Cardiac autonomic activity in patients with transient left ventricular apical ballooning.

To the Editor: Transient left ventricular apical ballooning (AB) is characterized as a reversible apical balloon-like left ventricular wall motion abnormality. In contrast to patients with acute myocardial infarction (MI), patients with AB do not have obstructive coronary heart disease (CHD) and experience almost complete recovery of cardiac function. Excess sympathetic activity and cardiac sympathovagal disbalance seems to play a major part in the origin of this syndrome. Experimental data suggest high catecholamine plasma concentrations and activation of cardiac adrenoreceptors (1); however, cardiac sympathovagal activity has not yet been studied in patients with AB. The aim of the present study was to investigate differences in reflex and tonic sympathovagal activity in patients with AB compared with patients with successfully reperfused acute anterior MI. We investigated 11 consecutive patients undergoing coronary angiography with clinical signs of ST-segment elevation acute MI who fulfilled morphologic criteria of AB in the left ventricular angiography: balloon-like left ventricular wall motion abnormality at the apex and absence of obstructive CHD. Exclusion criteria were history of a previous MI or structural/valvular disease, pheochromocytoma, myocarditis, atrial fibrillation, left bundle branch block, pacemaker rhythm and rhythm other than sinus, and invalid Holter electrocardiograph (ECG) recordings. Nine of 11 consecutive age-, gender-, BMI-, and left ventricular function-matched patients with ST-segment elevation acute MI who underwent successful direct percutaneous coronary intervention (PCI) of a proximal total occlusion of the left anterior descending artery within 12 h after onset of chest pain served as a control group. All patients underwent 24-h ECG recordings on the third day after hospital admission. Time and frequency domain heart rate variability (HRV) parameters were measured according to the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (2). Heart rate turbulence (HRT) was analyzed after single ventricular premature beats, as previously described (3). Continuous and categorical variables were compared with the Student t test and the Mann-Whitney U test. Data are presented as mean SD. A two-tailed significance level of 0.05 was used for the analyses. Among the 11 patients with AB, 9 fulfilled the clinical and technical inclusion criteria. There were no significant differences regarding demographic variables, left ventricular ejection fraction, medication, and TIMI risk score (4) between groups (Table 1). Peak cardiac enzyme release was significantly higher in MI patients. Measurements of HRT and HRV are depicted in Table 2. Standard deviation of NN intervals (SDNN) and high-frequency component were significantly higher in the AB group. Lowfrequency/high-frequency ratio revealed a shift towards sympathetic predominance in MI patients compared with AB patients. The AB patients also exhibited significantly higher values for turbulence slope. Mean RR-intervals tended to be higher in AB patients. The present study is the first to investigate cardiac sympathovagal activity in patients with AB. The principal finding was that, in contrast to matched patients with reperfused anterior MI, tonic and reflex autonomic activity is preserved in the subacute phase of AB. This observation might suggest a rapid attenuation of cardiac autonomic impairment in the subacute phase of AB, resulting in electrical stability and reduced oxygen demand of the affected myocardium. Although AB clinically mimics ST-segment elevation MI, invasive and laboratory findings suggest a nonischemic cause of the disease. Recent data suggest that excess sympathetic activity play a major role in the origin of the syndrome. In the majority of patients, history of emotional or physiological stress was observed immediately before the onset of the acute event. Interestingly, there are contrary results, thus far, regarding circulating catecholamine concentrations in AB (5). Owa et al. (6) suggested apical disturbance of cardiac sympathetic innervation and perfusion/innervation discrepancy as the origin of AB. The hypothesis of excess sympathetic activation in AB is