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Background Declining platelet counts may reveal platelet activation and aggregation in a postoperative prothrombotic state. Therefore, we hypothesized that nadir platelet counts after on-pump coronary artery bypass grafting (CABG) surgery are associated with stroke. Methods We evaluated 6,130 adult CABG surgery patients. Postoperative platelet counts were evaluated as continuous and categorical (mild vs. moderate to severe) predictors of stroke. Extended Cox proportional hazard regression analysis with a time-varying covariate for daily minimum postoperative platelet count assessed the association of day-to-day variations in postoperative platelet count with time to stroke. Competing risks proportional hazard regression models examined associations between day-to-day variations in postoperative platelet counts with timing of stroke (early: 0–1 days; delayed: ≥2 days). Results Median [interquartile range] postoperative nadir platelet counts were 123.0 [98.0, 155.0] × 109/L. The incidences of postoperative stroke were 1.09%, 1.50%, and 3.02% for platelet counts, >150×109/L, 100–150×109/L, and <100×109/L, respectively. The risk for stroke increased by 12% on a given postoperative day for every 30 × 109/L decrease in platelet counts (adjusted hazard ratio [HR], 1.12; 95% confidence interval [CI], 1.01–1.24; P=0.0255). On a given day, patients with moderate to severe thrombocytopenia were twice as likely to develop stroke (adjusted HR, 1.99; 95% CI, 1.18–3.34; P=0.0093) as patients with nadir platelet counts >150×109/L. Importantly, such thrombocytopenia, defined as a time-varying covariate, was significantly associated with delayed (≥2days after surgery; adjusted HR, 2.87; 95% CI, 1.49–5.55; P=0.0016), but not early postoperative stroke. Conclusion Our findings suggest an independent association between moderate to severe postoperative thrombocytopenia and postoperative stroke, and timing of stroke after CABG surgery.

Persistent postoperative pain (PPP) after cardiac surgery is a significant complication that negatively affects patient quality of life and increases health care system burden. However, there are no standards or guidelines to inform how to mitigate these effects. Therefore, in this review, we will discuss strategies to prevent and manage PPP after cardiac surgery. Adequate perioperative analgesia may prove instrumental in the prevention of PPP. Although opioids have historically been the primary analgesic approach to cardiac surgery, an opioid-sparing strategy may prove advantageous in reducing side effects, avoiding secondary hyperalgesia, and decreasing risk of PPP. Implementing a multimodal analgesic plan using alternative medications and regional anesthetic techniques may offer superior efficacy while reducing adverse effects.

These data demonstrate that human HCC is characterized by altered AQP 9 expression and AQP 9 localization in the NTL mass is dependent on underlying liver pathology. Given the central role of AQPs in normal liver function and the potential role of AQPs during transformation and progression, these data may prove valuable in future diagnostic and/or therapeutic strategies.

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