QJM Advance Access originally published online on May 4, 2007
QJM 2007 100(6):335-343; doi:10.1093/qjmed/hcm028
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Cardiac autonomic imbalance in patients with reversible ventricular dysfunction takotsubo cardiomyopathy
From the 1Division of Cardiology, Department of Internal Medicine, St Marianna University School of Medicine, Kawasaki, Japan,2Division of Applied Cachexia Research, Center for Cardiovascular Research, Charité Campus Mitte, Berlin, Germany,3Cardiology Unit, Department of Medical Pathophysiology, University La Sapienza, Rome, Italy and4Division of Laboratory Medicine, St Marianna University School of Medicine, Kawasaki, Japan
Address correspondence to Dr Y.J. Akashi, Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2161 Sugao Miyamae-district, Kawasaki-city, Kanagawa-prefecture, 2168511, Japan. email: johnny{at}marianna-u.ac.jp
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Background: Although in reversible takotsubo cardiomyopathy (TC), wall motion generally recovers dramatically within a few weeks, there are few data on changes in autonomic function in this condition.
Aim: To investigate cardiac autonomic function in the acute and chronic phases of TC.
Methods: Ten patients with TC (mean age 70.1 ± 13.7 years) underwent cardiac catheterization on the first hospital day, when left ventricular (LV) ejection fraction (EF) was calculated. A Holter electrocardiographic study was performed within 3 days after the onset of symptoms (0 months) and 3 months after discharge (3 months). The standard deviation of the mean cycle length of normalnormal RR (NN) intervals over 24 h (SDNN), and the 24-h standard deviation of the mean value of the difference between the NN intervals for each 5-min segment (SDANN), were calculated according to time-area analysis of heart rate variability over 24 h. Frequency domain analysis was also done.
Results: Coronary angiography in the acute and chronic phases revealed no significant stenosis in any TC patient. LV wall motion returned to normal in 17.6 ± 6.4 days. LVEF was 45.7 ± 8.8% in the acute phase and 69.8 ± 6.8% after the improvement of wall motion (p < 0.001). Between 0 months and 3 months, SDNN and SDANN improved significantly, from 88.8 ± 35.5 to 109.5 ± 33.4 ms (p = 0.01) and from 79.9 ± 34.7 to 99.3 ± 40.3 ms (p = 0.03), respectively. No significant changes were observed in frequency domain parameters.
Discussion: These results support our previous hypothesis that TC might be caused by neurogenic stunning of the myocardium, due to acute autonomic dysfunction.