myocardial damage. Meanwhile, soluble uric acid (sUA), before forming crystals, is also related to these diseases. This study was carried out to investigate whether sUA could also activate NLRP3 inflammasome in cardiomyocytes and to analyse the mechanisms. The cardiomyocyte activity was monitored, along with the levels of mature IL‐1β and caspase‐1 from H9c2 cells following sUA stimulus. We found that sUA was able to activate NLRP3 inflammasome, which was responsible for H9c2 cell apoptosis induced by sUA. By elevating TLR6 levels and then activating NF‐κB/p65 signal pathway, sUA promoted NLRP3, pro‐caspase 1 and pro‐IL‐1β production and provided the first signal of NLRP3 inflammasome activation. Meanwhile, ROS production regulated by UCP2 levels also contributed to NLRP3 inflammasome assembly and subsequent caspase 1 activation and mature IL‐1β secretion. In addition, the tlr6 knockdown rats suffering from hyperuricemia showed the lower level of IL‐1β and an ameliorative cardiac function. These findings suggest that sUA activates NLRP3 inflammasome in cardiomyocytes and they may provide one therapeutic strategy for myocardial damage induced by sUA. [ABSTRACT FROM AUTHOR]

In December 2019, the world started to face a new pandemic situation, the severe acute respiratory syndrome‐coronavirus 2 (SARS‐CoV‐2). Although coronavirus disease (COVID‐19) clinical manifestations are mainly respiratory, major cardiac complications are being reported. Cardiac manifestations etiology seems to be multifactorial, comprising direct viral myocardial damage, hypoxia, hypotension, enhanced inflammatory status, ACE2‐receptors downregulation, drug toxicity, endogenous catecholamine adrenergic status, among others. Studies evaluating patients with COVID‐19 presenting cardiac injury markers show that it is associated with poorer outcomes, and arrhythmic events are not uncommon. Besides, drugs currently used to treat the COVID‐19 are known to prolong the QT interval and can have a proarrhythmic propensity. This review focus on COVID‐19 cardiac and arrhythmic manifestations and, in parallel, makes an appraisal of other virus epidemics as SARS‐CoV, Middle East respiratory syndrome coronavirus, and H1N1 influenza. [ABSTRACT FROM AUTHOR]

Extensive investigations into long noncoding RNAs (lncRNAs) in various diseases and cancers, including acute myocardial infarction (AMI) have been conducted. The current study aimed to investigate the role of lncRNA solute carrier family 8 member A1 antisense RNA 1 (SLC8A1‐AS1) in myocardial damage by targeting solute carrier family 8 member A1 (SLC8A1) via cyclic guanosine 3′,5′‐monophosphate‐protein kinase G (cGMP‐PKG) signaling pathway in AMI mouse models. Differentially expressed lncRNA in AMI were initially screened and target relationship between lncRNA SLC8A1‐AS1 and SLC8A1 was then verified. Infarct size, levels of inflammatory factors, biochemical indicators, and the positive expression of the SLC8A1 protein in AMI were subsequently determined. The expression of SLC8A1‐AS1, SLC8A1, PKG1, PKG2, atrial natriuretic peptide, and brain natriuretic peptide was detected to assess the effect of SLC8A1‐AS1 on SLC8A1 and cGMP‐PKG. The respective contents of superoxide dismutase, lactate dehydrogenase (LDH), and malondialdehyde (MDA) were detected accordingly. Microarray data GSE66360 provided evidence indicating that SLC8A1‐AS1 was poorly expressed in AMI. SLC8A1 was verified to be a target gene of lncRNA SLC8A1‐AS1. SLC8A1‐AS1 upregulation decreased levels of left ventricular end‐systolic diameter, −dp/ dtmax, interleukin 1β (IL‐1β), IL‐6, transforming growth factor α, nitric oxide, inducible nitric‐oxide synthase, endothelial nitric‐oxide synthase, infarct size, LDH activity and MDA content, and increased IL‐10, left ventricular end‐diastolic pressure and + dp/ dtmax. Furthermore, the overexpression of SLC8A1‐AS1 was noted to elicit an inhibitory effect on the cGMP‐PKG signaling pathway via SLC8A1. In conclusion, lncRNA SLC8A1‐AS1, by downregulating SLC8A1 and activating the cGMP‐PKG signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage. In conclusion, long noncoding RNA (lncRNA) solute carrier family 8 member A1 antisense RNA 1 (SLC8A1‐AS1), by downregulating solute carrier family 8 member A1 (SLC8A1) and activating cyclic guanosine 3′,5′‐monophosphate‐protein kinase G (cGMP‐PKG) signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage. [ABSTRACT FROM AUTHOR]

Abstract: Aim: We investigated the clinical courses before and during pregnancy and after delivery in patients with repaired anomalous origin of the left coronary artery from the pulmonary artery to determine the impact of the hemodynamic changes and cardiac function on the selection of the appropriate mode of delivery. Methods: Six patients who underwent coronary artery reimplantation delivered 10 infants. We scrutinized the patients’ hemodynamic changes on echocardiographs and the plasma brain natriuretic peptide levels before and during pregnancy and after delivery, the perinatal outcomes and maternal and fetal events. Results: All patients were asymptomatic and categorized as having New York Heart Association functional class I before pregnancy. In 8 of 10 pregnancies, vaginal deliveries were performed; two elective cesarean sections were performed because of symptomatic heart failure. The hemodynamic parameters were stable throughout pregnancy and postdelivery, and no maternal or fetal events occurred in the patients who underwent vaginal deliveries. One cesarean section patient developed significant heart failure during the late second and third trimesters, which was accompanied by hemodynamic changes, including increased brain natriuretic peptide levels, left ventricular diastolic dysfunction and worsening arrhythmias, and thrombosis and post‐partum hemorrhage occurred postdelivery. The baby had intrauterine growth retardation and small for gestational age. None of the babies had congenital anomalies. Conclusion: Pregnancy was safe in most of the asymptomatic patients long after anomalous origin of the left coronary artery from the pulmonary artery was repaired. Symptomatic heart failure might occur during pregnancy in patients with persisting myocardial damage. Pregnancy and delivery should be carefully managed. [ABSTRACT FROM AUTHOR]

Background Cardiac troponin I ( cTnI) is a peripheral blood marker for myocardial damage. Because of the unavailability of goat-specific cTnI assays human cTnI assays may be validated for detection of myocarditis in goat kids. Objectives The purpose of the study was to evaluate 2 commercially available human cTnI assays in goat kids with myocardial damage, and to determine the cTnI expression in cardiac muscle. Materials and Methods Plasma cTnI concentrations were measured in healthy goat kids ( n = 7) and goat kids with myocardial damage ( n = 8) using the Beckman Coulter Access Accu TnI and the Biomérieux Vidas Ultra. The results were correlated with gross necropsy and histopathologic findings, and cTnI immunhistochemistry in cardiac tissue. Results Macro- and microscopic findings confirmed myocardial damage in the myocarditis group. Mean plasma cTnI concentration was significantly higher in the myocarditis group than in the healthy control group (104.82 vs 0.02 ng/mL). The overall mean plasma cTnI concentration measured by Biomérieux Vidas Ultra (61.75 ng/mL, 95% CI: 19.55-103.95) was comparable to the mean measured by Beckman Coulter Access Accu TnI (50.08 ng/mL, 95% CI: 24.11-76.06), and cTnI concentrations measured by these assays were highly correlated ( r = .977) with a −6.2% bias. Both assays were precise and accurate. Conclusion The human-specific Beckman Coulter Access Accu TnI and the Biomérieux Vidas Ultra can be used for diagnostic confirmation of myocardial damage in caprine medicine. [ABSTRACT FROM AUTHOR]

Vasostatin-1 (VS-1) plays important roles in myocardial ischemia/reperfusion injury. We have explored the protective effects of VS-1 on cardiomyocytes using cardiomyocyte-endothelial cells Transwell Co-culture System. Cardiomyocytes and rat aortic endothelial cells (RAECs) were prepared from ventricles and thoraco-abdominal aorta of Sprague-Dawley rats. The experiment used cardiomyocytes alone culture group (C) and cardiomyocytes-RAECs co-culture group (T), each with three subgroups: C-Ad-Null, C-Ad-VS-1, C-Hb (Ad-VS-1 + NO scavenger Hb), or T-Ad-Null, T-Ad-VS-1 transfection, T-Hb. After 48 h incubation, all groups were treated with hypoxia for 60 min and then reoxygenated for 120 min. We also investigated endothelial cells-mediated cardiomyocytes protection. RAECs were treated with hypoxia for 30 min and reoxygenated with normal cardiomyocytes for 120 min. The cardiomyocytes apoptosis rate, aspartate aminotransferase (AST) and creatine kinase isozyme MB (CK-MB) were recorded. As expected, cardiomyocytes apoptosis, AST and CK-MB were significantly increased in the T-Ad-Null group than in the C-Ad-Null group. VS transfection significantly reduced these levels. However, apoptosis, AST and CK-MB levels were increased again after Hb treatment, returning to the similar level of the C-Ad-null group in the C-Hb group, but still significantly lower in the T-Hb group compared with the T-Ad-null group. RAEC injury caused cardiomyocyte injury, and VS-1 transfection of the RAEC decreased apoptosis and the levels of AST and CK-MB. The findings suggest that VS-1 exerts protective effects on the cardiomyocytes directly or indirectly by cardiomyocyte-endothelial cells interaction. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Cardiac damage is a major complication of anorexia nervosa (AN). The present study evaluated the prevalence of myocardial damage in patients with AN by cardiac magnetic resonance imaging (CMR). Method This study was cross-sectional and observational. Forty consecutive female patients with a diagnosis of AN and 28 healthy female subjects were evaluated from January 2007 to 2011 at the Department of Psychiatry (University of Istanbul, Istanbul, Turkey). Following enrolment in the study, participants underwent a cardiac evaluation, a physical examination, a standard electrocardiogram (ECG), an echocardiography and a CMR. Results Body weight, body mass index and heart rate values were lower in patients with AN than in the control group. When compared with control groups, patients with AN showed reduced left ventricular mass with normal systolic function. Compared to control subjects, patients with AN had higher prevalence of pericardial effusion (30% in the AN group, 4% in the control group, p = .005) and mitral valve prolapses (23% in the AN group, 4% in the control group, p = .03). Myocardial fibrosis (detected as late gadolinium enhancement on CMR) was found in 23% of patients with AN. Myocardial fibrosis was not detected in any control subject ( p = .007). Conclusion A strong association was found between myocardial fibrosis and AN. Cardiac damage of myocardial fibrosis in asymptomatic patients with AN can be found by CMR examination. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:862-866) [ABSTRACT FROM AUTHOR]

Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence. We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations. Twenty-nine influenza-naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 10 EID EIV A/eq/Kentucky/91 6 months after vaccination. Six age-matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls. Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi-square, or clustered regression analyses were used to identify relationships between each group and cTnI. All EIV-infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was <0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups. This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 10 EID EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur. [ABSTRACT FROM AUTHOR]

Background: Irrigated radiofrequency (RF) ablation catheters may produce different lesion sizes dependent upon the electrode orientation to the tissue. This study examined the effect of irrigated electrode orientation on the lesion size and explores a potential mechanism for this effect. Methods and Results: Lesions were created in isolated porcine myocardium using an open irrigation, closed irrigation, and nonirrigated RF catheter (all 3.5–4 mm tips). Lesions were created with the electrodes with all permutations of electrode orientation (vertical or horizontal), contact pressure (6 or 20 g), and saline superfusate flow (0.2 or 0.4 m/sec) over tissue interface. The effect of electrode irrigation without RF delivery on tissue temperature was assessed with intramyocardial temperature probes and infrared thermal imaging. For both irrigated catheters, the horizontal orientation produced 25–30% smaller lesion volumes than the vertical orientation despite equal or greater power deliveries. The horizontal orientation produced larger lesion volumes for the nonirrigated catheter. Higher superfusate flow rates were associated with decreased lesion volumes for the irrigated catheters but greater lesion volumes for the nonirrigated catheter. Catheter irrigation alone without RF delivery reduced intramyocardial temperatures up to 4.9°C and the horizontal orientation produced a 2-fold greater area of tissue cooling than the vertical orientation. Conclusion: Horizontal electrode orientations reduce lesion volumes for irrigated RF catheters. This effect may be in part due to greater areas of active tissue cooling in the horizontal orientation. [ABSTRACT FROM AUTHOR]

Progress in cardiovascular disease understanding and management continues at an exponential pace. Our understanding of the molecular basis of disease is enhanced by newer molecular measurement techniques, sophisticated models of physiological protein functions, understanding of the genetic foundation for diseases, and the incorporation of population genetic tools in our clinical analysis. In this review, I discuss prevention and therapy of coronary stenosis impeding coronary flows, prevention of acute and chronic manifestation of coronary flow impairment, and interfering with myocardial manifestation of acute or chronic deprivation of coronary flow. Mechanical heart failure and arrhythmias are common causes of myocardial dysfunction that originate, in part, from the loss of myocardial tissue and function. Techniques for interfering with cardiac function, in order to address the molecular mechanisms associated with restenosis, range from pharmacologic to mechanical procedures including mechanical dilation and scaffolding of coronary stenosis. The use of stents with and without drug coating is leading the clinical world of revascularization side-by-side with cardiac bypass surgery. Other topics that are discussed here include managing myocardial damage and acute and chronic pump failure. Finally, population genetics of cardiac health and the potential for genetic therapeutic guidance in managing ischemic cardiovascular diseases are discussed. [ABSTRACT FROM AUTHOR]

Background: This randomized, double-blind, placebo-controlled study was designed to determine whether an intra-operative, intravenous infusion of glucose–insulin–potassium (GIK) could be helpful in the prevention of myocardial ischemia and in the maintenance of intra-operative cardiac performance in patients undergoing off-pump coronary artery bypass (OP-CAB) surgery. Methods: Eighty two adults undergoing elective OP-CAB surgery were randomly divided into two groups that received intravenously either 5% dextrose in water or GIK (50% dextrose in 500 ml of water; regular insulin, 125 IU; potassium, 80 mmol) at 0.75 ml/kg/h immediately before the induction of anesthesia to the end of surgery. To evaluate myocardial damage, creatine kinase MB and troponin T were measured before surgery, immediately after arrival in the intensive care unit and on the first post-operative day. To assess cardiac performance, hemodynamic data were obtained before and after the induction of anesthesia, before and after the bypass graft and after sternal closure. Blood glucose was measured at the same time. Results: There was no significant difference in cardiac enzymes, hemodynamic parameters and blood glucose between the two groups. The use of vasoactive, inotropic and/or anti-arrhythmic agents, insulin and supplemental glucose was not significantly different between the groups. Conclusion: The results suggest that the intravenous administration of GIK during OP-CAB surgery neither reduces myocardial damage nor improves intra-operative cardiac performance in patients without contractile dysfunction. [ABSTRACT FROM AUTHOR]

Over the last 40 years, great progress has been made in treating childhood and adult cancers. However, this progress has come at an unforeseen cost, in the form of emerging long-term effects of anthracycline treatment. A major complication of anthracycline therapy is its adverse cardiovascular effects. If these cardiac complications could be reduced or prevented, higher doses of anthracyclines could potentially be used, thereby further increasing cancer cure rates. Moreover, as the incidence of cardiac toxicity resulting in congestive heart failure or even heart transplantation dropped, the quality and extent of life for cancer survivors would improve. We review the proposed mechanisms of action of anthracyclines and the consequences associated with anthracycline treatment in children and adults. We summarise the most promising current strategies to limit or prevent anthracycline-induced cardiotoxicity, as well as possible strategies to prevent existing cardiomyopathy from worsening. [ABSTRACT FROM AUTHOR]

Aim: To measure serial cardiac troponin-T, creatine kinase, creatine kinase-MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase levels in asphyxiated newborn infants during the first 15 d of life. Methods: Troponin-T, creatine kinase, creatine kinase-MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (LDH) concentrations were measured prospectively in blood samples obtained from 45 asphyxiated and 15 healthy term neonates within the first 2–4 h, third, seventh and 15th days. Results: Infants with severe asphyxia had significantly higher cardiac troponin-T levels than grade I and II asphyxiated and healthy neonates within the first 2–4 h of life (0.34±0.21 ag/ml vs 0.07±0.03 ag/ml, 0.12±0.07 ag/ml, 0.04±0.02 ag/ml, respectively). Troponin-T levels remained high on days 3 and 7 in severely asphyxiated neonates. The creatinine kinase-MB levels were significantly higher in grade II and III asphyxiated neonates than grade I asphyxiated and healthy neonates within the first 2–4 h. No difference was found in creatinine kinase-MB on day 3. There was cardiac involvement in 12 (80%) newborns of group III on B mode echocardiographic images on day 1. However, no echocardigraphic pathology was found in the seventh- and 15th-day echocardiographic analysis in any groups. Conclusion: Our results suggest that asphyxia-related cardiac changes were significant but reversible in severely asphyxiated neonates, and troponin T is a good determinant of the degree of injury to the heart within the first week of life. Cardiac troponin T also has a wider diagnostic frame than other diagnostic markers of myocardial damage. [ABSTRACT FROM AUTHOR]

Aim. To investigate serum cardiac troponin I levels before and after magnesium sulfate treatment in preeclamptic pregnant women. Materials and methods. Fifty-five pregnant women were included in the prospectively planned study. Study group patients (n = 25) were pregnant women hospitalized with a preeclampsia diagnosis while the control group (n = 30) were pregnant women with no medical or obstetric problem who had been attending the antenatal clinic. Serum cardiac troponin I levels were compared in the normal pregnant women and in preeclamptic pregnant women. These levels were also compared in the preeclamptic women before and after magnesium sulfate treatment. Mann-Whitney U-test was used for statistical analysis. Results. Groups were similar with respect to age, gravity, parity, and gestational age. The median serum cardiac troponin I levels in preeclamptic patients was 0.20 ng/ml (0.02–4.53) before treatment and 0.09 ng/ml (0.02–3.91) after treatment, while it was 0.02 ng/ml (0.0–0.05) in the control group. The serum cardiac troponin I level in the preeclamptic group was significantly high (P<0.01), and pretreatment values in this group were significantly higher compared with post-treatment values (P<0.01) Conclusion. Cardiac troponin I is a sensitive parameter for indicating minor myocardial damage which may occur in preeclampsia and for evaluating the efficiency of magnesium sulfate treatment. [ABSTRACT FROM AUTHOR]

Aims: To determine the prevalence of myocardial damage in severe respiratory syncytial virus (RSV) disease as evident from elevated cardiac Troponin T (cTnT) levels. To assess the nature of the myocardial involvement as manifested in electro- and echocardiographic abnormalities. To compare severity of disease with and without myocardial involvement as evident from duration of ventilation, inotrope requirements and death. Methods: This was a prospective observational cohort study of children with RSV infection admitted to the paediatric intensive care unit at the Royal Liverpool Children's Hospital during the winter season 2002/2003. cTnT concentrations were measured using a third generation monoclonal sandwich immunoassay (Roche Diagnostics). Results: 34 children were included in our study. 12 (35%) had elevated cTnT levels. The levels measured after admission had a median [interquartile range (IQR)] of 50 pg/ml (37.5-67.5). There was no significant difference (p > 0.05) between patients with and without elevated cTnT levels with regards to gender, gestational age at birth, history of neonatal intensive care, presence of congenital heart disease, chronic lung disease, inotrope requirements, duration of ventilation, death, fractional shortening on echocardiogram or arrhythmias. Children with elevated cTnT levels were significantly younger [median (IQR): 1.4 months (0.8-2.0)] than children without [median (IQR): 4.0 months (1.7-6.6)] (p = 0.04). The systolic blood pressure on admission was lower in children with increased cTnT compared to those with undetectable cTnT (p = 0.01). Conclusions: Myocardial involvement is common in infants with severe RSV lung disease without congenital heart disease. cTnT level elevation was associated with hypotension. [ABSTRACT FROM AUTHOR]

We report the case of a young Caucasian man who presented with polyneuropathy and severe, ultimately fatal, congestive heart failure in the context of a chronic active Epstein–Barr virus (EBV) infection. Post-mortem examination revealed both monoclonal and polyclonal proliferation of EBV-positive atypical T lymphocytes within different organs. Predominant infiltration of the nervous system and heart with extensive myocardial scarring accounted for the clinical symptoms. The remarkable features of this case are (i) the occurrence in a Caucasian patient, (ii) the absence of detectable immunodeficiency, and (iii) the myocardial destruction by EBV-infected monoclonal T cells. [ABSTRACT FROM AUTHOR]

ROLLÁN, M.J., et al.: Acute Pulmonary Edema Secondary to Myocardial Damage After Electrical Cardioversion. Direct cardioversion used in the treatment of various cardiac arrhythmias is a highly effective and simple procedure with infrequent complications. An uncommon complication is the occurrence of pulmonary edema. This report describes a 68-year-old woman with normal coronary arteries who experienced pulmonary edema following cardioversion secondary to myocardial injury demonstrated by ECG changes and elevation of troponin T. (PACE 2003; 26:2330–2332) [ABSTRACT FROM AUTHOR]

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 Ca 2+ -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 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.