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Human stress cardiomyopathy mimicking acute myocardial syndrome
  1. D H SPODICK
  1. Saint Vincent Hospital,
  2. 25 Winthrop Street
  3. Worcester, MA 01604–4593, USA

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    Sir,—Pavin and colleagues’1 report of “human stress cardiomyopathy” is additional evidence of the probable catecholamine basis of the characteristic T wave change. Their figures 1B, 1C, and 2B neatly fit the ECG criteria established by us in a prospective investigation of 100 patients2 with a long follow up (mean, eight years).3 Since the response is diagnostically non-specific, we termed it “global T wave inversion” and speculated that it was a catecholamine effect.2 As with Pavin and colleagues, the complete (global) response was almost never on the initial ECG and it disappeared in a matter of days.2 3 Both their patients were women, as were 81 of ours. My only criticism of their report concerns fig 1D. It is not normal: P2, P3 (but not PaVF), and PV4–6 are all inverted. The ST segments are so elongated as to resemble those in hypocalcaemia. Can the authors explain those findings? This is not to criticise, but rather to augment a nice report.

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    This letter was shown to the authors, who reply as follows:

    Dr Spodick makes a pertinent remark about fig 1D, which is not normal. This ECG shows abnormalities of the P wave that seem to be isodiphasic (±) rather than inverted in leads D2, D3, V5, and V6. Unfortunately we cannot explain these findings. Indeed, this ECG was done by the patient’s physician during a routine visit late after the events described in the report and we have no information regarding metabolic or neurohumoral state at this time. We cannot exclude atrial conduction disturbances. However, I don’t think it is of major importance in this report, as this ECG was shown to illustrate the normalisation of QRS and T wave morphology.

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