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Echocardiographic evaluation in patients with autosomal dominant polycystic kidney disease and end-stage renal disease

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Echocardiographic evaluation in patients with autosomal dominant polycystic kidney disease and end-stage renal disease
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  Echocardiographic Evaluation in Patients WithAutosomal DominantPolycystic Kidney Disease and End-Stage Renal Disease AlbertoMartinez-Vea,MD,AlfredoBardajı´,MD,FESC,CristinaGutierrez,PhD,CarmenGarcia,MD,Carmen Peralta, MD, JosepAguilera, MD, Pere Sanchez, MD, Joan Vidiella, MD,PereAngelet, MD, Teresa Compte, MD, Cristobal Richart, MD, and Jesu´sAngel Oliver, MD ●  Cardiovascularabnormalitieshavebeenconsideredimportantextrarenalmanifestationsofautosomaldominantpolycystic kidney disease (ADPKD). However, little is known about their prevalence in patients with ADPKDundergoing hemodialysis (HD). To investigate whether cardiac abnormalities are more prevalent in these patients,clinical and echocardiographic manifestations of cardiovascular disease were evaluated in a group of 32 patientswith ADPKD and a matched control group of 32 patients without diabetes treated by chronic HD for more than 6months.Predialysissystolicanddiastolicbloodpressure(BP),prevalenceofhypertension,andnumberofpatientsrequiring antihypertensive medications were lower in the ADPKD group than controls. There was no difference inthe prevalence of cardiac events, including cardiac failure, ischemic heart disease, and arrhythmia. Systolicdysfunction, diastolic patterns, and left ventricular hypertrophy were similar in the two groups. In patients withADPKD,simpleregressionanalysisshowedleftventricularmass(LVM)indexwascorrelatedwithhemoglobinleveland predialytic systolic and diastolic BPs. In multiple regression analysis, predialysis systolic BP was the onlyindependentvariablelinkedtoLVMindex.Theprevalenceofaortic,mitral,andtricuspidvalvediseasedidnotdifferbetweengroups.Inconclusion,theoccurrenceofcardiovascularcomplicationsinpatientswithADPKDissimilartothatofHDpatientswithotherprimaryrenaldiseases,althoughhypertensionislessprevalent.   1999 by the National Kidney Foundation, Inc. INDEXWORDS:Polycystickidneydisease;end-stagerenaldisease;hemodialysis;cardiaccomplications;Dopplerechocardiography;valvularheartdisease. T HE PREVALENCE of autosomal dominantpolycystic kidney disease (ADPKD) in pa-tients undergoing renal replacement therapy(RRT) ranges between 3% to 11%. 1-3 Despite thelarge number of treated patients, little informa-tion is available on cardiac function and theoccurrence of cardiovascular complications dur-ing chronic dialysis. 4 Cardiac disease, the leading cause of death inthe general population undergoing RRT, 5 is alsothe most common cause of death in the ADPKDpopulation undergoing hemodialysis (HD). 1,6,7 Nev-ertheless, a lower cardiac mortality has been ob-served in patients withADPKD than in those with-out ADPKD undergoing HD, 4 suggesting ADPKDdoes not adversely affect survival during HD.The paradoxical lower cardiac mortality of patients with ADPKD contrasts with the highprevalence of cardiovascular abnormalities be-fore the onset of end-stage renal disease. A highprevalenceofcardiacvalvulardisease, 8 hyperten-sion, 9 and left ventricular hypertrophy (LVH) 10 has been reported in patients withADPKD, evenin its early stages. These disorders are assumedto progress during RRT, but their prevalence andconsequences for cardiac function in patients withADPKDundergoingHDarenotwellestablished.This study was designed to evaluate the occur-rence of cardiovascular complications in patientswithADPKD undergoing HD, with special atten-tion to echocardiographic manifestations of car-diovascular disease. METHODS Subjects Patients with ADPKD were selected from an originalpopulation of 40 patients undergoing HD treated at fivecenters that observed similar dialysis routines. Criteria forexclusion were dialysis duration less than 6 months (4patients) and suboptimal echocardiographic readings (4 pa-tients). Thirty-two patients were included on the study. Thediagnosis ofADPKD was established before the initiation of RRT by the usual criteria. 11 A control group of 32 HD patients without diabetes andwithout ADPKD, who had undergone dialysis for a mini-mum of 6 months and had a reliable echocardiographicstudy, were identified for the purposes of comparison. Pa- From the Nephrology Service, Cardiology Section, and  Research Unit, Hospital Universitari de Tarragona, Joan XXIII; Department of Medicine and Surgery, University Rovira i Virgili, Hospital de Santa Tecla; Reus Medical, Reus; Hospital de la Santa Creu, Tortosa; Tarragona, Spain. Received December 11, 1998; accepted in revised form March 23, 1999. Address reprint requests to Alberto Martinez-Vea, MD, Apartado de Correos 12, 43080 Tarragona, Spain. E-mail:amtz@hjxxiii.scs.es  1999 by the National Kidney Foundation, Inc. 0272-6386/99/3402-0011$3.00/0 264  American Journal of Kidney Diseases,  Vol 34, No 2 (August), 1999: pp 264-272  tients were matched for age, sex, body mass index, andduration of HD. The causes of renal failure were as follows:hypertensive kidney disease (n  8), chronic glomerulone-phritis (n    6), tubule interstitial disease (n    5), andundetermined (n  13).Three patients with ADPKD and four controls had previ-ously received a renal allograft.  HD Procedure Patients received dialysis three times weekly in sessionslasting 3.5 to 4 hours, using a dialysis system with bicarbon-ate dialysate and controlled ultrafiltration. The sodium con-tent of dialysis fluid was 140 mEq/L, and the calciumcontent was 2.5 to 3 mEq/L. Blood flow, dialyzer surfacearea, and time of treatment were adjusted to obtain a Kt/V of at least 3.0 per week, taking residual renal function intoaccount. Twenty-seven patients withADPKD were dialyzedthrough a native arteriovenous fistula, three patients througha polytetrafluoroethylene (PTFE) graft, and two patientsthrough a central venous catheter. Controls were dialyzedthrough a native arteriovenous fistula (n  29) or PTFE graft(n  3). Twenty patients with ADPKD and 23 controls hadno residual renal function, whereas the remainder were highlyoliguric(  200mL/24h). General Population Data Age, height, body mass index (dry weight/height 2 ), andmonths of dialysis were recorded. Blood pressure (BP) wasmeasured by a dialysis nurse with a mercury sphygmoma-nometer. Systolic and diastolic BPs were the averages of allpredialysis measurements obtained with the patient in su-pine position during the 3 months preceding the study andtotaled 34 to 38 determinations in each patient. Hyperten-sion was defined as systolic BP greater than 140 mm Hg ordiastolic BP greater than 90 mm Hg and/or treatment withantihypertensive medication. Interdialysis weight gain wasaveraged during the 3 months before the study and calcu-lated according to the following formula:Interdialysis weight gain (%)  (body weight before dialysis  body weight after dialysis: dry weight)  100.Other parameters recorded included the number and class of antihypertensive medication used and the patients receivingmaintenance recombinant human erythropoietin (rHuEPO)treatment. Antihypertensive medication was not discontin-ued during the study.Clinical events during HD treatment, such as cardiacfailure, ischemic heart disease, and arrhythmia, were alsorecorded. Some patients were admitted to an inpatient unitwith the specific diagnoses, whereas others were judged ortreated during dialysis. The following definitions were usedfor clinical events. 12 Cardiac failure was defined as dyspnea and cardiomegaly,detected by radiograph, plus two of the following: bibasilarcrackles,pulmonaryvenoushypertensionorinterstitialedemaon chest radiograph requiring hospitalization or extra ultra-filtration. The diagnosis of ischemic heart disease was madeby the presence of angina, defined by interview and/ormyocardial infarction. Arrhythmia was considered an atrialor ventricular rhythm disorder requiring therapy.  Laboratory Evaluation Fasting laboratory determinations of serum hemoglobin,alkaline phosphatase, parathyroid hormone (intact molecule,radioimmunoassay), calcium, and phosphorus levels wereperformed predialysis during the same time period.  Echocardiography and Doppler Studies Standard two-dimensional and two-dimensionally guidedM-mode echocardiography was performed with a Diasonic(Vigmed Sound, Horten, Norway) 800 recorder using a3.5-MHz transducer. All studies were performed and ana-lyzed by the same experienced echocardiographer (A.B.),who was unaware of data concerning the patients. Studieswere performed on a midweek nondialysis day. Two-dimensionally guided M-mode echocardiograms were per-formedaccordingtotheAmericanSocietyofEchocardiogra-phy guidelines. 13 Measurements included left ventricularinternal diameter at end-diastole (LVIDD) and end-systole(LVISD), interventricular septal thickness (IVS), posteriorwall thickness at end-diastole (PWT), aortic root dimension,and left atrium dimension. Two-dimensional studies wereperformed from the parasternal long-axis and short-axisviews, apical four-chamber and apical long-axis two-chamber views, and subcostal views.Left ventricular fractional shortening (FS) was defined as:FS  (LVIDD  LVIDS)/LVIDD.Systolic dysfunction was considered left ventricular shorten-ing of 25% or less. 12 Left ventricular mass (LVM) was calculated from thefollowing formula 14 :LVM (g)  0.8  1.04 [(LVIDD  IVS  PWT) 3  LVIDD 3 ]  0.6Relative wall thickness (RWT) was calculated from thefollowing formula:RWT  2  PWT/LVIDDwith less than 0.45 as the value from normality.LVM index was calculated by dividing LVM by bodysurface area.LVH was defined in absolute terms as an LVM indexgreater than 131 g/m 2 in men and 110 g/m 2 in women. 14 Thefollowing patterns were categorized: concentric remodeling(normalLVMindexandincreasedRWT),eccentrichypertro-phy (increased LVM index and normal RWT), and concen-tric hypertrophy (increased LVM index and RWT). 15 Pulsed Doppler Echocardiography Two-dimensional guided pulsed Doppler interrogation of left ventricular inflow was performed from the apical two- orfour-chamber inflow between the mitral annulus and theleaflet tips, and recordings of left ventricular inflow velocityprofile were made at the point of maximal velocity of earlyvelocity. Doppler indices were measured directly onlineduring the examination: peak early diastolic velocity (E CARDIAC DISEASE IN ADPKD HD PATIENTS 265  wave), peak atrial diastolic velocity (A wave), decelerationtime of early velocity (time from peak E velocity to theextrapolation of the decline of the velocity to the baselinevalue), and isovolumic-relaxation time (time from aorticvalve closure to mitral valve opening). The early to atrialpeak velocity ratio (E/Aratio) was calculated.Previously defined echocardiographic and pulsed Dopplercriteria for mitral, aortic, and tricuspid valve defects wereused. 16 Regurgitation valvular lesions were classified asmild, moderate, or severe according to the degree of regurgi-tation. Mitral valve prolapse on M-mode and two-dimen-sional studies was defined according to the recent guide-lines. 17 Calcification of the mitral annulus was defined asdense echoes behind the posterior leaflet of the mitral valvemoving parallel and anterior to the endocardium of theposterior left ventricular wall. 18 By M-mode, the degree of mitral annulus calcification was measured in millimeters atits widest point behind the echoes srcinating from themitral valve. Severity was considered mild (  5 mm), mod-erate (6 to 10 mm), or severe (  10 mm). Aortic valvecalcification was defined as bright dense echoes of greaterthan 1 mm in one or more cusps and decreased mobility of the involved cusp thickening of the aortic valve leaflets. 19 Calcification was considered severe when the leaflets weremore highly reflective than surrounding structures and stoodout in sharp contrast to the less dominant background.Significant aortic stenosis was defined by two-dimen-sional or M-mode criteria and a maximum aortic flowvelocity greater than 2.2 m/seconds.Intraobserver variability in measurements of M-modeechocardiography and Doppler indices was calculated as thedifference between two measurements performed in thesamepatientbyoneobserverdividedbythemeanvalue.Theintraobserver variability was 5% for isovolumic-relaxationtime, 4.8% for deceleration time of early velocity, 2% for Ewave, 1% for A wave, 2.7% for LVIDD, 2.1% for LVISD,2.8% for IVS, 1% for PWT, and 3.3% for LVM.Subjects gave informed consent, and the study was ap-proved by the hospital ethics committee. Statistical Analysis Comparisons were performed between matched groupsusing the statistical package SPSS/PC  (IMC, Chicago, IL).For normally distributed variables, mean values and SDswere calculated and the means compared using the two-sample  t  -test or analysis of variance. For variables withnonparametric distribution, median values and ranges weredeterminedandtheMann-Whitneytestwasusedforcompari-sons. Categorical variables were compared using the chi-squared or Fisher’s exact test. Linear regression analysis wasused to established relationships between variables. A multipleregression model was used to identify independent determinantsoftheLVMindex.The yearly incidence of a cardiac event was calculated bydividing the number of events by the number of patient-years at risk. The proportions of patients free of cardiacevents during the follow-up on HD were compared betweenthe groups with the use of a Tarone-Ware method andKaplan-Meier estimates. Statistical significance was definedas  P  less than 0.05. RESULTS  Demographic and Clinical Data Clinical characteristics of the patients withADPKDandcontrolsarelistedinTable1.Groupsdid not differ in terms of age, sex, body massindex, dialysis duration, and interdialysis weightgain. Patients with ADPKD showed lower meanpredialytic systolic and diastolic BPs than con-trols. The proportion of patients with ADPKDreceiving antihypertensive medication and theaverage number of antihypertensive drugs re-quired were also less than those in controls.Angiotensin-converting enzyme inhibitors aloneor in combination with calcium channel blockerswere used in the same proportion in theADPKDand control groups: 3 (50%) versus 9 (69%) and6 (100%) versus 13 (100%), respectively. Thenumber of patients receiving rHuEPO treatmentwas greater in the control group than in theADPKD group. Table 1. Demographic and Clinical Data Variable ADPKD Control  P  Age(y) 64.1  8.6 65.5  7.6 NSMalesex,no.(%) 16(59) 15(47) NSBMI(kg/m 2 ) 25.5  4.1 24.5  3.8 NSMonthsondialysis 37(7-169) 40.5(8-264) NSInterdialysisweightgain(%) 3.8  1.1 3.3  1 NSSystolicBP(mmHg) 133.6  22.7 149.5  18.4 0.003DiastolicBP(mmHg) 74.2  12.3 81.4  9.7 0.01Hemoglobin(g/dL) 10.4  2.2 10.1  1.4 NSCalcium(mmol/L) 2.47  0.23 2.47  0.18 NSPhosphorus(mmol/L) 1.84  0.5 1.7  0.4 NSAlkalinephospha-tase(U/L) 152(66-1,100) 179(111-1,252) NSPTH(pg/mL) 146(5-1,005) 168(6-1,183) NSAntihypertensivetreatment,no.(%) 6(19) 13(41) NSAntihypertensivedrugsperpatient(no.) 1 1.6(1-3) 0.01RhuEPOtreat-mentno.(%) 8(25) 27(84) 0.00001Abbreviations: BMI, body mass index; rHuEPO, recom-binant human erythropoietin; BP, blood pressure; PTH,parathyroid hormone; NS, not significant.266 MARTINEZ-VEA ET AL   Echocardiographic and Pulsed Doppler Data Left ventricular wall thickness, left ventricularand aortic root dimensions, LVM index, and leftventricular fractional shortening were similar inthe two groups (Table 2). Peak E and A waveswere lower in the patients with ADPKD than incontrols,butE/Aratio,E-wavedecelerationtime,and isovolumic-relaxation period were similar inthe two groups. In the patients with ADPKD,simple regression analysis showed LVM indexwas correlated with hemoglobin level (inversecorrelation) and predialytic systolic and diastolicBPs, but not to age, fractional shortening, E/Aratio, duration of dialysis treatment, parathyroidhormone level, or any other biochemical vari-ables (Table 3).There were no differences in LVM index be-tween men and women or between patients re-ceiving antihypertensive drugs or rHuEPO andthose not receiving these treatments. Subsequentmultipleregressionanalysisshowedthatpredialy-sis systolic BP ( t     3.14;  P    0.003) was theonly independent variable linked to LVM index. Cardiac Complications There was no difference between patients withADPKD and controls in the prevalence of car-diac events (Table 4). Q wave myocardial infarc-tion with creatine kinase level elevation occurredin one patient of each group. The average yearlyincidence of cardiac failure, ischemic heart dis-ease, and arrhythmia was 2.7%, 2%, and 5% inpatients with ADPKD, respectively, and 3.8%,1.4%, and 2.4% in controls, respectively. Therisk for a cardiac event was similar in the twogroups (Fig 1). Hypertension was less prevalentin the ADPKD group. Systolic dysfunction anddiastolic patterns, LVH, and the prevalence of concentric or eccentric hypertrophy and concen-tric remodeling were similar in the two groups. Table 2. Echocardiographic and Doppler Data ADPKD Control  P  LVIDD (mm) 47.5  8.2 48.0  8.1 NSLVISD (mm) 29.8  8.5 29.7  6.3 NSIVS (mm) 13.4  3.3 13.4  6.3 NSPWT (mm) 13.0  2.6 13.9  2.6 NSRWT 0.56  0.13 0.60  0.18 NSLVM (g) 255.0  93.8 270.5  86.8 NSLVM index (g/m 2 ) 154.6  58.4 170.9  49.9 NSLVM index (g/m 2 )Men 147.6  53.9 183.0  51.8 NSWomen 161.6  63.6 160.3  47 NSLA(mm) 39.1  8.4 40.0  9.4 NSAO (mm) 34.7  5.3 33.5  3.5 NSD time (ms) 230  84 229  72 NSIR time (ms) 126  22 116  21 NSFS (%) 39  13 37.2  8.3 NSPeak E wave (m/s) 0.64  0.20 0.87  0.38 0.01PeakAwave (m/s) 0.73  0.26 1  0.31 0.004E/Aratio 0.99  0.63 0.88  0.31 NSHeart rate (beats/min) 75  9.6 79  9.7 NSAbbreviations: LVIDD, left ventricular internal diameterat end-diastole; LVISD, left ventricular internal diameter atend-systole; IVS, interventricular septal thickness; PWT,posterior wall thickness at end-diastole; RWT, relative wallthickness;LVM,leftventricularmass;LA,leftatriumdimen-sion; AO, aortic root dimension; D time, deceleration time;IR time, isovolumic relaxation time; FS, left ventricularfractional shortening; NS, not significant. Table 3. Univariate Correlation With the LVM Index Variable ADPKD  P   Control  P  Hemoglobin   0.37 0.03   0.007 NSSystolic BP 0.49 0.004 0.33 0.05Diastolic BP 0.41 0.01 0.32 0.07Age 0.28 NS 0.22 NSFS   0.03 NS 0.40 0.02E/A   0.22 NS 0.27 NSDialysis duration 0.13 NS 0.27 NSPTH 0.10 NS   0.10 NSNOTE. Data expressed as  r   determined by Pearson’scorrelation.Abbreviations: BP, blood pressure; FS, fractional short-ening; PTH, parathyroid hormone; NS, not significant. Table 4. Prevalence of Cardiac Complications Variable ADPKD Control  P  Cardiac failure 4 (12.5) 8 (25) NSIschemic heart disease 3 (9.4) 3 (9.4) NSArrhythmia 7 (21.9) 4 (12.5) NSHypertension 13 (40.6) 26 (81.3) 0.002E/Aratio  1 15 (65.2) 22 (73.3) NSSystolic dysfunction 3 (9.6) 2 (6.3) NSLVH 20 (62.5) 27 (84.3) NSConcentric LVH 17 (53.1) 22 (68.8) NSEccentric LVH 3 (9.4) 5 (15.6) NSConcentric remodeling 8 (25) 4 (12.5) NSNOTE. Values expressed as number (percent).Abbreviations: LVH, left ventricular hypertrophy; NS, notsignificant.CARDIAC DISEASE IN ADPKD HD PATIENTS 267  Comparisons for the prevalence of hypertensionand LVH remained unchanged after excludingthe eight control patients with hypertensive kid-ney disease. Cardiac Valvular Abnormalities The prevalence of aortic, mitral, and tricuspidregurgitationwassimilarinthetwogroups(Table5). Moderate or severe aortic valve regurgitationwas encountered more often in the control groupthan in the ADPKD group: 7 of 13 versus 0 of 7patients, respectively. Severity of mitral regurgi-tation was similar in the two groups.The frequency of aortic valve calcificationwas similar in the two groups, but calcification of the mitral annulus was less common in the pa-tients with ADPKD than in controls. Severeaortic calcification was present in 1 of 10 patientswith ADPKD and 2 of 16 controls. A greaterprevalence of moderate or severe mitral annuluscalcification was found in controls than in pa-tients with ADPKD: 10 of 19 versus 0 of 8,respectively.In theADPKD group, mitral and aortic calcifi-cation were associated more frequently with mi-tral ( P    0.01) and aortic regurgitation ( P   0.001), respectively. LVM index did not differ inpatients with ADPKD with or without cardiacvalvularabnormalities.Nopatienthadendocardi-tis or required valve replacement. DISCUSSION This study essentially compared the echocar-diographic data of patients with ADPKD under-going HD with those observed in a matchedcontrol group. This comparison can define theactual role of ADPKD in the occurrence of cardiovascular complications that are not neces-sarily related to the disease. We found there wereno marked differences in the prevalence of car-diac events and left ventricular disorders (sys-tolic dysfunction and diastolic patterns, LVH,and valvular abnormalities), but hypertensionwas less prevalent in theADPKD population.In this study, the proportion of hypertensivepatients, levels of predialysis BP, and averagenumber of antihypertensive drugs were less inthe patients with ADPKD than controls. The useof the average of all predialysis BP determina-tions during the 3 months preceding the studyreinforces these findings. Our results are at vari-ance with the high prevalence of hypertensionnormally reported in ADPKD studies, ranging Fig1. Kaplan-Meiercurvesfor freedom from cardiaceventsinpatientswithADPKD(dotted line) and controls(solidline).Table 5. Prevalence of Valve Disease Variable ADPKD Control  P  Aortic valve diseaseRegurgitation 7 (22) 13 (41) NSStenosis 1 (3) 3 (9) NSCalcification 10 (31) 16 (50) NSMitral valve diseaseRegurgitation 9 (28) 12 (37.5) NSStenosis 1 (3) 1 (3) NSProlapse 4 (12.5) 0 (0) NSCalcification 8 (25) 19 (59.4) 0.01Tricuspid valve diseaseRegurgitation 1 (3) 1 (3) NSNOTE. Values expressed as number (percent).268 MARTINEZ-VEA ET AL
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