Ivica Šafradin

Modern antiplatelet management of coronary artery bypass patients: a role of platelet function testing in decision making.

We read with great interest the recently published study by Williams et al. [1]. The authors sought to determine the relationship between postoperative clopidogrel and clinical and angiographic outcomes following coronary artery bypass grafting (CABG) [1]. Although clopidogrel is now recommended as postoperative antiplatelet therapy in patients with recent acute coronary syndromes, some other circumstances such as off-pump CABG, performed endarterectomy, and extensive severe coronary artery disease with small target vessels, warrant the use of both clopidogrel and aspirin following surgical revascularization [2]. In present study by Williams et al. [1], postoperative antiplatelet therapy was left to physician discretion, thus creating patient selection bias since above mentioned circumstances requiring dual antiplatelet therapy (dAPT) could influence angiographic as well as clinical outcomes. Aortocoronary vein graft disease is composed of three distinct but interrelated pathological processes: thrombosis, intimal hyperplasia, and atherosclerosis [3]. Early thrombosis is a major cause of vein graft attrition during the first month after CABG [3]. Since the present study assessed clinical outcome [1] it would be interesting if authors included in analysis patients who died prior to 30 days postoperatively. It would be interesting to elucidate how many patients of those who died prior to 30 days postoperatively were on dAPT versus mono antiplatelet therapy early after CABG? In our opinion, the lack of data concerning objective quantification of the antiplatelet effect of aspirin and clopidogrel constitutes a major drawback of the study. Expected inhibition of platelet function is not always achieved after aspirin and/or clopidogrel administration. The frequency of low responsiveness for the 2 drugs has been reported to range from 1 to 45 % [4, 5] and such a phenomenon could certainly explain in some degree ischemic events after CABG. When assessing relationship between postoperative dAPT and both clinical and angiographic outcomes following CABG, the role of aspirin should inextricably be included into considerations. Within dAPT the possible impact of each antiplatelet agent (aspirin and clopidogrel) on clinical and angiographic outcomes should separately be assessed by drug specific platelet function tests, facilitating individual therapeutic approach for each antiplatelet agent postoperatively. Such an approach could distinguish patients with high residual platelet activity, thus proclivity to ischemic events, from those with enhanced platelet inhibition, thus proclivity to bleeding events (notably, not captured in present trial). In our recent study [5], we analyzed the proportion of patients with aspirin resistance, both preand postoperatively. Considering all CABG patients, we observed 31/99 (31.3 %) patients with aspirin resistance preoperatively [5]. Postoperatively, we registered 46/99 (46.5 %) CABG patients with aspirin resistance, suggesting platelet hyperactivity [5]. A postoperatively registered increase of 15.2 % in the proportion of patients with aspirin resistance was found to be significant (p = 0.04) as well as higher prevalence of aspirin resistance within diabetic subpopulation (58.5 vs 38 %, p = 0.04). Postoperatively, we observed significant increase in values of platelet function M. Petricevic (&) B. Biocina I. Safradin Department of Cardiac Surgery, University Hospital Center Zagreb, University of Zagreb School of Medicine, Kispaticeva 12, 10000 Zagreb, Croatia e-mail: petricevic.mate@gmail.com

Rewarming strategy and neuromonitoring are significant details in neurological outcome after surgical repair of type A aortic dissection

We with great interest read the article by Haldenwang et al. [1] on the evaluation of the risk factors for transient neurological dysfunction and adverse outcome after repair of acute type A dissection. We recognize the importance of their aim to assess preand intraoperative factors that can cause neurological impairment. We do, however, have a few comments and suggestions for more proper clinical management in such complex cases. One form of transient neurological deficit (TND) was defined by Haldenwang et al. as persistent loss of cognitive function without changes on computed tomography or complete resolution before discharge, which is, in our opinion, closer to the definition of permanent neurological damage. Morphological changes that cause persistent cognitive loss can be detected with more sensitive methods such as MR, but functional changes may regress or disappear before discharge because of brain plasticity [2]. Therefore, the evaluation of cognitive function requires the application of specific functional tests [3]. Axillary cannulation is technically difficult, but is associated with less local and systemic complications. In the case of emergency, an alternative, but safer approach often has to be used [4]. Haldenwang et al. did not specify what type of cannulation modality was used in patients with poor mental status prior to surgery (n = 36), which was found to be a significant predictor of adverse outcome and TND. Although the authors found a statistically significant correlation between femoral cannulation and stroke incidence, analysis of cannulation modality in this subset of patients with poor mental status may cast a different light on the stipulated correlation. Selective cerebral perfusion (SCP) is a widely accepted strategy for cerebral protection during aortic surgery. However, certain technical difficulties can occur during SCP. Therefore, the use of an additional method for neuromonitoring is required. Near-infrared spectroscopy and transcranial Doppler are safe and non-invasive methods that can detect the occurrence of embolization and significant decrease in regional cerebral saturation and blood flow, events that are associated with worse neurological outcome. That information could help the surgical team to act in a timely manner to prevent a neurological deficit [5]. An aggressive rewarming rate after HCA can cause brain hyperthermia. A rapid rewarming rate and large temperature variations during that process may cause imbalance between metabolic needs and inadequate cerebral perfusion as a result of impaired autoregulation of cerebral blood flow. Mismatch between cerebral oxygen supply–demand causes markedly decreased oxygen saturation in the jugular bulb, which receives most of the venous blood from the brain. It is known that oxygen desaturation in the jugular bulb is a risk factor for neurocognitive dysfunction. Also, hyperthermia >37°C 24 h after a surgical procedure is associated with poorer neurocognitive outcome after 6 weeks [6]. It is noteworthy that the authors did not specify the value of oxygen saturation in the jugular bulb, rewarming rate, target rewarming temperature or temperature maintenance in the intraoperative and postoperative periods. In conclusion, we believe that a proper rewarming strategy and additional neuromonitoring methods could increase the efficacy of routine cerebral protection during surgery. We congratulate the authors on their useful and clinically applicable research.