Platelet reactivity in overweight and obese patients undergoing cardiac surgery.

Body mass index (BMI) and specifically overweight and obesity have been associated with an increased platelet reactivity in different series of patients. This information is derived by different laboratory platelet function tests (PFTs) like mean platelet volume (MPV), platelet microparticles, thromboxane B2 metabolites, and others. Point-of-care PFT, which are often used in cardiac surgery, are rarely addressed. The present study aims to verify platelet reactivity using multiple-electrode aggregometry (MEA) as a function of BMI in cardiac surgery patients. One-hundred ninety-eight cardiac surgery patients free from the effects of drugs acting on the P2Y12 receptor and undergoing cardiac surgery received MEA-PFT immediately before surgery. Platelet reactivity was compared between normal weight and overweight-obese subjects. There were 99 underweight/normal (BMI < 25), 60 overweight (BMI ≥ 25) and 39 obese (BMI ≥ 30) patients. Overweight-obese patients did not show higher platelet counts nor a clear platelet hyper-reactivity, when tested with MPV and MEA ADP test. At TRAPtest, the overweight/obese patients had a significantly (P = 0.011) higher platelet reactivity (median 118, interquartile range 106-136) than controls (median 112, interquartile range 101-123) and a higher rate of platelet hyper-reactivity (odds ratio 2.19, 95% confidence interval 1.15-4.16, P = 0.016) in a multivariable model. A minor association was found between the BMI and platelet reactivity at TRAPtest, with a higher degree of activity for increasing BMI. The BMI determines an increased thrombin-dependent platelet reactivity in cardiac surgery patients. Thrombin is extensively formed during cardiac surgery, and this may explain the lower postoperative bleeding observed in obese patients in previous studies.

Markers of cardiogenic shock predict persistent acute kidney injury after out of hospital cardiac arrest.

OBJECTIVE: Ischemia and reperfusion injury (IRI) in cardiac arrest patients after return to spontaneous circulation causes dysfunctions in multiple organs. Kidney injury is generally transient but in some patients persists and contributes both to mortality and increased resource utilisation. Ongoing shock may compound renal injury from IRI, resulting in persistent dysfunction. We tested whether cardiac dysfunction was associated with the development of persistent acute kidney injury (PAKI) in the first 72 h after cardiac arrest. METHODS: We performed an observational retrospective study from January 2013 to April 2017. We included consecutive patients treated after out-of-hospital cardiac arrest at a single academic medical center with renal function measured and immediately and for 48 h post arrest. We also recorded each patient's pre arrest baseline creatinine, demographic and clinical characteristics. Our primary outcome of interest was PAKI, defined as acute kidney injury (AKI) on at least 2 measurements 24 h apart. We compared demographics and outcomes between patients with PAKI and those without, and used logistic regression to identify independent predictors of PAKI. RESULTS: Of 98 consecutive patients, we excluded 24 for missing data. AKI was present in 75% of subjects on arrival. PAKI developed in 35% of patients. PAKI patients had a longer hospital length of stay (median 21 vs 11 days) and lower hospital survival (47% vs 71%). Serum lactate levels, dosage of adrenaline during resuscitation and days of dobutamine infusion strongly predicted PAKI. CONCLUSIONS: Among patient who survive cardiac arrest, acute AKI is common and PAKI occurs in more than one third. PAKI is associated both with survival and with length of stay at the hospital. High doses of adrenaline, high serial serum lactate levels, and dose of dobutamine predict PAKI. Evaluation of the trajectory of renal function over the first few days after resuscitation can provide prognostic information about patient recovery.