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Aims Irreversible electroporation (IRE) ablation is a non-thermal ablation method based on the application of direct current between a multi-electrode catheter and skin electrode. The delivery of current through blood leads to electrolysis. Some studies suggest that gaseous (micro)emboli might be associated with myocardial damage and/or (a)symptomatic cerebral ischaemic events. The aim of this study was to compare the amount of gas generated during IRE ablation and during radiofrequency (RF) ablation. Methods and results In six 60–75 kg pigs, an extracorporeal femoral shunt was outfitted with a bubble-counter to detect the size and total volume of gas bubbles. Anodal and cathodal 200 J IRE applications were delivered in the left atrium (LA) using a 14-electrode circular catheter. The 30 and 60 s 40 W RF point-by-point ablations were performed. Using transoesophageal echocardiography (TOE), gas formation was visualized. Average gas volumes were 0.6 ± 0.6 and 56.9 ± 19.1 μL (P Conclusion Anodal IRE applications result in significantly less gas formation than both cathodal IRE applications and RF applications. This finding is supported by TOE observations.

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.Новая коронавирусная инфекция COVID-19 в превалирующем большинстве случаев манифестирует респираторными симптомами и лихорадкой, однако у некоторых пациентов могут отмечаться сердечно-сосудистые и гастроэнтерологические проявления. Особенностью клинического синдрома COVID-19 является развитие выраженных иммунопатологических реакций и нарушений гемостаза, ведущее к широкому спектру сердечно-сосудистых осложнений. Течение COVID-19 может осложниться развитием острого инфаркта миокарда, венозных и артериальных тромбозов и тромбоэмболий в различных сосудистых бассейнах, острого повреждения миокарда и миокардита. Среди гастроэнтерологических проявлений наиболее часто выявляются диарея, тошнота или рвота, а также абдоминальная боль. Эти симптомы могут предшествовать появлению респираторных признаков заболевания, а в некоторых случаях выходить на первый план в клинической картине заболевания. Помимо этого, у части больных наблюдаются лабораторные признаки поражения печени (повышение сывороточных трансаминаз). Точный патогенез описанных нарушений продолжает изучаться.

Introduction: At the end of 2019, a novel coronavirus was identified as the cause of a pneumonia cluster in Wuhan, China. Since then, the contagion has rapidly spread all over the world resulting in a global pandemic. Since frequent cardiovascular (CV) system involvement has soon been detected in patients occurring coronavirus disease 2019 (COVID-19), we would provide a simple review available to cardiologists who are going to be involved in the management of COVID-19 patients from several levels: from diagnosis to prevention and management of CV complications. Areas covered: We investigate the role of CV diseases in COVID-19: from incidence of CV comorbidities to their negative impact on prognosis. We also search Literature in order to identify the main CV manifestations in patients occurring virus infection and their management by cardiologists. Expert opinion: Specific treatments for CV involvement associated with COVID-19 are still debated. Results from ongoing trials are needed to further clarify issues about the therapeutic approach, which is constantly changing according the continuous flow of published evidences. Finally, it seems necessary to sensitize all population to raise awareness on CV diseases in COVID era, to hinder underestimation of both new-onset acute CV diseases and consequences of chronic mistreated CV diseases.

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.

Klotho is a type of single‑pass transmembrane protein that is important for the proper function of numerous organs. The aim of the present study was to investigate the role of Klotho in sepsis‑associated myocardial damage. In the present study, reverse transcription‑quantitative PCR, western blotting and ELISA were conducted to examine the expression levels of function genes, and flow cytometry was performed to detect cell apoptosis and reactive oxygen species. The present study demonstrated that Klotho expression was significantly downregulated in septic mice and that the myocardial function of septic mice improved after treatment with exogenous Klotho protein. It further demonstrated that indoxyl sulfate inhibited the expression of Klotho protein. In addition, decreased Klotho protein further led to activation of the reactive oxygen species‑p38 mitogen‑activated protein kinase signaling pathway, finally resulting in myocardial damage. In conclusion, Klotho protein may be a key regulator in the myocardial damage of cardiorenal syndrome in sepsis. It also has a potential to be a therapeutic target for sepsis‑associated myocardial damage in the future.

Hintergrund: Der Myokardinfarkt gilt als zweithäufigste kardiovaskuläre Todesursache in Deutschland. Zur Diagnostik eines Myokardschadens sind kardiale Biomarker von großer Bedeutung. Ziel dieser Arbeit ist es, Patienten zu analysieren und charakterisieren, die ein erhöhtes hochsensitives (hs-) Troponin T, jedoch keine koronare Obstruktion aufweisen. Dadurch soll eine bessere Prognoseeinschätzung und Risikobewertung dieser Patienten ermöglicht werden. Methodik: Analysiert wurden Daten von insgesamt 570 Patienten mit erhöhtem hs-Troponin T, die in den Jahren 2015 bis 2017 in der Charité – Universitätsmedizin Berlin, Campus Benjamin Franklin, eine Koronarangiographie erhalten hatten. Ausschlusskriterien waren ein normwertiges hs-Troponin T, eine koronare Herzkrankheit oder die Notwendigkeit einer koronaren Revaskularisation. Für jeden Patienten wurde ein Prüfbogen ausgefüllt. Die dokumentierten Daten wurden anschließend statistisch ausgewertet. Der primäre Endpunkt der Studie war die Gesamtsterblichkeit. Ergebnisse: Das Durchschnittsalter der Patienten betrug 69 Jahre bei nahezu ausgeglichenem Geschlechterverhältnis. Das Patientenkollektiv wies zahlreiche kardiovaskuläre Risikofaktoren auf. Die häufigsten Ursachen der Myokardschädigung waren Rhythmusstörungen, hypertensive Entgleisungen, andere kardiale Ursachen und Infektionen. Der Unterschied in der hs-Troponin T Erhöhung in diesen Gruppen war nicht signifikant. In den ersten 30 Tagen des Follow-ups verstarben 32 Patienten (5,6 %), davon 14 (2,5 %) aufgrund kardiovaskulärer Ursachen. Bei infektiöser Genese bestand eine signifikant erhöhte Mortalität. Als Prädiktoren der Gesamtmortalität konnten der Zustand nach Bypassoperation, die Nierenfunktion, der maximale CK-MB Wert (Creatine Kinase Myocardial Band) sowie der maximale hs-Troponin T-Wert identifiziert werden. Fazit: Patienten mit erhöhtem hs-Troponin und nicht-obstruktiven Koronarien stellen sich häufig mit dem Bild eines Nicht-ST-Hebungs-Myokardinfarkts und den Symptomen Angina pectoris und Dyspnoe vor. Eine genaue Diagnostik der Genese der Troponinerhöhung ist aufgrund des heterogenen Patientenkollektivs von hoher therapeutischer Relevanz. Dabei gebühren der Nierenfunktion als signifikanten Prädiktor der Gesamtmortiltät und den infektiösen Ursachen der hs-Troponin T Erhöhung besondere Aufmerksamkeit., Background: Myocardial infarction is the second most common cause of cardiovascular death in Germany. Cardiac biomarkers, like high-sensitive (hs-) troponin T, play an important role in the diagnosis of myocardial damage. The aim of this study is to analyse and characterize patients with an elevated hs-troponin T but without coronary obstruction, thereby contributing to an advanced characterisation and risk stratification of these patients. Methods: A total of 570 hs-troponin T positive patients who underwent coronary angiography at the Charité – Universitätsmedizin Berlin, Campus Benjamin Franklin, between 2015 and 2017 were included in the analysis. Exclusion criteria were normal hs-troponin T, obstructive coronary artery disease, or the need for coronary revascularisation. For every patient a case report form was completed and the documented data were evaluated statistically. The primary endpoint of the study was all cause mortality. Results: The mean age of the study population was 69 years with 47,2 % of the patients being women. The patients had numerous cardiovascular risk factors. The most common reasons for myocardial damage were rhythm disorders, hypertensive urgency / emergency, other cardiac disorders and infections. The hs-troponin T did not show a significant difference in these groups. During the first 30 days of the follow-up, a total of 32 patients (5,6 %) died, 14 (2,5 %) patients due to cardiovascular causes. Infectious diseases were significantly related to mortality. Predictors of all-cause mortality were prior coronary artery bypass grafting, kidney dysfunction, maximum hs-troponin T-values and maximum creatine kinase myocardial band-values. Conclusion: Patients with cardiac troponin elevation without obstruction of the coronary arteries presented mostly with non-ST-segment elevation myocardial infarction, angina and dyspnoea. Because of the heterogenous patient collective an exact diagnosis of the troponin etiology is therapeutically relevant. Especially kidney function as a significant all-cause mortality predictor and infectious causes of the hs-troponin T elevation may require special attention in the clinical setting.

Kardiyovasküler hastalıklar dünya çapında önde gelen en önemli ölüm nedenidir. Kardiyovasküler hastalıkların sekonder korumasında antiagregan tedaviler önemli bir yer tutmaktadır. Bu çalışma ile; akut koroner sendrom ile başvuran hastalarda, daha önceden düzenli asetilsalisilik asit kullanımının TIMI akımı ve miyokardiyal hasar üzerine olan etkileri araştırılacaktır. Yöntem: Çalışmaya retrospektif olarak akut koroner sendrom kliniği ile başvurmuş ve koroner anjiyografi yapılmış hastalar alındı. Hastalar daha önceden düzenli asetilsalisilik asit kullanan (grup 1) ve hiç asetilsalisilik asit kullanmayanlar olarak (grup 2) iki gruba ayrıldı. Gruplar arasında demografik veriler, laboratuvar verileri, TIMI akımları ve miyokardial hasar belirteci olarak troponin I değerleri karşılaştırıldı. Bulgular: Çalışmaya 440 hasta alındı. Grup 1’de 122 hasta (yaş ortalaması 64.9±1 yıl; 25 (%20.5) kadın) ve grup 2’de 318 hasta (yaş ortalaması 61±0.7 yıl; 83 (%26.1) kadın) yer aldı. Grup 1’de ileri yaş, hipertansiyon, diyabetes mellitus, hiperlipidemi ve koroner arter hastalığı öyküsü daha yüksek oranda gözlendi. Grup 1’deki hastalarda TIMI-0 akım grup 2’ye göre anlamlı olarak daha düşük oranda gözlendi (%30.3’e karşın, %47.8; p=0.004). Bunun yanı sıra; grup 1’deki hastaların maksimum ölçülen troponin I değerleri grup 2’deki hastalara göre anlamlı olarak daha düşük düzeyde bulundu (median 5486 pg/ml’ye karşın 15740 pg/ml; p, Cardiovascular diseases are the leading cause of death worldwide. Antiaggregant therapies have an important place in the secondary prevention of cardiovascular diseases. In this study, the effects of regular use of acetylsalicylic acid on TIMI flow grade and myocardial damage will be investigated in patients presenting with acute coronary syndrome. Methods: The patients who admitted with the clinic of acute coronary syndrome and underwent coronary angiography were included in the study, retrospectively. The patients were divided into two groups as those who used acetylsalicylic acid regularly (group 1) and those who never used acetylsalicylic acid (group 2). Demographic data, laboratory data, TIMI flow grade and troponin-I values as a marker of myocardial damage were compared between the groups. Results: 440 patients were included in the study. There were 122 patients in group 1(mean age 64.9±1.0 years; 25(20.5%) women) and 318 patients in group 2(mean age 61.0±0.7 years; 83(26.1%) women). Advanced age, hypertension, diabetes mellitus, hyperlipidemia and history of coronary artery disease were observed at a higher rate in group 1. TIMI-0 flow was observed at a significantly lower rate in patients in group 1(30.3% vs. 47.8%; p=0.004). Additionally, the maximum measured troponin values of the patients in group 1 were found significantly lower (median 5486 pg/ml vs. 15740 pg/ml; p

Synopsis The clinical manifestations of COVID-19 are widely variable and may involve several districts. Although the clinical course is mostly characterized by respiratory involvement, up to 30% of hospitalized patients have evidence of myocardial injury due to acute coronary syndrome, cardiac arrhythmias, myocarditis, and cardiogenic shock. In particular, myocarditis is a well-recognized severe complication of COVID-19 and is associated with fulminant cardiogenic shock and sudden cardiac death. The pathophysiology of cardiac injury remains poorly understood and the management and outcomes of myocarditis are not yet clarified. Our aim is to present a comprehensive review about COVID-19 related myocarditis, including clinical characteristics, diagnostic workup, and management.

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.

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 p p = 0.004], prior heart failure (HR 2.35; 95% CI 1.10–5.01; p = 0.027), high-sensitivity C-reactive protein (HR 1.08; 95% CI 1.03–1.11; p p p p = 0.011) and malnutrition (HR 2.30; 95% CI 1.13–4.67; p = 0.020) as significantly associated with MACCE. Furthermore, Cox proportional hazards models using malnutrition and hemodialysis revealed that patients with malnutrition and hemodialysis were at greater risk of MACCE after PCI than patients with neither malnutrition nor hemodialysis (HR 6.91; 95% CI 3.29–14.54; p Conclusions In CAD patients with myocardial damage, malnutrition (GNRI

Background: Abnormal aldosterone signaling is a recognized source of cardiovascular damage. Its influence on cardiomyocyte structure, function, and hormonal receptors when associated with heart failure is still unreported. Methods: Twenty-six consecutive patients with heart failure (LVEF &lt, 40%) and normal coronaries and valves underwent left ventricular endomyocardial biopsy (EMB) for evaluation of myocardial substrate. Biopsy samples were processed for histology, electron microscopy, immunohistochemistry, and Western blot analysis of myocardial aldosterone receptor and aquaporin-1 correlated with plasma aldosterone (AD) and renin activity (PRA). Eight patients with virus-negative inflammatory cardiomyopathy (ICM) had a control EMB after 6 months of immunosuppressive therapy and recovery of cardiac function with re-evaluation of cardiomyocyte structure and receptor expression. Results: EMB in addition to the diagnosis of myocarditis (15 cases), dilated cardiomyopathy CM (6), alcohol CM (2), and diabetic CM (3) showed vacuolar degeneration and cloudy swelling of cardiomyocytes corresponding at electron microscopy to ions and water accumulation into cytosol, membrane-bound vesicles, nucleus, and other organelles, and was associated with an increased AD, PRA, and myocardial expression of aldosterone receptor (2.6 fold) and aquaporin 1 (2.7 fold). In the 8 patients recovered from ICM, cardiomyocyte diameter reduced with disappearance of intracellular vacuoles and normalization of cytosol, nucleus, and cell organelles’ electron-density, along with down-regulation of aldosterone receptor and aquaporin-1. Conclusion: Human heart failure is associated with overexpression of myocardial aldosterone receptor and aquaporin-1. These molecular changes are paralleled by intracellular water overloading and cardiomyocyte swelling and dysfunction. Cardiac recovery is accompanied by down-regulation of hormonal receptors and normalization of cell structure and composition.

Acute myocardial infarction (AMI) is a form of cardiomyopathy in which a blocked coronary artery leads to an irreversible loss of cardiomyocytes due to inadequate blood and oxygen supply to the distal myocardium tissues, eventually leading to heart failure. Recently, studies have revealed that microRNA (miRNA/miR)-24 has diagnostic value in the pathogenesis of AMI by affecting multiple cell processes such as cell proliferation, differentiation and apoptosis. However, the specific mechanism of miR-24 in ischemia-reperfusion injury (IRI) after AMI remains to be fully elucidated. The present study aimed to investigate the effects and mechanisms of miR-24 in IRI. In vitro, the current study detected cellular apoptosis and apoptotic-related protein expression levels in the cardiomyocyte H9C2 cell line (negative control group, model group and miRNA group) via flow cytometry and western blot analysis. In the in vivo study, rats were randomly divided into sham, model and miRNA groups. The infarct area was observed using nitro blue tetrazolium staining, pathological changes of the myocardium were detected via hematoxylin and eosin staining and TUNEL staining was used to detect cardiomyocyte apoptosis. The expression levels of related proteins were evaluated via immunohistochemistry and western blot analysis. The in vitro and in vivo results demonstrated that miR-24 significantly inhibited cardiomyocyte apoptosis compared with the model group. Concurrently, the expression levels of proteins associated with the NF-κB/TNF-α pathway (NF-κB, caspase-3, Bax, Bcl-2, TNF-α, vascular cell adhesion molecule 1, intercellular adhesion molecule 1 and monocyte chemoattractant protein-1) in the miRNA group were significantly different from the model group (P

Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.

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: Remote ischemic preconditioning (RIPC) is promising for preventing periprocedural myocardial damage (pMD) in patients undergoing percutaneous coronary intervention (PCI). However, the impact of RIPC on pMD on smokers is not well elucidated. The aim of this study was to investigate an association between tobacco smoking and RIPC on pMD in patients planning to undergo PCI. Methods: This study used data from a multicenter randomized controlled trial involving patients with stable angina who planned to undergo elective PCI. We analyzed data for 262 patients in the control (n = 133) and upper-limb RIPC (n = 129) groups, including 166 current or former smokers. The major outcome was the pMD incidence following PCI, with pMD defined as an elevated level of highly sensitive cardiac troponin T or a creatine kinase myocardial band 12 or 24 h after PCI. Results: The incidence of pMD was significantly lower in the upper-limb RIPC group than in the control group (28/83 patients [33.8%] vs. 43/83 patients [51.8%], respectively; p = 0.018). In a multiple logistic regression model, tobacco smoking was an independent predictor of interacting with and enhancing the effect of RIPC on reducing the incidence of pMD after PCI (regression coefficient, −0.4 [95% confidence interval, −0.74 to −0.082]; p = 0.015). Conclusions: Tobacco smoking may have a beneficial effect on RIPC against pMD after PCI. Keywords: Myocardial damage, Percutaneous coronary intervention, Tobacco, Ischemic preconditioning

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.