Study of left ventricle hypertrophy, dilatation, and ejection fraction changes before and after kidney transplantation

Noha Mohamed Elkohly; Mohamed Abdelnasr Abdelkareem Abdelfadeel; Eman Mohamed Elsharqawy; Montasser Mohamed Zeid

doi:10.4103/jesnt.jesnt_30_21

ORIGINAL ARTICLES

Year : 2022 | Volume : 22 | Issue : 3 | Page : 154-162

Study of left ventricle hypertrophy, dilatation, and ejection fraction changes before and after kidney transplantation

Noha Mohamed Elkohly, Mohamed Abdelnasr Abdelkareem Abdelfadeel, Eman Mohamed Elsharqawy, Montasser Mohamed Zeid
Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt

Date of Submission	11-Oct-2021
Date of Acceptance	27-Dec-2021
Date of Web Publication	22-Jul-2022

Correspondence Address:
Dr. Noha Mohamed Elkohly
Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Semouha, Alexandria
Egypt

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/jesnt.jesnt_30_21

Abstract

Background People with end-stage renal disease (ESRD) are at risk of developing serious cardiovascular complications. Left ventricular hypertrophy is the most prevalent cardiac finding observed. Renal transplantation is the best renal replacement modality offered to these patients with an expected improvement in cardiovascular complications. The aim of this work the present study aims to compare changes in left ventricle hypertrophy, dilatation, and ejection fraction before and after kidney transplantation. Patients and methods This cross-sectional study included 30 renal transplant recipients. Echocardiography was performed for all patients before transplantation and 6–12 months after transplantation. Patients with a reported history of posttransplant rejection or heart failure were excluded from the study. All patients were on hemodialysis before transplantation, and the mean postrenal transplant duration was 10.33 ± 1.95 months. All patients received the same posttransplant immunosuppressive regimen. Results The mean left ventricular ejection fraction before and after renal transplantation was 59.70 ± 7.86 and 68.82 ± 7.93, respectively (P<0.001). The mean left ventricular mass index showed a significant improvement from 144.1 ± 44.15 before transplant to 115.1 ± 38.79 after transplant, with a P value of 0.002. Conclusion According to the results of this study, renal transplantation can improve left ventricle parameters in patients with ESRD.

Keywords: cardiovascular, chronic kidney disease, echocardiography, renal transplantation

How to cite this article:
Elkohly NM, Abdelfadeel MA, Elsharqawy EM, Zeid MM. Study of left ventricle hypertrophy, dilatation, and ejection fraction changes before and after kidney transplantation. J Egypt Soc Nephrol Transplant 2022;22:154-62

How to cite this URL:
Elkohly NM, Abdelfadeel MA, Elsharqawy EM, Zeid MM. Study of left ventricle hypertrophy, dilatation, and ejection fraction changes before and after kidney transplantation. J Egypt Soc Nephrol Transplant [serial online] 2022 [cited 2023 Mar 25];22:154-62. Available from: http://www.jesnt.eg.net/text.asp?2022/22/3/154/351711

Introduction

Uremia has been proven to affect the normal physiology of several organs, including the heart [1]. Echocardiography studies have revealed adverse changes in cardiac muscle structure and function related to end-stage renal disease (ESRD), which is termed uremic cardiomyopathy. These cardiac abnormalities, such as left ventricular hypertrophy (LVH) and systolic dysfunction, are more common in hemodialysis (HD) patients and are linked to high risk of adverse clinical outcomes [2]. Kidney transplantation is the treatment of choice for certain patients with ESRD. A successful kidney transplantation enhances the quality of life and decreases the mortality risk for most patients more than in patients who undergo maintenance dialysis [3].

LVH in chronic kidney disease (CKD) and ESRD

Although coronary atherosclerosis is the leading cause of cardiovascular (CV) mortality in the general population, LVH and vascular calcification are the leading and the most common CV abnormalities among patients with CKD. LVH is present in 75% of patients at the onset of dialysis [4,5].

Types of LVH

The relation between pressure and volume overload affects the type of subsequent LVH.

If the main stimulus is volume overload, there is an elevation in diastolic pressure, which initially leads to the addition of new sarcomeres followed by new sarcomeres in parallel, leading to an eccentric LVH where the increase in wall thickness is just adequate to counterbalance the increased radius, and consequently, the relative wall thickness in these patients (wall thickness/ventricular radius) is <0.45 [6].

If the main stimulus is pressure overload, then LVH is linked to systolic or pulse pressure. Pressure overload will lead to parallel addition of new sarcomeres with a disproportionate increase in ventricular wall thickness at normal radius, which is named concentric LVH. Because the left ventricle will not change its internal dimensions, the relative wall thickness for these patients is >0.45. Despite the increase in wall thickness, the ventricle does not increase in radius [7].

Both volume and pressure overload are present in patients with CKD and ESRD [6].

Causes and pathogenesis of LVH in CKD

The pathogenesis of LVH in patients with CKD is multifactorial [8].

We can generally divide the pathogenetic factors leading to LVH ESRD into three categories [9]:

(1) Afterload-related factors.

(2) Preload-related factors.

(3) No afterload- or preload-related factors.

Afterload-related factors

They include systemic elevated arterial blood pressure (BP), arterial resistance, and also large-vessel compliance [10].

The large vessel compliance may be linked to aortic “calcification,” which is detected in CKD and in ESRD.

These afterload-related factors lead to myocardial cell thickening and concentric LV remodeling [10].

RAS activation

Activation of the intracardiac renin-angiotensin system (RAS) appears to have a significant role in this pathway; nonetheless, angiotensin II and aldosterone can also be involved in the development of myocardial cell hypertrophy and fibrosis [11,12].

Hyperaldosteronemia leads to cardiac fibrosis, through the generation of signals that stimulate the production of profibrotic transforming growth factor β [13].

Preload-related factors

Multiple factors such as intravascular volume expansion are mainly owing to salt and fluid loading, anemia, as well as large flow arteriovenous fistulas (AVFs).

These factors lead to myocardial cell lengthening and eccentric LV remodeling.

This can result in progressive impairment in contractility and stiffening of myocardial wall, resulting in systolic and diastolic dysfunction and eventually to dilated cardiomyopathy and congestive heart failure. Moreover, intermyocardial fibrosis also leads to disorders in the electrical circuitry of the heart, leading to ventricular arrhythmogenesis is (e.g., ventricular fibrillation).

Other nonpreload- and nonafterload-related factors

These include iron and erythropoietin deficiency (associated with anemia), and carnitine deficiency may also promote LVH [14].

Vitamin D deficiency and LVH

Vitamin D deficiency can stimulate the intracardiac RAS, and the use of active vitamin D supplementation can lead to regression of LVH and/or cardiac fibrosis [15].

Role of AVFs in pathogenesis of LVH

AVFs can participate in LVH as suggested by findings that much lower frequency of LVH is observed in patients receiving continuous ambulatory peritoneal dialysis in comparison with HD [16].

High blood flow through an AVF can contribute to the development of LVH [16,17].

Role of hypoalbuminemia

Hypoalbuminemia has also been associated with an elevated risk of LVH among HD patients, and this may be owing to “microinflammation” or a “negative” acute phase response [18].

Hyperparathyroidism and LVH

Elevated levels of calcium and phosphorous are linked to secondary hyperparathyroidism and have been associated with the development of vascular calcification, and parathyroid hormone (PTH) has already been identified as a serious cardiotoxin in ESRD [19].

Although the exact mechanisms remain uncertain, PTH can stimulate the secretion of aldosterone, a known mediator of cardiac hypertrophy and myocardial fibrosis [20].

Parathyroidectomy has been revealed to cause a reduction in LV mass, supporting the pathologic role for high PTH levels in the generation of LVH [20].

Chronic inflammation and LVH

In brief, inflammation, as previously demonstrated, causes low serum albumin and high C-reactive protein (CRP) and appears to significantly contribute to the development and progression of LVH in patients with CKD [21].

Fibrinogen is now considered a conventional predictor of CV events [22,23].

LV mass assessment in patients with CKD and ESRD

Electrocardiographic study (ECG) was the first noninvasive investigation used to diagnose LVH, but its accuracy in excluding LVH is relatively unsatisfactory [24,25].

Cardiac magnetic resonance imaging (CMRI) is generally considered the “gold standard” method for assessing LV dimensions and can also evaluate fibrosis [26].

Cine-computed cardiac tomography can also precisely measure LV mass, but it includes radiation and its availability is limited [27].

Cardiac biomarkers

Cardiac biomarkers include troponin T and NT-pro-brain natriuretic peptide. These plasma biomarkers are evidenced to be valuable in the diagnosis and prognosis of myocardiopathy linked to further advanced stages of CKD. Nevertheless, they do not substitute CMRI or ECHO-based imaging procedures [28].

Echocardiography for LV assessment

To date, most LV mass estimations used linear measurements consequent from the M-mode ECHO.

LVM index

The LV mass is proportionate to body volume, and the indexation by body surface area has been usually used for this calculation in standard studies.

It is important to highlight that some of the variations in the LV geometry in uremic patients might be linked to the time when the echocardiogram is done. Shortly after a HD session, a decrease in the LV diastolic diameter is common as a direct result of volume depletion due to ultrafiltration. Likewise, evaluation made before the HD session can detect LV dilatation with eccentric hypertrophy, and that will be “transformed” into concentric at the end of the session. These variations can lead to assessment faults, which can be reduced by performing the examination on interdialytic days [29].

Renal transplantation

Structural and functional cardiac abnormalities after renal transplantation

Early evaluation of posttransplantation cardiac abnormalities using unidimensional echocardiography (M-mode) was revealed in the 1980 decade. Although with small samples, those studies had already indicated a tendency in the direction of decreased cardiac volumes after the operation [30], along with better parameters of systolic function [31] and quite early regression (3 weeks) of LV mass index [32].

In contrast, other studies have failed to prove any cardiac change after renal transplantation.

In the first study that included only children and adolescents, in which transplanted individuals were compared with patients on dialysis, only the latter just revealed a diastolic dysfunction [33]. More recent studies like Dudziak et al. [34] have proven improvement of diastolic function after renal transplantation, during an average follow-up time of about 30 months.

Factors responsible for cardiac changes after renal transplantation

Arteriovenous fistula (AVF)

A study of 20 renal transplant recipients, 4 months after AVF closure, reported a decrease in LV diastolic diameter and mass index [35]. Unger et al. [36] also detected a significant decrease in LV mass index with a 21-month follow-up study after AVF closure. Cridlig et al. [16] demonstrated in a recent case–control study that a patent AVF has a significant effect on LV mass and dimensions.

Immunosuppression drugs

Immunosuppressant drugs may have an effect on cardiac changes after renal transplantation. In a recent study, which extensively examined serum levels of cyclosporine, a substantially lower prevalence of diastolic dysfunction was detected at lower drug levels [37]. Paoletti et al. [38], in a nonrandomized, single-center study, illustrated that conversion from calcineurin inhibitor to sirolimus can favor LVH reversion after renal transplantation, in spite of variations in the arterial blood pressure.

Other factors

It is evident that systolic blood pressure control, improvement in graft function [39,40], normalization of hemoglobin level, and adequate decrease in nocturnal systolic blood pressure [41] are also significantly associated with LVH regression [42,43].

Cardiovascular complications after renal transplantation

The development of new CVD risk factors or deterioration of preexisting factors in the posttransplant period may develop hyperhomocysteinemia, renal allograft dysfunction, proteinuria, and elevated serum C-reactive protein concentrations, all of which could dependently have a substantial effect [44,45].

Aim of the work

The aim of this work was to investigate the changes in left ventricle hypertrophy, dilatation, and ejection fraction (EF) before and after kidney transplantation.

Patients

In this study, 30 patients with ESRD who underwent renal transplantation in Alexandria University Hospital were included.

By using G power 3 software for sample size calculation and based on the expected difference in the LVH before (2.35 ± 0.57) vs. after kidney transplantation (1.95 ± 0.51) (1), the minimum sample size required is 17 patients to achieve 80% study power within 95% confidence limits.

Inclusion criteria

The following were the inclusion criteria:

(1) All patients who received living kidney grafts.

(2) All evaluated patients were on HD treatment for more than 3 months before renal transplantation.

Exclusion criteria

The following were the exclusion criteria:

(1) Patients with acute rejection, chronic allograft nephropathy with progressive impairment of renal function in the first 3 posttransplant months.

(2) Patients with posttransplant heart failure.

(3) Patients older than 70 years or younger than 16 years.

Methods

All patients were subjected to the following:

(1) Full history taking including the duration of ESRD, hypertension, diabetes mellitus, medications, and duration of HD.

(2) Full clinical examination.

(3) Renal transplantation:
- (a) All patients had received living kidney grafts and received the same medical regimen, including tacrolimus, mycophenolate mofetil, and prednisone.
(4) Echocardiographic study was done for all patients before renal transplant procedure in the interdialytic day and then the echocardiogram is followed up for 6 months to 1 year after renal transplantation.

Echocardiography [46]

Standard transthoracic M-Mode, two-dimensional, continuous, and pulsed wave Doppler echocardiography were utilized to measure the following:

(1) Left ventricular end diastolic dimension (LVEDD).

(2) Left ventricular end systolic dimension (LVESD).

(3) Left ventricular posterior wall thickness (LVPWT).

(4) Interventricular thickness (IVST).

(5) Left ventricular wall thickness (LVM) was calculated according to the following formula (g/m²):

EF is the percentage change in LV volume between systole and diastole:

Detect any valvular abnormalities, calcification, pericardial effusion, or wall motion abnormalities.

Statistical analysis of the data

The data were fed to the computer and analyzed using IBM SPSS software package version 20.0 (IBM Corp., Armonk, NY).

The Kolmogorov–Smirnov test was used to verify the normality of distribution of variables. Paired t-test was used for comparison between two periods for normally distributed quantitative variables, whereas Wilcoxon signed-rank test was used for comparison between two periods for abnormally distributed quantitative variables. Significance of the obtained results was judged at the 5% level.

Results

In the studied group, 22 patients were males (73.3%), whereas 26.7% were females ([Table 1]).

Table 1: Distribution of the studied cases according to demographic data (n=30)

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The age ranged between 18 and 59 years, with a mean age of 34.13 ± 11.80 years ([Table 2]).

Table 2: Descriptive analysis of the studied cases according to duration (n=30) figure

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Duration of hemodialysis among the studied patients ranged from 3 to 60 months, whereas echo was done after transplantation at 6–12 months ([Table 2]).

The represented findings in the echocardiographic studies done for the patients before and after transplant revealed that the pretransplant echo was done while patients were on HD for a period ranging from 3 to 60 months, whereas the posttransplant echo was done after a period ranging from 6 to 12 months after the operation.

Regarding haemoglobin level, there was a significant difference between the two groups, with a significantly lower hemoglobin in the pretransplant dialysis patients, where hemoglobin (Hb) level ranged from 7.8–12 g/dl in the pretransplant group, whereas ranged from 11.9–15 g/dl in the posttransplant group ([Table 3]).

Table 3: Comparison between the two studied periods according to Hb (n=30)

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As for the prevalence of LVH in the pretransplant group calculated from left ventricular mass index (LVMI), LVH was found in 25 of 30 patients (83.3%) ([Table 4]).

Table 4: Distribution of the patients with CKD according to prevalence of LVH calculated according to LVMI (n=30)

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There was no significant correlation between hemoglobin level and LVMI in both studied groups ([Table 5]).

Table 5: Correlation between LVMI (kg/m²) and Hb (n=30)

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The mean EF before transplant was 59.70 ± 7.86% and after transplant was 68.82 ± 7.93% ([Table 6]).

Table 6: Comparison between the two studied periods according to ejection fraction (EF%) (n=30)

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There was a statistically significant increase in EF between the two studied periods (P<0.001) ([Table 6]).

There was a statistically significant decrease in LVEDD between the two studied periods (P<0.001), where LVEDD ranged from 37 to 71 mm in the pretransplant vs. 30 to 59 mm in the posttransplant group ([Table 7]).

Table 7: Comparison between the two studied periods according to LVEDD, LVESD, and IVS (n=30)

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There was a statistically significant difference between the studied periods regarding LVESD (P<0.001), where LVESD ranged from 22 to 56 mm in the pretransplant group vs. 15 to 42 mm in the posttransplant group ([Table 7]).

However, there was no statistically significant difference between the studied periods regarding IVS (P=0.305) ([Table 7]).

There was no statistically significant difference between the studied periods regarding posterior wall (PW) (P=0.535) ([Table 8]).

Table 8: Comparison between the two studied periods according to LV-PW, LVMI, and PW (n=30)

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There was a statistically significant difference between the two studied periods regarding LVMI that was significantly lower in the posttransplant group (P=0.002), where LVMI in the pretransplant group ranged from 65 to 228 kg/m² vs. 41 to 247 kg/m² in the posttransplant group ([Table 8]).

There was statistically significant difference between left atrium diameter between the two studied groups, where it was significantly lower in the posttransplant group (P<0.001), where LA diameter in the pretransplant group ranged from 28 to 54 mm vs. 27 to 41 mm in the posttransplant group ([Table 8]).

Discussion

CKD is considered as a major health problem for ~13% of the United States population [47].

CV disease is a main cause of morbidity and mortality in patients with CKD, particularly in those with ESRD undergoing three times HD weekly. Indeed, the CV-related mortality risk is 10- to 20-times higher in HD individuals [48,49].

LVH has been demonstrated in 40% of patients with moderate renal insufficiency, and 75% of those starting dialysis. Both forms of LVH (concentric and eccentric) are manifested in ESRD [49].

The present study included 30 patients (30 transplant recipients). The studied group consisted of 73.3% males and 26.7% females. This sex distribution shows a higher proportion of males more than females, and this may be owing to the relatively high prevalence of CKD among men compared with women [26]. The mean age was 34.13 ± 11.80 years, and there were 13 (43.3%) individuals less than 30 years.

Early evaluation of posttransplantation cardiac abnormalities using unidimensional echocardiography (M-mode) was done in 1980. Despite the small samples, these studies have already indicated a tendency toward decreased postcardiac volumes [30], along with the best parameters of systolic function [31] and quite early regression (3 weeks) of LV mass index [32]. Through evaluating a group of patients with juvenile diabetes, Larsson et al. [50] detected a significant decrease of 37% in ventricular mass, 44 months after the renal transplantation, in addition to a decrease of the LV systolic and diastolic volumes, with consequential rise of the EF and improved LV distensibility and filling patterns.

With the aid of bidimensional echocardiography, more robust studies have been published, with conflicting results. One of these studies, evaluating more than 40 patients, exhibited a significant decrease in the ventricular mass and cardiac volumes, although there was no effect on the diastolic function [51]. However, Hüting [52], in a quite prolonged follow-up study (>40 months), evaluated 24 patients on HD, and there was no decrease in ventricular mass.

Peteiro et al. [53] established a significant decrease of the LV mass and volumes, about 10 months after renal transplantation, especially in the subgroup with good arterial pressure control, and two other recent studies demonstrated significant cardiac changes after renal transplantation. One such study evaluated 50 patients before renal transplantation as well as 3 months after renal transplantation and revealed significant improvement in EF and reduction in the chamber diameters [54]. Another retrospective study in 30 individuals revealed a significant decrease in LVH and diastolic dysfunction about 1 year after renal transplantation [55]. Another study on a larger sample size, including more than 100 individuals, revealed a decrease in LVMI and of LV diastolic volume, after renal transplantation [56].

In contrast, other studies have failed to prove any cardiac change after renal transplantation. De Lima et al. [57] did not detect any significant decrease in ventricular hypertrophy, or any influence on LV systolic and diastolic functions during a 30-month follow-up after renal transplantation.

In the present study, we noticed a substantial effect of renal transplant on cardiac functions in general and the left ventricular function in particular. Not only did the echocardiographic parameters improve but also the patient’s performance. Patient performace was assessed with regular follow-up. There was significant improvement in effort tolerability and exercise, and there was also less dyspnea and fatiguability in comparison with the pretransplant period. These changes were attributed to improvement in several risk factors. Hypertension as a major risk factor for cardiac dysfunction was not cured but became easily controlled due to correction of the volume status. Uremic state as a chronic inflammatory condition and posttransplant anemia were also improved.

In the present study, there was a significant improvement in left ventricular functions after transplant. The EF increased, the left ventricular volumes (end systolic and end diastolic volumes) decreased, left ventricular post wall thickness and inter ventricular septum slightly decreased, and the LVMI significantly decreased.

These findings are supported by many studies including Hawwa et al. [58], who conducted a study on 232 recipients, found that there was a significant increase in EF and a significant decrease in LVMI and left ventricular dimensions. Garcia-Covarrubias et al. [59] obtained similar results and significant improvement in all echocardiographic, ECG, radiographic, and clinical parameters 6 months after renal transplantation.

Conclusions

From the present study, we can conclude the following:

(1) LVH is prevalent in patients with CKD owing to several risk factors that have been found in patients with CKD and ESRD and has been aggravated by HD.

(2) Renal transplantation is the preferred treatment for CKD, and it can reverse its bad effect on the CV system.

(3) Echocardiography can be used to assess the improvement in left ventricular functions and mass index after renal transplantation 6–12 months after transplant.

Recommendations

(1) Renal transplant is the treatment of choice for CKD, and it can improve cardiac functions.

(2) Echocardiography can assess improvement in cardiac functions and reverse remodeling in cardiac muscle after transplant.

Acknowledgements

The manuscript has been read and approved by all the authors, that the requirements for authorship as stated earlier in this document have been met, and that each author believes that the manuscript represents honest work, if that information is not provided in another form.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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