Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi

suck pdf from helios

10.1016/j.ahj.2020.04.025

http://scihub22266oqcxt.onion/10.1016/j.ahj.2020.04.025
suck pdf from google scholar
32497913!7252118!32497913
unlimited free pdf from europmc32497913    free
PDF from PMC    free
html from PMC    free
PDF vom PMID32497913  :  Publisher
PDF vom PMID32497913
PDF vom PMID32497913

suck abstract from ncbi

pmid32497913
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • 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]
  • |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]
  • |Takotsubo Cardiomyopathy/etiology[MESH]
  • |Virus Internalization[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    29 ä.226 2020