vasospazm

Vasospasm, also written as vasospazm in some languages, is a sudden and reversible constriction of a blood vessel, most often an artery, leading to reduced blood flow and tissue perfusion. It can affect vessels in different organs, with cerebral, coronary and peripheral vasospasm having the greatest clinical relevance.

In the brain, cerebral vasospasm commonly occurs after subarachnoid hemorrhage due to ruptured aneurysms and can cause delayed cerebral ischemia. In the heart, coronary vasospasm (often referred to as Prinzmetal or variant angina) produces transient chest pain and ischemic ECG changes. Peripheral vasospasm affects small arteries, notably in the digits, as seen in Raynaud’s phenomenon.

Pathophysiology involves contraction of vascular smooth muscle driven by imbalances between vasodilators and vasoconstrictors, endothelial injury, inflammation, and osmotic or oxidative stress. Calcium influx into smooth muscle cells, endothelin release, reduced nitric oxide availability, and sympathetic nervous system activity contribute to the constriction and its variability over time.

Risk factors include vascular injury (especially after subarachnoid hemorrhage), atherosclerosis, smoking, cocaine or other vasoconstrictive drugs, cold exposure, and autoimmune conditions. Diagnosis relies on clinical suspicion supported by imaging: transcranial Doppler or CT/MR angiography for cerebral vasospasm; ECG monitoring and coronary imaging for coronary vasospasm. Laboratory tests may exclude alternative causes of ischemia.

Treatment is location-specific. Cerebral vasospasm is managed with calcium channel blockers such as nimodipine, blood pressure optimization, and, in refractory cases, endovascular therapies with vasodilator infusions or angioplasty. Coronary vasospasm typically responds to calcium channel blockers and nitrates. The prognosis varies by location and severity, with cerebral vasospasm after subarachnoid hemorrhage posing a substantial risk of lasting deficits.