Archives ofDisease in Childhood 1993; 68: 637-643

Cardiac abnormalities in end stage renal failure andanaemia

K P Morris, J R Skinner, C Wren, S Hunter, M G Coulthard

AbstractThirteen anaemic children on dialysis wereassessed to determine the incidence of cardiacchanges in end stage renal failure. Ninechildren had an increased cardiothoracic ratioon radiography. The electrocardiogram wasabnormal in every case but no child had leftventricular hypertrophy as assessed by voltagecriteria. However, left ventricular hyper-trophy, often gross, was found on echo-cardiography in 12 children and affected theinterventricular septum disproportionately.Cardiac index was increased in 10 patients as aresult of an increased left ventricular strokevolume rather than heart rate. Left ventricularhypertrophy was significantly greater in thoseon treatment for hypertension and in thosewith the highest cardiac index. Abnormaldiastolic ventricular function was found in 6/11children.

Children with end stage renal failure havesignificant cardiac adnormalities that are likelyto contribute to the high cardiovascularmortality in this group. Anaemia and hyperten-sion, or its treatment, probably contribute tothese changes. Voltage criteria on electrocar-diogram are of no value in detecting leftventricular hypertrophy. Echocardiographymust be performed, with the results correctedfor age and surface area, in order to detect andfoliow these abnormalities.(Arch Dis Child 1993; 68: 637-643)

Department ofPaediatricNephrology, RoyalVictoria Infirmary,Newcastle upon TyneK P MorrisMG Coulthard

Department ofPaediatricCardiology, FreemanHospital, Newcastleupon TyneJR SkinnerC WrenS HunterCorrespondence to:Dr Malcolm G Coulthard,Department ofPaediatric Nephrology, RoyalVictoria Infirmary, Newcastleupon Tyne NEI 4LP.

Accepted 15 November 1992

Many studies in adult patients with end stagerenal failure have documented cardiac abnor-malities."'3 In addition to accelerated athero-sclerosis, an increased cardiac output and leftventricular hypertrophy are often found. Leftventricular systolic function usually remainsnormal despite these abnormalities but a

minority of patients develop left ventriculardysfunction and heart failure.4 Recent studieshave documented abnormal right and leftventricular diastolic function in these patients.5A number of factors may alter cardiovasculardynamics in renal failure including anaemia,hypertension, volume overload, ischaemic heartdisease, electrolyte imbalance, hyperlipidaemia,acidaemia, and arteriovenous fistulas. In addi-tion there is still debate about the existence of a

specific uraemic cardiomyopathy independent ofthese factors.6

Cardiovascular complications are the mostfrequent cause of death in children with chronicrenal failure.7 Children provide an ideal groupfor study as they are free ofpotentially confound-ing factors such as atherosclerosis, diabetes, andsmoking. There are only a few studies of cardio-

vascular function in paediatric patients with endstage renal failure,8"'2 and some of these concen-trate on systolic time interval assessments of leftventricular function without including an echo-cardiographic assessment.9 There have been nostudies of diastolic ventricular function in apaediatric population with end stage renalfailure.

Previous studies have assessed children pre-dominantly on haemodialysis. Haemodialysishas marked effects on both cardiac dimensionsand function, related to improvements in volumeoverload and possibly to removal of uraemictoxins; the timing of investigation in relation todialysis therefore dramatically alters cardio-vascular findings.'314 In addition, an arterio-venous fistula, the commonest form of access forhaemodialysis, can itself increase cardiac outputand alter left ventricular function.'561

Cardiac output has previously been measuredin children with end stage renal failure using theM mode 'cube method'; M mode echocardio-graphy is used to measure left ventricular enddiastolic diameter (LVEDD) and end systolicdiameter (LVESD). Left ventricular diastolicvolume (LVEDD3) and systolic volume(LVESD3) are then calculated and their differ-ence taken as an approximation of left ventricu-lar stroke volume. Developments in Dopplerultrasound now allow a more reliable non-invasive assessment ofcardiac output from directmeasurements of aortic stroke distance andaortic root cross sectional area (equation 1),'1 aswell as investigation of diastolic ventricularfunction. We therefore studied a group of 13anaemic children (haemoglobin concentration<90 g/l) with end stage renal failure on dialysis,12 of whom were on overnight peritoneal dialy-sis. In addition to conventional cross sectionaland M mode echocardiography, continuous andpulsed wave Doppler were used to determineaortic stroke distance and assess right and leftventricular diastolic function.

Patients and methodsWe studied 13 children (11 boys, two girls),median age 6-7 years (range 2-3-14-5), medianhaemoglobin concentrations 73 g/l (range 42-85). The range of underlying conditions andother clinical details are summarised in table 1.None of the conditions has recognised cardiacassociations. The median age at diagnosis ofchronic renal failure was 0 1 years (range 0-13 4)and the median duration of dialysis 2-9 years(range 0A4-7-9). They therefore represent agroup with early onset end stage renal failure;four started dialysis in infancy. All were ondialysis at the time of the study; peritoneal rapid

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Morris, Skinner, Wren, Hunter, Coulthard

Table I Clinical details ofthe 13 children studied

Patient Age Age at chronic renal Age at dialysis Duration of Mode of Diagnosis TreatnentforNo Sex (years) failure (years) (years) dialysis (years) dialysis hypertenswn

1 M 10-4 7-2 7-2 3-2 PROD Familial HUS Yes2 M 2-3 Newborn 1-3 1 PROD Infantile PCKD Yes3 F 4 5 Newborn 0 7 3-8 PROD Dysplasia No4 M 3 0-8 1-3 1-7 PROD Congenital nephrotic Yes

syndrome5 M 6-4 Newborn 3-3 3-1 Haemodialysis PUV No6 M 8-8 Newborn 0 9 7 9 PROD PUV No7 F 8-9 8 5 8-5 0 4 PROD Unknown Yes8 M 12-3 11-9 11.9 0-4 PROD FSGS Yes9 M 2-8 Newborn 0 3 2 5 PROD Dysplasia No10 M 6-7 Newborn 3-5 3-2 PROD Dysplasia No11 M 8-3 Newborn 5-4 2-9 PROD PUV Yes12 M 3-1 Newborn 0-1 3 PROD Dysplasia No13 M 14-5 13-4 14-1 0-4 PROD FSGS Yes

PROD=Peritoneal rapid overnight dialysis; HUS=haemolytic uraemic syndrome; PCKD=polycystic kidney disease; PUV=posteriorurethral valves; FSGS=focal segmental glomeruloscierosis.

overnight dialysis (PROD)'8 in 12 cases andhaemodialysis in one. Two children had afunctioning ateriovenous fistula.

Although seven children were receiving treat-ment for hypertension, six of these were normo-tensive,'9 assessed regularly at home using anautomatic blood pressure machine (WaeschleDS40). Six children were receiving a combina-tion of propranolol and hydralazine, one pro-pranolol alone, and three were also takingcaptopril.A detailed clinical examination was performed

in 11 children. Systolic and diastolic bloodpressure was measured by auscultation using thelargest cuff that could be applied to the upperarm. The cardiothoracic ratio was measured onchest radiography; a standard posteroanteriorviewwas taken in the oldest children (n=9) andanerect or supine anteroposterior view in theyoungest children (n=4). A standard 12 leadelectrocardiogram was performed in the semi-recumbent position after five minutes rest (Mar-quette Instruments). The measured parameters(table 2) were compared with the published stan-dards of Davignon et al20; a value lying above the95th centile or below the 5th centile for appro-priate age was classified as abnormal.A single experienced observer (JRS) per-

formed all the echocardiograms using the sameHewlett Packard Sonos 1000 machine. Thesubject was placed in a semirecumbent positionand the echocardiogram performed after fiveminutes rest, within six hours offinishing PRODor within 24 hours of the last haemodialysissession. One child required sedation with oraltrimeprazine and triclofos. Examinations were

Table 2 Parameters measured on electrocardiography and echocardiography

Electrocardiography P wave (II), Q wave (III, V5), R wave (aVR, V2, V5)S wave (V2, V5), T wave (V2, V5), PR interval (II)QRS axis, QRS interval (V5), QTc interval (V5)R/S ratio (VI, V5), RV5+SV2

EchocardiographyCross sectional Aortic root diameter (AoDiam)M mode Left atrial diameter

Interventricular septum (IVS)Left ventricular posterior wall (LVPW)Left ventricular end diastolic diameter (LVEDD)Left ventricular end systolic diameter (LVESD)

DoppeAortic stroke distance (AoSD)

PW Peak diastolic flow (E and A waves)Mitral and tricuspid flow

PW=pulsed wave, CW=continuous wave.

recorded and M mode measurements were madeaccording to standard techniques accepted bythe American Society of Echocardiography."' Alist of the measurements is shown in table 2.Aortic root diameter (AoDiam) was measuredfrom a cross sectional long axis view, immedi-ately below the insertion of the aortic valves.Aortic stroke distance (AoSD) was measuredwith continuous wave Doppler at the secondright intercostal space, the suprasternal notchand the apex. The highest value was assumed tobe most in line with the beam and was selectedfor analysis. A minimum of four consecutivebeats were averaged. Mitral and tricuspid valvediastolic flow were recorded from the apex, withthe pulsed Doppler sample at the tip of thevalves. A minimum of four consecutive beatswere analysed and peak 'E' and 'A' waves wereaveraged, and the ratio calculated (E:A ratio).From these measurements the following werederived:

Equation 1.Left ventricular stroke volume (SV)=

AoSDxntx(AoDiam/2)2Equation 2.

Stroke index (SI)= SV/body surface area

Equation 3.Cardiac output (CO)=SVx heart rate

Equation 4.Cardiac index (CI)=CO/body surface area

Equation 5.Left ventricular mass index=

0.77{(LVEDD+LVPW+IVS)'-(LVEDD)3} +2-4Body surface area

Equation 6.Fractional shortening=(LVEDD-LVESD)/LVEDD

As virtually all echocardiographic measure-ments vary with age and body surface area it wasnecessary to correct for these before comparingchildren of differing age and size. Henry et alstudied a large healthy paediatric population andgenerated prediction equations for most echo-cardiographic measurements based on age andbody surface area," allowing us to generatestandard deviation or z scores for each measure-ment and to make comparisons between indi-viduals.

ResultsOn examination nine of the 11 children had an

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I

aVR

aVF V3 V6

Figure I Electrocardiogram demonstrating the typical abnormalities in a year old boy.

Table 3 Abnormalities ofelectroencephalography (n= 13)

No ofabnormalities

QRS prolongation 10Small S wave V5 8Deep Q wave III/V5 8Increased R/S ratio V5 7Flat T wave V5 4QT prolongation 3Small R wave V2 3Tall R wave V2 2Small R wave V5 2Decreased RV5+ SV2 2Abnormal QRS axis 2

ejection systolic murmur best heard over thepulmonary area. Six children had a venous humheard in the right infraclavicular or supra-clavicular areas, there was a right ventricularheave in three, a left ventricular heave in four,and a displaced apex beat in three. There was nohepatomegaly or other clinical evidence of con-gestive heart failure and no additional heartsounds were heard. Twelve of 13 children werenormotensive at the time of investigation.The median cardiothoracic ratio was 53%

(range 44-61). The cardiothoracic ratio was

5

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Figure 2 The electrocardiographic sum ofR wave in lead V5and S wave in V2 against age. The 5th and 95th centiles for anormal population are also plotted.20

greater than 50% in nine and greater than 55% infour. There was no relationship between cardio-thoracic ratio and echocardiographic left ven-tricular dimensions or severity of left ventricularhypertrophy.The electrocardiogram was abnormal in every

child with at least three of the measurementslying outside the normal range on the centiles ofDavignon et al. The commonest abnormalitiesare shown in table 3 and a typical electrocardio-gram in fig 1. Many of these abnormalities arecompatible with left ventricular hypertrophy butthe more widely used voltage criteria of leftventricular hypertrophy, such as the height oftheR wave in V5 or V6, or the depth of the S wave inV1 or V2, or the sum ofRV5+SV2, were not metin any of the children. In 11 the sum of RV5+SV2 in fact lay below the 50th centile, with onechild well below the 5th centile (fig 2).

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Figure 3 Cardiac index represented by z scores. Solidhorizontal line represents normal mean value and doned lines95% confidence intervals.

Cardiac abnormalities in end stage renalfailure and anaemia

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Figure 4 Relationship between cardiac index and strokeindex.

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The cardiac index was raised in 10 children,and in two was more than three times normal (fig3). This resulted from an increase in stroke index(fig 4) rather than heart rate, which was notraised in any child (median z score -0-37; range-2106 to +1-14). Twelve children had hyper-trophy of the interventricular septum; in severalthe septal thickness was more than twice normal(fig 5). Septal hypertrophy was consistently moremarked than hypertrophy of the left ventricularposterior wall (LVPW) which was, however,present in seven children. As a result, the ratio ofinterventricular septum to LVPW was abnor-mally high in six children (median 1-26, range0 90-2-15; normal <1-33). The mean leftventricular mass index was well above thenormal mean value (106-5 v 70-0 g/m2).23 Thosewith the highest cardiac index had the highestleft ventricular mass index (fig 6). We found norelationship within the group between haemo-globin and either cardiac index or severity of leftventricular hypertrophy, but they were allanaemic. For the group as a whole there was noconsistent evidence of volume overload con-tributing to these abnormalities, though four ofthe 10 children with an increased cardiac indexwere found to have an increase in LVEDD andLVESD.

In the seven children on antihypertensivetreatment there was a significantly higher cardiacindex, as a result of a higher stroke index, andgreater ventricular hypertrophy compared withthe untreated group (table 4). However theirmean systolic blood pressure z score was only+0-63, well within the normal range (-2-00 to+2-00) and not significantly different from theuntreated children (-1 15). If the one child withpoorly controlled blood pressure is excluded, inwhom there was non-compliance with treat-ment, the blood pressure z scores for the twogroups become even more comparable but the

Table 4 Differencesfound in the groups having or not having antihypertensive treatment.Values expressed as mean (SD)

Antihypertensive No antiVypertensivetreatnent treatment p Value

Systolic blood pressure (z score) 0-63 (2 35) -1 15 (0 74) 0 100Cardiac index (1/min/m2) 8-74 (260) 6-17 (0-90) 01043Stroke index (mi/m2) 100-5 (33-3) 59-7 (8-24) 0-014Interventricular septal thickness fz score) 7-31 (3-68) 3-49 (2-78) 0-062Left ventricular mass index (g/m ) 124-8 (34-4) 85-2 (21-9) 0-034

Statistical analysis using unpaired t test (two tail).

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Figure 5 Interventricul septal (IVS) thickness representedas (A) z scores (with normal mean and 95% confienceintervals) and (B)plotted against body swface area (with 95%normal prediction limits).

differences in cardiac index and left ventricularhypertrophy persist.We found no evidence of left ventricular

systolic dysfunction; only one child had a

shortening fraction below the normal lower limitof 28% (median 35; range 27-43). No child hadmore than trivial mitral regurgitation, tricuspidregurgitation, or pulmonary regurgitation.Tricuspid regurgitation was pansystolic in one

child, the peak velocity predicting normalsystolic right ventricular and pulmonary arterialpressures (20mm Hg). None of the children hada pericardial effusion.

Abnormalities of right and left ventriculardiastolic function were found in six of the 11children with complete data. Normally there are

two phases of ventricular filling. The early (E)

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Figure 6 Relationship between left venricular mass indexand stroke index.

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Cardiac abnormalities in end stage renalfailure and anaemia

E E

B

AE iX-

A

Figure 7 An example of(A) normal and (B) abventricular diastolic function. E=early, A=atriacontraction.

rapid filling phase has a higher velocitlater phase coinciding with atrial c(

(A), such that the normal E:A ratiothan 1-0 (fig 7). Three children had a i

the normal tricuspid valve E:A ratio c< 1-0), one child a reversed mitral valveonly, and two had a reversal ofboth tricmitral E:A ratios. An example of ncabnormal tricuspid valve diastolic flouin fig 7.

DiscussionCardiac complications account for neajdeaths in children with chronic renaDespite this we have only a poor undeof the cardiac pathophysiology that iible. Peritoneal dialysis affects th(dynamic state less than haemodialyevidence suggests that left venticultrophy may even regress on changintoneal dialysis.24 Echocardiographic fipatients on haemodialysis are highly

on the timing of study in relation tperiod of haemodialysis whereas a

dialysis exchange produces no signifilcardiographic change.25 Althoughdialysis is now the preferred form of dsmall children with end stage renal faiare no reported cardiac studies in thisThe majority of children had an easi

flow murmur or venous hum in keepinfindings of Ulmer et al who used phcgraphy to study such murmurs.9 Sysmurmurs were attributed to functiostenosis and the diastolic murmurs toflow across the mitral valve and aorticence. Others have found pulmccompetence in addition to aortic inceat times of fluid overload with seve

tension.26 Although evidence of valvular regurgi-tation was found in several cases using colourDoppler, this technique is very sensitive and

A detects regurgitation in a high proportion ofnormal individuals. The regurgitation was

t haemodynamically trivial in all cases.None of our children had congestive heart

failure and all had normal left ventricular systolicfunction (shortening fraction). Most studies inadults on regular dialysis and the few in childrendescribe normal echocardiographic left ventricu-lar systolic function, as judged by shorteningfraction, ejection fraction, or velocity of circum-ferential fibre shortening.4 10 Other reports haveused systolic time intervals to assess left ven-tricular systolic function. O'Regan et al foundthat most children with chronic renal failure ofmixed severity had normal function," though a

Lfi small subgroup (17%) had abnormal systolictime intervals and a reduced shortening fractiontogether with clinical evidence of congestiveheart failure. Ulmer et al followed up 11 childrenprospectively through chronic renal failuremanaged conservatively to haemodialysis andsubsequently transplantation.9 Systolic time

normal right intervals were significantly prolonged even

during the predialysis period, deterioratedfurther during the time on dialysis, but slowlynormalised after transplantation. Altogether39% of their more complete chronic renal failure

y than the cohort and 24% of their haemodialysis popula-ontraction tion had evidence of congestive heart failure.27is greater In this group the cardiac index was increasedreversal of due to a high stroke index rather than an increase)nly (ratio in heart rate. The two children with arterio-E:A ratio venous fistulas were not significantly different touspid and the others. Studies that have included non-

)rmal and anaemic children with chronic renal failure havev is shown found an inverse relationship between cardiac

index and haemoglobin,8 and correction ofanaemia with erythropoietin has been shown toreduce the cardiac index in adults.28 The lack of arelationship between the cardiac index and

rly 50% of severity of anaemia in this study is probably dueil failure.7 to the fact that all the children studied were

zrstanding anaemic.s respons- One of the most striking findings was thee haemo- increase in left ventricular wall thickness,rsis, adult particularly affecting the interventricularLar hyper- septum. A ratio of interventricular septum toig to peri- LVPW thickness above 1-33 is indicative ofindings in asymmetric septal hypertrophy, as found independent hypertrophic cardiomyopathy associated with:o the last left ventricular outflow obstruction. It has also

peritoneal been reported in a variety of congenital heartcant echo- defects, as a normal developmental finding in theperitoneal human fetus and in infants of diabetic mothers.29iialysis for It has been reported in both adultsn0 and child-ilure there ren'2 with uraemia, particularly those withgroup. hypertension but, with one exception,'2 is notily audible accompanied by outflow obstruction. We foundIg with the no significant difference in the severity of asym-)nocardio- metric septal hypertrophy in those childrenstolic flow requiring antihypertensive treatment.)nal aortic The severity of left venticular hypertrophy iniincreased uraemia has been linked to hypertension,3'

28incompet- anaemia, circulating catecholamines,2 and to)nary in- myocardial calcium content and parathyroid)mpetence hormone concentration.32 The use of left ven-~re hyper- tricular mass as a measure of left ventricular

A

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Morris, Skinner, Wren, Hunter, Coulthard

hypertrophy is attractive as it represents a threedimensional measurement rather than a twodimensional thickness. It cannot however bemeasured directly and is derived from other leftventricular measurements.33 The existingformulas for deriving left ventricular mass werevalidated in populations with concentric ratherthan asymmetric ventricular hypertrophy, socare is needed when interpreting left ventricularmass values in such individuals.We found cardiac index and more particularly

stroke index to be strongly correlated with leftventricular mass index; thus the greatest leftventricular workloads are associated with thegreatest hypertrophy. This severity of left ven-tricular hypertrophy is of particular concern inview ofthe increasing evidence that left ventricu-lar hypertrophy, with or without renal disease, isthe single most powerful predictor of cardio-vascular mortality in adults.' We found norelationship between calcium, phosphate, orparathyroid hormone concentration and severityof left ventricular hypertrophy.While it may be that the higher left ventricular

mass index and stroke index in patients beingtreated for hypertension are explained byunidentified differences in blood pressure, forexample during exercise or stress, an alternativeexplanation is that the high cardiac output at restand more particularly any subsequent increasethat occurs during exercise can, in the presenceof j3 blockade, be maintained only at the expenseof a further increase in stroke index, leading tofurther compensatory left ventricular hyper-trophy. A drug with a primary vasodilatoryaction might therefore have theoretical advant-ages over a ,3 blocker provided it does not alsogreatly increase cardiac output.The incidence of pericardial effusion in pre-

vious paediatric reports has varied widely from12 to 40%. 1035 None of our series had an effusiononM mode or cross sectional echocardiography,although one child had previously required peri-cardiocentesis for a large effusion shortly afterdeveloping end stage renal failure secondary tofamilial haemolytic uraemic syndrome. Whetherthe apparent absence of pericarditis reflects thegreater efficiency of PROD in clearing urea orother possible toxins is uncertain.

It has been suggested that ventricular diastolicfunction is abnormal in adult patients with endstage renal failure,' based on peak inflow velocitymeasurements in the rapid early (E) filling phaseof diastole and the later atrially mediated phase(A). Typically the peak E wave velocity isdecreased and the A wave velocity increased, sothat the E:A ratio is also decreased. This hasbeen largely attributed to reduced compliance ofthe ventricle as a result of hypertrophy, but thisis almost certainly too simplistic since theseindices are not reliable measures of ventricularcompliance. Because we did not study diastolicfunction in a control group we can only commenton those with the grossest abnormalities, that iswhere there was a reversal of the normal E:Aratio from greater than 1I0 to less than 1-0. Wefound 6/11 children to have a reversed ratio, withdiastolic dysfunction of the right ventricle pre-dominating. There was no relationship betweenthe ratio and left ventricular mass index. The

clinical relevance of these findings is uncertain;adult studies link diastolic dysfunction to atendency to hypotension during haemodialysis36and to clinical decompensation, with congestiveheart failure, around the time of transplanta-tion.37 In addition ventricular filling might beseriously jeopardised by an atrial arrhythmia.The incidence of cardiomegaly found on chest

radiography depends on the definition used. Acardiothoracic ratio of>50% is found in as manyas two thirds of children on regular haemodialy-sis,27 and in nine of our 13 children, but clearlythis definition is inappropriate in a populationthat includes young children in whom anterio-posterior and supine views are necessary.Scharer and Ulmer suggested that radiographiccardiomegaly might represent a physiologicaladaptation to an increased stroke index ratherthan a pathological dilatation,27 but the presentstudy did not find a relationship between cardio-thoracic ratio and stroke index or other leftventricular dimensions.

Careful systematic evaluation of a standardelectrocardiogram revealed at least three abnor-malities in every child, contradicting claims thatelectrocardiographic changes are only rarelyobserved in paediatric patients with end stagerenal failure.8 The commonest abnormalities of aprolonged QRS complex and deep Q waves ininferior and anterolateral leads are compatiblewith left venticular hypertrophy but the muchmore frequently used voltage criteria such as theheight of an R wave in V5 or V6, or the depth ofan S wave in V1 or V2 were not met in any child,with values predominantly in the low normalrange. The same was true for the sum of RV5+SV2, a measure often calculated by generalpaediatricians but not generally regarded asvaluable by paediatric cardiologists. It is worthstressing that 50% of normal children aged 8 to12 years will have a sum in excess of 4-7 mV'0 sothat defining left ventricular hypertrophy as asum greater than 4 or even 5 mV, values oftenused, will include a substantial number ofnormal children. Electrocardiography should nolonger be used as the only tool to identify leftventricular hypertrophy in any population as itconsistently underestimates the prevalence ofleft ventricular hypertrophy confirmed echo-cardiographically in both adults-' andchildren.38Children with end stage renal failure on peri-

toneal dialysis have an increased cardiac index,an increased stroke index, and often gross ven-tricular hypertrophy, particularly of the inter-ventricular septum. These findings are mostmarked in children on antihypertensive treat-ment despite apparent optimal blood pressurecontrol. Systolic function is usually normal butdiastolic function may be abnormal with areversal of the normal E:A peak velocity ratio. Achest radiograph and electrocardiogram havevery limited usefulness, often failing to detecteven gross ventricular hypertrophy; a detailedechocardiogram must be performed with thenecessary corrections made for age and bodysurface area. The role of anaemia in the patho-genesis of these abnormalities will becomeclearer after studying the cardiac effects oferythropoietin in such a paediatric population.

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Cardiac abnormalities in end stage renalfailure and anaemia

We are grateful to the nursing staff of Clinic E, Freeman Hospitalfor their help with the study. Dr K P Morris and Dr J R Skinnerare research fellows in child health, funded by Newcastle DistrictResearch Committee and Child Kidney Fund (KPM), and theNational Heart Research Fund (JRS).

1 Cohen MV, Diaz P, Scheuer J. Echocardiographic assessmentof left ventricular function in patients with chronic uraemia.Cln Nephrol 1979; 12: 156-62.

2 Miach PJ, Dawborn JK, Louis WJ, McDonald IG. Leftventricular function in uremia: echocardiographic assess-ment in patients on maintenance dialysis. Clin Nephrol 1981;15: 259-63.

3 Cohen JL, Barooah B, Segal KR, Batuman V. Two-dimensional echocardiographic findings in patients onhemodialysis for more than six months. Am J Cardiol 1987;60: 743-5.

4 Huting J, Kramer W, Reitinger J, Kuhn K, Wizemann V,Schutterle G. Cardiac structure and function in continuousambulatory peritoneal dialysis: influence of blood purifica-tion and hypercirculation. Am Heartj 1990; 119: 344-52.

5 Huting J, Kramer W, Reitinger J, Kuhn K, Schutterle G,Wizemann V. Abnormal diastolic left ventricular filling bypulsed Doppler echocardiography in patients on continuousambulatory peritoneal dialysis. Clin Nephrol 1991; 36: 21-8.

6 Hung J, Harris PJ, Uren RF, Tiller DJ. Uremic cardiomyo-pathy - effect of hemodialysis on left ventricular function inend-stage renal failure. NEnglJMed 1980; 302: 547-51.

7 Broyer M, Brunner FP, Brynger H, Fassbinder W, GuillouPJ, Oules R. Demography of dialysis and transplantation inchildren in Europe 1984. Report from the registry. NephrolDial Transplant 1986; 1: 9-15.

8 O'Regan S. Cardiovascular abnormalities in pediatric patientswith end-stage renal disease. In: Fine RN, Gruskin AB, eds.End-stage renal disease in children. Philadelphia: WBSaunders, 1984: 359-74.

9 Ulmer HE, Heupel EW, Scharer K. Long term evaluation ofcardiac function utilizing systolic time intervals in childrenwith chronic renal failure. International Journal ofPediatricNephrology 1982; 3: 79-86.

10 Palcoux JB, Palcoux MC, Jouan JP, Gourgand JM, CassagnesJ, Malpuech G. Echocardiographic patterns in infants andchildren with chronic renal failure. International Journal ofPediatric Nephrology 1982; 3: 311-4.

11 O'Regan S, Matina D, Ducharme G, Davignon A. Echo-cardiographic assessment of cardiac function in childrenwith chronic renal failure. Kidney Int 1983; 24 (suppl 15):S77-82.

12 Drukker A, Urbach J, Glaser J. Hypertrophic cardiomyo-pathy in children with end-stage renal disease and hyper-tension. Proceedings of the European Dialysis and TransplantAssociation 1981; 18: 542-7.

13 O'Regan S, Villemand D, Revillon L, Robitaille P, DucharmeG, Davignon A. Effects of hemodialysis on myocardialfunction in pediatric patients. Nephron 1980; 25: 214-8.

14 Blaustein AV, Schmitt G, Foster MC, Hayes RV, Bronstein S.Serial effects on left ventricular load and contractility duringhemodialysis in patients with concentric hypertrophy.AmHeartJ 1986; 111: 340-6.

15 Dongradi G, Rocha P, Baron B, et al. Hemodynamic effects ofarteriovenous fistula in chronic hemodialysis patients at restand during exercise. Clin Nephrol 1981; 15: 75-9.

16 O'Regan S, Villemant D, Ducharme G, Davignon A,Robitaille P. Effects of Brescia-Cimino fistulae on myo-cardial function in pediatric patients. Dialysis and Transplant1981;10:202-5.

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doi: 10.1136/adc.68.5.637 1993 68: 637-643Arch Dis Child

 K P Morris, J R Skinner, C Wren, et al. failure and anaemia.Cardiac abnormalities in end stage renal

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