High-sensitivity cardiac troponin in acute conditions

Gualandro, Danielle Menosi; Puelacher, Christian; Müeller, Christian

doi:10.1097/mcc.0000000000000132

Cited by 43 publications

(52 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, troponin T (TnT) has been recognized as a biomarker of myocardial injury. 1,2 Numerous reports have demonstrated that the measurement of high -sensitivity TnT (hs -TnT) levels may have prognostic value in various cardiovascular disorders, such as coronary artery disease (CAD), 3 heart failure, 4 and pulmonary embolism.…”

mentioning

confidence: 99%

High‑sensitivity troponin T as a prognostic marker in patients undergoing aortic valve replacement

Duchnowski¹,

Hryniewiecki²,

Zatorska³

et al. 2017

Polish Archives of Internal Medicine

View full text Add to dashboard Cite

using EuroSCORE II. On the day before surgery, blood samples for the measurement of biomarker levels were collected from each patient. Complete blood count was performed with K 2 -EDTA samples, using a Cobas 6000 electronic counter (Roche, Mannheim, Germany). The plasma levels of cardiac TnT (cTnT) concentrations were measured by the Troponin T hs -STAT (Roche). The endpoint was all-cause death. Patients were followed by direct observation during hospitalization, telephone interviews, or clinic visits for 30 days after the surgery or until death. The study protocol was approved by an institutional review board.Statistical analysis A statistical analysis was performed using SAS version 9.2 (World Headquarters SAS Institute, Cary, North Carolina, United States). Logistic regression was used to assess relationships between variables. The following covariates were investigated for association with the endpoint in a univariate analysis: age, atrial fibrillation, body mass index, chronic obstructive pulmonary disease, CAD, current smoking, EuroSCORE II, hyperlipidemia, hypertension, insulin -dependent diabetes mellitus, left ventricular ejection fraction, New York Heart Association class, peripheral atherosclerosis, previous myocardial infarction, pulmonary blood pressure, history of stroke, tricuspid annulus plane systolic excursion, the levels of bilirubin, creatinine, high -sensitivity C -reactive protein, hs -TnT, hematocrit, hemoglobin, mean corpuscular hemoglobin, and N -terminal pro -B-type natriuretic peptide, glomerular filtration rate, mean corpuscular volume, and platelet and white blood cell counts.

show abstract

mentioning

confidence: 99%

High‑sensitivity troponin T as a prognostic marker in patients undergoing aortic valve replacement

Duchnowski¹,

Hryniewiecki²,

Zatorska³

et al. 2017

Polish Archives of Internal Medicine

View full text Add to dashboard Cite

show abstract

“…The septic patients can have an elevated cTn levels in the plasma in up to 60% of cases (Hamilton et al, 2012) in which its elevated levels is associated with increased mortality risk (Fromm, 2007; Gualandro et al, 2014). Septic patients with elevated cTn levels can have a 2–5 fold increased risk of death, even in the absence of known cardiovascular disease (Mantzouris et al, 2013).…”

Section: Non-invasive Methods To Assess Heart Function In Sepsismentioning

confidence: 99%

Complement and sepsis-induced heart dysfunction

Fattahi

Ward

2017

Molecular Immunology

View full text Add to dashboard Cite

It is well known that cardiac dysfunction develops during sepsis in both humans and in rodents (rats, mice). These defects appear to be reversible, since after “recovery” from sepsis, cardiac dysfunction disappears and the heart returns to its function that was present before the onset of sepsis. Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis. Use of a neutralizing antibody to C5a largely attenuates cardiac dysfunction and other adverse events developing during sepsis. The molecular basis for cardiac dysfunctions is linked to generation of C5a and its interaction with C5a receptors present on surfaces of cardiomyocytes (CMs). It is established that C5a interactions with C5a receptors leads to significant reductions involving faulty contractility and relaxation in CMs. In addition, C5a interactions with C5a receptors or CMs results in reductions in Na+/K+-ATPase in CMs. This ATPase is essential for intact action potentials in CMs. The enzymatic activity and protein for this ATPase were strikingly reduced in CMs during sepsis by unknown mechanisms. In addition, C5a interactions with C5aRs also caused reductions in CM homeostatic proteins that regulate cytosolic [Ca2+]i in CMs: sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2) and Na+/Ca2+ exchanger (NCX). In the absence of C5a receptors, defects in SERCA2 and NCX in CMs after sepsis are strikingly attenuated. These observations suggest new strategies to protect the heart from dysfunction developing during sepsis.

show abstract

“…We identified potential risk factors of troponin release through a search of the literature [3,5,6,[12][13][14][15][16][17][18][19][20][21][22] and classified them according the following clusters: (A) patient-level risk factors present at baseline, and (B) three categories of time-dependent risk factors: (1) markers of inflammation and coagulation, (2) determinants of myocardial oxygen supply-demand mismatch, and (3) other potential causes of troponin release. All patient-level and most time-dependent risk factors had been prospectively recorded within the MARS study, yet some required additional retrospective review of the medical chart in order to yield accurate classifications.…”

Section: Data Collectionmentioning

confidence: 99%