The Weight of Tissue Plasminogen Activator Dose in Overweight Patients With Strokes

Abstract

See related article, page 1615–1620 Obesity is a widespread problem, particularly in the cardiovascular disease and stroke population. The combination of hypertriglyceridemia, glucose intolerance, and inflammation is linked with increased production of the primary inhibitor of endogenous thrombolysis, plasminogen activator inhibitor-1, leading to deficient thrombolysis in overweight patients. Enhanced fibrin crosslinking has been shown to be, at least partially, responsible for delayed clot lysis among obsesses. Moreover, body mass index was directly associated with fibrinogen, Factor VII, plasminogen activator inhibitor-1 and tissue plasminogen activator (tPA) antigen, von Willebrand factor, and viscosity. In contrast, body mass index itself had no impact on in-hospital mortality in patients undergoing primary percutaneous coronary interventions for acute myocardial infarction. Obese patients with acute myocardial infarction have a lower risk for in-hospital, 6-month, and 12-month mortality and cardiovascular events than patients with a normal body mass index.1 This “obesity paradox” may be explained by the fact that obese patients were younger at presentation. tPA dose for stroke (0.9 mg/kg alteplase, maximum 90 mg) was chosen based on small dose-escalation studies. This body weight-based dose has …