Ahtarovski, Kiril Aleksov1; Iversen, Kasper Karmark7; Christensen, Thomas Emil3; Andersson, Hedvig1; Grande, Peer1; Holmvang, Lene1; Bang, Lia1; Hasbak, Philip3; Lønborg, Jacob Thomsen1; Madsen, Per Lav1; Engstrøm, Thomas1; Vejlstrup, Niels Grove1
1 Hjertemedicinsk Klinik, Hjertecentret Rigshospitalet, Rigshospitalet, The Capital Region of Denmark2 Department of Cardiology, Nephrology and Endocrinology, Nordsjællands Hospital, The Capital Region of Denmark3 Klinik for Klinisk Fysiologi, Nuklearmedicin og PET, Diagnostisk Center, Rigshospitalet, The Capital Region of Denmark4 Traumecenter og Akut Modtagelse, HovedOrtoCentret Rigshospitalet, Rigshospitalet, The Capital Region of Denmark5 Medical Center, Amager and Hvidovre Hospital, The Capital Region of Denmark6 Department of Cardiology, Medical Center, Amager and Hvidovre Hospital, The Capital Region of Denmark7 Cardiology, Herlev and Gentofte Hospital, The Capital Region of Denmark
AIMS: Takotsubo cardiomyopathy (TTC) is an entity mimicking acute myocardial infarction, characterized by transient severe systolic heart failure. Echocardiographic studies suggest that diastolic dysfunction is present in TTC at presentation; however, no reports exist regarding the time course of left ventricular (LV) recovery. This study describes the recovery of LV systolic and diastolic function in TTC. We hypothesized that, in TTC, there is diastolic dysfunction at admission, and that recovery is delayed compared with systolic function. METHODS AND RESULTS: We enrolled (consecutively 2010-12) 16 patients (mean age 66, range 39-84 years) diagnosed with TTC and 20 healthy matched controls. We performed cardiac magnetic resonance imaging (CMR) at admission, pre-discharge, and 3-month follow-up. Diastolic function was assessed by LV peak filling rate (LVPFR) and left atrial (LA) emptying volumes. At admission, LV ejection fraction was low, increased at pre-discharge (37 ± 6 vs. 58 ± 6%, P < 0.001), and normalized at follow-up (to 65 ± 5%, P = 0.01). LVPFR did not increase during hospitalization (80 ± 3 vs. 89 ± 4 mL/s/m(2), P = 0.21), but was normalized at follow-up (to 206 ± 19, P < 0.001; controls, 214 ± 13, P = 0.23). During hospitalization, LA passive emptying volume remained low (6 ± 2 vs. 8 ± 3 mL/m(2), P = 0.05) and LA active emptying volume remained high (17 ± 3 vs. 16 ± 3 mL/m(2), P = 0.71), whereas LA conduit volume increased (7 ± 3 vs. 23 ± 4 mL/m(2), P < 0.001). T2-weighted imaging demonstrated non-coronary distributed apical oedema without contrast enhancement. CONCLUSION: Patients with TTC undergo fast systolic recovery. However, at discharge, profound diastolic dysfunction is demonstrated by CMR. At follow-up, both LV systolic and diastolic function is normalized in patients with recovered TTC.
European Heart Journal Cardiovascular Imaging, 2014, Vol 15, Issue 8, p. 855-62