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Historically, it has been difficult for hospitals to change methods for activated clotting time (ACT) testing because of differences in ACT values obtained with different instruments, wide differences in target ranges used in different procedures, and the difficulty of performing crossover studies at the bedside in critical care situations. There are limited published data comparing the i-STAT (Abbott Point of Care, Princeton, NJ) kaolin ACT with the Medtronic ACT Plus (Medtronic, Minneapolis, MN). The i-STAT system can perform ACT testing in addition to testing of a number of critical care analytes and may offer potential advantages over other ACT analyzers. Comparison of ACT values on 121 simultaneous split-sample tests yielded an R² of 0.88 with i-STAT = 0.79 Medtronic + 72.0. The Pearson correlation was R = 0.94, indicating statistically significant correlation between the 2 methods. Based on this comparison, we were able to implement the i-STAT ACT throughout our institution without changing target ranges for any individual procedure. [ABSTRACT FROM AUTHOR]

Objectives: Point-of-care laboratory testing (POCT) offers reduced turnaround time and may promote improved operational efficiency. Few studies have been reported that document improvements from implementing POCT in primary care. Methods: We measured metrics of practice efficiency in a primary care practice before and after implementation of POCT, including the total number of tests ordered, letters and phone calls to patients, and revisits due to abnormal test results. We performed a cost and revenue analysis. Results: Following implementation of POCT, there was a 21% decrease in tests ordered per patient (P < .0001); a decrease in follow-up phone calls and letters by 89% and 85%, respectively (P < .0001 and P < .0001); and a 61% decrease in patient revisits (P = .0002). Estimated testing revenues exceeded expenses by $6.62 per patient, and potential cost savings from improved efficiency were $24.64 per patient. Conclusions: POCT can significantly improve clinical operations with cost reductions through improved practice efficiency. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The histidine-rich Ca-binding protein (HRC) is a Ca-storage protein in cardiac sarcoplasmic reticulum. Recent transgenic studies revealed that this protein inhibits the maximal rates of sarcoplasmic reticulum Ca-transport, leading to cardiac dysfunction. In view of the role of sarcoplasmic reticulum Ca-cycling in myocardial ischemia/reperfusion injury, we designed this study to gain further insight into the role of HRC during ischemia/reperfusion. Methods and results: The transgenic mouse model with cardiac-specific overexpression of HRC was utilized and cardiac contractile parameters were assessed before and after ischemia/reperfusion injury by Langendorff perfusion. After a 20-min stabilization period, the hearts were subjected to 40 min of global ischemia, followed by 60 min of reperfusion. We found that although transgenic (TG) hearts showed depressed cardiac function (25%) compared to wild types (WTs) at baseline, they exhibited better recovery of left ventricular developed pressure (86.6±2.6% in TGs vs. 58.3±4.0% in WTs of pre-ischemic values, P <0.05) and higher rates of contraction and relaxation after ischemia/reperfusion than WTs. This improvement was accompanied by smaller infarcts (23.1±1.7% in TGs vs. 41.1±2.5% in WTs of infarct region-to-risk region ratio, P <0.05) and lower creatine kinase release. Notably, the extent of apoptotic cell death was significantly attenuated, as evidenced by decreased DNA fragmentation, upregulation of the antiapoptotic protein Bcl-2, and downregulation of the active caspases (3, 9 and 12) following ischemia/reperfusion in TG hearts, compared with WTs. Extension of these studies to an in vivo model of 30-min myocardial ischemia, via coronary artery occlusion, followed by 24-h reperfusion, showed that the infarct region-to-risk region ratio was 9±0.9% in TGs, compared with 20.4±2.9% in WTs (P <0.05). Conclusions: Our findings suggest that increased cardiac HRC expression protects against ischemia/reperfusion injury in the heart, resulting in improved recovery of function and reduced infarction. [Copyright &y& Elsevier]