Affiliations: St. Luke’s Hospital, Bethlehem, PA,
Department of Cardiology, University Hospital Schleswig-Holstein, Campus Luebeck, Germany
Correspondence to: Sudip Nanda, MD, Department of Internal Medicine, St. Luke’s Hospital, 801, Ostrum St, Bethlehem, PA 18015; e-mail: firstname.lastname@example.org
We read with great interest the recent article in CHEST (September 2007) by Kurowski et al1and congratulate the authors for defining the frequency of stress cardiomyopathy. In addition to apical and mid-ventricular types of stress cardiomyopathy, other variants exist, and we have reported a new variant.2
The most common mechanisms suggested for stress cardiomyopathy are coronary vasospasm and catecholamine injury. Patients with stress cardiomyopathy, when compared with those with myocardial infarction, have markedly elevated plasma catecholamine levels, and this leads to the hypothesis of catecholamine-injury.3Variant cases with preserved distal territory contraction and dyskinetic proximal territory cannot be explained by vasospasm. Myocardial glucose metabolism was affected more than perfusion between 2 and 6 days and subsequently between 6 and 12 days after presentation. Kurisu et al4 have reported impairment of myocardial fatty acid metabolism with 123I-beta methyl-p-iodophenyl pentadecanoic acid (or BMIPP) initially at mean (± SD) time of 5 ± 3 days and subsequently at 29 ± 6 days after presentation. The heart normally acquires energy from glucose and fatty acid under well-oxygenated conditions when both are available. Failures to use either substrate in the presence of good perfusion suggest abnormalities in oxidation at the cellular level. Cyclic adenosine monophosphate (cAMP) modulates the enzymes involved in either oxidative pathway, and catecholamines are significant modulators of cAMP. An increased cAMP level causing reduced K+ channel activity will prolong depolarization and QT interval, as is frequently noticed in this disease. This implies a role for cAMP at some point in the pathogenesis.
Receptors mediating an increase in cAMP level include adrenergic β1, β2, and β3, and adenosine A2. Adrenergic α2, adenosine A1, and muscarinic M2 and M3 decrease cAMP levels. The differential distribution of such receptors in the myocardium will make different areas more susceptible. A recently described5 variant of stress cardiomyopathy had ventricular dyskinesia involving varying regions of the left ventricle at different hospital admissions. Myocardial receptor distribution may be a dynamic process, and assays will need to be performed at different times to track this process.
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
The authors have no conflicts of interest to disclose.
We fully agree with the authors’ statement1that stress cardiomyopathy may phenotypically present in different variants and, as we have described in our recent study,2is not limited to the apical region (“apical ballooning”). In addition to impairment of the left ventricle (“left ventricular dysfunction syndrome”), there is rising evidence that Tako-Tsubo cardiomyopathy can also effect the right ventricle.3
The recent and novel observation that recurrent episodes of Tako-Tsubo cardiomyopathy may even result in different patterns of left ventricular dysfunction4 can indeed be best explained by the fact that the location of wall motion abnormality is most likely not determined by preexisting anatomic structures (eg, the distribution or density of autonomic nerves) but is rather the result of a functional disarray (eg, on the level of receptors expression or the subsequent transmitter system).
It is well known that endogenous norepinephrine released from presynaptic sympathetic nerve endings is a significant modulator of cyclic adenosine monophosphate (cAMP). In a very recent functional study,5 we found a pronounced impairment of cardiac sympathetic neurotransmission related to the region of wall motion abnormality in patients with Tako-Tsubo cardiomyopathy. Since inhomogenous activation or differential distribution of β-adrenergic receptors may subsequently result in an impaired accumulation of cardiac cAMP, it is reasonable to assume that alterations in cAMP levels represent a potential pathophysiologic link for the impairment of left ventricular function found in patients with Tako-Tsubo cardiomyopathy.
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