The Effects of Vitamin D on Myocardial Function Demonstrated by Speckle Tracking Echocardiography in Children With Βeta Thalassemia

doi:10.21203/rs.3.rs-1751055/v1

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The Effects of Vitamin D on Myocardial Function Demonstrated by Speckle Tracking Echocardiography in Children With Βeta Thalassemia

https://doi.org/10.21203/rs.3.rs-1751055/v1

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Objective: β-thalassemia major is an inherited hemoglobin disorder resulting in chronic hemolytic anemia. Cardiac involvement is the main cause of death in patients. Speckle-tracking echocardiography is feasible method for the evaluation of cardiac function via an assessment of the longitudinal deformation of the myocardium through the cardiac cycle. The aim of our study is to evaluate the association of vitamin D deficiency and deformation of the left ventricular myocardium measured by speckle-tracking echocardiography in children with thalassemia major.

Methods: In this prospective study, 33 thalassemic patients with vitamin D deficiency were enrolled. Cardiac magnetic resonance T2* value, conventional echocardiography and speckle tracking, left ventricle longitudinal and circumferential strain values were measured. Vitamin D level <20 ng/ml deficient, 20-30 ng/ml insufficient, >30 ng/ml considered sufficient. Myocardial functions of patients with vitamin D deficiency or insufficiency were evaluated by speckle-tracking echocardiography before and after vitamin D replacement.

Results: The mean age of our patients was 15.4 ± 3.09 years, male / female ratio was 18/15. Vitamin D level was deficient in 30 (90%) and insufficient in 3 (10%) of our patients. Speckle-tracking analysis showed a significantly decreased absolute value of left ventricle global longitudinal strain before vitamin D replacement. A significant improvement in the global longitudinal strain of left ventricular after vitamin D replacement was detected (p<0.05). A statistically significant increase was observed in parameters showing left ventricular systolic and diastolic functions after vitamin D replacement.

Conclusion: Vitamin D deficiency are frequently observed and vitamin D deficiency causes decreased contractility and leads to an increase in cardiac iron in thalassemic patients. In our study, we observed that our patients cardiac functions had improved after vitamin D replacement therapy. Further prospective studies are needed to evaluate the relationship between vitamin D levels and cardiac function in patients with these patients.

Thalassemia major

vitamin D

cardiac function

Beta thalassemia major (β-TM) is an autosomal recessive disorder caused by the homozygous deletion of the β-globin chain gene and characterized by microcytic hypochromic anemia [1]. Frequent erythrocyte transfusion and iron chelation therapy are the mainstays of the treatment. Despite significant improvements in the treatment, due to frequent blood transfusions patients are susceptible to excess iron deposition in vital organs like the heart, liver, and endocrine glands [2]. Although iron-chelating agents have a vastly improved prognosis, iron overload may initiate structural changes in the myocardium which can eventually lead to heart failure which is considered the major cause of death in thalassemic patients [3].

Vitamin D deficiency is common in patients with β-TM due to decreased outdoor activities and limited sun exposure, genetic and cultural factors, or dark skin. Furthermore, vitamin D deficiency may be due to decreased synthesis of 25- hydroxyl-vitamin D (25-OH vitamin D) as a result of iron accumulation in the liver.

Epidemiologic studies have shown that vitamin D deficiency was associated with chronic diseases such as cancer, diabetes, autoimmune diseases, and cardiovascular disease (hypertension, coronary artery disease, peripheral artery disease, heart failure, and stroke) [4]. Vitamin D deficiency leads to an increase in serum parathyroid hormone (PTH). The PTH affects the myocardium directly through downstream actions of G protein-coupled receptors and is associated with a decrease in cardiac function, muscle weakness, and left ventricular hypertrophy [5, 6]. Also, vitamin D can also affect cardiac function by regulating the renin–angiotensin–aldosterone system, and regulating blood pressure effects. Activated vitamin D suppresses renin gene expression in vitro and regulates the growth and proliferation of vascular smooth muscle cells and cardiomyocytes [7].

However, the effect of vitamin D deficiency on the deformation parameters of the myocardium is very limited.

In thalassemic patients, conventional echocardiography which examines ejection fraction and fractional shortening are not exactly adequate for early diagnosis of cardiac iron overload and subclinical cardiac systolic dysfunction. Speckle-tracking echocardiography (STE) is a relatively novel and sensitive echocardiographic modality and appears to be capable of providing a useful regional functional assessment of myocardial segments via an assessment of the longitudinal deformation of the myocardium through the cardiac cycle. Speckle-tracking echocardiography can assess regional and/or globally subtle LV myocardial impairment with strain and strain rate measurements[8].

The aim of this study was to evaluate myocardial function using speckle STE methods in children with thalassemia major with no obvious heart disease. Speckle-tracking echocardiography is a method that has been recently developed that evaluates methods of myocardial function, even in the absence of clinical signs of abnormal cardiac function. To our knowledge, there is no study which used both TDI and STE to assess both left ventricle (LV) and right ventricle (RV) function in children with thalassemia major and the relationship between vitamin D levels and cardiac function in patients with these patients.

Study Population

This prospective study enrolled 33 patients with transfusion-dependent thalassemia who were followed at Pediatric Hematology-Oncology Department from April 2018-January 2021. Inclusion criteria were 1) Transfusion-dependent β-thalassemia major patients with regular monthly transfusions, 2) age between 5 and 25 years, 3) No active liver or kidney disease, 4) Serum 25-OHD3 < 30 ng/mL, 5) No history of vitamin D injection in the preceding 6 months. Exclusion criteria were 1) the presence of congenital heart disease, liver disease, renal disease, type 1 diabetes. Data including gender, age, hemoglobin levels, ferritin levels, chelation therapy type were obtained from medical records. Calcium, phosphate, alkaline phosphatase, PTH, and vitamin D levels were measured.

Clinical Data

Cardiac function, left ventricular ejection fraction (LVEF), and left ventricular shortening fraction (LVSF), was evaluated by conventional echocardiography, a commercially available ultrasound system (iE33, Philips, The Netherlands, Eindhoven), equipped with a broadband (1–5 MHz) S5 transducer was used to obtain 2D grayscale harmonic images at a frame rate of 60–80 frames per second (frames/s). Two-dimensional and M-mode echocardiography was used to measure left ventricular end-diastolic and endsystolic diameter, end-diastolic septal and posterior wall thickness, EF and shortening fraction (FS), according to the guidelines of the American Society of Echocardiography [9].

All two-dimensional STE analyses were performed by the same investigator to avoid inter-observer variability. Myocardial deformation parameters (S and SR) were measured using commercially available software (QLAB Advanced Quantification Software, version 6.0, TMQ, Philips Medical systems, Best, The Netherlands, Eindhoven) on standard 2D grayscale LV images from the standard apical 4-chamber view (AP4) for longitudinal strain and standard parasternal short axis at the papillary muscle level (PML) for circumferential strain. Two consecutive beats synchronized to a continous electrocardiography (ECG) were recorded with frame rate set to > 60 frames/s. The data were transferred to the QLAB software system for off-line analysis. The endocardial borders were identified manually to include the entire myocardium in all view areas. The following peak systolic LV and RV STE parameters were measured:

LVGLS: Left ventricular global longitudinal strain at AP4,
LVGLSR: Left ventricular global longitudinal strain rate at AP4,
LVGCS: Left ventricular global circumferential strain at PML,
LVGCSR: Left ventricular global circumferential strain rate at PML,
RVGLS: Right ventricular global longitudinal strain at AP4,
RVGLSR: Right ventricular global longitudinal strain rate at AP4.

Cardiac iron was determined by cardiac T2* magnetic resonance imaging (MRI). Cardiac iron overload was defined as cardiac T2∗ ≤ 20 ms. Vitamin D level < 20 ng/mL indicated deficiency; 20–30 ng/ml indicated insufficient, > 30 ng/ml indicated sufficient. PTH level > 65 pg/mL indicated hyperparathyroidism. Vitamin D replacement was given to patients with deficient or insufficient and it was observed that vitamin D levels came to normal. Myocardial functions of patients with vitamin D deficiency or insufficiency were evaluated by conventional echocardiography and STE before and after vitamin D replacement.

The study protocol was reviewed and approved by the Ethics Committee at the Ankara Children’s Hematology and Oncology Research and Training Hospital. Assent and informed consent were obtained from all participants and their parents or legal guardians.

Statistical analysis

SPSS for Windows (version 18; SPSS Inc., Chicago, IL, USA) was used for the statistical analysis. Kolmogorov-Smirnov test was used to analyze the distribution of continuous variables. Numeric variables are expressed as the mean ± standard deviation (SD) and median. Chi-square analysis were used to compare continuous and categorical variables between groups. Comparisons of demographic data and echocardiographic parameters between patients and controls were performed using Mann-Whitney U test for non-normally distributed variables. A difference was considered statistically significant at a p value of < 0.05. Spearman’s correlation coefficient was used to disclose possible correlations between vitamin D level and all echocardiographic data.

The study included 33 patients (18 M/15F); the mean age was 15.4 ± 3.09 years. Baseline urea, creatinine, alanine transaminase, and aspartate transaminase levels of the subjects were within normal limits. The mean pre-transfusion and post-transfusion hemoglobin level was 7.8 ± 0.9 g/dL and 11.8 ± 1.1 g/ dL, respectively. The mean serum ferritin level was 2017 ± 1573 ng/ml. All participants received iron chelation therapy; deferasirox in 25 patients, deferiprone in 2 patients, combined deferasirox, and deferiprone in 5 patients. Ten patients were splenectomized. In the study group, 30 of the patients had vitamin D deficiency and 3 had insufficiency. All patients had normal calcium, phosphorus, alkaline phosphatase, and parathyroid hormone levels. None of our patients received multivitamin and/or calcium channel blocker therapy. The characteristic of the patients and laboratory findings are shown in Table 1.

Twelve patients had cardiac iron overload with T2* MR < 20 msn. In echocardiographic evaluation, the mean LVEF of patients without cardiac iron overload was 66.5 ± 2,9% while LVEF of patients with cardiac iron overload was 65.3 ± 3,7% (p > 0.05).

Speckle-tracking analysis showed no statistically significant difference between patients with and without cardiac iron overload (absolute value of LVGLS, LVGCS, and RVGLS) (Table 2).

Vitamin D treatment was given to patients who had vitamin D deficiency or insufficiency. After 3 months later, cardiological evaluations of the patients were performed when patients’ vitamin D level was normal. Patients’ cardiological evaluations compared before and after vitamin D replacement. Any statistically significant difference in left ventricular functions before and after vitamin D replacement in conventional echocardiography was not detected (Table 3). In STE, the patients’ LVGLS and LVGCS were 19 ± 2.7% and 20 ± 2.8% before vitamin D replacement, and LVGLS and LVGCS after vitamin D replacement were 24 ± 2.7% and 25 ± 3.8% respectively (p < 0.05). Speckle-tracking analysis showed a significantly decreased absolute value of LVGLS (lower absolute values of strain parameters indicate dysfunction) before vitamin D replacement. A significant improvement in the global longitudinal strain of left ventricular after vitamin D replacement was detected. However, RVGLS were 19.4 ± 3.5% and 22.7 ± 4.1% before and after vitamin D replacement (p > 0.05). Right and left ventricular functions before and after vitamin D replacement were shown in Table 3.

Speckle tracking echocardiography could be used as a feasible method for evaluating subclinical myocardial dysfunction and has been recently started to use widely for children. Global longitudinal strain is widely accepted as being a sensitive tool in the assessment of left ventricular function and changes often occur in the LVGLS before overt changes in the LVEF [10].

Several factors are involved in the pathogenesis of the so called ‘‘thalassaemic cardiomyopathy’’. In the era of systematic transfusion therapy, myocardial iron overload is traditionally thought to be the main cause of thalassemia cardiomyopathy [11]. Cardiac function in patients with thalassemia is relatively complex. Patients usually have mild chronic anemia despite regular transfusion, which results in hyperdynamic circulation characterized by increased cardiac output [12]. Cardiac iron overload is part of the complexity that induces oxidative damage by generating reactive oxygen species and results in heart failure[13]. Another cause of cardiac dysfunction is nutritional deficiencies such as vitamin D, selenium, zinc, copper, and thiamine [14]. In thalassemia major patients, defective synthesis of 25-OH vitamin D has been described and becomes an important cause of morbidity [15]. The deficiency of vitamin D reduces contractility of the heart muscle and increases the production of PTH which in turn increases heart rate and cardiac hypertrophy and also increases cardiac iron uptake, leading to iron-induced cardiomyopathy[16]. Both PTH and 25-OH vitamin D appear to stimulate transmembrane calcium movement via L-type voltage-dependent calcium channels which are important in transporting non-transferrin-bound iron into the myocardium[17]. Because of this, vitamin D levels should be assessed in thalassemia patients and replacement should be started if these levels are low [18].

In patients with transfusion-dependent thalassemia, features of diastolic dysfunction appear to be present even the ejection fraction and the myocardial iron load is normal [19]. However, studies evaluating myocardial function in thalassemia patients with STE are limited in the literature [20]. Parsaee et al. reported a significant reduction in global longitudinal strain and basal segments longitudinal strain compared to the normal subjects and concluded STE helps to detect early stages of left ventricular dysfunction in thalassemic patients [21]. Abtahi et al. reported that global longitudinal strain had a statistically significant correlation with T2* MR values and when taking a threshold of 19.5 as the cut-off value, it could detect iron deposition with a sensitivity of 82.14% and specificity of 86.36%. Also, the assessment of global longitudinal strain can be used as a useful and less expensive tool for screening myocardial iron overload [22].

In our study, a significant positive correlation between vitamin D level and left ventricular diastolic functions was detected in transfusion-dependent thalassemia patients with vitamin D deficiency. The relationship between vitamin D deficiency and cardiac function in patients with thalassemia has also been shown. Wood et al. have reported that patients with low vitamin D levels have higher cardiac iron overload and significantly lower LVEF[18]. Ambarwati et al. reported that N-terminal pro-brain natriuretic peptide levels, which can be used to diagnose preclinical cardiac dysfunction, were higher in thalassemia major children with vitamin D deficiency than those with normal vitamin D levels. They also stated that thalassemic patients with cardiac dysfunction in conventional echocardiography have significantly lower vitamin D levels [23].

Although there are some studies comparing left ventricular global longitudinal strain and cardiac T2* MR in terms of cardiac functions in patients with thalassemia. These studies showed a significant correlation between LVGLS and cardiac T2*MR in patients with β-TM that patients with cardiac iron overload had a lower GLS than those without [22, 24]. But, we did not find a statistically significant difference in the absolute value of LVGLS, LVGCS, and RVGLS between patients with and without cardiac iron overload.

In patients with β-TM, diastolic functions deteriorate earlier than systolic functions in iron overload and cardiac effects due to other causes. Nadar et al. showed the presence of significant diastolic dysfunction with STE even in the presence of normal systolic function [19]. In our study, we also demonstrated that patients’ diastolic functions had improved after vitamin D replacement therapy. Inversely, in a recent study, it was found that vitamin D deficiency was associated with systolic dysfunction in patients with thalassemia [25].

Our study has some limitations such as the small number of patients. Compliance with chelation therapy was self-reported but during every monthly visit, the importance of compliance to the chelating therapy was emphasized to the patients and their families. The effects of other nutritional deficiencies on cardiac dysfunction were not assessed in this study. Indeed, repeated vitamin D level and LVGLS measurements across time could be useful to support our hypothesis.

In conclusion, vitamin D deficiency is a severe complication of transfusion-dependent thalassemia in children. This study demonstrated that lower vitamin D levels were significantly associated with impaired myocardial deformation parameters, sufficient vitamin D substitution can be beneficial to improve the cardiac functions in patients with thalassemia major and the STE can be used as a cheap and easy supply non-invasive technique for the follow-up of patient's cardiac functions. Therefore, patients need regular monitoring of serum vitamin D levels with a view to diagnosing vitamin D deficiency early and reducing its complications. Further studies with more subjects and a longer follow-up period will be needed for a more precise assessment.

β-TM	Beta thalassemia major
PTH	Parathyroid hormone
STE	Speckle-tracking echocardiography
LVEF	Left ventricular ejection fraction
LVSF	Left ventricular shortening fraction
LVGLS	Left ventricle global longitudinal strain
LVGCS	Left ventricle regional global circumferential strain
RVGLS	Right ventricle global longitudinal strain

Conflict of Interest Disclosures: The authors have indicated they have no conflicts of interest relevant to this article to disclose.

Contributors’ Statement

Dr. Yozgat, Dr. Azak, and Prof Dr. Yaralı conceptualized and designed the study, drafted the initial manuscript, collected data, carried out the initial analyses, and reviewed and revised the manuscript.
Dr. Kaçar, Dr. Işık, Dr. Bilir, Dr. Güzelküçük, Prof Dr. Çetin, and Prof Dr. Özbek conceptualized and designed the study, coordinated, and supervised data collection.

All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

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Table 1

Clinical characteristic and laboratory parameters of study group
Paramaters	Patients (n = 33)	Range
Age (year)	15.4 ± 3.09	8–22
Sex (Male/Female)	18/ 15
Heart rate (beat/min)	96 ± 14	68–122
Systolic BP (mmHg)	109 ± 10	88–132
Diastolic BP (mmHg)	70 ± 8	56–92
Ferritin serum (mg/dl)	2017 ± 1573	474–7240
AST (U/L)	35.3 ± 10.6	19–60
ALT (U/L)	46 ± 15.6	20–74
Urea (mg/dl)	23.7 ± 5.6	13–45
Cr (mg/d)	0.35 ± 0.07	0.23–0.54
BP: Blood pressure, AST: Aspartate transaminase, ALT: Alanine transaminase Cr: Creatinine

Table 2

Echocardiographic and speckle-tracking echocardiographic evaluation of patients with and without iron overload in T2* MR
	T2* MR > 20 msn (n:21)	T2* MR < 20 msn (n: 12)
LVEF,%	66.5 ± 2.9	65.3 ± 3.7	p > 0.05
LVGLS,%	19.6 ± 2.8	20.4 ± 3.9	p > 0.05
LVGCS,%	20.9 ± 2.7	20.8 ± 2.3	p > 0.05
RVGLS,%	19.4 ± 3.4	19.9 ± 3.7	p > 0.05
LVEF: Left ventricular ejection fraction, LVGLS: left ventricle global longitudinal strain, LVGCS: left ventricle regional global circumferential strain, RVGLS: right ventricle global longitudinal strain

Table 3

Left ventricular function and speckle tracking echocardiography measurements of patients before and after vitamin D replacement
	Before vitamin D replacement	After vitamin D replacement	P
LVEF,%	64 ± 4.7	65.1 ± 5.2	p > 0.05
LVSF,%	34.2 ± 3.8	35 ± 3.7	p > 0.05
LVGLS,%	19 ± 2.7	24 ± 2.7	0.04
LVGLSR, s^− 1	0.8 ± 0.2	0.91 ± 0.19
LVGCS,%	20 ± 2.8	25 ± 3.8	0.03
LVGCSR, s^− 1	0.78 ± 0.2	0.88 ± 0.21
RVGLS,%	19.4 ± 3.5	22.7 ± 4.1	> 0.05
RVGLSR, s^− 1	0.71 ± 0.21	0.8 ± 0.2
LVEF: Left ventricular ejection fraction, LVSF: Left ventricular fraction of shortening, LVGLS: Left ventricle global longitudinal strain, LVGCS: Left ventricle regional global circumferential strain, RVGLS: Right ventricle global longitudinal strain

No competing interests reported.

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The Effects of Vitamin D on Myocardial Function Demonstrated by Speckle Tracking Echocardiography in Children With Βeta Thalassemia

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Abstract

Introduction

Materials And Methods

Study Population

Clinical Data

Statistical analysis

Results

Discussion

Abbreviation

Declarations

References

Tables

Additional Declarations

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