Regional alterations in myocardial sympathetic innervation in patients with transient left-ventricular apical ballooning (Tako-Tsubo cardiomyopathy)

Abstract

Background: Excess sympathetic nervous activity was proposed to play a crucial role in the pathogenesis of transient left-ventricular apical ballooning (TLVAB, also known as Tako-Tsubo cardiomyopathy). This study was conducted to assess presynaptic adrenergic alterations in the dysfunctional myocardium of patients with TLVAB.

Methods and results: Ten consecutive patients undergoing coronary angiography for acute coronary syndrome who fulfilled the proposed Mayo Clinic criteria for the diagnosis of TLVAB were investigated. Myocardial iodine-123 metaiodobenzylguanidine ((123)I-MIBG) studies (planar and single-photon emission computed tomography [SPECT]) were performed to evaluate adrenergic innervation. Concomitantly, myocardial perfusion was assessed by means of technetium-99m methoxyisobutylisonitrile ((99m)Tc-MIBI) SPECT. In all patients, angiography revealed typical ballooning of the left-ventricular (LV) apex and hyperkinesis of the basal LV segments (overall ejection fraction, 41% +/- 5% [mean +/- SEM]). Planar (123)I-MIBG scans revealed decreased heart-to-mediastinum ratios at early (20 minutes) and delayed (4 hours) images (2.1 +/- 0.1 and 1.9 +/- 0.1, respectively). The cardiac washout rate of (123)I-MIBG on the late images was increased to 34% +/- 3%. The (123)I-MIBG uptake on SPECT scans was obviously reduced in the akinetic LV apex (defect score, 3.30 +/- 0.34), whereas (99m)Tc-MIBI SPECT indicated normal or only mildly reduced perfusion within this region (defect score, 0.89 +/- 0.35).

Conclusions: Our study indicates a functional alteration in presynaptic sympathetic neurotransmission in patients with TLVAB, and suggests a pathophysiologic explanation of the impairment of LV function.