Does the Heart Behave Abnormally in Children on Dialysis? |
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Patients on dialysis have a very high risk of developing disease of the heart and blood vessels (cardiovascular disease). This is also true for young people. For example, in 20-30 year olds, the chance of dying from cardiovascular disease is the same as that of an 85 year old. One cause for this is that the haemodialysis treatment itself puts a lot of strain on the heart. The heart is similar to other organs in the body in that it needs a good blood supply to work properly. During haemodialysis it is necessary to remove the fluid from the blood that the patient has drunk and that the kidneys have not been able to get rid of. This can result in a drop in the amount of fluid in the blood vessels so that the blood pressure drops. This occurs in about one quarter of dialysis sessions, even in children. It is known as intradialytic hypotension and produces symptoms such as headaches and stomach cramps. If anybody, whether or not they are on dialysis, has a fall in their blood pressure, the heart pumps harder to ensure that sufficient blood still reaches the brain and other important organs in the body. The heart itself is also vulnerable, as its blood supply is also reduced. If the blood supply to the heart falls below a critical level this injures the heart muscle and is known as myocardial ischaemia. The sections of injured heart muscle do not contract or move normally and the heart’s function is reduced. Adults develop myocardial ischaemia during dialysis, which persists after dialysis finishes. This is known as myocardial stunning; gradually the heart function is restored and the effect is not permanent. However we know that in adults with coronary heart disease, repeated episodes of reduced blood flow to the heart and repeated episodes of myocardial stunning can cause myocardial hibernation. This describes a situation when part of the heart goes into a state of hibernation, with reduced contraction or not contracting at all, behaving like scarred or permanently damaged heart tissue. If prolonged or severe, this contributes to the development of heart failure. It was originally believed that children with renal disease were protected and the heart is only affected in adults. We now know this to be untrue. We have shown that children on dialysis have stiff blood vessels, calcium deposits in their heart and their blood vessels, atherosclerosis and abnormally large left ventricles (the part of the heart that pumps blood around the body), known as ventricular hypertrophy. These disease processes can predispose patients to reduced blood flow to the heart. Combined with the possibility of further reduction in heart blood flow during haemodialysis children also are likely to be at risk of developing myocardial stunning. We propose a pilot study to determine whether children on haemodialysis and peritoneal dialysis develop myocardial stunning and have abnormal heart and circulatory responses to stress. We will do this using non-invasive ultrasound measurements. We will restudy any child who goes on to be transplanted, to see if the abnormalities persist. The potential for identification of cardiac abnormalities at an early stage will enable development of therapies that reduce the cardiovascular stress of dialysis. Such therapies can then be invoked before irreversible disease occurs, hence reducing cardiovascular mortality in these young patients. Therefore, if myocardial stunning is present, we plan a future studies, the first of which will be cooling the haemodialysis fluid, a technique that reduces myocardial stunning in adults. The long-term outcome of all patients will be followed up through the paediatric renal registry.
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