Name (Synonyms) | Correlation | |
---|---|---|
D007238 | Infarction NIH | 0.53 |
D009203 | Myocardial Ischemia NIH | 0.41 |
D009205 | Myocarditis NIH | 0.25 |
Name (Synonyms) | Correlation | |
---|---|---|
HP:0001658 | Myocardial infarction HPO | 0.41 |
HP:0012819 | Myocarditis HPO | 0.25 |
There are 2 clinical trials
Myocardial injury, as assessed by elevation of cardiac troponins (Tnc), is frequent among patients with COVID-19. Although rare autopsy cases reported COVID-19 related myocardial inflammation, the origin of Tnc elevation is unknown to date. Several cardiac causes, such as myocarditis, non-ischemic myocardial injury (NIMI), or myocardial infarction (MI) may lead to Tnc kinetic. Our work will test the hypothesis that during SARS-Cov2 infection, the elevation of cardiac biomarkers could be linked to the occurrence of myocarditis.
Description: Myocardtitis diagnosis in patients COVID+ and troponin+
Measure: characterize the myocardial damage associated with CoV-2 SARS infection Time: Through study completion, an average of 1 yearThe COVID-19 pandemic highlights the importance of the prognosis of co-morbidities, such as coronary artery disease, which significantly increase the risk of mortality in patients infected with SARS-CoV2. Investigators have recently studied the complex links between respiratory infections, particularly pneumonia, and type 2 myocardial infarction (MI) in many respects. The etiology of type 2 MI is based on an imbalance of myocardial oxygen supply/need in the absence of rupture/erosion of atheromatous plaques. Based on the RICO survey data, the investigators investigated whether COVID-19-related sepsis and/or respiratory failure could be an underlying mechanism of MI2.