The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of
ticlopidine are reviewed.
Ticlopidine appears to inhibit platelet aggregation induced by
adenosine diphosphate.
Ticlopidine hydrochloride is rapidly absorbed after
oral administration, and maximum antiplatelet effects occur one to three hours after the dose. In multicenter, randomized, double-blind trials,
ticlopidine was more effective than
aspirin or placebo in preventing
stroke,
myocardial infarction, or death caused by vascular events.
Ticlopidine was more effective than
aspirin in preventing recurrent
transient ischemic attacks after six months of
therapy.
Ticlopidine has also been used to prevent occlusion and improve patency of
aortocoronary bypass grafts, to prevent ischemic
ulcers in patients with chronic
arterial occlusive disease, and to slow the progression of
diabetic microangiopathy. The most serious adverse effect,
neutropenia, occurred in about 1% of patients. The most frequently reported adverse effects are
diarrhea,
nausea,
vomiting, and
abdominal cramps.
Ticlopidine is indicated for reducing the risk of
thrombotic stroke in patients who have experienced a minor
stroke,
transient ischemic attack, or completed
thrombotic stroke. The recommended dosage is 500 mg/day in two divided doses taken with food.
Ticlopidine is an alternative agent for the primary and
secondary prevention of
stroke. Because of the risk of
neutropenia and
agranulocytosis and the high cost of
therapy,
ticlopidine should be reserved for patients who are intolerant of or lack benefit from
aspirin.