Copyright © 2007, The European Society of Cardiology
Microvascular dysfunction in left apical ballooning syndrome: Primary cause or secondary phenomenon?
Cardiology, Department of Cardiological, Thoracic and Vascular Sciences, Centro "V. Gallucci", University of Padova-Policlinico, Via Giustiniani 2, 35128 Padova, Italy
Received 8 May 2007; .
* Corresponding author. Tel.: +39 49 8212348; fax: +39 49 876 1764. francescotona{at}hotmail.com
We read with great interest the recent report from Meimoun et al.1 indicating the time course of transthoracic coronary flow reserve in the left anterior descending artery in a patient who suffered a transient left apical ballooning syndrome. The authors conclude that serial non-invasive measurements of coronary flow reserve in that case suggest transient impairment of the coronary microcirculation during the acute phase of the syndrome. The improvement of the microcirculation parallels the regression of the wall motion abnormalities suggesting a relationship between these two features.
Several pathophysiological mechanisms have been proposed to explain the unusual features of this syndrome, such as multivessel coronary vasospasm, catecholamine-mediated cardiotoxicity and abnormalities in coronary microvascular function.2 However, the precise aetiology and pathophysiology of this syndrome remain unknown.
Some authors evaluated the microcirculation using Doppler guidewire or contrast echocardiography.3,4 Their findings suggest that abnormalities in the coronary microcirculation do not contribute significantly to the syndrome. In contrast, other authors found that TIMI frame count, a validated index of coronary blood flow, was significantly higher in patients with transient left ventricular apical ballooning syndrome when compared with controls during both acute phase and follow-up.5,6 These investigators interpreted their findings as indicative of diffuse coronary microvascular dysfunction and suggested that this abnormality may play a significant role in the pathogenesis of this syndrome.
In the paper of Meimoun et al. as well as in the other reports, the presence of a myocarditis has not been excluded. As recently stated in the "Mayo Clinic Criteria" for the diagnosis of the left ventricular apical ballooning syndrome, a key point is the exclusion of myocarditis.7 According to the current WHO definition, the diagnosis of myocarditis is based upon endomyocardial biopsy, using the Dallas histological criteria with the adjunct of immunological and immunohistochemical criteria.8 In the lack of the biopsy, magnetic resonance imaging may suggest though not prove myocarditis.9 Meimoun et al. did not perform either endomyocardial biopsy or magnetic resonance imaging.
Diminished coronary flow reserve associated with wall motion abnormalities, has been described in animal models and in patients with biopsy-proven myocarditis. Klein et al. described 29 patients with biopsy-proven inflammatory infiltrates and coronary flow reserve impairment, suggesting that the coronary reserve is diminished in most patients with inflammatory heart disease.10 This may be due to the involvement of the intramural coronary vasculature in inflammatory heart disease. Saraste et al. recently demonstrated that coronary flow reserve, measured with transthoracic Doppler echocardiography, is reduced in coxsackievirus myocarditis in mice.11
Moreover, the most common presenting clinical symptoms of apical ballooning syndrome are chest pain and dyspnoea. However, most serious clinical presentations such as cardiogenic shock and ventricular fibrillation are frequent.2 All these clinical symptoms are also common in myocarditis.
Therefore the improvement of the microcirculation with the regression of the wall motion abnormalities suggests the diagnosis of myocarditis. We think that if myocarditis is not excluded, it is inappropriate to suggest that microvascular dysfunction is an etiopathogenetic factor in the apical ballooning syndrome. It remains unclear whether microvascular dysfunction is the primary cause of the syndrome or a secondary phenomenon.
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- Meimoun P., Malaquin D., Benali T., Tribouilloy C. Assessment of coronary flow reserve by transthoracic Doppler echocardiography in left apical ballooning syndrome. Eur J Echocardiogr (2007) doi:10.1016/j.euje.2007.01.002.
- Gianni M., Dentali F., Grandi A.M., Summer G., Hiralal R., Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J (2006) 27:1523–1529.
[Abstract/Free Full Text] - 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] - Kurisu S., Inoue I., Kawagoe T., Ishihara M., Shimatami Y., Nakamura S., et al. Time course of electrocardiographic changes in patients with tako-tsubo syndrome: comparison with acute myocardial infarction with minimal enzymatic release. Circ J (2004) 68:77–81.[CrossRef][Web of Science][Medline]
- Gibson C.M., Cannon C.P., Daley W.L., Dodge J.T. Jr., Alexander B. Jr., Marble S.J., et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation (1996) 93:879–888.
[Abstract/Free Full Text] - Bybee K.A., Prasad A., Barsness G.W., Lerman A., Jaffe A.S., Murphy J.G., et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol (2004) 94:343–346.[CrossRef][Web of Science][Medline]
- Prasad A. Apical ballooning syndrome. An important differential diagnosis of acute myocardial infarction. Circulation (2007) 115:e56–e59.
[Free Full Text] - Richardson P., McKenna W., Bristow M., Maisch B., Mautner B., O'Connell J., et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation (1996) 93:841–842.
[Free Full Text] - Mahrholdt H., Goedecke C., Wagner A., Meinhardt G., Athanasiadis A., Vogelsberg H., et al. Cardiovascular magnetic resonance assessment of human myocarditis. A comparison to histology and molecular pathology. Circulation (2004) 109:1250–1258.
[Abstract/Free Full Text] - Klein R.M., Schwartzkopff B., Gabbert H.E., Strauer B.E. Diminished coronary reserve in patients with biopsy-proven inflammatory infiltrates. Cardiology (2003) 100:120–128.[CrossRef][Web of Science][Medline]
- Saraste A., Kyto V., Saraste M., Vuorinen T., Hartiala J., Saukko P. Coronary flow reserve and heart failure in experimental coxsackievirus myocarditis. A transthoracic Doppler echocardiography study. Am J Physiol Heart Circ Physiol (2006) 291:H871–H875.
[Abstract/Free Full Text]
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