Evaluation of P-Wave Dispersion, Ventricular Functions, and Atrial Electromechanical Coupling in Children with Type 1 Diabetes Mellitus.
INTRODUCTIONType 1 DM is one of the most common chronic diseases in adolescents and children. Poorly controlled type 1 DM is associated with many complications such as nephropathy, neuropathy, retinopathy and cardiovascular diseases. There is an increased risk of cardiovascular diseases such as ischemic heart diseases, systolic and diastolic heart failure, conduction system abnormalities and arrhythmias in patients with type 1 DM (1, 2). Atrial fibrillation, which is associated with high mortality and morbidity, is frequently encountered in daily practice (3). It is known that prolonged intra- and inter-atrial conduction delay and non-homogenous distribution of sinus impulses increase predisposition to Atrial fibrillation (AF). Risk of this predisposition can be determined by noninvasive methods such as P wave dispersion (Pd) and tissue doppler imaging (TDI) (4, 5).
There are a few studies conducted on pediatric cases in the literature. Similar to the methodology and design of the previous study conducted by Irdem et al. (6) on pediatric patients with hypothyroidism, we aimed to evaluate ventricular diastolic function, inter- and intra-atrial conduction delay and P wave dispersion in pediatric patients with type 1 DM.
METHODS
Thirty pediatric patients (18 females, 12 males, mean age 9.6+2.4 years) who have been diagnosed with type 1 DM in accordance with the criteria of the American Diabetes Association (7), who have received insulin therapy for at least one year and have been followed for a mean time period of 3.0+1.2 years in our clinic, as well as 30 healthy children (16 females, 14 males, mean age 8.4+3.6 years), as the control group, were enrolled in this study. Pediatric cases with hypertension, cardiomyopathy, valvular heart disease, branch block in ECG, atrioventricular conduction disorders, thyroid function disorder, kidney disease, lung disease, hypercholesterolemia and a bad presentation in ECG and Transthoracic echocardiography (TTE) in both type 1 DM and control groups were excluded from the study. In addition, individuals in both groups were not using any drugs that could affect heart rhythm and they had sinusoidal heart rhythm. P wave dispersion was measured as described by Dilaveris et al. (8) in resting ECG. Individuals in both groups provided written informed consent was obtained before the study. Ethics committee approval was not received. The current research was performed in accordance with the principles of the Helsinki Declaration as revised in 2008. We used the method from our previous study on pediatric patients with subclinical hypothyroidism while planning this study (6).
Transthoracic echocardiography (TTE) (Vivid S5 Pro device, GE, Horten, Norway, 2-4MHz phased-array transducer) was performed with 2-dimensional, M-mode, pulse and color flow Doppler imaging on all cases. A recording was made with one lead ECG throughout the TTE. Using conventional TTE, the mean values of the mitral and tricuspid early diastolic E wave, late diastolic A wave, isovolumetric relaxation times (IVRT), deceleration time (DT) and E/A ratio were calculated from three cycles obtained with Doppler and evaluated according to the American Echocardiography Association guidelines (9). Left atrial (LA) diameter was measured from the parasternal long axis, whereas left ventricular end diastolic diameter (LVEDd) and left ventricular end systolic diameter (LVEDs) as well as ejection fraction (EF) were measured using M-mode.
Atrial Electromechanical Coupling and tissue Doppler imaging assessments were performed using minimal optimal gain and adjusting spectral pulse Doppler signal filters until reaching Nyquist limit 0.15-0.20 m/s with transducer frequencies between 3.5-4 MHz in Tissue Doppler echocardiography. LV lateral mitral annulus, septal mitral annulus and RV tricuspid annulus TDI measurements were obtained using pulse Doppler in the Apical 4 chamber. Atrial electromechanical delay (PA), the time interval from the onset of P wave to the beginning of the late diastolic (Am) wave on surface ECG was measured in milliseconds from the LV lateral mitral annulus (PA lateral), septal mitral annulus (PA septal) and RV tricuspid annulus (PA tricuspid) (10). Values were calculated by averaging the measurements from 3 sequential beats. The difference between lateral and tricuspid PA (lateral PA-tricuspid PA) was defined as inter-atrial electromechanical delay, and the difference between septal PA and tricuspid PA (septal PA - tricuspid PA) was defined as intra-atrial electromechanical delay.
In calculating the P wave in 12-lead resting ECG, the beginning of the first positive wave deflecting upwards from the isoelectric line or the beginning of the first negative wave deflecting downwards from the isoelectric line was determined as the beginning of the P wave. The point where the wave returned to the isoelectric line was determined as the end of the P wave. The longest ([P.sub.max]) and shortest ([P.sub.min]) P wave in any derivation of the twelve-derivation ECG were measured in milliseconds in order to calculate P wave dispersion (Pd) (Pd=[P.sub.max]-[P.sub.min]). All measurements were performed by two experienced investigators who did not have any information about the clinical condition of the patients. Among the variables measured by two investigators, only those with less than 5% difference were included in the study.
Statistical Analysis
All analyses were performed using Statistical Package for the Social Sciences 11.0 (SPSS Inc.; Chicago, IL, USA) software. All continuous variables were described as mean+standard deviation, and categorical variables as percentage. Categorical variables were compared with the Chi-square test. The relationship between the two variables was analyzed using the Pearson Correlation analysis. Student t test was used in comparing continuous variables between the two groups. P<0.05 was accepted as statistically significant.
RESULTS
Age, gender, body weight, height, body mass index, systolic and diastolic pressures, LA diameter, LVEDd, LVEDs and LV EF were similar in both groups (p>0.05) (Table 1). Maximum P wave duration and Pd values were found to be significantly higher in patients with type 1 DM (p<0.001) (Table 1). The mean [HbA.sub.1c] level was 8.1+0.7% and the mean duration of the disease was 3.0+1.2 years in patients with type 1 DM.
Isovolumetric relaxation times was higher in the type 1 DM group as compared to the control group (p<0.001) (Table 2). Mitral and tricuspid E, A wave velocities and DT were similar in both groups (p>0.05) (Table 2). Mitral E/A ratio was significantly lower in the type 1 DM group as compared to the control group (p=0.017) (Table 2).
LV septal [S.sub.m], [E.sub.m] velocities and [E.sub.m]/[A.sub.m] ratio were significantly lower in the type 1 DM group as compared to the control group (p=0.047, p=0.003, p=0.001, respectively) (Table 2). [A.sub.m] velocity and E/[E.sub.m] ratio, on the other hand, were significantly higher in patients with type 1 DM in comparison to the control group (p=0.010, p=0.038, respectively) (Table 2). LV lateral Em velocity and [E.sub.m]/[A.sub.m] ratio were significantly lower in the type 1 DM group as compared to the control group (p=0.009, p=0.012, respectively) (Table 2).
Patients with type 1 DM were found to exhibit a significantly prolonged PA lateral, PA septum, PA tricuspid, inter-atrial (PA lateral-PA tricuspid) and intra-atrial conduction delay (PA septum-PA tricuspid) in comparison to the control group (p<0.001, p<0.001, p=0.001, p<0.001, p<0.001, respectively) (Table 3).
No correlation was found between the duration of disease and [HbA.sub.1c], atrial conduction delay (r=0.003, p=0.493; r=-0.092, p=0.315, respectively).
DISCUSSION
It is known that type 1 DM constitutes a risk of heart disease. In addition, DM increases the risk of heart failure by directly affecting the heart without the presence of coronary heart disease and also causes functional and structural changes in individuals with impaired glucose tolerance without the presence of microvascular disease (11-13). Cardiac dynamic changes (increased heart rate, arrhythmia etc.) due to autonomic nervous system dysfunction, systolic and diastolic dysfunction in the heart, and cardiomyopathy can manifest in patients with DM (14, 15). Patients with DM can frequently have heart rhythm disorders with advancing age. The most common of such disorders is atrial fibrillation (AF) (16). Previous studies showed that conditions which cause left atrial enlargement lead to inter-atrial conduction delay (4, 5). Filtered P wave analysis is useful in detecting atrial electrophysiological abnormalities in paroxysmal AF. Atrial electromechanical delay can be measured by various methods (17, 18). Today, it is frequently measured by calculating the time interval between the onset of P wave on ECG and the onset of Am wave in both ventricles on TDI in milliseconds while performing TTE. Studies have shown that patients with paroxysmal AF and mitral stenosis also had intra- and inter-atrial conduction delay (4, 5). There was intra- and inter-atrial conduction delay in our study despite the normal size of the left atrium.
The decrease in mitral or tricuspid early systolic A velocity correlated with reduced atrial contraction. Both parameters are affected by many cardiac conditions such as heart rate, preload and afterload (19). Previous studies have reported different results regarding left ventricular systolic and diastolic function in patients with DM; i.e. some of these studies reported systolic dysfunction whereas others reported diastolic dysfunction (20-23). However, impaired glucose tolerance leads to systolic and diastolic dysfunction in the heart also in the early phase of DM (13, 21, 24). Left ventricular systolic dysfunction may improve by itself if serum glucose concentrations return to normal levels (11). In our study, although ventricular systolic functions were normal in patients with type 1 DM, some parameters of the ventricular diastolic function were moderately impaired. The reason why our patients exhibited diastolic dysfunction in both ventricles and especially in the right ventricle, although mean duration of the disease was short, can be attributed to high [HbA.sub.1c] levels.
Intra- and inter-atrial conduction time can be determined by calculating P wave dispersion and maximum P wave duration in twelve-lead ECG. It is known that non-homogenous sinus impulses constitute a risk factor for AF. It was reported that interatrial electromechanical delay measured using TDI has a correlation with P wave dispersion (10, 22). Increased atrial heterogenous electrical activity facilitates developing atrial fibrillation/atrial flutter by causing atrial reentry. Pd and Pmax have been used to predict the risk of AF development in many studies (3-5, 25). It is known that an increase in the left atrial diameter is significant for AF development. However, studies demonstrated that [P.sub.d] increased in patients with AF, although the atrial diameter was normal. Our study also revealed that maximum P wave duration and Pd were significantly higher in patients with Type 1 DM, although LA diameter was normal. Consequently, patients with type 1 DM have higher atrial conduction delay in comparison to healthy individuals and this may indicate an increased risk of developing atrial rhythm disturbance in patients with type 1 DM.
Our study has more than one limitation. The limiting factors of this study include the low number of cases in the study, short duration of follow-up, lack of LV posterior wall thickness measurements and lack of LA mechanical measurements.
CONCLUSION
In our study, it was seen that there was atrial electromechanical delay, i.e. left atrium was affected in patients with type 1 DM. In addition, we found in tissue Doppler imaging that systolic and diastolic functions of the left ventricle were sub-clinically affected in patients with type 1 DM.
Ethics Committee Approval: Authors declared that the research was conducted according to the principles of the World Medical Association Declaration of Helsinki "Ethical Principles for Medical Research Involving Human Subjects", (amended in October 2013).
Informed Consent: Written informed consent was obtained from patients and healthy children and their parents who participated in this study.
Peer-review: Externally peer-reviewed.
Author Contributions: Concept--M.S., A.I., O.B., D.A.S., M.Ker.; Design--M.S., A.I., D.A.S.; Supervision--M.Ker., O.B., M.S.; Materials--M.Kes., A.I., D.A.S.; Data Collection and/or Processing--A.I., D.A.S., O.B., M.Ker., M.Ki.; Analysis and/or Interpretation--M.Ker., A.I., O.B., D.A.S.; Literature Search -- D.A.S., A.I.; Writing Manuscript--D.A.S., A.I. Critical Review--O.B., M.Ker., M.Ki., M.Kes.
Conflict of Interest: The authors have no conflicts of interest to declare.
Financial Disclosure: The authors declared that this study has received no financial support.
REFERENCES
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(20.) Peterson LR, Waggoner AD, de las Fuentes L, Schechtman K, McGrill JB, Gropler RJ, et al Alterations in left ventricular structure and function in type-1 diabetics: a focus on left atrial contribution to function. J Am Soc Echocardiogr 2006; 19: 749-55. [CrossRef]
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How to cite:
Aydin Sahin D, Irdem A, Kervancioglu M, Baspinar O, Sucu M, Keskin M, et al. Evaluation of P-Wave Dispersion, Ventricular Functions, and Atrial Electromechanical Coupling in Children with Type 1 Diabetes Mellitus. Eur J Ther 2018; 24(4): 250-4.
Derya Aydin Sahin (1) [iD], Ahmet irdem (1) [iD], Mehmet Kervancioglu (1) [iD], Osman Baspinar (1) [iD], Murat Sucu (2) [iD], Mehmet Keskin (3) [iD], Metin Kilinc (1) [iD]
(1) Division of Pediatric Cardiology, Gaziantep University School of Medicine, Gaziantep, Turkey
(2) Department of Cardiology, Gaziantep University School of Medicine, Gaziantep, Turkey
(3) Division of Pediatric Endocrinology, Gaziantep University School of Medicine, Gaziantep, Turkey
ORCID IDs of the authors: D.A.S. 0000-0002-8520-2335; A.I. 0000-0002-2565-5674; O.B. 0000-0002-9307-0344; M.S. 0000-0002-3695-5461.
Corresponding Author: Derya Aydin Sahin E-mail: [email protected]
Received: 24.05.2018 * Accepted: 05.06.2018
DOI: 10.5152/EurJTher.2018.785
Table 1. Clinical and laboratory characteristics of the patient and
control groups
Patients Control
(n=30) (n=30) p
Age (Years) 9.6[+ or -]2.4 8.40[+ or -]3.6 0.120
Female (n, %) 18 (60) 16 (53.3) 0.602
Body mass index (kg/m2) 16.3[+ or -]2.2 15.9[+ or -]3.7 0.615
Height (cm) 130.9[+ or -]12.0 124.5[+ or -]19.9 0.136
Systolic pressure (mmHg) 100.2[+ or -]7.9 97.9[+ or -]9.8 0.320
Diastolic pressure (mmHg) 61.5[+ or -]4.7 63.3[+ or -]5.6 0.200
Heart rate (beats/min) 90.75[+ or -]13.0 87.1[+ or -]16.7 0.352
Pmax (ms) 106.2[+ or -]12.0 91.3[+ or -]8.0 <0.001
Pmin (ms) 77.5[+ or -]9.9 74.3[+ or -]7.9 0.173
Pd (ms) 28.6[+ or -]8.2 16.9[+ or -]7.3 <0.001
HbA1c (%) 8.1[+ or -]0.7 - -
Duration of disease
(years) 3.0[+ or -]1.2 - -
LVEDd: left ventricular end diastolic diameter;
LVESd: left ventricular end systolic diameter; [P.sub.max]: maximum
P-wave; [P.sub.min]: minimum P-wave; Pd: P-wave dispersion
Table 2. Comparison of the variables measured using conventional and
tissue Doppler imaging between patients and control groups
Patients Control
(n=30) (n=30)
Conventional Doppler parameters
Ejection fraction (%) 70.9[+ or -]3.7 70.2[+ or -]4.8
LVEDd (cm) 3.9[+ or -]0.3 3.7[+ or -]0.5
LVESd (cm) 2.4[+ or -]0 2.3[+ or -]0.3
Left atrial diameter (cm) 2.3[+ or -]0.2 2.2[+ or -]0.3
Mitral E velocity (m/s) 0.92[+ or -]0.16 0.99[+ or -]0.17
Mitral A velocity (m/s) 0.57[+ or -]0.09 0.54[+ or -]0.15
Mitral E/A 1.67[+ or -]0.46 1.95[+ or -]0.43
DT (ms) 160.4[+ or -]14.5 154.7[+ or -]14.2
IVRT (ms) 74.5[+ or -]7.0 63.3[+ or -]5.2
Tricuspid E velocity (m/s) 0.70[+ or -]0.12 0.65[+ or -]0.10
Tricuspid A velocity (m/s) 0.46[+ or -]0.09 0.44[+ or -]0.10
Tricuspid E/A 1.45[+ or -]0.18 1.46[+ or -]0.29
Tissue Doppler parameters
Septal LV
[S.sub.m] (m/s) 0.09[+ or -]0.02 0.11[+ or -]0.01
[A.sub.m] (m/s) 0.07[+ or -]0.01 0.06[+ or -]0.01
[E.sub.m] (m/s) 0.12[+ or -]0.0 0.14[+ or -]0.0
[E.sub.m]/[A.sub.m] 1.7[+ or -]0.6 2.2[+ or -]0.5
E/[E.sub.m] 7.8[+ or -]1.6 7.0[+ or -]1.2
Lateral LV
[S.sub.m] (m/s) 0.10[+ or -]0.02 0.08[+ or -]0.02
[A.sub.m] (m/s) 0.07[+ or -]0.02 0.07[+ or -]0.02
[E.sub.m] (m/s) 0.13[+ or -]0.04 0.15[+ or -]0.03
[E.sub.m]/[A.sub.m] 1.8[+ or -]0.6 2.1[+ or -]0.4
E/[E.sub.m] 7.3[+ or -]1.7 6.5[+ or -]1.6
RV lateral annulus
[S.sub.m] (m/s) 0.12[+ or -]0.02 0.12[+ or -]0.0
[A.sub.m] (m/s) 0.10[+ or -]0 0.11[+ or -]0.0
[E.sub.m] (m/s) 0.13[+ or -]0.0 0.16[+ or -]0.02
[E.sub.m]/[A.sub.m] 1.4[+ or -]0.4 1.5[+ or -]0.4
p
Conventional Doppler parameters
Ejection fraction (%) 0.528
LVEDd (cm) 0.067
LVESd (cm) 0.087
Left atrial diameter (cm) 0.143
Mitral E velocity (m/s) 0.128
Mitral A velocity (m/s) 0.406
Mitral E/A 0.017
DT (ms) 0.132
IVRT (ms) <0.001
Tricuspid E velocity (m/s) 0.128
Tricuspid A velocity (m/s) 0.512
Tricuspid E/A 0.816
Tissue Doppler parameters
Septal LV 0.047
[S.sub.m] (m/s) 0.010
[A.sub.m] (m/s) 0.003
[E.sub.m] (m/s) 0.001
[E.sub.m]/[A.sub.m] 0.038
E/[E.sub.m]
Lateral LV 0.001
[S.sub.m] (m/s) 0.906
[A.sub.m] (m/s) 0.009
[E.sub.m] (m/s) 0.012
[E.sub.m]/[A.sub.m] 0.068
E/[E.sub.m]
RV lateral annulus
[S.sub.m] (m/s) 0.813
[A.sub.m] (m/s) 0.125
[E.sub.m] (m/s) 0.001
[E.sub.m]/[A.sub.m] 0.243
DT: deceleration time; IVRT: isovolumetric relaxation time; LV: left
ventricle; [S.sub.m]: septal systolic velocity; [E.sub.m]: early
diastolic velocity; [A.sub.m]: late diastolic velocity; RV: right
ventricle
Table 3. Atrial electromechanical interval measurement results obtained
from tissue Doppler
Patient Control
(n=30) (n=30) p
PA lateral (ms) 69.8[+ or -]4.8 53.2[+ or -]4.7 <0.001
PA septum (ms) 46.3[+ or -]2.3 41.1[+ or -]2.9 <0.001
PA tricuspid (ms) 40.6[+ or -]3.5 37.8[+ or -]3.1 0.001
PA lateral-PA tricuspid
(ms) (a) 29.1[+ or -]6.1 15.4[+ or -]5.5 <0.001
PA septum-PA tricuspid
(ms) (b) 5.6[+ or -]4.4 3.3[+ or -]3.9 <0.001
Data was provided in mean [+ or -] standard deviation. PA; the time
interval from the onset of P wave to the beginning of the late
diastolic wave ([A.sub.m]) on ECG measured by tissue Doppler.
(a) inter-atrial electromechanical delay.
(b) intra-atrial electromechanical delay
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| Title Annotation: | Original Research |
|---|---|
| Author: | Sahin, Derya Aydin; Irdem, Ahmet; Kervancioglu, Mehmet; Baspinar, Osman; Sucu, Murat; Keskin, Mehmet |
| Publication: | European Journal of Therapeutics |
| Article Type: | Report |
| Date: | Dec 1, 2018 |
| Words: | 4099 |
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