Importance of Inflammation and Neurohumoral Activation in Takotsubo Cardiomyopathy

Abstract 

Background

To gain more insight into the involvement of inflammatory response and neurohumoral activation in Takotsubo cardiomyopathy (TTC), we investigated C-reactive protein (CRP), leukocytes, plasma catecholamines levels, iodine 123 meta-iodobenzylguanidine (¹²³I-mIBG) myocardial uptake, myocardial perfusion (thallium 201 [²⁰¹Tl] or technetium [Tc] 99m-tetrofosmin myocardial single photon emission computed tomography [SPECT]), and metabolism (fluorine 18-fluorodeoxyglucose positron emission tomography).

Methods and Results

Inflammatory status and brain natriuretic peptide (BNP) levels in 17 patients with TTC were compared with 14 age-matched patients. In TTC, elevated levels of CRP were evidenced on admission, reaching a peak in the following days (P < .01). CRP levels were correlated to baseline left ventricular ejection fraction (LVEF) and BNP levels (P < .05). Leukocytes were correlated to BNP and noradrenaline levels. Myocardial ¹²³I-mIBG SPECT showed a reduced activity in the midventricle and apex corresponding to 35% ± 23% of the total myocardial mass, partially reversible at follow-up. An identical pattern was retrieved when assessing myocardial glucose metabolism. At rest, no relevant abnormalities of myocardial perfusion could be evidenced at the subacute phase.

Conclusion

Inflammatory status in TTC was related to LVEF impairment and to the extent of neurohormonal activation. The hypothesis of a catecholamine-induced myocardial “stunning” is emphasized by the evidence of a reduced ¹²³I-mIBG myocardial activity, impairment of myocardial glucose metabolism, and wall motion kinetic after the same temporospatial distribution.

Key Words: Takotsubo cardiomyopathy, plasma catecholamines, ballooning syndrome, myocardial stunning, inflammatory response, brain natriuretic peptide