LETTER TO THE EDITOR
Transient left ventricular apical ballooning and outflow tract obstruction: Reply
Yoshiteru Abe, MD
Division of Cardiology, Shimada Municipal Hospital, 1200-5 Noda, Shimada City, Shizuoka, 427-8502, Japan
y-a{at}zephyr.dti.ne.jp
We appreciate the comments and acknowledge the concerns of Dr. Penas-Lado and colleagues regarding the etiology of transient left ventricular apical ballooning described in our report (1). It may be quite reasonably argued that transient dynamic left ventricular outflow tract obstruction contributes to the pathogenesis of this syndrome (2). Tsuchihashi et al. (3) speculated on the inclusion of stress cardiomyopathy caused by vigorous stress (catecholamine exposure), dynamic midventricular obstruction due to basal hypercontraction, and/or secondary myocardial ischemia (increased wall tension) as an important etiological cause of this syndrome. However, they reported that only 18% of patients (12/72 patients) had left ventricular outflow tract obstruction and an intraventricular pressure gradient >30 mm Hg during the acute phase.
We did not discuss findings of left ventricular outflow tract obstruction in our report (1) for the following reasons. No patient showed left ventricular outflow tract obstruction with an intraventricular pressure gradient >30 mm Hg among 9 patients who underwent pressure recording during catheter withdrawal from the left ventricle and/or an accelerated flow in the left ventricular outflow tract in any of the 17 patients who underwent Doppler echocardiography during the acute phase. Moreover, little evidence was seen of geometric predisposition (sigmoid intraventricular septum, small left ventricular outflow tract, abnormal orientation of a slack mitral apparatus, reduced left ventricular volume) in our patients. However, pathological findings of the specimen obtained from left ventricular endomyocardial biopsy during the acute phase differed from those of myocardial ischemia (1,3,4). Moreover, Tawarahara et al. (5) recently reported a variant type of reversible severe left ventricular wall-motion abnormality of the basal segment with hypercontraction at the apex. It was considered that left ventricular outflow obstruction did not contribute to the etiology of this type of transient left ventricular abnormality. Thus, these findings suggested that left ventricular outflow obstruction was not a primary cause of this syndrome.
Kono et al. (6) reported that the mechanism of neurogenic stunned myocardium in patients with subarachnoid hemorrhage was mediated by the direct toxic effect of norepinephrine. Mann et al. (7) demonstrated the mechanism of catecholamine-mediated cardiac toxicity was that adrenergic stimulation leads to cyclic AMP-mediated calcium overload of cultures of adult cardiac muscle cells exposed to norepinephrine. Doshi et al. (8) reported that individual necrotic muscle fibers surrounded by macrophages and inflammatory cells and small foci of inflammatory cells between the muscle fibers with or without the presence of necrotic muscle fibers were observed histologically in patients with subarachnoid hemorrhage. These reports suggest that the direct toxicity of catecholamines could lead to myocyte damage.
Because none of our patients demonstrated neither significant left ventricular outflow tract obstruction nor intraventricular pressure gradient nor the evidence of geometric predisposition in our study, left ventricular outflow obstruction was not considered a primary cause. Therefore, we considered that this syndrome might be caused by the direct toxicity of catecholamines.
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References
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- Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol. 2003;41:737–742[Abstract/Free Full Text]
- Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning and left ventricular outflow tract obstruction. Mayo Clin Proc. 2001;76:79–83[Medline]
- Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol. 2001;38:11–18[Abstract/Free Full Text]
- Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy ("Takotsubo" cardiomyopathy)—reversible left ventricular dysfunction with ST segment elevation. Jpn Circ J. 2000;64:156–159[CrossRef][Medline]
- Tawarahara K, Matoh F, Odagiri K, Saitoh N. Nuclear cardiac imaging in "Tsubo-like (Pod-like)" transient left ventricular dysfunction. Jpn Circ J. 2001;65(Suppl 1A):420
- Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol. 1994;24:636–640[Abstract]
- Mann DL, Kent RL, Parsons B, Cooper G IV. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation. 1992;85:790–804[Abstract/Free Full Text]
- Doshi R, Neil-Dwyer G. A clinicopathological study of patients following a subarachnoid hemorrhage. J Neurosurg. 1980;52:295–301[Medline]
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