Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens' ECG pattern) in Tako-Tsubo cardiomyopathy.
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BACKGROUND
Tako-Tsubo cardiomyopathy (TTC) presents with chest pain, ST-segment elevation followed by T-wave inversion and QT interval prolongation (Wellens' electrocardiographic [ECG] pattern), and left ventricular dysfunction, which may mimic an acute coronary syndrome.
OBJECTIVE
To assess the pathophysiologic basis of the Wellens' ECG pattern in TTC by characterization of underlying myocardial changes by using cardiac magnetic resonance (CMR).
METHODS
The study population included 20 consecutive patients with TTC (95% women; mean age 65.3 ± 10.4 years) who underwent CMR studies both in the initial phase and after 3-month follow-up by using a protocol that included cine images, T2-weighted sequences for myocardial edema, and post-contrast sequences for late gadolinium enhancement. Quantitative ECG indices of repolarization, such as maximal amplitude of negative T waves, sum of the amplitudes of negative T waves, and maximum corrected QT interval (QTc max), were correlated to CMR findings.
RESULTS
At the time of initial CMR study, there was a significant linear correlation between the apicobasal ratio of T2-weighted signal intensity for myocardial edema and the maximal amplitude of negative T waves (ρ = 0.498; P = .02), sum of the amplitudes of negative T waves (ρ = 0.483; P = .03), and maximum corrected QT interval (ρ = 0.520; P = .02). Repolarization indices were unrelated to either late gadolinium enhancement or quantitative cine parameters. Wellens' ECG abnormalities and myocardial edema showed a parallel time course of development and resolution on initial and follow-up CMR studies.
CONCLUSIONS
Our study results show that the ischemic-like Wellens' ECG pattern in TTC coincides and quantitatively correlates with the apicobasal gradient of myocardial edema as evidenced by using CMR. Dynamic negative T waves and QTc prolongation are likely to reflect the edema-induced transient inhomogeneity and dispersion of repolarization between apical and basal left ventricular regions.
