Background: Most studies examining the prognostic value of preoperative coagulation testing are too small to examine the predictive value of routine preoperative coagulation testing in patients having noncardiac surgery. Methods: Using data from the American College of Surgeons National Surgical Quality Improvement database, the authors performed a retrospective observational study on 316,644 patients having noncardiac surgery who did not have clinical indications for preoperative coagulation testing. The authors used multivariable logistic regression analysis to explore the association between platelet count abnormalities and red cell transfusion, mortality, and major complications. Results: Thrombocytopenia or thrombocytosis occurred in 1 in 14 patients without clinical indications for preoperative platelet testing. Patients with mild thrombocytopenia (101,000–150,000 µl−1), moderate-to-severe thrombocytopenia (<100,000 µl−1), and thrombocytosis (≥450,000 µl−1) were significantly more likely to be transfused (7.3%, 11.8%, 8.9%, 3.1%) and had significantly higher 30-day mortality rates (1.5%, 2.6%, 0.9%, 0.5%) compared with patients with a normal platelet count. In the multivariable analyses, mild thrombocytopenia (adjusted odds ratio [AOR], 1.28; 95% CI, 1.18–1.39) and moderate-to-severe thrombocytopenia (AOR, 1.76; 95% CI, 1.49–2.08), and thrombocytosis (AOR, 1.44; 95% CI, 1.30–1.60) were associated with increased risk of blood transfusion. Mild thrombocytopenia (AOR, 1.31; 95% CI, 1.11–1.56) and moderate-to-severe thrombocytopenia (AOR, 1.93; 95% CI, 1.43–2.61) were also associated with increased risk of 30-day mortality, whereas thrombocytosis was not (AOR, 0.94; 95% CI, 0.72–1.22). Conclusion: Platelet count abnormalities found in the course of routine preoperative screening are associated with a higher risk of blood transfusion and death.

No abstract

Key Words: mitochondrial ATP-sensitive potassium channel Ⅲ ischemia/reperfusion Ⅲ ischemic preconditioning Ⅲ fluoxetine T he mitochondrial ATP-sensitive potassium channel (mK ATP ) is thought to be essential for cardioprotection recruited by ischemic preconditioning (IPC), 1,2 but despite intense research the molecular identity of this channel remains unclear. The simplest thesis is that mK ATP channels are derivative of surface K ATP channels, and thus composed of inward rectifying K ϩ channels (K IR ) and sulfonylurea receptors (SURs). The cardiomyocyte surface K ATP channel is comprised of K IR 6.2 and SUR2A isoforms, 3 but efforts to conclusively assign these proteins to the cardiac mK ATP have been unsuccessful to date.Neither K IR 6 nor SUR genes contain mitochondrial target sequences, and K IR 6/SUR proteins are not found in mitochondrial proteome databases or prediction engines. 4,5 Furthermore, immune-based methods to detect K IR /SUR subunits in mitochondria are plagued by issues of antibody specificity 6 and mitochondrial purity/contamination. Several of the key pharmacological reagents used to study mK ATP channels (eg, the agonist diazoxide and antagonist 5-hydroxydecanoate) are also known to exhibit off-target effects. 7,8 Targeted gene deletion in mice to identify the mK ATP channel involved in IPC has proven futile, because of the confounding cardiovascular effects of knocking out K IR 6 and SUR genes (Kcnj8, Kcnj11, Abcc8, and Abcc9) on surface K ATP channel function. In general, K IR and SUR knockouts exhibit profound defects in glucose/insulin handling, 9 -12 which impacts the response to IPC. 13 A recent study using custom-made antibodies and SUR knockout mice identified short-form splice variants of SUR2 in mitochondria. 14 Furthermore, recent pharmacological evidence suggests that complex II of the respiratory chain (succinate dehydrogenase) may be a regulatory component of the mK ATP channel. 15,16 However, both these findings leave the identity of the K ϩ channel-forming subunit of mK ATP unknown. In this regard, mK ATP is similar to other mitochondrial ion channels which exist at a phenomenological level but have not been molecularly identified (eg, the mitochondrial Ca 2ϩ uniporter). A major obstacle in studying the mK ATP channel has been the availability of a reliable assay. Most studies to date have used an isolated mitochondrial rapid swelling assay, in which Original received October 20, 2009; resubmission received December 18, 2009; revised resubmission received January 28, 2010; accepted February 12, 2010. From K ϩ uptake into mitochondria is followed by osmotically-obliged water, leading to mild swelling that is assayed as light scattering in a spectrophotometer. 17,18 This assay has been criticized as irreproducible by some laboratories, 19 with the precise timing of mitochondrial isolation appearing to be a critical factor. 20 Studying the literature on surface K ATP channels, two key biochemical properties that appeared to have been overlooked in the mK ATP channel field...