class=""h4"">BackgroundTo 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).class=""h4"">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 c; .01). CRP levels were correlated to baseline left ventricular ejection fraction (LVEF) and BNP levels (P c; .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.
class=""h4"">Conclusion
Inflammatory status in TTC was related to LVEF impairment and to the extent of neurohormonal activation. The hypothesis of a catecholamine-induced myocardial ȁc;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.
