The refreshing report of Rao et al. 1 about 2 patients with reversible mitral regurgitation (MR), left ventricular (LV) outflow tract pressure gradient (LVOTPG), and systolic anterior motion (SAM) of the mitral valve, attributed to Takotsubo syndrome (TTS), who were admitted with a picture of acute coronary syndrome, strikes a chord for this author, preoccupied for some time with the notion that transient MR and/or LV wallmotion abnormalities (WMAs) with subsequent amelioration, or complete resolution at repeat echocardiography (ECHO), observed particularly in postmenopausal women are formes frustes of TTS, and are common. 2 Although the 2 cases presented by the authors are very convincing, as to the underlying pathophysiology, one wonders whether milder cases of MR, without LVOTPG and SAM, and/or WMAs, represent cases of TTS. The authors, discussing the mechanism of the SAM-related MR in TTS, attribute it to the "the hyperdynamic function of the basal LV walls in response to apical akinesis," modeled after the hyperdynamic response of the noninfarcted myocardium in patients with an acute myocardial infarction-induced akinetic/dyskinetic territory. However, there is a possibility that in TTS the hypercontractility of the basal region and the akinesis/dyskinesis of the LV apex are "part and parcel" of the pathophysiological neuromechanical derangement, mediated by the catecholamine-induced stimulation of the b 1-, and b 2 -adrenergic receptors, and the latter's switch from cardiostimulatory to cardiodepressive functionality. 3,4 It is conceivable that if the dynamic character of the WMAs noted in the rat model of TTS, 4 is also found in the human TTS, the degree of MR, LVOTPG, SAM, and WMAs is continuously varying in the clinical course of the disease. Of course this is not appreciated with the currently implemented routine of obtaining one ECHO on admission, usually after coronary arteriography, and a repeat ECHO prior to discharge or at followup aimed at confirming restoration of LV function to the baseline. Accordingly, it is conceivable that the MR, LVOTPG, and SAM of the 2 presented patients was even more severe earlier in their clinical course; the electrocardiograms of the 2 patients on admission showed T-wave inversions which usually follow the very acute phase of TTS characterized by ST-segment elevations. Greater pathophysiological insights of TTS are going to be gained only by very frequent implementation of ECHOs particularly during the hyperacute and acute phase of the disease, starting in the Emergency Room upon arrival of patients, suspected of TTS. Perhaps ECHOs performed with handheld devices, and employed as often as currently the stethoscope is used to monitor patients, may be required to unravel the dynamic course of patients with TTS. This may not be the solution, but there should not be any doubt that ECHO, in some form, will provide the answers.
References1. Rao RV, Wright D, Dokainish H: Acute mitral regurgitation in suspected acute coronary syndrome: What is the cause? Echocardiography 201...