Cardiovascular Death in Dialysis Patients

Cardiovascular events are the dominant cause of death in patients with ESRD. Until recently, plaque rupture due to atherogenic dyslipoproteinemias was presumed to be a major mechanism of cardiovascular events in dialysis patients. But how reasonable was that hypothesis and was it entirely discredited by the results of 4D and AURORA? This article places the conventional lipids-cholesterol and triglyceride-within the more physiologic framework of the apoB lipoproteins. Viewed from the perspective of atherogenic particle number, the failure of statins to lower cardiovascular mortality in hemodialysis patients versus the continuing potential for success in peritoneal dialysis patients becomes comprehensible. In the former, apoB is characteristically not elevated and therefore apoB-lowering therapy can have only limited effect; in the latter, apoB is characteristically high and therefore apoB-lowering therapy might have considerable clinical benefit. Nevertheless, plaque rupture is only one mechanism leading to cardiac death. In addition to those previously noted, a new mechanism is suggested for consideration-recurrent reperfusion injury. The coronaries of dialysis patients are often narrowed, the microcirculation underdeveloped, and the left ventricle hypertrophied-all of these plus transient hypotension could produce severe ischemia followed by reperfusion necrosis. The minor but common elevations of troponin that are so well known yet widely disregarded may be markers of an adverse sequence of events that could each trigger a fatal arrhythmia and tend to reduce left ventricular function. Thus sudden death due to arrhythmia and slow progressive death due to heart failure could be manifestations of reperfusion injury.