|Year : 2013 | Volume
| Issue : 3 | Page : 127-132
Right ventricular dysfunction in patients with end-stage renal disease on regular hemodialysis
Mohamed Momtaz1, Hussein Al Fishawy1, Ula Mabid Aljarhi1, Rabei Z. Al-Ansi2, Mohamed A. Megid2, Mahmoud Khaled3
1 Department of Internal Medicine, Cairo University Hospital, Cairo, Egypt
2 Department of Cardiology, Cairo University Hospital, Cairo, Egypt
3 Department of Critical care, Cairo University Hospital, Cairo, Egypt
|Date of Submission||15-Apr-2013|
|Date of Acceptance||29-Jun-2013|
|Date of Web Publication||2-Jul-2014|
MD, Department of Internal Medicine, Cairo Hospital, 41 Manialstreet, 11451 Cairo
Source of Support: None, Conflict of Interest: None
Although there are considerable data on the changes in left ventricular function in hemodialysis (HD) patients, only a few studies on right ventricular (RV) function can be found in the literature. We investigated the changes in RV function in HD patients.
We examined 74 individuals grouped as follows: healthy controls (n=24) and HD patients (n=50). Echocardiography including tissue Doppler imaging (TDI) of the RV was performed in all patients.
HD patients had significantly lower RV systolic indices than control participants in right ventricle fractional area change (normal 35–63%) (37.54±9.86 vs. 43.5±4.8%, P<0.001), tricuspid plane systolic excursion (normal 1.6–3 cm) (2.09±0.49 vs. 2.61±0.36 cm, P<0.001), STDISº wave (7.99±1.37 vs. 9.66±1.86 cm/s, P<0.001), and LTDISº wave (peak systolic velocity at lateral tricuspid annulus; normal: 10–19 cm/s) (11.86±2.86 vs.16.04±3.60, P<0.001). HD patients had statistically significantly higher systolic pulmonary pressure (normal<35 mmHg at rest) compared with those in the control group (32.75±10.11 vs. 25.23±3.99, P<0.001). There were no statistically significant correlations between systolic pulmonary pressure and RV dimensions or RV function indices.
Subclinical RV dysfunction – as estimated by RV function indices; tricuspid plane systolic excursion, right ventricle fractional area change, and LTDISº – is increased among HD patients. A high prevalence of pulmonary hypertension was found among HD patients and this was not associated significantly with RV or left ventricular dysfunction in these patients.
Keywords: hemodialysis, pulmonary hypertension, right ventricular dysfunction
|How to cite this article:|
Momtaz M, Al Fishawy H, Aljarhi UM, Al-Ansi RZ, Megid MA, Khaled M. Right ventricular dysfunction in patients with end-stage renal disease on regular hemodialysis. Egypt J Intern Med 2013;25:127-32
|How to cite this URL:|
Momtaz M, Al Fishawy H, Aljarhi UM, Al-Ansi RZ, Megid MA, Khaled M. Right ventricular dysfunction in patients with end-stage renal disease on regular hemodialysis. Egypt J Intern Med [serial online] 2013 [cited 2020 May 31];25:127-32. Available from: http://www.esim.eg.net/text.asp?2013/25/3/127/135853
| Introduction|| |
Chronic renal failure (CRF) is associated with significantly increased morbidity and mortality. Chronic renal failure affects almost every system of the body and results in various functional and structural abnormalities. Cardiovascular complications are the main cause of death in patients with chronic kidney disease (CKD) undergoing hemodialysis (HD) therapy 1, 2, accounting for 40% of deaths in international registries 3.
The traditional risk factors for cardiovascular disease do not completely explain this high risk, which seems to be influenced by the so-called nontraditional risk factors associated with CKD 4. This set of factors accelerates the course of coronary artery disease 5 and is associated with a higher prevalence of ventricular hypertrophy, myocardial fibrosis, valvulopathies, arrhythmias, and sudden death 6.
The prevalence of clinical manifestations of cardiac disease at the start of end-stage renal disease (ESRD) therapy is high and these manifestations predict death independently 7,8. More than 50% of the individuals starting a dialysis program present some type of pre-existent cardiovascular disease 9. Clinical manifestations of cardiovascular disease were highly prevalent at the start of ESRD therapy: 14% had coronary artery disease, 19% had angina pectoris, 31% had cardiac failure, 7% had dysrhythmia, and 8% had peripheral vascular disease 10.
There is increasing evidence of the pivotal role of echocardiography in the improvement of quality of global clinical evaluation of advanced CKD patients. The current literature and clinical practice have emphasized the usefulness of the method for the diagnosis of clinical and subclinical cardiac dysfunction, the prediction of cardiovascular risk, and in the orientation and follow-up of treatment strategies. Guidelines recommend the echocardiogram for all HD patients 1–3 months after the start of renal replacement therapy and in intervals of 3 years subsequently, irrespective of the symptoms 11.
ESRD is associated with a variety of cardiac alterations including left ventricular hypertrophy (LVH), left ventricular (LV) dilation, and reduction in systolic and diastolic function, with only 16% of new dialysis patients presenting with normal cardiac morphology and function 12
On echocardiography, 15% had systolic dysfunction, 32% had LV dilatation, and 74% had LVH 13. Patients undergoing chronic HD show an increased prevalence of pulmonary hypertension during treatment, 15–20% 1,2.
However, although most available studies focused on LV function in dialysis patients, the impact of dialysis treatments on the development of right ventricular dysfunction (RVD) has not been fully investigated. However, recently, a retrospective study in which Paneni et al. 14 investigated the impact of different dialysis treatments on right ventricular (RV) function showed that compared with peritoneal dialysis, HD increases the risk of RVD, particularly in the presence of brachial ateriovenous fistula (AVF). A limitation of this study is its retrospective design.
| Patients and methods|| |
This is a prospective study that included 50 patients with end-stage renal failure on regular HD (group I). They were recruited from the nephrology and dialysis department, Cairo University (Kasr El-Ainy) hospital, from May 2011 to December 2011. We also included 24 age-matched and sex-matched healthy volunteers (without any cardiac or renal diseases) who served as the control group (group II).
Selection of patients
Patients on HD had been on regular 4 h HD sessions three times per week for at least 3 months using bicarbonate-buffered dialysate. All patients underwent full clinical evaluation and they also underwent chest radiography, standard 12-lead ECG, and arterial blood gas analysis. The exclusion criteria were defined by clinical or echocardiographic evidence of ischemic heart disease, LV dysfunction, valvulopathy, or previous renal transplantation. We also excluded patients with clinical conditions that might predispose to pulmonary hypertension (chronic obstructive pulmonary disease, interstitial lung diseases, connective tissue disorders, chronic thromboembolic disease, congenital left-to-right shunts, and primary pulmonary hypertension). Every participant provided informed consent and all the diagnostic procedures were approved by our institute’s ethics committee.
The entire study population underwent transthoracic echocardiography, including both conventional and tissue Doppler imaging (TDI) of the LV and the RV. Echocardiography was performed within 1 h after the completion of HD while the patients were at optimal dry weight to avoid any overestimation of pulmonary pressure because of volume overload. Images were obtained using a Philips iE33 (Philips Healthcare, Massachusetts, USA) with 2 and 2.5 MHz sector transducer equipped with the TDI mode. The study was carried out according to the criteria of the American Society of Echocardiography 15. LV volumes were estimated using the z-derived method. Ejection fraction (EF) of the LV was calculated using the Teicholz formula 16 and further confirmed using Simpson’s technique in the four-chamber view. The maximal tricuspid regurgitation velocity was measured by continuous wave Doppler echocardiography from the apical four-chamber view. The highest peak velocity was recorded and the average peak velocities from three beats were calculated. RV diameters were measured in the long axis view. EF of the RV was calculated using Simpson’s formula from the apical four-chamber view.
Data management and statistical analysis
The data were coded and entered on an IBM compatible computer using the statistical package SPSS version 16.0 (IBM Corporation, Armonk, New York, USA). All data sets were assessed for normality and distribution and appropriate tests were used accordingly. Descriptive statistics using the suitable measures of central tendency and dispersion were calculated to summarize the given data sets. The mean and the SD were mostly used for quantitative data. For qualitative data sets, percentages were used. Inferential statistics were used to assess differences between the studied groups and their comparison. Student’s t-test was used to assess differences between two unrelated groups in normally distributed quantitative variables. Qualitative variables were assessed using the χ2-test. The association between two quantitative variables was tested using the univariate analysis approach for quantitative variables, namely, simple linear correlation – regression. The Pearson correlation coefficient (r) was used to test the strength of the relationship, which varies from −1 to 1, where 0 indicates no relationship and 1 indicates a perfect linear relationship. The sign identifies the direction of the relationship, whether direct in case of a positive sign or inverse in case of a negative sign. All the above-mentioned statistical levels rejected the null hypothesis at a P value less than 0.05.
| Results|| |
No statistically significant differences were found among the groups in their age, sex, BMI and smoking, and systolic blood pressure; however, there was a significant increase in diastolic blood pressure and heart rate [Table 1].
Laboratory investigations showed a significant increase in blood urea, serum creatinine, potassium, and phosphors in the HD group compared with the control group and a statistically significant decrease in blood hemoglobin and calcium [Table 2].
By echocardiography, compared with the control group, the HD group showed a statistically significant increase in interventricular septal thickness (IVST; 0.99±0.21 vs. 0.83±0.13 cm, P<0.001), posterior ventricular wall thickness (PWT; 1.01±0.17 vs. 0.83±0.13 cm, P<0.001), and LV mass index (117.43±46.72 vs. 80.13±13.40 g/m2, P<0.001) [Table 3]. The prevalence of LVH by ECG was 28% (14 patients) versus 52% (26 patients) by echocardiography. The sensitivity and specificity was 50 and 95.83%, respectively, and the positive predictive value and negative predictive value were 92.85 and 63.88%, respectively [Table 4].
However, patients on HD showed a nonsignificant increase in RV dimensions compared with the control group, except for the long dimension of RV, which was higher in the HD group (7.23±0.87 vs. 6.36±0.79 cm, P<0.001) [Table 5]. The prevalence of an increase in RV diameters according to the mean lower limits of RV dimensions is shown in [Table 6]. Compared with the control group, HD patients had significantly lower RV systolic indices and there was a statistically significant decrease in right ventricular fractional area change (RVFAC; 37.54±9.86 vs. 43.5±4.8%, P<0.001), tricuspid plane systolic excursion (TAPSE; 2.09±0.49 vs. 2.61±0.36 cm, P<0.001), STDISº wave (7.99±1.37 vs. 9.66±1.86 cm/s, P<0.001), and LTDISº wave (11.86±2.86 vs. 16.04±3.60, P<0.001) [Table 7].
From [Table 8], it is clear that there were positive correlations between RV long, right atrium (RA) major, RA minor diameters and E and E/A. Also, there were positive correlations between RV mid cavity, proximal right ventricle outflow tract, RA minor diameters and left atrium diameter.
Patients on HD had statistically significantly higher systolic pulmonary pressure (SPAP) compared with those in the control group (32.75±10.11 vs. 25.23±3.99, P<0.001) [Table 9]. There were no correlations between SPAP and EF, IVST, and PWT. There were no statistically significant correlations between SPAP and RV dimensions or RV function indices [Table 10].
|Table 10: Correlations between SPAP and right-side, left-side parameters|
Click here to view
| Discussion|| |
Cardiovascular disease is the leading cause of mortality in patients undergoing dialysis, accounting for 50% of deaths 17. In particular, congestive heart failure is the most common finding in these patients and is associated with a poor prognosis 18.
HD, which is usually carried out through a surgically created native AVF, has been associated with an increased risk of pulmonary hypertension. In HD patients, AVF causes a left-to-right shunt, leading to chronic volume overload, independent of the increase in total body water, thus worsening RV overload 2.
Previous studies on the relation between pulmonary hypertension and dialysis have mostly investigated the impact of volume overload on TDI indices of LV function, showing an increased prevalence of diastolic dysfunction in these patients 19. However, although most available studies focused on LV function in dialysis patients, the impact of dialysis treatments on the development of RVD has not fully been investigated. However, in 2010, a retrospective study in which Paneni et al. 14 investigated the impact of different dialysis treatments on RV function showed that HD increases the risk of RVD, particularly in the presence of brachial AVF. One of the important limitations of that study was its retrospective nature.
In the present study, we investigated RV involvement in HD patients, in an attempt to determine the prevalence of RV dysfunction in these patients and find the correlates of RV dysfunction. Our study was prospective and was designed to investigate the impact of chronic dialysis therapy on RV function.
Patients on HD in our study showed a significant increase in LV mass index compared with the controls (117.43±46.72 vs. 80.13±13.40 g/m2, P<0.001); also, in our study, it was found that HD patients, compared with controls, showed a statistically significant increase in both IVST (0.99±0.21 vs. 0.83±0.13 cm, P<0.001) and PWT (1.01±0.17 vs. 0.83±0.13 cm, P<0.001). This finding was similar to that of the study of Said et al. 20 who found that HD led to an increase in IVST (1.1 vs. 1.0 cm, P=0.01) and PWT (1 vs. 0.95 cm, P=0.009); the LV mass index was 133.7 g/m2 (95–186.5 g/m2) (mean, range).
The prevalence of LVH by ECG in our study was 28% (14 patients) versus 52% (26 patients) by echocardiography. The sensitivity and specificity of ECG criteria were 50 and 95.83%, respectively, and the positive predictive and negative predictive values were 92.85 and 63.8%, respectively. In a recent comparable study carried out by Esquitin et al. 21 LV was detected better by echocardiography than by any of the ECG criteria (69 and 34%, respectively, of their study population).
Similar to Said et al. 20, we found no difference in the left ventricle ejection fraction (LVEF) between the HD group and the control group (62.50±11.6, 64.54±15.20%, P=0.525, respectively). However, Paneni et al. 14 found that the EF was significantly lower in HD patients than in peritoneal dialysis patients and controls (56.1±8.6, 62.4±9.8, 68.3±5.7%, P=0.001, respectively). The difference may be attributed to a relatively shorter duration of dialysis in our study patients than that in the study of Paneni and colleagues (37±18, 44±29 months, respectively).
No difference in RV dimensions was found between the two groups of our study, except for the long dimension of RV, which was higher in the HD group compared with the controls (7.23±0.87 vs. 6.36±0.79 cm, P<0.001). More importantly, a positive correlation was found between E/A and RV long diameters (P=0.005). This means that diastolic dysfunction of LV had an impact on RV dimensions.
The TAPSE is a good parameter to evaluate the RV function and it correlates closely with RVEF and RVFAC in a variety of patient populations 22. In our study, TAPSE was reduced (<1.6 cm) in 28% of the patients in the HD group. This may not only have been because of the effects of uremia on RV function but also the effect of hyperdynamic circulation because of AVF 23.
RVFAC is another measure of RV systolic function that has been shown to correlate well with RV EF by MRI 24. RVFAC was reduced in 20 patients (40%) of the HD group. A statistically significant decrease in RVFAC in the HD group than the control group was observed (37.54±9.86 vs. 43.5±4.8%, respectively, P<0.001). However, no correlation was detected between RVFAC and duration of HD, SPAP, LVEF, LV mass index, or E/A. Thus, the reduction in RVFAC was independent of LVH, diastolic dysfunction of the LV, and pulmonary hypertension. Further studies are needed to explore the cause for reduction in RVFAC in HD patients.
Twelve HD patients (24%) showed an abnormal decrease in lateral TDISº. Patients with HD had statistically significant lower lateral TDISº compared with the controls (11.86±2.86, 16.04±3.60 cm/s, P<0.001). Similar results were obtained by Paneni et al. 14 and Said et al. 20. Similar to the reduction in RVFAC, the decrease in lateral TDISº in the HD group was also independent of LVH, LV diastolic dysfunction, and pulmonary hypertension.
SPAP of 35 mmHg represents the cutoff value for pulmonary hypertension assessed by Doppler echocardiography 25. The long-term HD patients have a high prevalence of pulmonary hypertension 26. In our study, SPAP was increased in 17 HD patients (34%). The mean SPAP was 32.75±10.11 mmHg in HD patients and 25.23±3.99 in the control group (P<0.001). Comparable prevalence of pulmonary hypertension in HD patients was found by previous two studies in Egypt. Abdelwhab and Elshinnawy 27, Amin et al. 28; both detected increased SPAP among their HD populations (44.4 and 29%, respectively).
In the current study, on the basis of the Pearson linear correlation coefficient, there was a positive correlation between SPAP and left atrium (P=0.019), E wave (P=0.001), E/A ratio (P=0.027), right ventricle outflow tract proximal diameter (P=0.012), and septal TDISº (P=0.009). However, no significant correlation was found between SPAP and systolic right indices, RVFAC (P=0.223), LTDISº (P=0.335), TAPSE (P=0.223), or LVEF% (P=0.072). This means that the increased SPAP in the HD population could be attributed to left atrium and LV diastolic dysfunction, and may also be because of AVF, which causes a left-to-right shunt, leading to chronic volume overload.
| Conclusion|| |
This study confirmed a high prevalence of pulmonary hypertension among HD patients and that is not significantly associated with RV dysfunction in these patients. Subclinical RV dysfunction, as estimated by RV function indices, TAPSE, RVFAC, and LTDISº, is increased among HD patients. The reduction in RV systolic indices was independent of LVH, diastolic dysfunction of the LV, or pulmonary hypertension, whereas diastolic dysfunction of LV had an impact on RV dimensions.
| References|| |
|1.||No authors listed in this article. Causes of death. USRDS United States Renal Data System. Am J Kidney Dis 1997; 30:S107–S117. |
|2.||Foley RN, Parfrey PS, Sarnak MJ.Clinical epidemiology of cardiovascular disease in chronic renal disease.Am J Kidney Dis1998;32Suppl 3S112–S119. |
|3.||Fassbinder W, Brunner FP, Brynger H, Ehrich JHH, Geerlings W, Raine AEG, et al..Combined report on regular dialysis and transplantation in Europe, XX, 1989.Nephrol Dial Transplant1991;6Suppl 15–35. |
|4.||Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL, et al..Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association councils on kidney in cardiovascular disease, high blood pressure research, clinical cardiology and epidemiology and prevention.Circulation2003;108:2154–2169. |
|5.||Stenvinkel P, Pecoits Filho R, Lindholm B.Coronary artery disease in end-stage renal disease: no longer a simple plumbing problem.J Am Soc Nephrol2003;14:1927–1939. |
|6.||Parfrey PS, Foley RN.The clinical epidemiology of cardiac disease in chronic renal failure.J Am Soc Nephrol1999;10:1606–1615. |
|7.||Hutchinson TA, Thomas CD, Mac Gibbon B.Predicting survival in adults with end-stage renal failure: an age-equivalence index.Ann Intern Med1982;96:417–423. |
|8.||Collins AJ, Ma JZ, Umen A, Keshaviah P.Urea index and other predictors of hemodialysis patient survival.Am J Kidney Dis1994;23:272–282. |
|9.||Foley RN, Herzog CA, Collins AJ.Smoking and cardiovascular outcomes in dialysis patients: the United States renal data system wave 2 study.Kidney Int2003;63:1462–1467. |
|10.||Foley RN, Parfrey PS, Harnett JD, Kent GM, Martin CJ, Murray DC, et al..Clinical and echocardiographic disease in patients starting end-stage renal disease therapy.Kidney Int1995;47:186–192. |
|11.||No authors listed in this article. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis 2005; 45(Suppl 3):S1–S153. |
|12.||Curtis BM, Parfrey PS.Congestive heart failure in chronic kidney disease: disease-specific mechanisms of systolic and diastolic heart failure and management.Cardiol Clin2005;23:275–284. |
|13.||Greaves SC, Sharpe DN.Cardiovascular disease in patients with end-stage renal failure.Aust N Z J Med1992;22:153–159. |
|14.||Paneni F, Gregori M, Ciavarella GM, Sciarretta S, De Biase L, Marino L, et al..Right ventricular dysfunction in patients with end-stage renal disease.Am J Nephrol2010;32:432–438. |
|15.||Sahn DJ, DeMaria A, Kisslo J, Weyman A.Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements.Circulation1978;58:1072–1083. |
|16.||Teichholz LE, Kreulen T, Herman MV, Gorlin R.Problems in echocardiographic volume determinations: echocardiographic angiographic correlations in the presence or absence of asynergy.Am J Cardiol1976;37:7–11. |
|17.||Mohi Ud Din K, Bali HK, Banerjee S, Sakhuja V, Jha V.Silent myocardial ischemia and high-grade ventricular arrhythmias in patients on maintenance hemodialysis.Ren Fail2005;27:171–175. |
|18.||Trespalacios FC, Taylor AJ, Agodoa LY, Bakris GL, Abbott KC.Heart failure as a cause for hospitalization in chronic dialysis patients.Am J Kidney Dis2003;41:1267–1277. |
|19.||Gulel O, Soylu K, Yuksel S, Karaoglanoglu M, Cengiz K, Dilek M, et al..Evidence of left ventricular systolic and diastolic dysfunction by color tissue Doppler imaging despite normal ejection fraction in patients on chronic hemodialysis program.Echocardiography2008;25:569–574. |
|20.||Said K, Hassan M, Baligh E, Zayed B, Sorour K.Ventricular function in patients with end-stage renal disease starting dialysis therapy: a tissue Doppler imaging study.Echocardiography2012;29:1054–1059. |
|21.||Esquitin R, Razzouk L, Peterson GE, Wright JT Jr., Phillips RA, De Backer TL, et al..Left ventricular hypertrophy by electrocardiography and echocardiography in the African American Study of Kidney Disease Cohort Study.J Am Soc Hypertens2012;6:193–200. |
|22.||López Candales A, Dohi K, Rajagopalan N, Edelman K, Gulyasy B, Bazaz R.Defining normal variables of right ventricular size and function in pulmonary hypertension: an echocardiographic study.Postgrad Med J2008;84:40–45. |
|23.||Di Lullo L, Floccari F, Polito P.Right ventricular diastolic function in dialysis patients could be affected by vascular access.Nephron Clin Pract2011;118:c257–c261. |
|24.||Anavekar NS, Gerson D, Skali H, Kwong RY, Kent Yucel E, Solomon SD.Two-dimensional assessment of right ventricular function: an echocardiographic-MRI correlative study.Echocardiography2007;24:452–456. |
|25.||Nakhoul F, Yigla M, Gilman R, Reisner SA, Abassi Z.The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access.Nephrol Dial Transplant2005;20:1686–1692. |
|26.||Tarrass F, Benjelloun M, Medkouri G, Hachim K, Benghanem MG, Ramdani B.Doppler echocardiograph evaluation of pulmonary hypertension in patients undergoing hemodialysis.Hemodial Int2006;10:356–359. |
|27.||Abdelwhab S, Elshinnawy S.Pulmonary hypertension in chronic renal failure patients.Am J Nephrol2008;28:990–997. |
|28.||Amin M, Fawzy A, Hamid MA, Elhendy A.Pulmonary hypertension in patients with chronic renal failure: role of parathyroid hormone and pulmonary artery calcifications.Chest2003;124:2093–2097. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10]