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Dr. Rishard Sear
Cases Journal
Dear Dr. Richard Sear,
we have some considerations about your comments.
Recently Hahn et al. showed some differences between patients with apical and non
apical ballooning; the firth (non apical ballooning syndrome) have cardiogenic shock or
pulmonary edema on admission less frequently than the typical apical syndrome;
furthermore they suggested that wall motion abnormalities in patients with non apical
ballooning resolve more rapidly than in those with apical ballooning. Moreover they
showed that atypical transient left ventricular ballooning may develop in patients with fewer
coronary risk factors than classic left ventricular apical ballooning.
Some authors have reported in the past that vasospasm of the coronary artery caused
acute and reversible cardiomiopathy in a few patients (Tsuchihashi et al. J Am Coll Cardiol
2001; Karisu et al Am Heart J 2002). In our case report the total absence of changes of
aspect of the right coronary artery at the ostial tract, before and after injection of nitrates, is
not in favour of a ostial spasm.
Furthermore the hypothesis that the ventricular ballooning syndrome is an expression of
an acute myocarditis is not confirmed be the rare cases in which endomyocardial biopsy
(Abe et al. J Am Coll Cardiol 2003) and CMR were performed (Sharkey et al. Circulation
2005)
As described in the text the apical preponderance of ballooning is not understood.
Although myocardial responsiveness to adrenergic stimulation is increased in the apical
myocardium, norepinephrine content is lower in the apex than in the base; furthermore
heterogeneous nerve distribution exists in the human heart. The apex may not be more
vulnerable to cathecolamine excess than mid ventricle, the base or other walls in all
patients. Rather, individual variation in the regional myocardial vulnerability may determine
the location of regional wall motion abnormality. This evidence can explain the atypical
localization of ventricular ballooning.
In our case the diagnosis of atypical “tako – tsubo – like” syndrome was based on many
factors: sex, age, clinical picture, mild elevation of myocardial markers, ttoal absence of
coronary lesions, akinesia of a little district of the left ventricle with absolute normalization
after the acute phase. In the cases so far described the absence of coronary artery was
defined as “absence of significant angiographic stenosis”; Ibanez et al (Heart 2005) have
documented, through an intravascular ultrasound, plaque rupture in a limited number of
patients.
Finally in the literature we found two cases with atypical ventricular ballooning involving
the anterior wall described by Suzuki et al. (Intern Med 2004) after discontinuation of
intake of alcohol in a person from ethanol and Mazzarotto et al. (Ital Heart J Suppl 2005) in
a young woman.
So, according to all these data, we confirm our diagnosis of atypical left ventricular
ballooning involving the inferior wall