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Clinical
manifestations
Ischaemic symptoms
This group of presenting
symptoms includes angina, acute coronary syndrome and myocardial
infarction.
Coronary ischaemia is
a result of an imbalance between supply and demand. In the general
population, this is largely determined by either occlusion or narrowing
of the coronary vessels, but in the renal population other factors
are important. These include:
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excess
of left ventricular hypertrophy, increasing the burden; |
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decreased
oxygen delivery due to anaemia; and |
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abnormal
cellular energetics, possibly related to abnormalities of calcium
metabolism. |
There are also observational
data showing increased coronary artery calcification in young dialysis
patients, but the pathological significance of this is unclear.
Moreover, small-vessel disease in diabetics is common by the time
such patients are on dialysis.
The rates of ischaemic
symptoms, including myocardial infarction are increased in patients
with end-stage renal failure.
Arrhythmias
Many arrhythmias
may be seen in dialysis patients both during, and between, dialysis.
These can be related
to abnormalities of the conduction system through calcification
and ischaemia or may be mediated by changes in the haemodynamics
or metabolic milieu during dialysis.
Atrial fibrillation is
particularly common, and may be either paroxysmal or persistent.
Left-ventricular hypertrophy
This is an almost universal
finding in patients on dialysis. The process
is probably an adaptive one to anaemia and hypertension which has
become maladaptive, with a high associated mortality rate owing
to heart failure and acute coronary events.
Pericardial disease
Pericardial disease may
reflect under dialysis or infection, such as tuberculosis
Valvular disease
Valvular disease
may be divided into valvular calcification and endocarditis.
Infective endocarditis
is an important complication within the dialysis population, occurring
in one to five percent of patients on haemodialysis.
It is more common in
patients who are dialysing through long-term cuffed subcutaneous
venous catheters and with PTFE grafts. However, a major predisposing
factor is valvular calcification.
Abnormalities of valve
function are also relatively common, with increased rates of calcifications
of both aortic and mitral valves, resulting in stenosis. In addition,
there is a high prevalence of mitral, aortic and tricuspid regurgitation.
Much of the aetiology of this is related to poor volume control,
so correction of volume may result in regression of these functional
regurgitant lesions.
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