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DOI 10.1161/strokeaha.107.497362

Медицинская библиотека · Stroke · 2008

Vasomotion in multiple spontaneous cervical artery dissections.

Baracchini Claudio, Tonello Simone, Vitaliani Roberta, Giometto Bruno, Meneghetti Giorgio, Ballotta Enzo

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Аннотация

BACKGROUND AND PURPOSE: The etiology of spontaneous cervical artery dissection (sCAD) is still unknown, even though an underlying arteriopathy impairing vasomotion has often been suspected. This study was undertaken to investigate: (1) spontaneous, (2) endothelial-dependent, and (3) endothelial-independent vasodilation in patients with multiple sCAD.

METHODS

In 19 consecutive patients with multiple carotid or vertebral artery dissections high-resolution ultrasound was used to assess spontaneous and endothelial-independent dilations (isosorbide dinitrate-mediated) in the common carotid, vertebral and brachial arteries, and endothelial-dependent dilation (flow-mediated arterial dilation) in the brachial arteries alone. The same parameters were measured in 19 healthy subjects matched for age, sex, and height (controls). Ultrasound studies were performed by one investigator, and off-line analysis by another investigator who was blinded to the clinical data and study status (patient or control).

RESULTS

Spontaneous and endothelial-independent dilations were significantly impaired in the carotid (P=0.0006 and P<0.0001, respectively) and vertebral arteries (P=0.0121 and P=0.0047, respectively) of patients as compared with controls, whereas no statistically significant differences were found in the brachial arteries; conversely, endothelial-dependent dilation of the brachial arteries was significantly lower in patients as compared with controls (P<0.0001).

CONCLUSIONS

Patients with multiple sCADs have a significantly impaired vasomotion, which may predispose to dissection.

Для цитирования: Baracchini Claudio, Tonello Simone, Vitaliani Roberta, Giometto Bruno, Meneghetti Giorgio, Ballotta Enzo. Vasomotion in multiple spontaneous cervical artery dissections.. Stroke. 2008. DOI: 10.1161/strokeaha.107.497362.

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