Transient left ventricular dysfunction syndrome: patho-physiological bases through nuclear medicine imaging.

BACKGROUND: Takotsubo cardiomyopathy (TTC) is a novel heart disease, mimicking acute myocardial infarction. The term "transient left ventricular dysfunction syndrome" (TLVDS) seems to be more appropriate since variant forms of TTC sparing apical segments (mid-ventricular ballooning syndrome (MVBS) and inverted TTC) have been described. Patho-physiological bases of TLVDS remain poorly understood and its optimal management is until now empirical. Our aim was to characterize patho-physiological mechanisms of TLVDS by means of nuclear medicine procedures and to discuss the clinical usefulness of isotopic imaging for a non-invasive diagnosis of TLVDS. METHODS AND RESULTS: During the sub acute phase, eighteen patients with TLVDS (13 TTC and 5 MVBS) underwent myocardial (99m)Tc-tetrofosmin or (201)Thallium Gated Single Photon Emission Computed Tomography (G-SPECT) (n=11), (123)I-mIBG SPECT (n=8) and (18)F-FDG Gated Positron Emission Tomography (G-PET) (n=15), assessing respectively LV perfusion, sympathetic innervation and glucose metabolism. Hypocontractile LV segments were characterized by normal perfusion but reduced uptake of (18)F-FDG and (123)I-mIBG. Topography and extent of metabolic defects and innervation abnormalities were largely overlapping. Follow-up (123)I-mIBG SPECT and (18)F-FDG G-PET were performed in selected patients showing rapid normalization of LV motion and progressive improvement of both glucose metabolism and sympathetic innervation. DISCUSSION: With the hypothesis of neurogenic stunned myocardium as the central causative mechanism of TLVDS, (123)I-mIBG SPECT seems to be the most specific diagnostic technique. Sympathetic function and glucose metabolism seem to be strictly correlated in the hypocontractile LV segments. Finally, our results underline the role of nuclear imaging in the setting of patho-physiological mechanisms of TLVDS.

Importance of inflammation and neurohumoral activation in Takotsubo cardiomyopathy.

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.