High‐sensitivity cardiac troponin T 30 days all‐come mortality in patients with acute heart failure. A Propensity Score‐Matching Analysis Based on the EAHFE Registry. TROPICA4 Study

2020 ◽  
Vol 50 (6) ◽  
Author(s):  
Alex Roset ◽  
Javier Jacob ◽  
Pablo Herrero‐Puente ◽  
Aitor Alquézar ◽  
Francisco Javier Martín‐Sanchez ◽  
...  
Keyword(s):  
Heart Failure ◽  
Propensity Score ◽  
Propensity Score Matching ◽  
Acute Heart Failure ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Propensity Score Matching Analysis

scholarly journals High-sensitivity cardiac troponin T and N-terminal pro-B-type natriuretic peptide in acute heart failure: Data from the ACE 2 study

2020 ◽  
Author(s):  
Kristian Berge ◽  
Magnus Nakrem Lyngbakken ◽  
Peder Langeland Myhre ◽  
Jon Brynildsen ◽  
Ragnhild Røysland ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Natriuretic Peptide ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Failure Data

scholarly journals Serial high sensitivity cardiac troponin T measurement in acute heart failure: insights from the RELAX-AHF study

2015 ◽  
Vol 17 (12) ◽  
pp. 1262-1270 ◽  
Author(s):  
G. Michael Felker ◽  
Robert J. Mentz ◽  
John R. Teerlink ◽  
Adriaan A. Voors ◽  
Peter S. Pang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T

Abstract 15285: Prognostic Value of 6-year Change in High Sensitivity Cardiac Troponin-T for Risk of Heart Failure, Heart Failure Subtype, and Death

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bill Mcevoy ◽  
Chiadi E Ndumele ◽  
Yuan Chen ◽  
Scott D Solomon ◽  
Michael Steffes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Troponin ◽  
Proportional Hazards ◽  
Troponin T ◽  
High Sensitivity ◽  
Sensitivity Analyses ◽  
Cardiac Troponin T ◽  
Reduced Ejection Fraction ◽  
Relative Change

Background: Serial changes in high-sensitivity cardiac troponin-T (hs-cTNT) indicate progressive subclinical myocardial damage and have been associated with heart failure (HF) and death in asymptomatic older adults. Whether these associations exist in middle-age and whether serial hs-cTNT is more strongly associated with HF with reduced ejection fraction (HFREF) or HF with preserved ejection fraction (HFPEF) is poorly understood. Methods: We studied 8,838 participants of the Atherosclerosis Risk in Communities Study, initially free of coronary heart disease and HF, who had hs-cTNT measured at two time-points, 6 years apart. Using proportional hazards regression, we examined the association of absolute and relative change in hs-cTNT with incident HF hospitalization or death. Sensitivity analyses for HFPEF and HFREF were also conducted. Results: Mean age at baseline was 57 years, 57% were female and 21% were black. Over a maximum of 16 years follow-up there were 965 HF events and 1813 deaths. In adjusted models, incident detectable hs-cTNT (≥5ng/L) was associated with subsequent HF (Hazard Ratio [HR] 1.86, 95% Confidence Interval [CI] 1.53-2.25) and death (1.46 [1.28-1.68]). HRs were larger for incident hs-cTNT elevation (≥14ng/L) but similar for those with a relative increase >50% from baseline hs-cTNT (Table). In contrast, risk was lower for relative reductions >50% from baseline hs-cTNT. Temporal increases in hs-cTNT were associated with both HFREF and HFPEF in categorical analyses, however, when modeled continuously (per SD increase), absolute 6-year hs-cTNT change appeared to be more strongly associated with HFPEF hospitalization (HR 1.30 [1.06-1.60]) than with HFREF hospitalization (1.08 [0.88-1.33]). Conclusions: Absolute and relative change in hs-cTNT were independently associated with incident CHD, HF and death, even after adjustment for baseline hs-cTNT. Associations were generally consistent for both the HFREF and HFPEF phenotypes

P3532Quantifying hemodynamic cardiac stress and cardiomyocyte injury in hypertensive and normotensive acute heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Kozhuharov ◽  
D Wussler ◽  
R Twerenbold ◽  
J Walter ◽  
J Du Fay De Lavallaz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Natriuretic Peptide ◽  
Cardiac Troponin ◽  
Validation Cohort ◽  
Troponin T ◽  
Plasma Concentrations ◽  
Cardiac Troponin T ◽  
Cardiac Stress ◽  
Derivation Cohort

Abstract Background Better characterization of the different pathophysiological mechanisms involved in normotensive and hypertensive acute heart failure (AHF) might help to develop novel individualized treatment strategies. Methods The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring B-type natriuretic peptide (BNP) as well as high-sensitive cardiac troponin T (hs-cTnT) in 1,152 unselected patients presenting with AHF to the emergency department (derivation cohort). Systolic blood pressure (SBP) of 90 - 140 mmHg at presentation was used to define normotensive AHF. Findings regarding hemodynamic cardiac stress and cardiomyocyte injury were validated in a second independent AHF cohort (validation cohort; n=324). Results In the derivation cohort 667 (58%) patients had hypertensive AHF. Hemodynamic cardiac stress, as quantified by BNP levels, was significantly higher in normotensive AHF as compared to hypertensive AHF (1,105 pg/mL versus 827 pg/mL, p<0.001). In addition, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF (41 ng/L versus 33 ng/L, p<0.001). These findings were confirmed in the validation cohort. Table 1. Cardiac stress and myocardial necrosis as quantified by BNP and hs-cTnT plasma concentrations Overall Hypertensive AHF Normotensive AHF p-value BNP in pg/ml, median (IQR) 974 (536–1,712) 827 (448–1,419) 1,105 (611–1,956) <0.001 hs-cTnT in ng/L, median (IQR) 37 (22–67) 33 (19–59) 41 (24–71) <0.001 BNP = B-type natriuretic peptide; hs-cTnT = high-sensitivity cardiac Troponin T; IQR = inter-quartile range. Figure 1 Conclusion Biomarker profiling revealed that the extent of hemodynamic stress and cardiomyocyte injury is different in patients with normotensive and hypertensive AHF. This characterization could help to understand AHF phenotypes better, which in turn may lead to more specific management in future, thus improving the dismal prognosis in these patients. Acknowledgement/Funding European Union, Swiss National Science Foundation, Swiss Heart Foundation, Cardiovascular Research Foundation Basel, University of Basel

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