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Persistent left superior vena cava (PLSVC) can be problematic when device implantation is scheduled from the left side because of the technical difficulty in delivering leads. Right-sided implantation is an alternative method, but there is a risk of a high defibrillation threshold (DFT). Transvenous implantation of an implantable cardioverter defibrillator (ICD) was scheduled for a 54-year-old man with idiopathic dilated cardiomyopathy and monomorphic non-sustained ventricular tachycardia, but computed tomography revealed the presence of a PLSVC. Right-sided ICD implantation was performed first; however, an ICD shock at 35 J failed to terminate the induced ventricular fibrillation (VF). Re-implantation via the PLSVC by a left subclavian approach with a dual coil lead was performed next. The dual coil right ventricular lead was successfully implanted via the PLSVC, and the induced VF was terminated by a single shock at 25 J. In the present case, the proximal coil was located in the coronary sinus (CS) and it enabled an antero-posterior defibrillation vector across the left ventricle. In addition to the re-location of the ICD generator from the right side to the left side, the new positioning of the proximal coil inside the CS is likely to have contributed to the great improvement of the DFT. < Learning objective: In cases with persistent left superior vena cava, left-sided implantationof an implantable cardioverter defibrillator (ICD) can be problematic because of the technical difficulty, but right-sided implantation has a risk of a high defibrillation threshold (DFT). Leftsided ICD via the persistent left superior vena cava with a dual coil lead enables an antero-posterior defibrillation vector across the left ventricle by positioning of the proximal coil inside the coronary sinus and contributes to a great improvement of the DFT.> [ABSTRACT FROM AUTHOR]

Background: Men and women have specific patterns in an electrocardiogram (ECG) differentiated by J-point elevation and ST-segment angle. Although gender-affirming hormone treatment is one of the treatments for gender dysphoria, its influence on an ECG has not been clarified yet.Objective: The purpose of this study was to investigate ECG changes induced by gender-affirming hormone treatment.Methods: The study population consisted of 29 transgender males and 8 transgender females and 37 age- and sex-matched cisgender females and males. Male pattern was defined as J-point elevation > 0.1 mV and ST-segment angle > 20° in precordial leads.Results: In the comparison between 29 transgender males and cisgender females, the prevalence of the male pattern (89.7% vs 6.9%; P < .001), prevalence of the early repolarization pattern (51.7% vs 17.2%; P = .01), J-point elevation (leads V1-V6), T-wave amplitudes (leads V1-V6), QRS amplitudes (leads II, III, V1-V6), and P-wave amplitudes (leads V1-V3) were significantly higher in transgender males. The prevalence of the male pattern was lower in transgender females than in cisgender males (25.0% vs 87.5%; P = .04). In the analysis of transgender males for whom ECGs were available before and after gender-affirming hormone treatment (n = 13), J-point elevation and T-wave amplitudes significantly increased after gender-affirming hormone treatment, leading to a higher prevalence of the male pattern (23.1% vs 92.3%; P < .001). The prevalence of the early repolarization pattern and QRS amplitudes also significantly increased after the treatment, but the augmentation of P-wave amplitudes was modest.Conclusion: Gender-affirming hormone treatment for gender dysphoria is accompanied by a change in ECG phenotype toward affirming gender, in which change in androgen level may be involved. [ABSTRACT FROM AUTHOR]

Background Deep vein thrombosis (DVT) develops after major orthopedic surgery despite the current use of prophylaxis. DVT frequently develops in the soleal vein (SV) and might develop easily at the site of SV dilatation because of blood flow stasis. However, whether preoperative SV dilatation detected by ultrasonography predicts DVT after major orthopedic surgery remains unknown. Objective We examined whether SV dilatation detected by preoperative ultrasonography predicts DVT after major orthopedic surgery. Methods Ultrasonography was performed preoperatively and postoperatively in 243 patients with orthopedic diseases (mean age of 67 ± 13 years, 77% women) who underwent total hip arthroplasty (THA, n = 180) or total knee arthroplasty (TKA, n = 63). Presence of DVT was diagnosed by ultrasonography and SV diameter ≥10 mm was defined as SV dilatation. Patients with preoperative DVT were excluded. Results Sixty-nine patients (28%) developed postoperative DVT. SV dilatation was found in 24 patients (10%), and 16 (67%) of those patients had postoperative DVT. Multivariate logistic regression analysis showed that female gender [odds ratio (OR): 4.09, p = 0.004], TKA (OR: 2.52, p = 0.011), and SV dilatation (OR: 6.67, p < 0.001), but not presence of comorbidities, medications, or plasma d -dimer value, independently predict postoperative DVT. Subgroup analyses according to the operation site showed that female gender (OR: 3.27, p = 0.043) and SV dilatation (OR: 3.72, p = 0.022) were independent predictors of postoperative DVT in the THA group. SV dilatation (OR: 12.0, p = 0.027) was an independent predictor of postoperative DVT also in the TKA group. Conclusions In addition to gender and TKA, SV dilatation detected by ultrasonography is an independent predictor of DVT after major orthopedic surgery. Determination of SV diameter by ultrasonography before major orthopedic surgery is useful for assessing the risk of postoperative DVT. [ABSTRACT FROM AUTHOR]

Background Pulmonary hypertension (PH) is a strong predictor of mortality in patients with interstitial lung disease (ILD). However, patients with ILD often have poor outcomes even in the absence of PH. Pulmonary vascular resistance (PVR) assessed by right heart catheterization is a predictor of mortality in patients with ILD. However, the clinical utility of PVR assessed by Doppler echocardiography (PVRecho) as a predictor of the outcome in patients with ILD remains unclear. The aim of this study was to examine whether PVRecho independently predicts mortality in patients with ILD. Methods Echocardiographic examinations were performed in 133 consecutively enrolled patients with ILD (age, 67 ± 9 years; 53% men). Tricuspid annular plane systolic excursion (TAPSE) was measured, and PVRecho was calculated by the following formula: PVRecho = [TRV × 10/time-velocity integral of right ventricular outflow (RVOT-VTI)] + 0.16. Data for parameters of pulmonary functional tests and for serum biomarkers, which were measured within 3 months before or after the echocardiographic examinations, were collected. Results During a mean follow-up period of 18 ± 7 months, 13 patients died due to respiratory failure ( n = 10), heart failure ( n = 1), or unknown causes ( n = 2). In univariate analysis, body mass index, idiopathic pulmonary fibrosis, use of an antifibrotic drug (AD), RVOT-VTI, PVRecho, percentage of predicted vital capacity (%VC), percentage of predicted forced expiratory volume in 1 second, and percentage of predicted diffusion capacity of the lungs for carbon monoxide (%DLco), but not TAPSE or serum biomarkers, were significantly associated with mortality. Cox proportional hazard multivariate analysis indicated that %VC [hazard ratio (HR): 0.92, p = 0.001], use of AD (HR: 4.05, p = 0.043), and PVRecho (HR: 3.79, p = 0.029) independently predict mortality in patients with ILD. Replacement of %VC with %DLco in the multivariate analysis did not change the results: %DLco (HR: 0.90, p = 0.001), use of AD (HR: 7.53, p = 0.029), and PVRecho (HR: 3.65, p = 0.020). Conclusions In addition to parameters of pulmonary function tests and use of AD, increased PVRecho is an independent predictor of mortality in patients with ILD who were evaluated for screening of PH by echocardiography. [ABSTRACT FROM AUTHOR]

Background Degenerative mitral stenosis (DMS) is found in the elderly population. However, there are a few reports regarding the prevalence rate of DMS and, its clinical characteristics. The aim of this study was to determine the relationship between age, gender, and the prevalence rate of DMS. Methods Patients with DMS and rheumatic mitral stenosis (RMS) were searched retrospectively in consecutive patients who underwent echocardiography from January 2011 to December 2013 in a community hospital. DMS was defined as presence of both turbulent antegrade flow with a mean transmitral pressure gradient (PG) of ≥2 mmHg and mitral annular calcification without restriction of leaflets tip motion. Results We identified 19 patients (17 female and 2 male) with DMS (0.22%) and 19 patients with RMS in 8683 patients. The prevalence rate of DMS significantly increased with aging, especially in patients >90 years old. There was no significant difference in the prevalence rates of RMS among the age groups. Patients with DMS were older (86 ± 8 years vs. 73 ± 10 years, p < 0.01) and had higher rates of hypertension and aortic stenosis, larger left ventricular mass index, and mean PG of aortic valve, smaller aortic valve area, less degree of left atrial dilatation, and lower rate of atrial fibrillation, compared with those values in patients with RMS. Conclusions DMS is rare (0.22%) and almost exclusively found in females in routine echocardiography. The prevalence of DMS increases with aging to 2.5% in patients >90 years of age, and DMS is often associated with aortic valve stenosis. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to determine the effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) treatment on both the repair process and ventricular function after myocardial infarction (MI). Background: The M-CSF and G-CSF have multiple potential effects on cells involved in wound repair. Methods: Myocardial infarction was induced by 45- or 90-min coronary occlusion and reperfusion in rats with or without subsequent injection of M-CSF (106 IU/kg/day) or G-CSF (50 μg/kg/day) for five days. We examined histology and messenger ribonucleic acid (mRNA), and assessed left ventricular function in situ using a conductance catheter. Results: Five days after MI, M-CSF increased the number of ED-1–positive cells, mRNA levels of transforming growth factor-β-1, collagen I and III, and collagen fibers within the infarct. Fourteen days after MI, induced by 45-min ischemia, left ventricular end-systolic elastance (Ees) was reduced (1,191 ± 87 mm Hg/ml vs. 1,812 ± 150 mm Hg/ml) and both isovolumic relaxation time constant (τ) (11.9 ± 0.9 ms vs. 8.5 ± 0.4 ms) and left ventricular end-diastolic volume (LVEDV) (0.225 ± 0.014 ml vs. 0.172 ± 0.011 ml) increased versus sham-operated rats. These alterations after MI were attenuated by M-CSF (Ees = 1,650 ± 146, τ = 9.7 ± 0.7, LVEDV = 0.199 ± 0.012) but not by G-CSF. This beneficial effect of M-CSF on Ees was also detected in hearts with MI induced by 90-min ischemia. Furthermore, M-CSF increased collagen content within infarcts and reduced the proportion of thin collagen fibers 14 days after MI. The Ees significantly correlated with infarct collagen content. Nevertheless, neither M-CSF nor G-CSF modified infarct size. Conclusions: The M-CSF treatment attenuates deterioration of left ventricular function after MI by accelerating infarct repair. [Copyright &y& Elsevier]

Abstract: Summary: Origin of myofibroblasts in infarcted myocardium was examined by using rats in which bone marrow of green fluorescent protein (GFP)-transgenic mice had been transplanted. GFP was not detected in myofibroblasts at either 3 or 7 days after infarction, suggesting that proliferating myofibroblasts in infarcted myocardium are derived from resident fibroblasts rather than circulating precursor cells of bone marrow origin. Background: Myofibroblasts play important roles in the repair process of myocardial infarct, and their origin has been assumed to be interstitial fibroblasts in the heart. However, bone marrow-derived myofibroblasts have recently been identified in pathological fibrosis in extracardiac tissues. In this study, we aimed to determine whether some of the myofibroblasts in infarcted myocardium are derived from circulating precursor cells of bone marrow origin. Methods and Results: Bone marrow (BM) of GFP-transgenic mice was transplanted into nude rats, and their coronary arteries were occluded for 60 min and reperfused for 3 or 7 days. Non-BM-transplanted rats served as controls. At 3 days after infarction, some endothelial cells were GFP-positive, indicating that they were of bone marrow origin. Predominant cells in infarcted regions were macrophages and neutrophils, and there were only a small number of vimentin-positive cells and fewer myofibroblasts, both of which were GFP-negative. At 7 days after infarction, there were numerous myofibroblasts in granulation tissue replacing necrotic myocytes, and none of them showed GFP signals, whereas some cells were positive for both GFP and vimentin. Appearance of myofibroblasts and extent of the infarct repair in BM-transplanted and those in non-transplanted rats were similar. Conclusions: The findings in this study suggest that proliferating myofibroblasts in infarcted myocardium are derived from resident fibroblasts rather than circulating precursor cells of bone marrow origin. [Copyright &y& Elsevier]

: ObjectivesThis study aimed to examine: 1) whether nicorandil protects the ischemic myocardium by activating sarcolemmal adenosine triphosphate (ATP)-sensitive K+ (sarcKATP) channels or the mitochondrial KATP (mitoKATP) channels, and 2) whether protein kinase C (PKC) activity is necessary for cardioprotection afforded by nicorandil.: BackgroundNicorandil is a hybrid of nitrate and a KATP channel opener that activates the sarcKATP and mitoKATP channels. Both of these KATP channels are regulated by PKC, and this kinase may be activated by nitric oxide and also by oxygen free radicals (OFR) generated after mitoKATP channel opening.: MethodsIn isolated rabbit hearts, infarction was induced by 30-min global ischemia/2-h reperfusion with monitoring of the activation recovery interval (ARI), an index of action potential duration. Protein kinase C translocation was assessed by Western blotting.: ResultsNicorandil did not change ARI before ischemia, but it accelerated ARI shortening after the onset of ischemia and reduced infarct size by 90%. A sarcKATP channel selective blocker, HMR1098, abolished acceleration of ischemia-induced ARI-shortening by nicorandil and eliminated 40% of nicorandil-induced infarct size limitation. A mitoKATP channel selective blocker, 5-hydroxydecanoate, abolished the protection afforded by nicorandil without affecting ARI. Cardioprotection by nicorandil was inhibited neither by an OFR scavenger, N-2-mercaptopropionylglycine nor by a PKC inhibitor, calphostin C, at a dose that was capable of inhibiting PKC-&epsiv; translocation after preconditioning.: ConclusionsBoth the sarcKATP and mitoKATP channels are involved in anti-infarct tolerance afforded by nicorandil, but PKC activation induced by nitric oxide or OFR generation, if any, does not play a crucial role. [Copyright &y& Elsevier]

Objective: This study aimed to clarify the role of adenosine triphosphate-sensitive K(+) (K(ATP)) channels in the no-reflow phenomenon and in its extension by hypercholesterolemia.Background: The no-reflow phenomenon is an important target of therapy in patients with acute myocardial infarction, but its mechanism remains unclear.Methods: The left circumflex coronary artery was occluded for 30 or 60 min and reperfused in rabbit hearts in situ. The no-reflow zone, area at risk, and infarct size were determined by thioflavin-S, Evans blue, and tetrazolium staining, respectively. No-reflow zone size was expressed as a percentage of infarct size (%NR/IS). Hypercholesterolemia was induced by two weeks of cholesterol-enriched diet.Results: A K(ATP) channel blocker, glibenclamide (0.3 mg/kg), increased %NR/IS after 30-min ischemia/90-min reperfusion from 33.6 +/- 1.9% to 45.9 +/- 1.6% and %NR/IS after 60-min ischemia/90-min reperfusion from 32.8 +/- 3.4% to 46.1 +/- 1.7%. However, N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthase inhibitor, and nicorandil, a hybrid of K(ATP) channel opener and nitrate, failed to significantly modify %NR/IS. Hypercholesterolemia increased %NR/IS to 61.6 +/- 0.6%, which was not further enlarged by glibenclamide, and delayed infarct healing during the subsequent five days of reperfusion. These effects of hypercholesterolemia were significantly suppressed by nicorandil. Neither glibenclamide, L-NMMA, nicorandil, nor hypercholesterolemia modified infarct size.Conclusions: The K(ATP) channel activation, but not NO, is a major mechanism of protection against microvascular injury, causing the no-reflow phenomenon in the heart. Suppression of K(ATP) channel opening may underlie the hypercholesterolemia-induced extension of no-reflow, which delays infarct healing. [ABSTRACT FROM AUTHOR]

: ObjectivesThis study aimed to clarify the role of adenosine triphosphate-sensitive K+ (KATP) channels in the no-reflow phenomenon and in its extension by hypercholesterolemia.: BackgroundThe no-reflow phenomenon is an important target of therapy in patients with acute myocardial infarction, but its mechanism remains unclear.: MethodsThe left circumflex coronary artery was occluded for 30 or 60 min and reperfused in rabbit hearts in situ. The no-reflow zone, area at risk, and infarct size were determined by thioflavin-S, Evans blue, and tetrazolium staining, respectively. No-reflow zone size was expressed as a percentage of infarct size (%NR/IS). Hypercholesterolemia was induced by two weeks of cholesterol-enriched diet.: ResultsA KATP channel blocker, glibenclamide (0.3 mg/kg), increased %NR/IS after 30-min ischemia/90-min reperfusion from 33.6 ± 1.9% to 45.9 ± 1.6% and %NR/IS after 60-min ischemia/90-min reperfusion from 32.8 ± 3.4% to 46.1 ± 1.7%. However, NG-monomethyl-l-arginine (l-NMMA), a nitric oxide (NO) synthase inhibitor, and nicorandil, a hybrid of KATP channel opener and nitrate, failed to significantly modify %NR/IS. Hypercholesterolemia increased %NR/IS to 61.6 ± 0.6%, which was not further enlarged by glibenclamide, and delayed infarct healing during the subsequent five days of reperfusion. These effects of hypercholesterolemia were significantly suppressed by nicorandil. Neither glibenclamide, l-NMMA, nicorandil, nor hypercholesterolemia modified infarct size.: ConclusionsThe KATP channel activation, but not NO, is a major mechanism of protection against microvascular injury, causing the no-reflow phenomenon in the heart. Suppression of KATP channel opening may underlie the hypercholesterolemia-induced extension of no-reflow, which delays infarct healing. [Copyright &y& Elsevier]

Sir2 (silent information regulator 2) is an NAD+-dependent histone deacetylase that contributes to longevity in yeast. SIRT1, a mammalian Sir2 ortholog, deacetylates histones and various transcription factors, including p53, FOXO proteins, and peroxisome proliferator-activated receptor-α. We found that its subcellular localization varied in different tissues of the adult mouse. Some subsets of neurons predominantly expressed SIRT1 in the cytoplasm, but ependymal cells expressed it in both the nucleus and cytoplasm. On the other hand, spermatocytes expressed SIRT1 only in the nucleus. Cardiomyocytes in the day 12.5 mouse embryo expressed SIRT! exclusively in the nucleus, but in the adult heart, they expressed it in both the cytoplasm and nucleus. C2C12 myoblast cells expressed SIRT1 in the nucleus, but it localized to the cytoplasm after differentiation. LY294002, an inhibitor of phosphoinositide 3-hydroxykinase, strongly inhibited the nuclear localization of SIRT1 in undifferentiated C2C12 cells. In a heterokaryon assay, SIRT1 shuttled between the nucleus and cytoplasm, and leptomycin B, an inhibitor of CRM1-mediated nuclear exportation, inhibited this shuttling. Two nuclear localization signals and two nuclear export signals were identified by deletion and site-directed mutation analyses. Overexpressed nuclear (but not cytoplasmic or dominant-negative) SIRT1 enhanced the deacetylation of histone H3 in C2C12 cells. Moreover, only the nuclear form suppressed the apoptosis of C2C12 cells induced by antimycin A, an oxidative stressor. These findings indicate that nucleocytoplasmic shuttling is a novel regulatory mechanism of SIRT1, which may participate in differentiation and in inhibition of cell death. [ABSTRACT FROM AUTHOR]

To investigate roles of sarcopenia indexes in prediction of development of insulin resistance in nondiabetic older adults. A 2-year follow-up cohort. The Tanno-Sobetsu study, a prospective observational cohort, included 194 community-dwelling nondiabetic older adults during 2017-2019. Lower limb, upper limb, appendicular, and trunk muscle masses by a bioelectrical impedance analysis, grip strength, knee extension torque, and walking speed were measured in study participants aged ≥65 years (79 men and 115 women) at baseline. Muscle mass and strength were divided by the weight, and then multiplied by 100 to calculate the weight ratio (%). Insulin resistance was assessed by homeostasis model (HOMA-IR) at baseline, and the study participants whose HOMA-IR was less than 1.73 at baseline were followed for a maximum of 2 years. The study endpoint was development of insulin resistance defined as HOMA-IR ≥1.73. The adjusted hazard ratio (HR) of each sarcopenia component for development of insulin resistance was calculated. Lower limb muscle mass (HR 0.88, 95% CI 0.79-0.98) and appendicular muscle mass (HR 0.89, 95% CI 0.81-0.99), but not other sarcopenia components, were associated with the development of insulin resistance, independently of sex and age, HOMA-IR, and waist circumference at baseline. The loss of lower limb muscle mass is a significant risk factor for development of insulin resistance independently of obesity in nondiabetic older adults. The lower limb muscle mass may be a novel target of interventions for the prevention of diabetes in older adults. [ABSTRACT FROM AUTHOR]

Cardiomyopathy is the main cause of death in Duchenne muscular dystrophy. Here, we show that oral administration of resveratrol, which leads to activation of an NAD+-dependent protein deacetylase SIRT1, suppresses cardiac hypertrophy and fibrosis and restores cardiac diastolic function in dystrophindeficient mdx mice. The pro-hypertrophic co-activator p300 protein but not p300 mRNA was up-regulated in the mdx heart, and resveratrol administration down-regulated the p300 protein level. In cultured cardiomyocytes, cardiomyocyte hypertrophy induced by the α1-agonist phenylephrine was inhibited by the overexpression of SIRT1 as well as resveratrol, both of which down-regulated p300 protein levels but not p300 mRNA levels. In addition, activation of atrial natriuretic peptide promoter by p300 was inhibited by SIRT1. We found that SIRT1 induced p300 down-regulation via the ubiquitin-proteasome pathway by deacetylation of lysine residues for ubiquitination. These findings indicate the pathological significance of p300 up-regulation in the dystrophic heart and indicate that SIRT1 activation has therapeutic potential for dystrophic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Abstract: Background: Single nucleotide polymorphisms (SNPs) of the adenosine deaminase, RNA-specific (ADAR) gene were reported to be associated with human longevity. There are possibilities that ADAR is associated with major risk factors of atherosclerotic cardiovascular diseases (CVD), such as hypertension, diabetes, dyslipidemia, and obesity. Objective: To investigate the association between SNPs of the ADAR gene and clinical data associated with major risk factors of atherosclerotic CVD. Subjects: A total of 1504 general population residents (586 males and 918 females) of two towns, Tanno-cho and Sobestu-cho, in Hokkaido, Japan. Methods: Clinical data associated with risk factors of atherosclerotic CVD were collected from these study subjects. DNA from peripheral blood and written informed consent were obtained. Three single nucleotide polymorphisms of ADARB1 and ADARB2 , which were previously reported to be associated with longevity, were genotyped employing the TaqMan PCR method. The associations between SNPs in ADARB1 and ADARB2 and clinical parameters related to risk factors of atherosclerosis were analyzed. Results: On uni- and multivariate analyses, rs2805533 in ADARB2 was significantly associated with the abdominal circumference, body mass index, serum triglyceride level, and serum adiponectin level. The subjects with the AA genotype of rs2805533 had a greater abdominal circumference, higher body mass index, higher triglyceride level, and lower adiponectin level than those with AG and GG genotypes. Conclusion: The SNP in ADARB2 related to longevity is associated with metabolic disorders. This finding suggests that genetic factors modulate human longevity via the regulation of metabolic factors such as abdominal obesity and lipid profiles. [Copyright &y& Elsevier]

Oxidative stress plays a pivotal role in chronic heart failure. SIRT1, an NAD+-dependent histone/protein deacetylase, promotes cell survival under oxidative stress when it is expressed in the nucleus. However, adult cardiomyocytes predominantly express SIRT1 in the cytoplasm, and its function has not been elucidated. The purpose of this study was to investigate the functional role of SIRT1 in the heart and the potential use of SIRT1 in therapy for heart failure. We investigated the subcellular localization of SIRT1 in cardiomyocytes and its impact on cell survival. SIRT1 accumulated in the nucleus of cardiomyocytes in the failing hearts of TO-2 hamsters, postmyocardial infarction rats, and a dilated cardiomyopathy patient but not in control healthy hearts. Nuclear but not cytoplasmic SIRT1-induced manganese superoxide dismutase (Mn-SOD), which was further enhanced by resveratrol, and increased the resistance of C2C12 myoblasts to oxidative stress. Resveratrol's enhancement of Mn-SOD levels depended on the level of nuclear SIRT1, and it suppressed the cell death induced by antimycin A or angiotensin II. The cell-protective effects of nuclear SIRT1 or resveratrol were canceled by the Mn-SOD small interfering RNA or SIRT1 small interfering RNA. The oral administration of resveratrol to TO-2 hamsters increased Mn-SOD levels in cardiomyocytes, suppressed fibrosis, preserved cardiac function, and significantly improved survival. Thus, Mn-SOD induced by resveratrol via nuclear SIRT1 reduced oxidative stress and participated in cardiomyocyte protection. SIRT1 activators such as resveratrol could be novel therapeutic tools for the treatment of chronic heart failure. [ABSTRACT FROM AUTHOR]

Abstract: Background: Visceral injury is a life-threatening complication of cardiopulmonary resuscitation (CPR); however, the clinical significance has been masked by the lethal outcome of out-of-hospital cardiac arrest (OHCA). Objective: The objective is to share our experience of successful treatment of OHCA patients with serious, CPR-related visceral complications. Case Reports: We report two cases of cardiac-origin OHCA with liver injury exacerbated by heparinization during mechanical circulatory support. Although both patients presented with delayed massive liver bleeding (intrahepatic or peritoneal) that compromised hemodynamic status, one patient was successfully treated by selective transcatheter arterial embolization and the other by a surgical procedure. Conclusion: Preventive measures such as careful CPR, as well as interventional or surgical repair after the early diagnosis of visceral injury, are required to improve the outcome in some cases of OHCA. [Copyright &y& Elsevier]