WHAT THIS PAPER ADDSThis study shows the additional value of measuring pre-operative young, reticulated platelets (pRP) in patients undergoing major non-cardiac surgery to predict post-operative myocardial injury (PMI) and 30 day mortality. Measuring pRP could identify patients with an increased risk of PMI and 30 day mortality. Future, prospective studies with consequent adjustment of cardiovascular risk management after pRP measurement, should determine the clinical relevance.Objective: A pre-operative marker for identification of patients at risk of peri-operative adverse events and 30 day mortality might be the percentage of young, reticulated platelets (pRP). This study aimed to determine the predictive value of pre-operative pRP on post-operative myocardial injury (PMI) and 30 day mortality, in patients aged ! 60 years undergoing moderate to high risk non-cardiac surgery.Methods: The incidence of PMI (troponin I > 0.06 mg/L) and 30 day mortality was compared for patients with normal and high pRP (!2.82%) obtained from The Utrecht Patient Orientated Database. The predictive pRP value was assessed using logistic regression. A prediction model for PMI or 30 day mortality with known risk factors was compared with a model including increased pRP using the area under the receiving operator characteristics curve (AUROC). Results: In total, 26.5% (607/2289) patients showed pre-operative increased pRP. Increased pRP was associated with more PMI and 30 day mortality compared with normal pRP (36.1% vs. 28.3%, p < .001 and 8.6% vs. 3.6%, p < .001). The median pRP was higher in patients suffering PMI and 30 day mortality compared with not ( 2.21 [IQR: 1.57e3.11] vs. 2.07 [IQR: 1.52e1.78], p ¼ .002, and 2.63 [IQR: 1.76e4.15] vs. 2.09 [IQR: 1.52e3.98], p < .001). pRP was independently related to PMI (OR: 1.28 [95% CI: 1.04e1.59], p ¼ .02) and 30 day mortality (OR: 2.35 [95% CI: 1.56e3.55], p < .001). Adding increased pRP to the predictive model of PMI or 30 day mortality did not increase the AUROC 0.71 vs. 0.72, and 0.80 vs. 0.81. Conclusion: In patients undergoing major non-cardiac surgery, increased pre-operative pRP is related to 30 day mortality and PMI.
Patients on P2Y inhibitors may still develop thrombosis or bleeding complications. Tailored antiplatelet therapy, based on platelet reactivity testing, might reduce these complications. Several tests have been used, but failed to show a benefit of tailored antiplatelet therapy. This could be due to the narrowness of current platelet reactivity tests, which are limited to analysis of platelet aggregation after stimulation of the adenosine diphosphate (ADP)-pathway. However, the response to ADP does not necessarily reflect the effect of P2Y inhibition on platelet function in vivo. Therefore, we investigated whether measuring platelet reactivity toward other physiologically relevant agonists could provide more insight in the efficacy of P2Y inhibitors. The effect of in vitro and in vivo P2Y inhibition on αIIbβ3-activation, P-selectin and CD63-expression, aggregate formation, release of alpha, and dense granules content was assessed after stimulation of different platelet activation pathways. Platelet reactivity measured with flow cytometry in 72 patients on P2Y inhibitors was compared to VerifyNow results. P2Y inhibitors caused strongly attenuated platelet fibrinogen binding after stimulation with peptide agonists for protease activated receptor (PAR)-1 and -4, or glycoprotein VI ligand crosslinked collagen-related peptide (CRP-xl), while aggregation was normal at high agonist concentration. P2Y inhibitors decreased PAR-agonist and CRP-induced dense granule secretion, but not alpha granule secretion. A proportion of P2Y-inhibitor responsive patients according to VerifyNow, displayed normal fibrinogen binding assessed with flow cytometry after stimulation with PAR-agonists or CRP despite full inhibition of the response to ADP, indicating suboptimal platelet inhibition. Concluding, measurement of platelet fibrinogen binding with flow cytometry after stimulation of thrombin- or collagen receptors in addition to ADP response identifies different patients as nonresponders to P2Y inhibitors, compared to only ADP-induced aggregation-based assays. Future studies should investigate the value of both assays for monitoring on-treatment platelet reactivity.
To assess the diagnostic value of automatic embolus detection software (AEDS) in transcranial Doppler (TCD) monitoring for the detection of solid microemboli in patients at risk for perioperative stroke during carotid endarterectomy (CEA). In 50 patients undergoing CEA, perioperative TCD registration was recorded. All recorded events, identified and saved by the AEDS, were analyzed off-line doubly by two human experts (HEs) within a time frame of> 4 months. The inter- and intraobserver variability was assessed. The overall agreement with the HEs, the sensitivity, specificity, negative and positive predictive values (NPV and PPV) of the AEDS were computed for different cut-offs (patient displaying perioperative 5, 10, 20, 25, or 50 microemboli). 77 233 events were analyzed. The inter- and intraobserver variability was good (min κ = 0.72, max κ = 0.79). AEDS and the HEs identified 760 and 470 solid emboli, respectively. The agreement between AEDS and the HEs for solid emboli detection was poor (κ = 0.24, SE = 0.016). The specificity and NPV were high (99.2 % and 99.6 %) but the sensitivity and PPV were low (30.6 % and 19.8 %). Applying a threshold of> 20 microemboli resulted in the best sensitivity (100.0 %), specificity (84.4 %), PPV (42.7 %), NPV (100.0 %) and area under the curve (0.898). However, 58.3 % of the patients were false positive as classified by AEDS. In this validation cohort, AEDS has insufficient agreement with HEs in the identification of solid emboli. AEDS and HEs disagree with respect to the identification of specific patients at risk. Therefore, AEDS cannot be used as a standalone system to identify patients at risk for perioperative stroke during CEA.
Objective/Background: The objective was to investigate renal outcomes following endovascular repair of thoraco-abdominal aortic aneurysms (TAAA) comparing fenestrations with branches for the renal arteries. Methods: Renal outcomes following TAAA endovascular repair performed with renal branches were collected from five high volume European centers and compared with renal outcomes following TAAA endovascular repair performed with renal fenestrations at one center. Renal re-intervention and occlusion rates, and freedom from any renal outcome and death were analyzed by patient and target vessel. Estimated glomerular filtration rate (eGFR) was calculated and collected pre-operatively and at the last available follow up. Results: In total, 449 patients were included in this retrospective study (235 treated with branched devices [BEVAR] and 214 with fenestrated devices [FEVAR]). Altogether, 856 renal vessels were analyzed (445 perfused by branches and 411 by fenestrations). Both groups were comparable except for sex and smoking habits. Technical success rates were 95% and 99%, respectively. Mean 6 SD follow up was 19 6 18 months after BEVAR and 24 6 20 months after FEVAR. During follow up, renal re-intervention rates were similar in both groups (4.7% vs 5.2%). The renal occlusion rate was significantly higher following BEVAR (9.6% vs 2.3%; P < .01), and the 2 year freedom for renal occlusion rate was 90.4% (SE 85.8%-95.3%) following BEVAR and 97.1% (SE 94.6%-99.7%) following FEVAR (P < .01). During follow up, a 12% median decrease in eGFR was observed following BEVAR versus 9% following FEVAR (non-significant). The 2 year survival rates were 73.4% (SE 66.6%-80.9%) and 81.8% (SE 76.1%-87.9%) following BEVAR and FEVAR, respectively. Conclusion: Mid-term renal outcomes following endovascular repair of TAAA are satisfactory. Endograft designs incorporating renal fenestrations rather than renal branches are associated with significantly lower occlusion rates. A prospective trial is now required to confirm these results.
HCPR is present in PAD patients and research on HCPR is needed in this population; timing of tests is relevant and standardisation of tests is needed. The optimal conditions for platelet function testing should be determined.
Background: Following carotid endarterectomy (CEA), cerebrovascular hemodynamic may be hampered by ipsilateral restenosis or development of contralateral stenosis. It remains to be clarified if these patients need follow-up for identifying development of contralateral stenosis. Identification of risk factors contributing to development of contralateral stenosis could allow more specific follow-up. In this current study, we assessed clinical risk factors and plaque characteristics of patients undergoing CEA with development of new contralateral stenosis during mid-term follow-up. Methods: Seven hundred and sixty patients undergoing CEA between 2003 and 2011 at UMC Utrecht were included. Atherosclerotic plaques were excised and analyzed for smooth muscle cells (SMCs), collagen, macrophages, lipid core, plaque hemorrhage and vessel density. Patients underwent clinical and duplex ultrasound follow-up at 3 and 12 months and yearly thereafter. Association between plaque- and patient characteristics with development of contralateral stenosis ≥50% was assessed with univariate and multivariate analysis. Clinical outcome during follow-up was associated with development of new contralateral stenosis. Results: After a median follow-up time of 2.5 years, development of contralateral stenosis was observed in 108 patients (20%). Presence of high collagen (p = 0.025) and high SMC (p = 0.027) was associated with development of new contralateral stenosis, whereas large lipid core was negatively associated with new development of contralateral stenosis (p = 0.034). The same plaque characteristics were related to contralateral occlusion. History of coronary artery disease (p = 0.031) and asymptomatic presentation (p = 0.000) were univariably associated with development of contralateral stenosis. Multiple regression analysis indicated that asymptomatic status was independently associated with contralateral stenosis (p = 0.001). Patients with new development of contralateral stenosis more often showed symptoms during follow-up (p = 0.049). Conclusion: Dissection of a lipid-poor, collagen-rich or SMC-rich plaque yielded an association with development of new contralateral stenosis during mid-term follow-up after CEA. Asymptomatic patients had a significantly higher risk for development of contralateral stenosis. New contralateral stenosis was related to the presence of new cerebral symptoms. These findings may help to develop individual treatment algorithms for patients with cerebrovascular atherosclerotic burden.
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