Comment on “DKA-Induced Takotsubo Cardiomyopathy in Patient with Known HOCM”

Abstract EN

I very much enjoyed reading the contribution by Gordon et al., published on April 3, 2017 [1], about a 66-year-old man with known history of hypertrophic cardiomyopathy (HOCM) who suffered diabetic ketoacidosis- (DKA-) triggered Takotsubo syndrome (TTS) in the setting of newly detected diabetes mellitus (DM).

There have been 2 previously reported cases of TTS associated with DKA, mentioned by the authors as their references #4 and #6 and also summarized elsewhere [2], but that report is the 1st in the United States associating TTS, HOCM, and DKA, as they state [1].

The authors did a marvelous job in working up and managing the patient, considering the complex pathophysiology which could ensue in patients with TTS superimposed on HOCM with previously detected intraventricular gradient and systolic anterior motion of mitral valve, further compounded by the triggering pathology of new DM with complicated DKA.

The authors discuss the importance of the DKA-induced increases in serum catecholamines [1, 3], although in patients with established DM a decrease in norepinephrine and epinephrine release by the autonomic sympathetic nervous system and the adrenals, respectively, is also reported [4].

Although it has been reported that patients with TTS have low prevalence of DM, in comparison with the general population [4], there is still a close association of TTS and DM; in a meta-analysis of all 32,809 patients collectively reported as case series in the international literature, 17% had DM, and in 1,083 patients individually reported, 10.2% had DM [4].

Probably the 10.2% reflects the actual TTS-DM association, since the 17% refers to large cohorts of patients, encompassing repeated reporting of expanding groups of patients with TTS from the same world research centers.

The elevated HgbA1c (11.8%) suggests that DM was present for some time; however, the exact onset of DM cannot be ascertained in this patient.

Perhaps the authors could supply some information, whether the patient continued to show evidence of DM after the recovery from TTS and whether he had evidence of peripheral neuropathy or other end-organ diabetic changes, which occasionally presage the emergence of chronic hyperglycemia of chemical DM.

Indeed, a neurologic work-up in the reported patient with HOCD, DM, and TTS is indicated.