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10.1016/j.ahj.2020.04.025 http://scihub22266oqcxt.onion/10.1016/j.ahj.2020.04.025 32497913!7252118!32497913     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+Heart+J 2020 ; 226 (ä): 29-44 Nephropedia Template TP {{tp|p=32497913|t=2020. A current review of COVID-19 for the cardiovascular specialist |pdf=|usr=}}{{32497913}} gab.com Text A current review of COVID-19 for the cardiovascular specialist JO: Am Heart J http://www.kidney.de/pget.php?&tw=1&pmid=32497913 #FOAvip Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19. Twit Text FOAVip A current review of COVID-19 for the cardiovascular specialist ????Am Heart J http://www.kidney.de/pget.php?&tw=1&pmid=32497913 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32497913 #FOAvip English Wikipedia <ref>{{Cite pmid|32497913}}</ref> A current review of COVID-19 for the cardiovascular specialist #MMPMID32497913 Lang JP; Wang X; Moura FA; Siddiqi HK; Morrow DA; Bohula EA Am Heart J 2020[Aug]; 226 (ä): 29-44 PMID32497913show ga Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19. |*Betacoronavirus/immunology/pathogenicity[MESH] |Adenosine Monophosphate/analogs & derivatives/therapeutic use[MESH] |Alanine/analogs & derivatives/therapeutic use[MESH] |Antimalarials/therapeutic use[MESH] |Antiviral Agents/therapeutic use[MESH] |Biomarkers/blood[MESH] |COVID-19[MESH] |Cardiovascular Diseases/*complications[MESH] |Chloroquine/therapeutic use[MESH] |Coronavirus Infections/*complications/drug therapy[MESH] |Humans[MESH] |Hydroxychloroquine/therapeutic use[MESH] |Hypoxia/complications[MESH] |Pandemics[MESH] |Plasma/immunology[MESH] |Pneumonia, Viral/*complications/drug therapy[MESH] |Receptor, Angiotensin, Type 2/metabolism[MESH] |Risk Factors[MESH] |SARS-CoV-2[MESH] |Takotsubo Cardiomyopathy/etiology[MESH]A current review of COVID-19 for the cardiovascular specialist (epmc).pdf DeepDyve Pubget Overpricing