| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-107 |
Sentence |
denotes |
COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. |
| T2 |
108-234 |
Sentence |
denotes |
The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. |
| T3 |
235-376 |
Sentence |
denotes |
We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. |
| T4 |
377-581 |
Sentence |
denotes |
While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. |
| T5 |
582-662 |
Sentence |
denotes |
Risk of severe infection and mortality increase with advancing age and male sex. |
| T6 |
663-790 |
Sentence |
denotes |
Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. |
| T7 |
791-1126 |
Sentence |
denotes |
The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). |
| T8 |
1127-1397 |
Sentence |
denotes |
Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. |
| T9 |
1398-1553 |
Sentence |
denotes |
This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). |
| T10 |
1554-1696 |
Sentence |
denotes |
While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. |
| T11 |
1697-1746 |
Sentence |
denotes |
Hence, patients should not discontinue their use. |
| T12 |
1747-1844 |
Sentence |
denotes |
Moreover, renin-angiotensin-aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. |
| T13 |
1845-2012 |
Sentence |
denotes |
Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. |
| T14 |
2013-2219 |
Sentence |
denotes |
Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. |
| T15 |
2220-2315 |
Sentence |
denotes |
Preventive measures (social distancing and social isolation) also increase cardiovascular risk. |
| T16 |
2316-2582 |
Sentence |
denotes |
Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed. |
| T1 |
0-107 |
Sentence |
denotes |
COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. |
| T2 |
108-234 |
Sentence |
denotes |
The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. |
| T3 |
235-376 |
Sentence |
denotes |
We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. |
| T4 |
377-581 |
Sentence |
denotes |
While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. |
| T5 |
582-662 |
Sentence |
denotes |
Risk of severe infection and mortality increase with advancing age and male sex. |
| T6 |
663-790 |
Sentence |
denotes |
Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. |
| T7 |
791-1126 |
Sentence |
denotes |
The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). |
| T8 |
1127-1397 |
Sentence |
denotes |
Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. |
| T9 |
1398-1553 |
Sentence |
denotes |
This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). |
| T10 |
1554-1696 |
Sentence |
denotes |
While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. |
| T11 |
1697-1746 |
Sentence |
denotes |
Hence, patients should not discontinue their use. |
| T12 |
1747-1844 |
Sentence |
denotes |
Moreover, renin-angiotensin-aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. |
| T13 |
1845-2012 |
Sentence |
denotes |
Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. |
| T14 |
2013-2219 |
Sentence |
denotes |
Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. |
| T15 |
2220-2315 |
Sentence |
denotes |
Preventive measures (social distancing and social isolation) also increase cardiovascular risk. |
| T16 |
2316-2582 |
Sentence |
denotes |
Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed. |