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Background: Feedback on “quality indicators” collected from chart audit is a widely used quality-improvement strategy. Skeptics argue that temporal change in practice patterns or improvement of documentation as a result of implementation of chart audit can affect change in quality indicators rather than change in practice due to feedback. This study compared the effectiveness in quality improvement for stroke care of chart audit and feedback versus chart audit only. Methods: Data were examined on quality indicators constructed from the performance measures abstracted from chart audit for 1953 stroke patients admitted to 13 hospitals. Seven of the 13 hospitals were provided with feedback on quality indicators from baseline audit, and 6 hospitals had chart audit only. Results: Least-squares estimation was used to estimate the adjusted mean change in quality indicators between follow-up and baseline audits and differences in mean change between feedback and nonfeedback groups. Differences in adjusted mean change (with 90% confidence interval) were: deep vein thrombosis prophylaxis, 8.46 (−9.46 to 26.38); dysphagia screening, −3.78 (−21.37 to 13.81); antithrombotic therapy within 48 hours of hospitalization, 3.63 (−6.59 to 13.84); discharged on antithrombotic, −0.31 (−6.26 to 5.63); patients with atrial fibrillation discharged on warfarin/coumadin, 44.73 (−13.14 to 102.60); lipid screening, 19.93 (2.99 to 36.86); and smoking counseling, 17.47 (−12.13 to 47.08). Conclusions: Although not statistically significant, results suggest a potential for improvement with data feedback. There is a need for evaluation of the effectiveness of a multifaceted approach in a community setting. [Copyright &y& Elsevier]

Thrombotic thrombocytopenic purpura (TTP) is a fulminant disease characterized by platelet aggregates, thrombocytopenia, renal insufficiency, neurologic changes, and mechanical injury to erythrocytes. Most idiopathic cases of TTP are characterized by a deficiency of ADAMTS13 (a disintegrin and metalloprotease, with thrombospondin-1-like domains) metalloprotease activity. Ironically, use of anti-platelet agents, the thienopyridine derivates clopidogrel and ticlopidine, is associated with drug induced TTP. Data were abstracted from a systematic review of English-language literature for thienopyridine-associated TTP identified in MEDLINE, EMBASE, the public website of the Food and Drug Administration, and abstracts from national scientific conferences from 1991 to April 2008. Ticlopidine and clopidogrel are the two most common drugs associated with TTP in FDA safety databases. Epidemiological studies identify recent initiation of anti-platelet agents as the most common risk factor associated with risks of developing TTP. Laboratory studies indicate that most cases of thienopyridine-associated TTP involve an antibody to ADAMTS13 metalloprotease, present with severe thrombocytopenia, and respond to therapeutic plasma exchange (TPE); a minority of thienopyridine-associated TTP presents with severe renal insufficiency, involves direct endothelial cell damage, and is less responsive to TPE. The evaluation of this potentially fatal drug toxicity can serve as a template for future efforts to comprehensively characterize other severe adverse drug reactions.Kidney International (2009) 75, S20–S24; doi:10.1038/ki.2008.613 [ABSTRACT FROM AUTHOR]

Objectives: We sought to describe clinical and laboratory findings for a large cohort of patients with thienopyridine-associated thrombotic thrombocytopenic purpura (TTP). Background: The thienopyridine derivatives, ticlopidine and clopidogrel, are the 2 most common drugs associated with TTP in databases maintained by the U.S. Food and Drug Administration (FDA). Methods: Clinical reports of TTP associated with clopidogrel and ticlopidine were identified from medical records, published case reports, and FDA case reports (n = 128). Duration of thienopyridine exposure, clinical and laboratory findings, and survival were recorded. ADAMTS13 activity (n = 39) and inhibitor (n = 30) were measured for a subset of individuals. Results: Compared with clopidogrel-associated TTP cases (n = 35), ticlopidine-associated TTP cases (n = 93) were more likely to have received more than 2 weeks of drug (90% vs. 26%), to be severely thrombocytopenic (84% vs. 60%), and to have normal renal function (72% vs. 45%) (p < 0.01 for each). Compared with TTP patients with ADAMTS13 activity >15% (n = 13), TTP patients with severely deficient ADAMTS13 activity (n = 26) were more likely to have received ticlopidine (92.3% vs. 46.2%, p < 0.003). Among patients who developed TTP >2 weeks after thienopyridine, therapeutic plasma exchange (TPE) increased likelihood of survival (84% vs. 38%, p < 0.05). Among patients who developed TTP within 2 weeks of starting thienopyridines, survival was 77% with TPE and 78% without. Conclusions: Thrombotic thrombocytopenic purpura is a rare complication of thienopyridine treatment. This drug toxicity appears to occur by 2 different mechanistic pathways, characterized primarily by time of onset before versus after 2 weeks of thienopyridine administration. If TTP occurs after 2 weeks of ticlopidine or clopidogrel therapy, therapeutic plasma exchange must be promptly instituted to enhance likelihood of survival. [Copyright &y& Elsevier]

The Duke Treadmill Score (DTS) has been shown to predict mortality in women who have symptomatic heart disease, but its ability to do so in asymptomatic women is unknown, as is its comparative advantage to exercise capacity. We investigated whether a decreased DTS is associated with increased mortality in a prospective cohort of 5,636 asymptomatic women. A symptom-limited exercise treadmill test using Bruce’s protocol was performed at baseline. DTS was calculated using exercise time, exercise-induced angina, and ST-segment depression. Exercise capacity was measured in METs. Deaths and cause of death were identified from 1992 to 2000. After adjusting for the Framingham Risk Score, the risk of death decreased by 9% for each unit increase in DTS and by 17% for every 1-MET increase (p &#60;0.001). Those who had a DTS &#60;5 (moderate or high risk) had hazard ratios for death and cardiac death that were 2.2 and 2.5 times greater, respectively, than did those who had a DTS ≥5 (low risk), after adjusting for Framingham Risk Score (p &#60;0.001). Receiver-operating characteristic curves for the DTS model and the exercise capacity model were not significantly different. In conclusion, we have demonstrated that, although the DTS is an independent predictor of mortality and cardiac mortality in asymptomatic women, it does not appear to be a better predictor than exercise capacity alone. The role of ST-segment changes and symptoms with stress testing in asymptomatic women does not provide additional prognostic information. [Copyright &y& Elsevier]

Thrombotic thrombocytopenic purpura (TTP) is a fulminant disease characterized by platelet aggregates, thrombocytopenia, renal insufficiency, neurologic changes, and mechanical injury to erythrocytes. Most idiopathic cases of TTP are characterized by a deficiency of ADAMTS13 ( a d isintegrin a nd m etalloprotease, with t hrombo s pondin-1-like domains) metalloprotease activity. Ironically, use of anti-platelet agents, the thienopyridine derivates clopidogrel and ticlopidine, is associated with drug induced TTP. Data were abstracted from a systematic review of English-language literature for thienopyridine-associated TTP identified in MEDLINE, EMBASE, the public website of the Food and Drug Administration, and abstracts from national scientific conferences from 1991 to April 2008. Ticlopidine and clopidogrel are the two most common drugs associated with TTP in FDA safety databases. Epidemiological studies identify recent initiation of anti-platelet agents as the most common risk factor associated with risks of developing TTP. Laboratory studies indicate that most cases of thienopyridine-associated TTP involve an antibody to ADAMTS13 metalloprotease, present with severe thrombocytopenia, and respond to therapeutic plasma exchange (TPE); a minority of thienopyridine-associated TTP presents with severe renal insufficiency, involves direct endothelial cell damage, and is less responsive to TPE. The evaluation of this potentially fatal drug toxicity can serve as a template for future efforts to comprehensively characterize other severe adverse drug reactions. [ABSTRACT FROM AUTHOR]