Author + information
- Jasmin Ortak, MD,
- Volkhard Kurowski, MD,
- Uwe K.H. Wiegand, MD,
- Frank Bode, MD,
- Gunther Weitz, MD,
- Iris Wilke, MD,
- Franz Hartmann, MD,
- Heribert Schunkert, MD and
- Hendrik Bonnemeier, MD⁎ ()
- ↵⁎Medizinische Klinik II, Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany
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 ttest and the Mann-Whitney Utest. 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. Low-frequency/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 supported by experimental data, showing that stress induces reversible left ventricular apical hypokinesia (1). Furthermore, in the apical region of the heart, a higher adrenergic receptor density and myocardial responsiveness to adrenergic stimulation has been described (7). The findings of the present study support the hypothesis that, not increased sympathetic autonomic activity directed to the heart, but rather, increased myocardial adrenergic responsiveness might be the underlying pathophysiologic mechanism. Indeed, low-frequency component, associated with cardiac sympathetic modulation, was not significantly elevated in AB. Furthermore, sympathovagal balance and baroreflex function were even more preserved in patients with AB. Therefore, the absence of the deleterious effects on reflex afferent and efferent autonomic function and tonic autonomic modulation in transient left ventricular AB suggest a preserved cardiac autonomic control. The blunted turbulence slope in patients with MI either suggests a faster recovery of baroreflex control in AB patients or a significant impact of coronary artery disease (CAD) on autonomic reflexes beyond acute myocardial ischemia.
Complete reperfusion of the infarct-related artery is associated with a significant restoration of baroreflex sensitivity, whereas incomplete reperfusion causes persistent impairment of baroreflex response, reflecting a more severe microvascular dysfunction (8). Despite angiographic evidence of complete epicardial perfusion, patients with MI, in contrast to patients with AB, might have a mismatch between vascular patency and myocardial perfusion. Accordingly, microvascular dysfunction has been previously ruled out also by measurements of coronary flow reserve, contrast echocardiography, and positron emission computer tomography in patients with AB (9). Serum cardiac troponin T, which is related to the amount of microvascular damage and dysfunction, was also not significantly elevated in AB patients. Therefore, significantly higher turbulence slope, surrogate marker for baroreflex sensitivity, might reflect a significant rapid improvement of the transient perfusion/innervation mismatch in AB patients.
The present study is the first to demonstrate significant differences of cardiac autonomic modulation in patients with acute ST-segment elevation MI with and without obstructive CAD. In contrast to AB patients, there is a delayed recovery of tonic and reflex autonomic nervous modulation in MI patients. These differences in autonomic modulation represent a previously unrecognized phenomenon that needs further investigation for understanding the underlying pathophysiological mechanisms in AB. Improved cardiac autonomic function might explain, in part, the rapid recovery of left ventricular function and favorable prognosis in patients with AB.
- American College of Cardiology Foundation
- Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology
- ↵Morrow DA, Antman EM, Parsons L, et al. Application of the TIMI risk score for ST elevation MI in the National Registry of Myocardial Infarction 3. JAMA 286:1356–9.
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