With the exception of near-occlusion, CEA is of overall benefit for selected patients with recent symptomatic carotid stenosis =50% (NASCET method), provided surgical stroke/death risk is low. The benefit is greater with greater stenosis, men, the elderly (aged =75y), most recent ischaemic event within 2w, irregular plaque surface, and impaired cerebral perfusion reserve. Patients with recent symptomatic carotid territory ischaemic events should be screened by Doppler ultrasonography, MRA, or CTA, confirming substantial stenosis with a second non-invasive investigation. Catheter angiography may be required to confirm uncertain results. The surgical peri-operative stroke and death rate (7% in RCTs) is higher in women, hypertension, peripheral arterial disease, and occlusion of the contralateral ICA or ipsilateral ECA. The experience of the surgeon and hospital are crucial, and audited peri-operative complication rates should be publically available. Carotid stenting is less invasive than CEA and causes fewer local complications (cranial neuropathy and neck haematoma), but carries a higher procedural risk of stroke. Stenting should be considered in younger patients, or those at increased risk from CEA. While stenting is of high risk for intracranial vertebral artery stenosis, risk is low for extracranial stenosis and should be considered for recurrent symptoms despite optimal medical therapy.

For hypertensive patients without prior stroke, TIA, or other symptomatic vascular disease, anti-hypertensive therapy reducing SBP by 10 mm Hg, is associated with reductions in recurrent stroke (by about one-quarter) and of combined stroke, MI, and vascular death (by about one-fifth). Benefit extends across all ages, race-ethnicities, and pathological stroke subtypes. Combined pharmacological and non-pharmacological therapy to lower blood pressure is indicated in all individuals with SBP> 140 or DBP> 90, and in individuals with SBP 130–139 or DBP 80–89 who have additional vascular risk factors. Non-pharmacological blood pressure lowering is indicated in individuals with SBP 130–139 or DBP 80–89 without important additional vascular risk factors. After an ischaemic stroke or TIA, treatment may be gradually started as early as 24–72 hours after onset. The absolute benefits of antihypertensive therapy increase with greater reductions in BP, and are higher for preventing recurrent stroke than for preventing MI, in both primary and secondary prevention. The degree of BP reduction more greatly influences vascular event prevention than does pharmacological agent class. Nonetheless, unless otherwise indicated, beta-blockers are not a preferred agent, as they show less efficacy for stroke prevention. Calcium channel antagonists, ACE inhibitors, and thiazide diuretics are particularly well-studied.

In broad, relatively unselected patients with acute ischaemic stroke, immediate high-dose anticoagulation therapy to avert early stroke progression or recurrence reduces recurrent ischaemic stroke compared with control during the treatment period but this benefit is offset by an increase in intracranial haemorrhage (ICH) and extracranial haemorrhage (ECH). Immediate antiplatelet therapy has similarly efficacy as anticoagulation in averting early stroke progress or recurrence, and is safer when used as an immediate agent (see Chapter 9). In acute ischaemic stroke patients with atrial fibrillation, after start of antiplatelet therapy on presentation, early switchover to anticoagulation therapy 2 -14 days after stroke onset is reasonable, but caution should be taken in certain subgroups of patients with high risk of bleeding. In broad, relatively unselected ischaemic stroke patients, low-dose, venous prophylaxis anticoagulation compared with control reduces the occurrence of asymptomatic deep venous thrombosis (DVT) and shows a tendency to reduce pulmonary embolism, but also shows off-setting tendencies to increase ICH and ECH, without conferring a clear net clinical benefit. Low-molecular-weight heparins (LMWH) or heparinoids, compared with unfractionated heparin, appear to further decrease the occurrence of DVT and PE but potentially further increase ICH, but there are too few data to provide reliable information.

In the year 2010, an estimated 16.9 million strokes occurred worldwide at an incidence rate of 258 per 100,000 persons per year. Approximately 70% of these strokes occurred in low- and middle-income countries. The 16.9 million incident strokes were added to a pool of 33 million prevalent stroke survivors. There were 5.9 million deaths and 102 million disability-adjusted life-years (DALYs) lost due to stroke in 2010, making stroke the second leading cause of death and the third leading cause of DALYs worldwide. In the preceding two decades, between 1990 and 2010, the incidence rate of stroke remained stable but the absolute number of incident strokes increased by 68%, the prevalence rate increased modestly yet the absolute number of stroke survivors nearly doubled, the rate of DALYs lost due to stroke decreased but the absolute number of DALYs lost increased by 12%, and the mortality rate fell but the absolute number of stroke-related deaths increased by 26%. Most of the burden of stroke is in low-income and middle-income countries, which bear 63% of incident ischaemic strokes and 80% of haemorrhagic strokes. The average age of incident ischaemic and haemorrhagic strokes was 6 years younger in low- and middle– than high–income countries.

Aspirin 160–300 mg daily started within 48 h of onset of acute ischaemic stroke is associated with a small beneficial reduction in recurrent ischaemic stroke (6 fewer per 1000 patients treated) and pulmonary embolism (1.5 fewer per 1000) that outweighs increased risk of bleeding (2 extra symptomatic ICHs and 4 extra major extracranial haemorrhages). The net effect is that, for every 1000 patients treated early with aspirin, 22 have reduced long-term disability, including 11 more achieving full recovery. Only two single antiplatelet regimens have been compared head to head against aspirin alone: cilostazol (a phosphodiesterase inhibitor) performed similarly to aspirin; ticagrelor (a GP IIa/IIIb receptor antagonist) showed tended to reduce ischaemic events but increased minor bleeding and dyspnea. In minor, non-cardioembolic ischaemic stroke or TIA, early dual antiplatelet therapy (DAPT) has shown advantages over early monotherapy. Most well-studied is clopidogrel and aspirin, with similar findings for dipyridamole and aspirin. DAPT reduces all-type (ischaemic and haemorrhagic) recurrent stroke (27 fewer per 1000 treated patients), but minimally increases major extracranial bleedings (3 more per 1000). Confining DAPT to the first 3 w maximizes the benefit to harm ratio. Anticoagulants alone and arterial-dose anticoagulants added to antiplatelet agents offer no net advantages over antiplatelet drugs alone. Venous prophylaxis-dose anticoagulants and aspirin, compared with aspirin alone, reduced recurrent ischaemic stroke more than it tend increased major extracranial haemorrhage.