LETTER TO THE EDITOR
Transient left ventricular apical ballooning and outflow tract obstruction
Manuel Penas-Lado, MD*
* Complexo Hospitalario de Pontevedra, Cardiology Service, Mourente-Montecelo, Pontevedra, Galicia 36071 Spain
Roberto Barriales-Villa, MD, FESC* and
Javier Goicolea, MD
manuel.penas.lado{at}sergas.es
In the interesting syndrome of transient left ventricular apical ballooning (TLVAB) without coronary artery stenosis mimicking acute myocardial infarction, originally described by Tsuchihashi et al. (1), clinical manifestations in most patients were preceded by severe physical or emotional stress, suggesting a catecholamine-mediated mechanism. In a recent issue of the Journal, Abe et al. (2) described the clinical characteristics of a new series of 17 patients with TLVAB and disscuss and investigate different possible pathogenic mechanisms for this syndrome. The investigators could not identify any specific cause, suggesting neurogenic myocardial stunning induced by emotional or physical stress as the most probable etiology. Surprisingly, the previously suggested (1) possible role of a transient dynamic left ventricular outflow tract (LVOT) obstruction in the pathogenesis of this syndrome was not investigated by these researchers, who did not even mention the possible existence of such gradients in their patients. However, we believe there is much evidence indicating that this relation actually exist. In fact, a transient dynamic LVOT gradient was detected at initial evaluation in a substantial proportion of the patients described by Tsuchihashi et al. (1), and in other cases of this syndrome described elsewhere (3,4). In these patients, the clinical and hemodynamic situation improved as the gradient disappeared. Moreover, in some of the patients presenting with cardiogenic shock, this situation persisted until the dynamic obstruction was diagnosed and specifically treated (3).
Thus, at least in some patients, a possible mechanism for TLVAB could be a dynamic LVOT obstruction preceding the ischemic event. Once present, the dynamic obstruction elevates left ventricular filling pressures, increasing myocardial oxygen demand at the mid-to-apical cavity. If this situation persists, apical hypoperfusion and ischemia may result, with eventual apical infarction. In fact, it is well known that, even in normal hearts, exposure to an exogenous catecholamine, such as dobutamine infusion, can precipitate dynamic LVOT obstruction (5). Some patients, primarily women, may have geometric predisposition (sigmoid interventricular septum, small LVOT, reduced left ventricular volume) to dynamic LVOT obstruction, which may manifest only in the setting of intense adrenergic stimulation or hypovolemia (3,5). In these susceptible patients, increased adrenergic tone might produce primary LVOT obstruction leading to secondary ischemia and focal wall-motion abnormalities. Thus, the intense physical or emotional stress that precedes apical ischemia in most patients with TLVAB could be the trigger for the acute development of LVOT obstruction capable of producing severe apical ischemia.
Identification of acute dynamic LVOT obstruction as the possible initial mechanism in some of these patients may have important clinical and therapeutic implications, as the use of traditional measures to treat patients with chest pain and evidence of myocardial ischemia, including nitrates and afterload reduction, would actually increase the LVOT gradient, causing further clinical deterioration, while abolishing the gradient (with beta-blockers, intravenous fluids, or alpha-adrenergic receptor stimulation) might be beneficial and even life-saving (3). Moreover, treatment for secondary prevention would depend also on the suspected underlying mechanism. Eventually, in those patients in whom an acute dynamic LVOT obstruction mechanism is suspected, the possibility of performing tests of provocation, such as dobutamine stress echocardiography, should be considered.
 |
References
|
|---|
1. 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]
2. 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]
3. Haley JH, Sinak LJ, Tajik AJ, Ommen SR, Oh JK. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock. Mayo Clin Proc. 1999;74:901–906[Abstract]
4. Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning and left ventricular outflow tract obstruction. Mayo Clin Proc. 2001;76:79–83[Abstract]
5. Luria D, Klutstein MW, Rosenmann D, Shaheen J, Sergey S, Tzivoni D. Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography. Eur Heart J. 1999;20:386–392[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
C.-C. Fang, Yeun Tarl Fresner Ng Jao, Yi-Chen, C.-L. Yu, C.-L. Chen, and S.-P. Wang
Transient Left Ventricular Apical Ballooning Syndrome: The First Series in Taiwanese Patients
Angiology,
May 1, 2008;
59(2):
185 - 192.
[Abstract]
[PDF]
|
|
|
|
Top
References