Vasospastica

Vasospastica refers to episodes of constriction of the smooth muscle in blood vessel walls, resulting in a reduced luminal diameter and diminished blood flow. The term can describe normal physiologic responses to cold or stress, as well as pathologic processes in several conditions. Notable examples include coronary vasospasm (variant angina), cerebral vasospasm after subarachnoid hemorrhage, and peripheral vasospasm seen in Raynaud phenomenon.

The underlying mechanism involves increased vascular smooth muscle reactivity, endothelial dysfunction, and an imbalance between vasodilators and vasoconstrictors. Endothelial-derived factors such as nitric oxide may be reduced, while constrictive mediators like endothelin can be elevated. Autonomic nervous system influences and external triggers (smoking, cocaine or other vasoconstrictors, cold exposure) can precipitate episodes.

Diagnosis depends on the clinical context and targeted testing. Coronary vasospasm is evaluated with patient history and angiography, sometimes using provocative testing. Cerebral vasospasm is monitored with imaging such as transcranial Doppler, CT or MRI perfusion studies after subarachnoid hemorrhage. Peripheral vasospasm is typically assessed clinically, with duplex ultrasonography or other vascular imaging as indicated.

Management centers on prevention and relief of symptoms. Calcium channel blockers are commonly used to reduce episodes, with nitrates for vasodilatory relief. In cerebral vasospasm after subarachnoid hemorrhage, nimodipine is frequently employed. Avoidance of triggering agents (eg, tobacco, illicit drugs) and treatment of associated conditions are important. The prognosis varies with the underlying cause and promptness of treatment; some patients experience recurrent episodes, while others have single events with complete recovery. Etymology derives from Latin vas, vessel, and Greek spasmos, spasm.