Cardiovascular Disease Research Paper

1. INTRODUCTION

Cardiovascular disease is the leading cause of death in renal failure patients. The morbidity and mortality in patients with chronic kidney disease is high and the presence of chronic kidney disease worsens outcomes of cardiovascular disease. Cardiovascular disease often begins before end-stage renal disease and patients with reduced kidney function are more likely to die of cardiovascular disease than to develop end-stage renal disease. 40-50% of all deaths in the end-stage renal disease population are of cardiovascular origin [1]. The majority of deaths among patients with predialysis kidney disease were due to cardiovascular disease (Wannamethee SG et al., 1997). The cardiovascular mortality risk is substantially higher

Most patients with end-stage renal disease should have renal replacement therapy programme involving either peritoneal or hemodialysis. A unique feature of cardiovascular disease in patients with primary renal disease is that retarding or preventing progression of progressive renal disease will reduce cardiac risk. The second feature of specific importance in progressive renal disease is the role of volume dependent mechanisms involved in hypertension and heart failure. The most extreme example of this is seen in anuric patients on haemodialysis, who accumulate on average 2–3 litres of fluid between dialysis sessions. Hypertension in such patients is volume dependent, and high weight gains are also associated with the development of pulmonary oedema in susceptible individuals. Fluid retention increases progressively with deteriorating renal function and thus contributes to the development of heart failure and hypertension. The third unique feature is the nature of vascular disease in this population, which has led to scepticism about the adoption of treatments and treatment strategies proven in the general population. The characteristic feature of the vessels is calcification- to a large extent the result of hyperparathyroidism in renal disease in peripheral and coronary vessels (Allan J Collins et al., 2003). The extent to which atherosclerosis in such vessels differs from the general population and the efficacy of established treatments such as statins—remains uncertain and unproven. Finally the mode of death in advanced renal disease is atypical, classical myocardial infarction being relatively unusual and