Journal of Medical Internet Research - International Scientific Journal for Medical Research, Information and Communication on the Internet

Coronavirus disease 2019 (COVID-19) is still an ongoing pandemic worldwide. COVID-19 is an age-related disease with a higher risk of organ dysfunction and mortality in older adults. Coagulation disorders and thrombosis are important pathophysiological changes in COVID-19 infection. Up to 95% of COVID-19 patients have coagulation disorders characterized by an elevated D-dimer, a prolonged prothrombin time, a low platelet count and other laboratory abnormalities. Thrombosis is found in critical cases with an increased risk of death. Endothelial cells are prone to be affected by the novel SARS-CoV-2 and express angiotensin-converting enzyme 2. The evidence, such as the presence of the virus, has been identified, leading to the inflammation and dysfunction. Endothelial cell activation and dysfunction play a pivotal role in the hypercoagulation status in COVID-19 patients. In addition to the direct exposure of subendothelial tissue to blood, Weibel-Palade bodies within the endothelium containing coagulants can be released into the circulation. Endothelial nitric oxide synthase may be impaired, thus facilitating platelet adhesion. Moreover, anti-β2-glycoprotein I antibodies may also contribute to the coagulopathy in COVID-19 by inducing the upregulation of proinflammatory mediators and adhesion molecules. To conclude, coagulation disorders and thrombosis are vital and predict a poor outcome in COVID-19 patients, especially in severe cases. Endothelial cell activation and dysfunction may play an important role in causing clot formation. More basic and clinical research is warranted to further our understanding of the role of coagulopathy and their possible mechanism in COVID-19 patients.

Background: Heart failure (HF) is a global health problem with high morbidity and mortality. Recently, the association between peak atrial longitudinal strain (PALS) and clinical outcomes of HF has gained increasing attention. Our aim was to systematically assess the prognostic value of PALS for adverse events in HF.Methods: PubMed, Embase, and Scopus databases were systematically searched from inception to 30 April 2022. Studies in which PALS was assessed to predict adverse outcomes in adult patients with HF were included. Study selection, quality assessment, and data extraction were performed independently by two authors. The primary endpoints were all-cause death and cardiac hospitalization.Results: Among 7,787 patients in 17 included studies, 3,029 (38.9%) experienced the primary endpoint. Patients with events had lower PALS than those without events [weighted mean difference (WMD) 6.17, 95% confidence interval (CI) 3.09–9.26, p < 0.001]. Each unit increment of PALS was independently associated with decreased risk for the primary endpoint [hazard ratio (HR) 0.96, 95% CI 0.94–0.98, p < 0.001]. The addition of PALS significantly improved the predictive power of conventional risk models [net reclassification index (NRI) 0.22, 95% CI 0.06–0.39, p = 0.008].Conclusion: Peak atrial longitudinal strain was an independent predictor for all-cause mortality and cardiac hospitalization in patients with HF, highlighting the clinical importance of left atrial (LA) deformation in the prognosis of HF.Systematic Review Registration: [www.crd.york.ac.uk/prospero/], identifier [CRD42020185034].

Currently, cardiac involvement is used to describe all eosinophilic granulomatosis with polyangiitis (EGPA) cardiac problems. However, heterogeneity exists among them. We aimed to depict the disease spectrum of EGPA cardiac involvement and identify high-risk population. We included EGPA patients hospitalized in our center from 2012 to 2023 and in public databases. Based on the cardiac enzymes, cardiac magnetic resonance imaging, and endomyocardial biopsy results, the patients were divided into 3 groups: eosinophilic myocarditis (EGPA-EM), chronic inflammatory cardiomyopathy (EGPA-ICM) and EGPA-Control. Their clinical, laboratory, imaging results and prognoses were collected and compared. A total of 193 EGPA patients were included, 118 with cardiac involvement (74 EGPA-EM, 44 EGPA-ICM) and 75 control. Among EGPA-control, EGPA-ICM and EGPA-EM, eosinophil increased (6.12/8.71/10.42 × 10⁹/l, p< 0.01), ANCA positivity decreased (41.33/31.82/14.86%, p< 0.01), and lung involvement reduced (73.33/72.73/43.24%, p= 0.02). In EGPA-EM, cardiac troponin further elevated (0.27 vs 6.00 ng/ml, p< 0.01), ejection fractions decreased (57.79 vs 33.20%, p< 0.01), while more ST-T abnormality was observed (41.89 vs 20.45%, p= 0.02). The prognosis of EGPA-EM was significantly worse, with 14.86% death rate, and 2-year event-free survival rate below 50%. Further, we proposed a LATE-EAST diagnostic score (7 items, 9 points) to discriminate EGPA-EM from EGPA-ICM using 4 points as threshold [AUC 0.85 (95%CI 0.78–0.92), sensitivity 0.78, specificity 0.86]. We first proposed different subtypes of cardiac involvement in EGPA. Identification and treatment of EGPA-EM needs improvement. LATE-EAST score could recognize the high-risk EGPA-EM effectively. Multi-disciplinary treatment is warranted, immunosuppressive therapy should be given timely and anti-IL-5 antibodies be tested in trials.

With anti-PD-1 antibodies serving as a representative drug, immune checkpoint inhibitors (ICIs) have become the main drugs used to treat many advanced malignant tumors. However, immune-related adverse events (irAEs), which might involve multiple organ disorders, should not be ignored. ICI-induced myocarditis is an uncommon but life-threatening irAE. Glucocorticoids are the first choice of treatment for patients with ICI-induced myocarditis, but high proportions of steroid-refractory and steroid-resistant cases persist. According to present guidelines, tumor necrosis factor alpha (TNF-α) inhibitors are recommended for patients who fail to respond to steroid therapy and suffer from severe cardiac toxicity, although evidence-based studies are lacking. On the other hand, TNF-α inhibitors are contraindicated in patients with moderate-to-severe heart failure. This review summarizes real-world data from TNF-α inhibitors and other biologic agents for ICI-induced myocarditis to provide more evidence of the efficacy and safety of TNF-α inhibitors and other biologic agents.

Polymyositis (PM) and dermatomyositis (DM) are autoimmune diseases characterized by inflammation of skeletal muscle, primarily manifesting as chronic muscle weakness. Extramuscular organs can also be affected. Cardiac involvement is one of the visceral organ damages whose prevalence is underestimated and is a marker of poor prognosis leading to irreversible dysfunction or even death. Although early and accurate recognition of cardiac involvement remains a key barrier to improving survival in PM/DM patients, considerable progress has been made, and an overview will be provided in this review. The new concept of multimodality imaging, which involves an integrated approach of echocardiography (Echo), cardiac magnetic resonance and sometimes positron emission tomography (PET), can facilitate diagnosis. The development of ultrasound technology, including strain analysis, stress Echo and contrast-enhanced Echo, helps disclose early cardiac dysfunction more sensitively than conventional Echo. Cardiac magnetic resonance unveils silent, acute or chronic myocarditis in PM/DM and is used to monitor treatment efficacy due to its excellent tissue characterization. PET can be useful thanks to the appearance of new tracers that can eliminate the effects of glucose uptake by normal cardiomyocytes. The sensitivity of endomyocardial biopsy may be increased by targeted sampling with the guidance of cardiac imaging. Troponin I is specific to cardiac injury, and investigations into antibodies against cardiac tissue are being carried out. Disease-specific mechanisms and therapies are also discussed to give more insights into cardiac involvement in PM and DM.