N-Terminal Pro-Brain Natriuretic Protein Levels in Takotsubo Cardiomyopathy
Do N-terminal probrain natriuretic peptide (NT-proBNP) levels correlate with inflammatory markers, catecholamines, and/or cardiopulmonary hemodynamics in takotsubo cardiomyopathy (TCC)?
Consecutive patients (n = 56) with TCC underwent echocardiography and laboratory assessment (NT-proBNP, troponin, C-reactive protein, normetenephrine levels) at baseline, 10 days, and 3 months after diagnosis. All patients underwent angiogram at baseline to exclude significant coronary disease and n = 34 and n = 42 had a right heart catheterization and cardiac magnetic resonance imaging (MRI), respectively, on index presentation. Correlations between NT-proBNP, baseline wedge pressure, wall stress by MRI, and wall motion score index by echocardiogram were examined using Spearman’s correlation analysis.
The mean ± standard deviation patient age was 69 ± 11 years, 96% (n = 54) were female, and 81% had experienced an acute stressor in life. At baseline, mean left ventricular ejection fraction (LVEF) was 53 ± 13%, 100% had an elevation of troponin T (median [interquartile range] = 0.32 [0.2-0.55]), and 36% had ST elevation on admission electrocardiogram. Median baseline NT-proBNP level was 1325 [448, 4284] pg/ml) at presentation, and levels increased significantly (NT-proBNP = 4382 [2440, 9019] pg/ml, p = 0.001) within 24 hours of presentation, with a slow and incomplete normalization by 3 months. Median baseline plasma norepinephrine concentrations (998 [547, 1144 pmol/L) were significantly correlated (r = 0.53, p = 0.001) with peak NT-proBNP levels. Correlations with C-reactive protein were weak (r = 0.3, p = 0.05). Likewise, NT-proBNP correlated with baseline LVEF (r = -0.39, 0.008) and the extent of impaired wall motion (r = 0.37, p = 0.008) found on echocardiogram. No significant correlation was found between NT-proBNP levels and baseline wedge pressures (mean 15 ± 7 mm Hg; r = 0.10, p = 0.58) or regional LV systolic wall stress by MRI. LVEF (62 ± 10%) and wall motion index 10 days after presentation did not correlate with follow-up NT-proBNP (p > 0.05).
The authors concluded that TTC is associated with elevated NT-proBNP levels, and these levels correlate with catecholamine increases and decrements in LV systolic function.
The authors provide interesting insight into TCC. By demonstrating that NT-proBNP continues to increase after admission, they suggest that the hormone increment is likely the result of increased synthesis rather than release of pre-formed peptides in response to catecholamine stress. Baseline wedge pressures and wall stress by MRI did not correlate with natriuretic peptide levels, and no correlation was noted between NT-proBNP and follow-up LVEF and wall motion index. The authors hypothesize that NT-proBNP and its continued elevation may be related to nonhemodynamic cardiac stressors. Since catecholamine stress is associated with myocardial calcium toxicity (contraction band necrosis) and inflammation (cytokines, interleukins) is a cardiac depressant, perhaps unmeasured extracellular and intracellular biochemical imbalances and perturbations are at play in this interesting disease.
Keywords: C-Reactive Protein, Biological Markers, Takotsubo Cardiomyopathy, Cardiac Catheterization, Catecholamines, Magnetic Resonance Imaging, Hemodynamics, Troponin, Echocardiography, Natriuretic Peptide, Brain
< Back to Listings