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Clonal hematopoiesis of indeterminate potential (CHIP) is linked to leukemia gene mutations and associates with an increased risk for coronary artery disease and poor prognosis in ischemic cardiomyopathy. Two recurrently mutated genes in CHIP and adult acute myeloid leukemia (AML) encode for isocitrate dehydrogenases 1 and 2 ( IDH1 and IDH2 ). Global expression of mutant IDH2 in transgenic mice-induced dilated cardiomyopathy and muscular dystrophy. In this retrospective observational study, we investigated whether mutant IDH1/2 predisposes to cardiovascular disease in AML patients. Among 363 AML patients, IDH1 and IDH2 mutations were detected in 26 (7.2%) and 39 patients (10.7%), respectively. Mutant IDH1 patients exhibited a significantly higher prevalence of coronary artery disease (26.1% vs. 6.4%, p  = 0.002). Applying inverse probability-weighting analysis, patients with IDH1/2 mutations had a higher risk for a declining cardiac function during AML treatment compared to IDH1/2 wild type patients [left ventricular ejection fraction pretreatment compared to 10 months after diagnosis: 59.2% to 41.9% ( p  < 0.001) vs 58.5% to 55.4% ( p  = 0.27), respectively]. Mechanistically, RNA sequencing and immunostaining in hiPS-derived cardiomyocytes indicated that the oncometabolite R-2HG exacerbated doxorubicin mediated cardiotoxicity. Evaluation of IDH1/2 mutation status may therefore help identifying AML patients at risk for cardiovascular complications during cytotoxic treatment.

To determine whether cardiac sympathetic nervous dysfunction is present, in this single center prospective, non-randomized trial non-invasive SPECT/CT imaging using the radiotracer 123 I-metaiodobenzylguanidine was performed in 33 recovered COVID-19 patients without pre-existing cardiac conditions. Increased cardiac sympathetic activity, as indicated by late HMR, was observed in 67.7% of patients. At 6–8 months, 82% of these subjects (27/33) received follow-up, and cardiac sympathetic innervation abnormalities were still present in 70.4% (19/27). Additionally, at 12–15 months post-diagnosis, persistently abnormal HMRs were found in 9 individuals who initially had abnormal sympathetic innervation. Further follow-up is needed to investigate potential long-term cardiovascular consequences of COVID-19.

Background Anticoagulant treatment is recommended for at least three months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related acute pulmonary embolism (PE), but the persistent pulmonary clot burden after that time is unknown. Methods Lung perfusion was assessed by ventilation-perfusion (V/Q) SPECT/CT in 20 consecutive patients with SARS-CoV-2-associated acute PE after a minimum of three months anticoagulation therapy in a retrospective observational study. Results Remaining perfusion defects after a median treatment period of six months were observed in only two patients. All patients (13 men, seven women, mean age 55.6 ± 14.5 years) were on non-vitamin K direct oral anticoagulants (DOACs). No recurrent venous thromboembolism or anticoagulant-related bleeding complications were observed. Among patients with partial clinical recovery, high-risk PE and persistent pulmonary infiltrates were significantly more frequent (p < 0.001, respectively). Interpretation Temporary DOAC treatment seems to be safe and efficacious for resolving pulmonary clot burden in SARS-CoV-2-associated acute PE. Partial clinical recovery is more likely caused by prolonged SARS-CoV-2-related parenchymal lung damage rather than by persistent pulmonary perfusion defects.

We integrated molecular data with available prognostic factors in patients undergoing allogeneic hematopoietic cell transplantation (alloHCT) for myelodysplastic syndrome (MDS) or secondary acute myeloid leukemia (sAML) from MDS to evaluate their impact on prognosis. Three hundred four patients were sequenced for mutations in 54 genes. We used a Cox multivariate model and competing risk analysis with internal and cross validation to identify factors prognostic of overall survival (OS), cumulative incidence of relapse (CIR), and non-relapse mortality (NRM). In multivariate analysis, mutated NRAS , U2AF1 , IDH2 , and TP53 and/or a complex karyotype were significant prognostic markers for OS besides age above 60 years, remission status, IPSS-R cytogenetic risk, HCT-CI > 2 and female donor sex. Mutated NRAS , IDH1 , EZH2 , and TP53 and/or a complex karyotype were genetic aberrations with prognostic impact on CIR. No molecular markers were associated with the risk of NRM. The inclusion of molecular information results in better risk prediction models for OS and CIR when assessed by the Akaike information criterion. Internal cross validation confirmed the robustness of our comprehensive risk model. In summary, we propose to combine molecular, cytogenetic, and patient- and transplantation-associated risk factors into a comprehensive risk model to provide personalized predictions of outcome after alloHCT.

To determine whether cardiac sympathetic nervous dysfunction is present, in this single center prospective, non-randomized trial non-invasive SPECT/CT imaging using the radiotracer I-metaiodobenzylguanidine was performed in 33 recovered COVID-19 patients without pre-existing cardiac conditions. Increased cardiac sympathetic activity, as indicated by late HMR, was observed in 67.7% of patients. At 6-8 months, 82% of these subjects (27/33) received follow-up, and cardiac sympathetic innervation abnormalities were still present in 70.4% (19/27). Additionally, at 12-15 months post-diagnosis, persistently abnormal HMRs were found in 9 individuals who initially had abnormal sympathetic innervation. Further follow-up is needed to investigate potential long-term cardiovascular consequences of COVID-19.