Acute ischemic coronary artery disease and ischemic stroke: similarities and differences.
Although acute myocardial infarction (MI) and acute ischemic stroke share similarities, physicians need to recognize important differences in pathophysiology and how these differences affect acute treatment and prevention to provide optimal patient care. Potential causes of acute ischemic stroke are substantially more heterogeneous than for acute MI, and available acute therapies are substantially more limited. In acute ischemic stroke patients, diagnostic evaluation is paramount in determining eligibility for treatment with the only approved therapy, which must be administered within 3 hours after stroke onset. For patients having acute MI, reperfusion therapy by percutaneous intervention or thrombolytic drug therapy is well established. Because atherosclerosis is a common pathway to acute MI and acute ischemic stroke, modifying associated known risk factors is required for primary and secondary prevention of both conditions. Pharmacologic therapies recommended for secondary prevention include beta-blockers and angiotensin-converting enzyme inhibitors for MI, oral anticoagulants for stroke, and statins and antiplatelet agents for both conditions. Aspirin is recommended for preventing recurrence of both MI and stroke; agents inhibiting the adenosine diphosphate pathway of platelet activation, such as ticlopidine and clopidogrel, are also beneficial. Recent studies suggest the benefits associated with adding aspirin to clopidogrel do not outweigh the significant increase in bleeding risk. The synergistic effects of aspirin plus extended-release dipyridamole make this combination twice as effective than aspirin alone in secondary prevention of ischemic stroke. An ongoing study is directly comparing the combination of aspirin plus extended-release dipyridamole with clopidogrel for the prevention of recurrent stroke.
Fisher
Marc
M
Department of Neurology, Division of Cardiology, University of Massachusetts Medical School, Worcester, MA 01605, USA. fisherm@ummhc.org
Folland
Edward
E
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D020521:Stroke / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000925:Anticoagulants; D005343:Fibrinolytic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors