Manuel Vidalón1. 1. Department of Cardiology and Neurology, Promitra Center for Research and Treatment of Stress, São Carlos Hospital, Curitiba, Brazil.
Abstract
OBJECTIVE: The aim of the present study was to evaluate cardiac performance of patients with migraine attacks during the overload produced by phenylephrine infusion. Background.-It is known that circulatory changes occur during migraine. However, the relationship between this finding and transient cardiac dysfunction is still unknown. METHODS: By means of two-dimensional direct M-mode echocardiography, we measured fractional shortening, ejection fraction, and mean velocity of circumferential fibers shortening in 18 patients with migraine and in 10 normal subjects as a control group. These measures were performed in two different periods: during attack-free intervals and during attacks. Pain intensity of typical migraine attack was evaluated on a 0 to 10 scale. RESULTS: Cardiac size and function were normal at rest in both groups. However, during migraine attacks, phenylephrine infusion provoked significant decrease in fractional shortening, EF, and mean velocity of circumferential fibers shortening, followed by concomitant increase of headache severity. On the other hand, during the attack-free interval and in the control group phenylephrine infusion did not show significant changes in cardiac function parameters. CONCLUSIONS: Our data suggest that left ventricular dysfunction during the phenylephrine test could participate in the complex pathophysiological mechanism of migraine attacks.
OBJECTIVE: The aim of the present study was to evaluate cardiac performance of patients with migraine attacks during the overload produced by phenylephrine infusion. Background.-It is known that circulatory changes occur during migraine. However, the relationship between this finding and transient cardiac dysfunction is still unknown. METHODS: By means of two-dimensional direct M-mode echocardiography, we measured fractional shortening, ejection fraction, and mean velocity of circumferential fibers shortening in 18 patients with migraine and in 10 normal subjects as a control group. These measures were performed in two different periods: during attack-free intervals and during attacks. Pain intensity of typical migraine attack was evaluated on a 0 to 10 scale. RESULTS: Cardiac size and function were normal at rest in both groups. However, during migraine attacks, phenylephrine infusion provoked significant decrease in fractional shortening, EF, and mean velocity of circumferential fibers shortening, followed by concomitant increase of headache severity. On the other hand, during the attack-free interval and in the control group phenylephrine infusion did not show significant changes in cardiac function parameters. CONCLUSIONS: Our data suggest that left ventricular dysfunction during the phenylephrine test could participate in the complex pathophysiological mechanism of migraine attacks.