vasospasme

Vasospasm, or vasospasme in French, is the sudden, sustained narrowing of a blood vessel due to contraction of vascular smooth muscle. This reduces distal blood flow and can cause tissue ischemia. It can involve any vessel but is most clinically important in the brain and the coronary arteries.

Cerebral vasospasm commonly follows aneurysmal subarachnoid hemorrhage and is a major cause of delayed cerebral ischemia. Coronary vasospasm occurs with or without underlying coronary disease and produces episodic chest pain and ischemia. Vasospasm can also affect peripheral arteries, such as the digital vessels.

Pathophysiology is multifactorial. In cerebral vasospasm, breakdown products of blood irritate vessels and disrupt autoregulation; endothelin-1, reduced nitric oxide, oxidative stress, inflammation, and smooth muscle hyperreactivity contribute. In coronary vasospasm, hyperreactivity of smooth muscle and endothelial dysfunction play similar roles, sometimes triggered by cocaine, nicotine, or other stimulants.

Clinical features: After SAH, patients may develop new focal deficits or altered consciousness about 3–14 days later. Coronary vasospasm presents with chest pain and transient ECG changes. Peripheral vasospasm presents with color changes or pain in affected limbs.

Diagnosis: Cerebral vasospasm is assessed with transcranial Doppler ultrasound, CT perfusion, or arterial angiography. Coronary vasospasm is suspected with ischemic symptoms and ECG changes and confirmed by coronary angiography showing vasoconstriction.

Treatment: For cerebral vasospasm, nimodipine, careful fluid management, and sometimes induced hypertension; refractory cases may need intra-arterial vasodilators or angioplasty. For coronary vasospasm, calcium-channel blockers and nitrates are used; identify and avoid triggers; urgent reperfusion if infarction occurs.

Prognosis: Outcomes depend on severity and prompt treatment; untreated cerebral vasospasm can cause stroke or death, while prompt management improves prognosis.