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Quantifying Cardiac Hemodynamic Stress and Cardiomyocyte Damage in Ischemic and Nonischemic Acute Heart Failure
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Background—
The early and noninvasive differentiation of ischemic and nonischemic acute heart failure (AHF) in the emergency department (ED) is an unmet clinical need.
Methods and Results—
We quantified cardiac hemodynamic stress using B-type natriuretic peptide (BNP) and cardiomyocyte damage using 2 different cardiac troponin assays in 718 consecutive patients presenting to the ED with AHF (derivation cohort). The diagnosis of ischemic AHF was adjudicated using all information, including coronary angiography. Findings were validated in a second independent multicenter cohort (326 AHF patients). Among the 718 patients, 400 (56%) were adjudicated to have ischemic AHF. BNP levels were significantly higher in ischemic compared with nonischemic AHF (1097 [604–1525] pg/mL versus 800 [427–1317] pg/mL;
P
<0.001). Cardiac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly higher in ischemic compared with nonischemic AHF patients (0.040 [0.010–0.306] μg/L versus 0.018 [0.010–0.060] μg/L [
P
<0.001]; 0.024 [0.008–0.106] μg/L versus 0.016 [0.004–0.044 ] μg/L [
P
=0.002]). The diagnostic accuracy of BNP, cTnT, and s-cTnI for the diagnosis of ischemic AHF, as quantified by the area under the receiver-operating characteristic curve, was low (0.58 [95% CI, 0.54–0.63], 0.61 [95% CI, 0.57–0.66], and 0.59 [95% CI,0.54–0.65], respectively). These findings were confirmed in the validation cohort.
Conclusions—
At presentation to the ED, patients with ischemic AHF exhibit more extensive hemodynamic cardiac stress and cardiomyocyte damage than patients with nonischemic AHF. However, the overlap is substantial, resulting in poor diagnostic accuracy.
Ovid Technologies (Wolters Kluwer Health)
Title: Quantifying Cardiac Hemodynamic Stress and Cardiomyocyte Damage in Ischemic and Nonischemic Acute Heart Failure
Description:
Background—
The early and noninvasive differentiation of ischemic and nonischemic acute heart failure (AHF) in the emergency department (ED) is an unmet clinical need.
Methods and Results—
We quantified cardiac hemodynamic stress using B-type natriuretic peptide (BNP) and cardiomyocyte damage using 2 different cardiac troponin assays in 718 consecutive patients presenting to the ED with AHF (derivation cohort).
The diagnosis of ischemic AHF was adjudicated using all information, including coronary angiography.
Findings were validated in a second independent multicenter cohort (326 AHF patients).
Among the 718 patients, 400 (56%) were adjudicated to have ischemic AHF.
BNP levels were significantly higher in ischemic compared with nonischemic AHF (1097 [604–1525] pg/mL versus 800 [427–1317] pg/mL;
P
<0.
001).
Cardiac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly higher in ischemic compared with nonischemic AHF patients (0.
040 [0.
010–0.
306] μg/L versus 0.
018 [0.
010–0.
060] μg/L [
P
<0.
001]; 0.
024 [0.
008–0.
106] μg/L versus 0.
016 [0.
004–0.
044 ] μg/L [
P
=0.
002]).
The diagnostic accuracy of BNP, cTnT, and s-cTnI for the diagnosis of ischemic AHF, as quantified by the area under the receiver-operating characteristic curve, was low (0.
58 [95% CI, 0.
54–0.
63], 0.
61 [95% CI, 0.
57–0.
66], and 0.
59 [95% CI,0.
54–0.
65], respectively).
These findings were confirmed in the validation cohort.
Conclusions—
At presentation to the ED, patients with ischemic AHF exhibit more extensive hemodynamic cardiac stress and cardiomyocyte damage than patients with nonischemic AHF.
However, the overlap is substantial, resulting in poor diagnostic accuracy.
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