Cardiovascular disease is the principal cause of morbidity and mortality in
dialysis patients. The principal alterations responsible are left ventricu
lar hypertrophy and arterial disease characterized by an enlargement and hy
pertrophy of arteries and the high prevalence of atheromatous plaques. Left
ventricular hypertrophy is the consequence of combined effects of chronic
hemodynamic overload and nonhemodynamic biochemical and neurohumoral factor
s characteristic of uremia. The hemodynamic overload is due to how and pres
sure overload. The flow overload is tightly related to hyperkinetic circula
tion caused by anemia, arteriovenous fistula, or overhydration and is chara
cterized by an enlargement of the left ventricular cavity. The pressure ove
rload in these patients is more tightly related to abnormal geometry and fu
nction of large conduit arteries, principally the stiffening of arterial tr
ee. The flow overload is also in large part responsible for remodeling of a
rterial tree, and as the heart and vessels are a coupled interactive physio
logical system, cardiac and vascular alterations occur in parallel, being i
nduced to a great extent by the same hemodynamic abnormalities. The princip
al clinical consequences of left ventricular hypertrophy and arterial alter
ations are heart failure, ischemic heart disease, and peripheral artery, di
sease. Cardiovascular alterations are only partly reversible, and efforts s
hould be directed toward early prevention.