Is coronary vasospasm really the cause of Takotsubo syndrome?

I enjoyed reading the case report by McKernan et al (1) and the accompanying editorial by Schussler (2), published in the April 2014 issue, about a 77-year-old woman who suffered Takotsubo syndrome (TTS) following a thoracic epidural steroid injection for postherpetic neuralgia. The authors and the editorialist opined appropriately that many factors, along with the procedure, had conspired for the emergence of TTS in this patient. However, what surprised me was the statement of the editorialist about the cause of TTS, that “it is becoming clearer that the final common pathophysiology pathway may be coronary spasm, although the details remain to be worked out,” citing the work by Patel et al (3). Patel et al studied the coronary vascular reactivity (both coronary epicardial and microvascular responses) of 10 women at a median of 5 months after an episode of TTS, employing intracoronary infusions of acetylcholine, nitroglycerine, and adenocine, and measured the percent change in coronary vessel diameter and in coronary blood flow. The authors found in their patients mild epicardial vasoconstriction, and markedly decreased coronary blood flow reserve, in comparison with a reference cohort of 211 women from their laboratory (3). Although Patel et al documented severe, primarily microcirculatory, impairment in these 10 patients with prior TTS, which conceivably “may be a central feature of the pathophysiology of TTS,” they added that “since the coronary physiological assessment was performed after the episode of TTS, we cannot be certain as to whether the abnormality on coronary vasomotion detected was present prior to the onset of the cardiomyopathy.” Considering that many myocardial derangements (e.g., myocardial edema and electrocardiogram QTc interval prolongation) persist long after the normalization of the left ventricular function after a bout of TTS, it is imperative that an assessment of the epicardial vessel and microcirculation function be carried out many more months after full recovery of patients after TTS. Otherwise, what was found by Patel et al (3) may not be the cause, but the consequence (epiphenomenon), a lingering effect of the affliction. Indeed, one could go further to speculate that even chronic microcirculation dysfunction in some postmenopausal women may predispose them to TTS (facilitator), in the emergence of a pathophysiological mechanism (cause) not yet discovered.

Kudos

The white coat lecture by Dr. Knowlan is so thoughtful. Would it be possible to get offprints of the speech to place in my waiting room? As always, I really enjoy reading the BUMC Proceedings.

—Sam Marynick, MD

Dallas, Texas