High-Sensitivity Cardiac Troponin-T and I

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The primary objective was to directly compare the prognostic accuracy of hs-cTnT versus hs-cTnI for the prediction of death in patient with pneumonia.

 

The prognostic accuracy of high sensitivity (hs)-cTnT and hs-cTnI was directly compared among patients presenting with dyspnea to the emergency department and centrally adjudicated by two independent experts to have pneumonia. Blood samples for the blinded measurement of hs-cTnT and hs-cTnI, as well as NTproBNP were obtained at ED presentation. CURB-65 was calculated as the multivariate risk score recommended in current guidelines. Primary endpoints were all-cause and cardiovascular (CV) mortality at 1 year.

 

Pneumonia is a common reason for presentation to the emergencydepartment (ED) associated with substantial short and long-termmortality with more than 4 million deaths worldwide annually. Thepathophysiological link between pneumonia and death is incompletelyunderstood. Recent studies indicate an increased risk for acutemyocardial infarction and acute heart failure (HF) among patientswith pneumonia provided evidence for the heart as a possiblecontributor. In addition, pilot studies have documented thathemodynamic cardiac stress as quantified by B-type natriuretic peptide(BNP) and NT-proBNP, and cardiomyocyte injury as quantified bycardiac troponin (cTn) T and I seem increased and are associated withmortality in patients with pneumonia. These biomarkers may beuseful in the early and rapid risk-stratification of patients withpneumonia and may complement or even replace at times complexmultivariable risk scores.

 

It is unknown, which of thebiomarkers quantifying cardiomyocyte injury, cTnT or cTnI, should bepreferred in the prediction of mortality in patients with pneumonia.With the development of high-sensitivity (hs) cTn assays, severalstudies demonstrated that, there are pathophysiological and analyticaldifferences between hs-cTnT and hs-cTnI [16]. First, hs-cTnT plasmaconcentrations exhibit a diurnal rhythm, while hs-cTnI does not.

 

This study also has limitations. First, this was a secondary analysis ofthe large prospective BASEL-V study. As such, no specific sample sizecalculation was performed. Second, as patients with severe renaldysfunction were excluded, we cannot comment on the preferredbiomarker in these high-risk patients. Third, we cannot comment onthe preferred biomarker in patients with pneumonia, who do notreport dyspnea at presentation. It is conceivable, although unlikely, thatother and/or additional mechanisms leading to cardiomyocyte injuryaffect the risk of death in these patients. Fourth, as an observationaldiagnostic study, BASEL-V did not interfere with patient management.Further studies are necessary to directly implement the hs-cTnTconcentration into clinical decision-making. Possible consequences ofdetecting a high risk of death by elevated hs-cTnT concentrationsinclude hospital admission, intense hemodynamic monitoring, cardiacwork-up using echocardiography and possibly non-invasive stressimaging for functionally relevant CAD, and optimization ofcardiovascular risk factors.

 

In conclusion, hs-cTnT, but not hs-cTnI, seems to be the preferredbiomarker quantifying cardiomyocyte injury in the prediction of deathamong patients presenting with pneumonia to the ED.

Media Contact: 

Liza Parker
Journal Manager 
Microbiology: Current Research
Email: aamcr@microbialjournals.com

High-Sensitivity Cardiac Troponin-T and I

 

The primary objective was to directly compare the prognostic accuracy of hs-cTnT versus hs-cTnI for the prediction of death in patient with pneumonia.

 

The prognostic accuracy of high sensitivity (hs)-cTnT and hs-cTnI was directly compared among patients presenting with dyspnea to the emergency department and centrally adjudicated by two independent experts to have pneumonia. Blood samples for the blinded measurement of hs-cTnT and hs-cTnI, as well as NTproBNP were obtained at ED presentation. CURB-65 was calculated as the multivariate risk score recommended in current guidelines. Primary endpoints were all-cause and cardiovascular (CV) mortality at 1 year.

 

Pneumonia is a common reason for presentation to the emergencydepartment (ED) associated with substantial short and long-termmortality with more than 4 million deaths worldwide annually. Thepathophysiological link between pneumonia and death is incompletelyunderstood. Recent studies indicate an increased risk for acutemyocardial infarction and acute heart failure (HF) among patientswith pneumonia provided evidence for the heart as a possiblecontributor. In addition, pilot studies have documented thathemodynamic cardiac stress as quantified by B-type natriuretic peptide(BNP) and NT-proBNP, and cardiomyocyte injury as quantified bycardiac troponin (cTn) T and I seem increased and are associated withmortality in patients with pneumonia. These biomarkers may beuseful in the early and rapid risk-stratification of patients withpneumonia and may complement or even replace at times complexmultivariable risk scores.

 

It is unknown, which of thebiomarkers quantifying cardiomyocyte injury, cTnT or cTnI, should bepreferred in the prediction of mortality in patients with pneumonia.With the development of high-sensitivity (hs) cTn assays, severalstudies demonstrated that, there are pathophysiological and analyticaldifferences between hs-cTnT and hs-cTnI [16]. First, hs-cTnT plasmaconcentrations exhibit a diurnal rhythm, while hs-cTnI does not.

 

This study also has limitations. First, this was a secondary analysis ofthe large prospective BASEL-V study. As such, no specific sample sizecalculation was performed. Second, as patients with severe renaldysfunction were excluded, we cannot comment on the preferredbiomarker in these high-risk patients. Third, we cannot comment onthe preferred biomarker in patients with pneumonia, who do notreport dyspnea at presentation. It is conceivable, although unlikely, thatother and/or additional mechanisms leading to cardiomyocyte injuryaffect the risk of death in these patients. Fourth, as an observationaldiagnostic study, BASEL-V did not interfere with patient management.Further studies are necessary to directly implement the hs-cTnTconcentration into clinical decision-making. Possible consequences ofdetecting a high risk of death by elevated hs-cTnT concentrationsinclude hospital admission, intense hemodynamic monitoring, cardiacwork-up using echocardiography and possibly non-invasive stressimaging for functionally relevant CAD, and optimization ofcardiovascular risk factors.

 

In conclusion, hs-cTnT, but not hs-cTnI, seems to be the preferredbiomarker quantifying cardiomyocyte injury in the prediction of deathamong patients presenting with pneumonia to the ED.

Media Contact: 

Liza Parker
Journal Manager 
Microbiology: Current Research
Email: aamcr@microbialjournals.com