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For many patients with ST-segment elevation myocardial infarctions (STEMIs), the time from presentation to percutaneous coronary intervention exceeds established goals. This study was conducted to examine the effects of formalized data assessment and systematic feedback on treatment times. All patients with STEMIs treated with percutaneous coronary intervention in a semi-rural 3-hospital network from January 1, 2006, to December 31, 2006, were prospectively analyzed (n = 114). Patients presenting during the first 3-month period (January 1, 2006, to March 31, 2006) were included as the reference group (n = 33). Time points from initial contact with the medical system to revascularization were assessed, analyzed, and presented in an interactive session to hospital and emergency services staff members. Data from patients with STEMIs presenting during the next 3 quarters were presented in the same manner (n = 28, 25, and 28). The median contact-to-balloon time was 113 minutes in the reference quarter, decreasing to 83, 66, and 74 minutes in the intervention groups (p <0.0001), whereas the median door-to-balloon time decreased from 54 minutes in the reference group to 35, 31, and 26 minutes in the intervention groups (p <0.0001). The proportion of patients with contact-to-balloon times <90 minutes increased from 21% to 79% (p <0.0001). There were significant reductions in the durations of initial treatment on location and in the emergency room and in puncture-to-balloon-time in the catheterization laboratory, and more patients were transported directly to the catheterization laboratory, bypassing the emergency room (from 23% in the reference quarter to 76% in the last intervention quarter, p <0.0001). In conclusion, formalized data feedback leads to marked reduction in revascularization times in patients with STEMIs.

The extent of luminal involvement of atherosclerotic vascular disease and platelet reactivity portend subsequent cardiovascular events. This study was designed to determine whether platelet reactivity correlates with the extent of the territorial distribution of vascular disease. Blood was obtained from 130 patients who had known atherosclerotic vascular disease categorized as being in > or =1 of the following territories: coronary artery disease (CAD; n = 89), cerebrovascular disease (n = 36), and peripheral arterial disease (n = 61). Platelet reactivity, i.e., the activation of platelets in response to a low concentration of adenosine diphosphate (0.2 micromol/L), was measured using flow cytometry. Patients with vascular disease in >1 territory compared with those with disease in only 1 territory had greater platelet reactivity with respect to P-selectin expression (p = 0.01). The percentages of platelets expressing P-selectin (mean +/- SD) were 6.4 +/- 4.2 in patients who had involvement of 1 territory (n = 88), 10.0 +/- 6.8 in those who had involvement of 2 territories (n = 28), and 10.1 +/- 9.9 in those who had involvement of 3 territories (n = 14). Patients who had CAD and diabetes mellitus had greater P-selectin expression than did those who had CAD without diabetes (p <0.02 for interaction). Thus, platelet reactivity is greater in patients who have more extensive territorial distribution of atherosclerotic vascular disease and in those who have CAD and diabetes mellitus. Accordingly, patients who have more widely distributed vascular disease are likely to derive particular benefit from antiplatelet regimens that suppress platelet function to a greater extent.

Hyperglycemia has been linked to adverse outcomes after myocardial infarction. We characterized the effect of selected concentrations of glucose or mannitol on platelet function in whole blood samples from healthy volunteers and from patients with and without diabetes mellitus. Activation of platelet glycoprotein IIb/IIIa and P-selectin expression was increased similarly after addition of isosmotic concentrations of glucose and mannitol, suggesting that increased osmolarity associated with hyperglycemia increases platelet reactivity.