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The evidence is increasing that left ventricular noncompaction cardiomyopathy as it is currently defined does not represent a failure of compaction of pre-existing trabecular myocardium found during embryonic development to form the compact component of the ventricular walls. Neither is there evidence of which we are aware to favour the notion that the entity is a return to a phenotype seen in cold-blooded animals. It is also known that when seen in adults, the presence of excessive ventricular trabeculations does not portend a poor prognosis when the ejection fraction is normal, with the risks of complications such as arrhythmia and stroke being rare in this setting. It is also the case that images of "noncompaction" as provided from children or autopsy studies are quite different from the features observed clinically in asymptomatic adults with excessive trabeculation. Our review suggests that the presence of an excessively trabeculated left ventricular wall is not in itself a clinical entity. It is equally possible that the excessive trabeculation is no more than a bystander in the presence of additional lesions such as dilated cardiomyopathy, with the additional lesions being responsible for the reduced ejection fraction bringing a given patient to clinical attention. We, therefore, argue that the term "noncompaction cardiomyopathy" is misleading, because there is neither failure of compaction nor a cardiomyopathic process in most individuals that fulfill widely used diagnostic criteria.

Chapter 2. Surgical and endovascular interventions for promoting arteriovenous fistula maturation 2.1. We suggest using regional block anaesthesia rather than local anaesthesia for arteriovenous fistula creation in adults with end-stage kidney disease. (2C) 2.2. We suggest there is insufficient evidence to support endof-vein to side-of-artery over side-of-vein to side-ofartery anastomosis for arteriovenous fistula creation in adults with end-stage kidney disease (2C) peri-and postoperative care of AV fistulas and grafts ii3

Access flow (Qa) has an important effect on systemic hemodynamics in dialysis patients. A Qa : cardiac output (CO) ratio higher than 0.3 is considered a risk factor for high-output cardiac failure. However, the effect of different types of vascular access in hemodialysis patients has not yet been studied. The aim of the present study was to assess the relationship between Qa and systemic hemodynamics and to compare systemic hemodynamics between patients with elbow/upperarm access with forearm access types. Qa, CO, cardiac index (CI), central blood volume (CBV), and peripheral vascular resistance (PVR) were studied by the saline dilution technique in 58 hemodialysis patients (18 with elbow/upperarm access; 40 with forearm access types). This article found that Qa was significantly and positively related to CO and CI, and inversely related to PVR. CBV, Qa, and presence of cardiac failure were independent determinants of CI. Qa and the Qa : CO ratio were significantly higher, and PVR significantly lower, in patients with elbow/upperarm access compared to patients with forearm access types. When patients with cardiac failure were excluded, CO and CI were also significantly higher in patients with elbow/upperarm access types. Eleven percent of patients with elbow/upperarm fistula had a Qa : CO ratio above 0.3. In conclusion, Qa is strongly related to systemic hemodynamics in dialysis patients. In patients without cardiac failure, CO and CI are significantly higher in patients with elbow/upperarm access compared to patients with forearm access types. However, only a small percentage of patients with elbow/upperarm fistulae appeared to be in the risk zone for development of high-output cardiac failure.