Neurogenic stunned myocardium vs. Takotsubo syndrome: We should stop making a distinction John E. Madias PII: DOI: Reference:

S0167-5273(14)01835-X doi: 10.1016/j.ijcard.2014.09.115 IJCA 18891

To appear in:

International Journal of Cardiology

Received date: Accepted date:

9 September 2014 20 September 2014

Please cite this article as: Madias John E., Neurogenic stunned myocardium vs. Takotsubo syndrome: We should stop making a distinction, International Journal of Cardiology (2014), doi: 10.1016/j.ijcard.2014.09.115

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Neurogenic stunned myocardium vs. Takotsubo

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syndrome: we should stop making a distinction

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John E. Madias, MD, FACC, FAHA

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Running Head: Neurogenic stunned myocardium vs. Takotsubo syndrome

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From the Icahn School of Medicine at Mount Sinai, New York, NY, and the Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY

Correspondence to John E. Madias, MD, Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, Tel: (718) 334-5005, Fax: (718) 334-5990, E-mail: [email protected]

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To the Editor:

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The data of Inamasu et al [1], published ahead of print in the

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August 23, 2014 issue of the Journal, exploring for possible differences between 12 patients with neurogenic stunned (NSM)

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to

aneurysmal

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myocardium

subarachnoid

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hemorrhage, and 19 patients with Takotsubo syndrome (TTS),

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are compelling and can make us think twice before making a

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distinction between these two entities: they are one and the same

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[2]. The Doppler E/E’ was higher in TTS than in NSM patients, difference that the authors appropriately attributed to the older

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age of the TTS patients by a mean of 14 years, and that these patients were “more likely to have had prior cardiac events” and that the “stiffened myocardium in that group might have resulted in worse diastolic dysfunction”. The higher frequency of T-wave inversion in the admission electrocardiogram (ECG) which was significantly higher in TCM than in the NSM patients is in keeping with a later presentation of the TTS than in NSM patients, as the authors commented, by which time a conversion of the 2

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ST-segment

elevations

to

ST-segment

elevations/T-wave

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inversions, or merely T-wave inversions, had taken place [3].

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Subsequent to the admission ECGs, recorded in the NSM patients, could have confirmed this assumption. The plasma epinephrine

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(EP) was 4 times as high, and the plasma norepinephrine (NE)

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was 2 times as high in NSM, than in TTS patients, and the authors are commenting on the “short half-life of epinephrine”

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[4], and that “the epinephrine/norepinephrine coefficient may

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vary substantially with the timing of blood collection”,

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presumably implying that had the TTS and NSM patients had their plasma catecholamines measured at similar times, after the

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onset of their illness, perhaps no differences would be detected in these 2 groups of patients. Are subsequent to the first assessment of plasma EP and NE available in the NSM patients, to substantiate this assumption? It is conceivable in regards to the magnitude of secretion and the role of EP and NE in the pathogenesis of TTS and NSM that: 1) there are no differences between TTS and NSM, and that the difference in plasma EP and

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NE is a reflection of the earlier clinical presentation of NSM

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patients; 2) at any time point after admission the plasma EP and

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NE are higher in NSM than in TTS; 3) the damage to the myocardium, mediated by EP and/or NE is inflicted early on in

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both TTS and NSM, and that subsequent levels of the plasma

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catecholamines are not of any significant pathogenetic relevance; 4) EP and NE continue to exert a myocardial damaging effect in

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both SM and TTS; and 5) EP and NE continue to exert a

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myocardial damaging effect in the case of NSM, but not in TTS.

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All the above could only become clarified by serial echocardiography

assessment,

and

repeat

EP

and

NE

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measurements in patients with TTS and NSM.

Conflicts of interest None.

References 1. Inamasu J, Watanabe E, Okuda K, et al. Are there differences

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between Takotsubo cardiomyopathy and neurogenic stunned

Aug

23.

pii:

S0167-5273(14)01629-5.

doi:

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2014

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myocardium? A prospective observational study. Int J Cardiol.

10.1016/j.ijcard.2014.08.084. [Epub ahead of print].

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2. Madias JE. Why the current diagnostic criteria of Takotsubo

2014 Jul 1;174(3):468-70.

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syndrome are outmoded: a proposal for new criteria. Int J Cardiol.

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3. J.E. Madias. Plausible mechanisms of the rapid conversion of

Int J Cardiol, 168 (2013), pp. 4593–4595.

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syndrome

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ST-segment elevation to T-wave inversion in Takotsubo

4. A.R. Lyon, P.S. Rees, S. Prasad, P.A. Poole-Wilson, S.E. Stress

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Harding.

(Takotsubo)

cardiomyopathy:

a

novel

pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med, 5 (2008), pp. 22–29.

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