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In 2020, the pandemic led to a reduction of this activity by 96% for the surgery performed overseas and 86% for the interventions carried out in Italy. In conclusion our study shows the important quantitative impact of the pandemic on the Italian humanitarian cardiac surgical activity overseas and in Italy. This shocking result highlights the failure of the systems adopted so far to solve the problem of CHD in developing countries.Myocardial infarction is a prevalent and life-threatening cardiovascular disease. The main goal of existing interventional therapies is to restore coronary reperfusion while few are designed to ameliorate the pathology of heart diseases via targeting the post-translational modifications of those critical proteins. Small ubiquitin-like modifier (SUMO) proteins are recently discovered to form a new type of protein post-translational modifications (PTM), known as SUMOylation. SUMOylation and deSUMOylation are dynamically balanced in the maintenance of various biological processes including cell division, DNA repair, epigenetic transcriptional regulation, and cellular metabolism. Importantly, SUMOylation plays a critical role in the regulation of cardiac functions and the pathology of cardiovascular diseases, especially in heart failure and myocardial infarction. This review summarizes the current understanding on the effects of SUMOylation and SUMOylated proteins in the pathophysiology of myocardial infarction and identifies the potential treatments against myocardial injury via targeting SUMO. Ultimately, this review recommends SUMOylation as a key therapeutic target for treating cardiovascular diseases.We report on an impressive case of a previously healthy 47-year-old female Caucasian SARS-CoV-2 positive patient who died within 48 h after initial cardiac symptoms. Autopsy revealed necrotizing myocarditis and extensive microthrombosis as the cause of death. The interesting feature of this case is the combination of both myocarditis and extensive localized microthrombosis of cardiac capillaries. Microthrombosis was not present in other organs, and the patient did not show typical features of diffuse alveolar damage in the lungs. Taken together, our morphologic findings illustrate the angiocentric, microangiopathic, thromboinflammatory disease with significant thrombotic diathesis prevalent in COVID-19, which has been previously described in the literature, likely warranting thromboprophylaxis even in oligosymptomatic circumstances. This case also delineates several potential etiologies for microthrombosis, i.e., inflammatory reactions and primary hypercoagulative states. Further systematic analyses on risk stratification for receipt of prophylactic anticoagulation in COVID-19 are urgently required.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein binds to angiotensin-converting enzyme 2 (ACE2) receptor on vascular cells. As a consequence, patients with COVID-19 have an increased incidence of thromboembolic complications of the SARS-CoV-2 infection and subsequent endothelial cell damage with consequence of development of systemic vasculitis and diffuse intravascular coagulation. The present case describes a COVID-19 female patient with ischemic dilated cardiomyopathy, who presented with congestive heart failure and echocardiographic evidence of biventricular apical thrombi. The peak antegrade longitudinal velocity (Va) of each thrombotic mass was measured by pulsed wave tissue Doppler imaging (PW-TDI). Both left ventricular and right ventricular apical thrombi were found with a TDI-derived mass peak Va less then 10 cm/s. There was no clinical evidence of neither systemic nor pulmonary embolization, probably due to the hypomobility of both left and right ventricular masses.Background When an implantable-cardioverter defibrillator (ICD) lead becomes non-functional, a recommendation currently exists for either lead abandonment or removal. Lead abandonment and subcutaneous ICD (S-ICD) implantation may represent an additional option for patients who do not require pacing. The aim of this study was to investigate the outcomes of a strategy of lead abandonment and S-ICD implantation in the setting of lead malfunction. Methods We analyzed all consecutive patients who underwent S-ICD implantation after abandonment of malfunctioning leads and compared their outcomes with those of patients who underwent extraction and subsequent reimplantation of a single-chamber transvenous ICD (T-ICD). Results Forty-three patients underwent S-ICD implantation after abandonment of malfunctioning leads, while 62 patients underwent extraction and subsequent reimplantation of a new T-ICD. The two groups were comparable. In the extraction group, no major complications occurred during extraction, while the procedure failed and an S-ICD was implanted in 4 patients. During a median follow-up of 21 months, 3 major complications or deaths occurred in the S-ICD group and 11 in the T-ICD group (HR 1.07; 95% CI 0.29-3.94; P = 0.912). Minor complications were 4 in the S-ICD group and 5 in the T-ICD group (HR 2.13; 95% CI 0.49-9.24; P = 0.238). Conclusions In the event of ICD lead malfunction, extraction avoids the potential long-term risks of abandoned leads. Nonetheless the strategy of lead abandonment and S-ICD implantation was feasible and safe, with no significant increase in adverse outcomes, and may represent an option in selected clinical settings. Further studies are needed to fully understand the potential risks of lead abandonment. Clinical Trial Registration URL ClinicalTrials.gov Identifier NCT02275637.Background Renalase has been implicated in chronic heart failure (CHF); however, nothing is known about renalase discriminatory ability and prognostic evaluation. The aims of the study were to assess whether plasma renalase may be validated as a predictor of ischemia in CHF patients stratified to the left ventricular ejection fraction (LVEF) and to determine its discriminatory ability coupled with biomarkers representing a range of heart failure (HF) pathophysiology brain natriuretic peptide (BNP), soluble suppressor of tumorigenicity (sST2), galectin-3, growth differentiation factor 15 (GDF-15), syndecan-1, and cystatin C. Methods A total of 77 CHF patients were stratified according to the LVEF and were subjected to exercise stress testing. Receiver operating characteristic curves were constructed, and the areas under curves (AUC) were determined, whereas the calibration was evaluated using the Hosmer-Lemeshow statistic. A DeLong test was performed to compare the AUCs of biomarkers. Results Independent predictors for ischemia in the total HF cohort were increased plasma concentrations BNP (p = 0.008), renalase (p = 0.012), sST2 (p = 0.020), galectin-3 (p = 0.018), GDF-15 (p = 0.034), and syndecan-1 (p = 0.024), whereas after adjustments, only BNP (p = 0.010) demonstrated predictive power. In patients with LVEF 45%. Conclusion Plasma renalase concentration provided significant discrimination for the prediction of ischemia in patients with CHF and appeared to have similar discriminatory potential to that of BNP. Although further confirmatory studies are warranted, renalase seems to be a relevant biomarker for ischemia prediction, implying its potential contribution to ischemia-risk stratification.Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder with overlapping myelodysplastic and myeloproliferative features. The disease is generally characterized by blood monocytosis, bone marrow dysplasia, cytopenia, and hepatosplenomegaly. While malignant blood diseases are frequently associated with a high risk of thromboembolism, CMML is often accompanied by immune-mediated hemorrhagic diathesis. Indeed, very few reports in literature report thrombotic complications of CMML patients. We will briefly present here the case of a patient with CMML who developed a massive right atrial thrombus. We aim to highlight the non-negligible thrombotic burden of the disease, and we will get through the differential diagnosis of right atrial masses and the management of right atrial thrombi, which are a rare and poorly known entity.Purpose Thyroid hormones (TH) play a central role for cardiac function. TH influence heart rate and cardiac contractility, and altered thyroid function is associated with increased cardiovascular morbidity and mortality. The precise role of TH in onset and progression of heart failure still requires clarification. Methods Chronic left ventricular pressure overload was induced in mouse hearts by transverse aortic constriction (TAC). One week after TAC, alteration of TH status was induced and the impact on cardiac disease progression was studied longitudinally over 4 weeks in mice with hypo- or hyperthyroidism and was compared to euthyroid TAC controls. Serial assessment was performed for heart function (2D M-mode echocardiography), heart morphology (weight, fibrosis, and cardiomyocyte cross-sectional area), and molecular changes in heart tissues (TH target gene expression, apoptosis, and mTOR activation) at 2 and 4 weeks. Results In diseased heart, subsequent TH restriction stopped progression of maladaptive cardiac hypertrophy and improved cardiac function. In contrast and compared to euthyroid TAC controls, increased TH availability after TAC propelled maladaptive cardiac growth and development of heart failure. This was accompanied by a rise in cardiomyocyte apoptosis and mTOR pathway activation. Conclusion This study shows, for the first time, a protective effect of TH deprivation against progression of pathological cardiac hypertrophy and development of congestive heart failure in mice with left ventricular pressure overload. Whether this also applies to the human situation needs to be determined in clinical studies and would infer a critical re-thinking of management of TH status in patients with hypertensive heart disease.Background Treadmill exercise testing (TET) is commonly used to measure exercise capacity. Studies have shown that cardiopulmonary exercise testing (CPET) is more accurate than TET and is, therefore, regarded as the "gold standard" for testing maximum exercise capacity and prescribing exercise plans. To date, no studies have reported the differences in exercise capacity after percutaneous coronary intervention (PCI) using the two methods or how to more accurately measure exercise capacity based on the results of TET. Saracatinib ic50 Aims This study aims to measure maximum exercise capacity in post-PCI patients and to recommend exercise intensities that ensure safe levels of exercise. Methods We enrolled 41 post-PCI patients who were admitted to the Cardiac Rehabilitation Clinic at the First Medical Center, the Chinese PLA General Hospital, from July 2015 to June 2016. They completed CPET and TET. The paired sample t-test was used to compare differences in measured exercise capacity, and multiple linear regression was applied to analyze the factors that affected the difference. Results The mean maximum exercise capacity measured by TET was 8.89 ± 1.53 metabolic equivalents (METs), and that measured by CPET was 5.19 ± 1.23 METs. The difference between them was statistically significant (p = 0.000) according to the paired sample t-test. The difference averaged 40.15% ± 2.61% of the exercise capacity measured by TET multiple linear regression analysis showed that the difference negatively correlated with waist-hip ratio (WHR). Conclusion For the purpose of formulating more accurate exercise prescription, the results of TET should be appropriately adjusted when applied to exercise capacity assessment. Clinical Trial Registrationhttp//www.chictr.org.cn/ number, ChiCTR2000031543.