Abstract
Dear Sir,
We read with great interest the article ‘Status migrainosus as a potential stressor leading to takotsubo cardiomyopathy’ by Jalan et al. (1). The authors present an important clinical observation on a presumably underestimated relationship between migraine and takotsubo cardiomyopathy. By presenting a similar case vignette we wish to emphasize this hypothesis.
A hitherto healthy 48-year-old woman developed for the first time blurred vision and scotoma, followed by a severe throbbing headache in the right temporo-parietal region. She felt pronounced phono- and photophobia and preferred to stay in bed. As the symptoms continued she took some over-the-counter analgesics. She described her headache as unbearable and as the most severe in her life. As her pain continued over 48 hours she consulted neurological care. The clinical neurological examination revealed a normal neurological status. Cranial computed tomography (CCT) was unremarkable, as was lumbar puncture. The patient received intravenous paracetamol leading to an improvement of her headache. The ECG on admission showed T-wave inversion in V3 to V6, I, II, aVL and aVR (Figure 1) prompting cardiological examination.
The 12-lead-electrocardiogramm (10 mm/mV; 50 mm/s; filter 50 Hz) on admission showed T-wave inversion in aVL, I, aVR, II, and V3 to V6.
Troponin T high was 0.017 ng/ml (normal <0.1). Echocardiographically a slightly impaired systolic left ventricular function was detected. The left ventricle was dilated (left ventricular endiastolic 61 mm) and the apex of the heart was hypokinetic. The cardiac catheter examination confirmed these findings and takotsubo syndrome was diagnosed. The coronary arteries were unremarkable without any signs of obstructive coronary disease. From the history the patient did not suffer severe migraine attacks and had had no thoracic complaints. However, some days before she had reported psychological stress due to familiar differences. The institutional regular work-up of takotsubo cardiomyopathy did not reveal other pathologies (2).
The coincidence of a severe prolonged migraine attack with visual disturbances on the one side and cardiological abnormalities according to the diagnosis of takotsubo cardiomyopathy on the other side raises the question on a potential causal relationship. Jalan and co-workers describe in detail the current knowledge on such a connection proposing increased catecholamine levels in migraine as the pathophysiological basis for takotsubo cardiomyopathy (1). Otherwise a vice versa scenario is thinkable, whereby a stress-induced takotsubo cardiomyopathy can trigger a migraine attack as is known from some patients with acute stroke (3). Also psychological stress itself, as the patient reported, can be a common precursor of both migraine and takotsubo cardiomyopathy. Along with Jalan et al., we wish to sensitize our colleagues on a possible link between migraine and takotsubo cardiomyopathy.