Thrombotic strokes can affect large or small arteries in the brain. Drugs to prevent
atherosclerosis complication such as
thrombotic strokes, should be drugs able to prevent the accumulation of intravascular fat, reduce vascular proliferation, decrease blood pressure levels with the resulting shear stress, reduce platelet aggregation, and possibly partially or totally reverse carotid plaques. Any of the commonly used
antihypertensive drugs lower the incidence of
stroke, with larger reductions in BP resulting in larger reductions in risk. Experimental and clinical data suggest that reducing the activity of the renin-angiotensin aldosterone system (RAAS) may have beneficial effects beyond the lowering of blood pressure to reduce
stroke incidence. In clinical trials,
statins consistently reduced the risk of
ischemic stroke in patients with or without CHD whereas the data on the effects of other
lipid modifying drugs on
stroke risk are limited. Approximately 25% of
strokes are recurrent. Antiplatelet
therapy is indicated for the prevention of recurrent
stroke in patients with a history of noncardioembolic minor
stroke or
transient ischemic attack (TIA). Although clinicians may choose
acetylsalicylic acid (ASA) as first-line
therapy for
secondary prevention, clinical guidelines and evidence from trials suggest that ASA may not be the most effective strategy. A recent review discussed results from clinical trials that have compared the efficacy of ASA monotherapy versus ASA + extended release
dipyridamole in secondary
stroke prevention. Therefore it is difficult to extrapolate the real benefit of pharmacological prevention strategies against atherothrombotic subtype for excellence in the TOAST classification subtype that is represented by the LAAS and also with regard to lacunar subtype as an expression of lipohyalinosis process which is a further aspect of
atherosclerosis.