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ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 2  |  Page : 407-412

Left ventricular dyssynchrony in hypertensive patients with normal systolic function: tissue synchronization imaging study


Department of Cardiology, Faculty of Medicine, Menoufia University, Menufia, Egypt

Date of Submission20-Jul-2013
Date of Acceptance27-Oct-2013
Date of Web Publication26-Sep-2014

Correspondence Address:
Mohammed A Ahmed
MBBCh, Cardiology Department, Faculty of Medicine, Menoufia University, Menufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.141716

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  Abstract 

Objective
The objective of our study was to assess left ventricular (LV) dyssynchrony in hypertensive patients with normal systolic function using tissue synchronization imaging (TSI).
Background
LV systolic and diastolic dyssynchrony are not uncommon in patients with hypertension. Dyssynchrony is associated with increasing incidence of heart failure, cardiovascular morbidity, and mortality.
Patients and methods
A total of 71 individuals were enrolled in this study. They were divided into two groups.
Group A included 51 hypertensive patients with good LV systolic function (ejection fraction≥ 50%) and narrow QRS on the ECG (<120 ms). We excluded individuals with any of the following: acute coronary syndrome, diabetes mellitus, atrial fibrillation, significant valvular heart disease, chronic renal failure, pulmonary hypertension, or myocardial or pericardial disease.
Group B included 20 age-matched and sex-matched healthy volunteers and represented the control group.
All participants underwent standard two-dimensional echocardiography and TSI.
Results
The hypertensive group had significantly higher septal wall and posterior wall thickness than the control group. In addition, the LV mass was significantly higher in hypertensive patients than in controls (P < 0.05). The delay between the septal and lateral walls was significantly higher in hypertensive patients than in controls (67.882 ± 53.536 in HTN vs. 44.400 ± 39.495 in controls) (P < 0.05). The severity of dyssynchrony is significantly related to the LV mass, septal wall thickness, posterior wall thickness, and left ventricular end-diastolic dimension.
Conclusion
Patients with systemic hypertension and normal systolic function may demonstrate LV dyssynchrony by TSI. The severity of dyssynchrony is significantly related to LV mass, septal wall thickness, posterior wall thickness, and left ventricular end-diastolic dimension. Systolic dyssynchrony may identify hypertensive patients at risk for the development of congestive heart failure, and who may benefit from more intensive hypertension control at an earlier stage in their disease process.

Keywords: Dyssynchrony, hypertension, tissue synchronization imaging


How to cite this article:
Soliman MA, Yaseen RI, Ahmed MA. Left ventricular dyssynchrony in hypertensive patients with normal systolic function: tissue synchronization imaging study. Menoufia Med J 2014;27:407-12

How to cite this URL:
Soliman MA, Yaseen RI, Ahmed MA. Left ventricular dyssynchrony in hypertensive patients with normal systolic function: tissue synchronization imaging study. Menoufia Med J [serial online] 2014 [cited 2019 Nov 20];27:407-12. Available from: http://www.mmj.eg.net/text.asp?2014/27/2/407/141716


  Introduction Top


Hypertension is an important public health challenge in both economically developing and developed countries [1].

Recent analyses have shown that as of the year 2000, there were 972 million people living with hypertension worldwide, and it is estimated that this number will escalate to more than 1.56 billion by the year 2025 [2].

Dyssynchrony means differences in the timing of contraction or relaxation between the different myocardial segments [3].

There are different classifications of dyssynchrony:

  1. Electrical or mechanical.
  2. Atrioventricular, interventricular, or intraventricular.
  3. Systolic or diastolic [4].


Dyssynchrony can be assessed by several methods such as: [5]

  1. Pulsed-wave Doppler to assess interventricular dyssynchrony by measuring the time delay between initiation of RV and left ventricular (LV) ejection known as presystolic ejection period.
  2. Septal to posterior wall motion delay assessed by M-Mode in parasternal long-axis and short-axis view to detect intraventricular dyssynchrony.
  3. Tissue Doppler imaging (TDI) uses pulsed-wave Doppler to record myocardial velocities at the basal septum and basal lateral wall close to the mitral valve annulus, measuring time from the onset of the QRS to peak of systolic velocity.
  4. Tissue synchronization imaging (TSI) allows for color guidance of myocardial activation.
  5. Strain imaging that incorporates velocity sampling in the two nearby points, and then the difference divided by the separation distance is proportional to strain rate, which, when integrated over time, can provide the strain value.
  6. Speckle tracking used to assess for LV strain (speckles are the hyperechoic areas of the myocardium tracked through the cardiac cycle).
  7. Tagged MRI [5].


Automated TSI enables rapid, reproducible intraventricular dyssynchrony assessment and overcomes some of the limitations of conventional techniques in sinus and nonsinus rhythm [6].


  Patients and methods Top


The study was conducted on 51 hypertensive patients (defined as SBP≥140 and/or DBP≥90 or on antihypertensive medications) with good LV systolic function [ejection fraction (EF)≥50%] and narrow QRS on ECG (<120 ms) presented to the cardiology outpatient clinic, Menoufia University Hospital. A total of 20 age-matched and sex-matched healthy individuals formed the control group.

Participants were excluded if they had LV systolic dysfunction, history of congestive heart failure, history of coronary artery disease, significant valvular heart disease, congenital or primary myocardial and pericardial disease, chronic renal failure, atrial fibrillation, pulmonary hypertension, diabetes mellitus, and bad echogenic window.

Written informed consent for participation was obtained, and the hospital ethics committee approved the protocol.


  Methods Top


All the participants included in the study were subjected to the following: full history taking, thorough clinical examination, 12-lead surface ECG, and echocardiographic examination.

Echocardiography examination

Transthoracic echocardiographic examination was conducted using a commercially available system (Vivid 9; GE Vingmed Ultrasound AS, Horten, Norway) using a 5-s phased array probe with simultaneous ECG tracing. Echocardiography was performed in the left lateral position according to the recommendations of the American Society of Echocardiography [7].

Conventional echocardiogram

M-Mode
: in parasternal long-axis view with M-Mode cruser perpendicular to intraventricular septum and posterior wall at the level of mitral valve tips for measuring left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), septal wall thickness in diastole (IVSTD), posterior wall thickness in diastole (PWTD), fractional shortening, EF, and calculating LV mass using the Devereux formula [8].



Doppler:

  1. Transmitral Doppler to measure the peak of early diastolic (E) velocity wave and the peak of late diastolic (A) velocity wave, and E/A ratio with Doppler (PW) sample volume placed in the middle of the LV inflow tract, 1 cm below the plane of mitral annulus in the apical four-chamber view.
  2. Transaortic Doppler (CW) in an apical five-chamber view or apical three-chamber view for time of aortic valve opening and aortic valve closure.


Tissue synchronization imaging

To prevent the TSI system from measuring peak systolic velocities outside the ejection phase, the event-timing tool was used to manually adjust the start and end times of the aortic valve ejection [9].

TSI shows regional dyssynchrony on two-dimensional (2D) echocardiography and allows immediate visual assessment of regional delay in systole. In addition, quantitative measurement of regional delay was derived from 2D TDI and automatically color-coded time to peak myocardial velocity (Ts ) from green to red, with reference to the QRS signal [Figure 1] [9],[10].
Figure 1:


Click here to view


In other words, Ts suggests the time to reach regional peak systolic tissue velocity. The median Ts measured by a 6-mm sample volume manually positioned within the 2D TSI for 12 LV segments. The 12 LV segments are six basal and six midwall segments of opposing LV walls in apical two-chamber, apical three-chamber, and apical 4-chamber views. At least three consecutive beats on TSI were stored, and the images were analyzed offline by a customized software package (EchoPac for PC; GE Vingmed Ultrasound AS) [Figure 1] [9],[10].

Parameters of systolic dyssynchrony were computed using the software. Parameters included SD of Ts of the 12 LV segments (dyssynchrony index), septal-lateral delay, septal-posterior delay, and all-segmental maximum difference. Dyssynchrony index is the most widely used parameter for LV dyssynchrony. LV systolic dyssynchrony is defined as dyssynchrony index of more than 34.4 ms assessed by TSI [11]. Moreover, LV systolic dyssynchrony is defined as (septal-lateral delay) or (septal-posterior delay)≥ (control+2 SD) [12].

Statistical analysis

Statistical analysis was carried out using the IBM-SPSS (version 20; USA) software. Mean and SD were calculated for all quantitative variables. Student's t-test was used to compare quantitative data between the two groups, and the c2-test was used for qualitative data. Pearson's correlation test was conducted to compare the two quantitative data.


  Results Top


This study included 51 hypertensive patients with mean age 52.02 ± 10.009 (11 male and 40 female), and the control group included 20 individuals with mean age 49.55 ± 7.104 (10 male and 10 female).

There was no significant difference between patients and controls regarding age (P > 0.05).

Septal wall thickness and posterior wall thickness were significantly higher in hypertensive patients than in the controls (P < 0.001) [Table 1].
Table 1: Conventional echo parameters in the studied groups

Click here to view


In addition, the LV mass was significantly higher in hypertensive patients than in controls (P < 0.05) [Table 1].

There was a significant delay between the septal and lateral walls in hypertensive patients than in controls (P < 0.05) [Table 2].
Table 2: Tissue synchronization imaging parameters in the studied groups

Click here to view


A significant correlation was present between conventional echo parameters and TSI parameters in patients and controls.

In the hypertensive group, there was a significant positive correlation between septal-lateral delay and each of LVEDD (P < 0.05, r = 0.38) and LV mass (P < 0.05, r = 0.34) [Table 3].
Table 3: Correlations between conventional echo parameters and tissue synchronization imaging parameters in patients and controls

Click here to view


Similarly, there was a significant negative correlation between septal-posterior delay and each of septal wall thickness (P < 0.05, r = -0.35) and posterior wall thickness (P < 0.05, r = −0.41) in hypertensive patients [Table 3].

There was also a significant positive correlation between all-segmental maximum difference and each of LVEDD (P < 0.05, r = 0.38) and LV mass (P < 0.05, r = 0.32) in the hypertensive group. However, there was a significant negative correlation with each of septal wall thickness (P < 0.05, r = −0.67) and LV mass (P < 0.05, r = −0.46) in the control group [Table 3].

Finally, there was a significant positive correlation between dyssynchrony index and each of LVEDD (P < 0.05, r = 0.43) and LV mass (P < 0.05, r = 0.35) in the hypertensive group, but there was a significant negative correlation with septal wall thickness in the control group (P < 0.05, r = −0.58) [Table 3].


  Discussion Top


Electrical dyssynchrony caused by left bundle branch block has been discerned to lead to further deterioration of LV systolic function in congestive heart failure, and is regarded as a surrogate for cardiac resynchronization therapy (CRT). However, a widening of the QRS duration did not necessarily identify responders to CRT, and a narrow QRS duration did not guarantee the absence of mechanical dyssynchrony in a recent study [13]. Furthermore, a number of myocardial imaging techniques based on echocardiography have been proven to be valuable for assessing mechanical dyssynchrony. Besides patients with systolic heart failure or wide QRS complexes, LV systolic or diastolic dyssynchrony evaluated through these myocardial imaging techniques has been revealed to be more prevalent than expected with prevalence of 25.0 or 21.7%, respectively, in patients with a preserved LV systolic function (EF>50%), and these did not occur in parallel [13]. Patients with heart failure and preserved LV systolic function constitute as many as 50% of the heart failure population. The presence of this clinical entity is well recognized and appears to be related to age, sex, and the presence of systemic hypertension. The mechanism by which heart failure occurs in certain patients meeting this clinical profile but not in others is less clear [12].

Among various echocardiographic techniques, TDI has gained its acceptance by virtue of the ability to define regional timing and contractility, and is highly reproducible. Recently, TDI has evolved into another technical modality, TSI. TSI portrays regional asynchrony on 2D echocardiography by transforming the timing of regional peak velocity into color codes that allows immediate visual identification of regional delay in systole by comparing the color mapping of orthogonal walls. In addition, quantitative measurement of regional delay is possible. However, the ability of TSI to assess systolic asynchrony and predict a positive response to CRT has not been explored [14].

Yu et al. [11] studied 373 patients with diastolic and systolic heart failure; LV dyssynchrony was observed in 39% of patients with normal LV systolic function. Hypertensive heart disease was found in 60% of the cohort studied. The study by Wang et al. [15] also assessed LV dyssynchrony in patients with heart failure and preserved systolic function, of whom 66% were hypertensive. Our study extended the findings of these studies, and demonstrated LV dyssynchrony in hypertensive patients without clinically overt congestive heart failure or evidence of conduction abnormalities.

Our study investigated a total of 51 hypertensive patients with normal LV systolic function (EF≥50%) and narrow QRS on the ECG (<120 ms), and 20 healthy individuals, age-matched and sex-matched, representing the control group.

In our study, we found that hypertension was more prevalent in women, especially in the postmenopausal (age>55 years) period, which was in agreement with previous studies [16].

In our study, we found that septal wall and posterior wall thickness significantly increased in hypertensive patients than in controls.

Izzo and Gradman [17] explained that increased LV wall thickness was associated continuously with the level of blood pressure and age.

In addition, Kiris et al. [18] studied LV dyssynchrony and its effects on cardiac function in 48 patients with newly diagnosed hypertension, and 33 controls.

They found that septal wall and posterior wall thickness were significantly increased in hypertensive patients than in controls [18].

In our study, we investigated LV dyssynchrony by four parameters using TSI. The four parameters were septal-lateral delay, septal-posterior delay, all-segmental maximum difference, and dyssynchrony index. The delay between septal and lateral walls in our study was significantly higher in hypertensive patients than in controls. This was in agreement with Schuster et al. [19], who studied 20 patients with structurally normal hearts to measure the time aspect of the regional longitudinal LV systolic movement, and defined synchronization as peak systolic delay between interventricular septum and lateral free wall less than ± 25 ms [19].

Normally, the intraventricular septum was activated first followed by LV lateral wall, with delay not more than 25 ms because of delay in impulse spreading through the Purkinje fibers. In hypertensive patients, the septal-lateral delay became more significant and exceeded the normal limit owing to LVH, with large ventricular mass and minor fibrosis between muscle fibers.

The other dyssynchrony parameters in our study do not significantly differ between patients and controls, which agreed with the previous studies on the assessment of LV dyssynchrony that depends on one parameter to diagnose LV dyssynchrony; the most sensitive of them is septal-lateral delay as in the study by Schuster and colleagues and Yang and colleagues [12],[13],[14],[15],[16],[17],[18],[19].

On the contrary, Kýrýs et al. [18] studied 48 newly diagnosed hypertensive patients and 33 controls, and diagnosed LV dyssynchrony in hypertensive patients with TSI by prolongation of dyssynchrony index and all-segmental maximum difference in hypertensive patients [18].

Yang et al. [12] who studied LV dyssynchrony in 42 hypertensive patients without congestive heart failure also detected LV dyssynchrony in hypertensive patients, but with TDI. In this study, dyssynchrony detected by T-P max (maximal difference of interval from onset of QRS to peak systolic velocity of two opposing LV walls such as septal and lateral walls). They considered T-P max prolonged if it exceeds control value by 2 SD [12].

In our study, we calculated LV mass and found that there was a significant increase in LV mass in hypertensive patients.

Izzo and Gradman [17] explained that increased LV mass correlated with the level of BP and age.

In the present study, the correlations between conventional echo parameters and TSI parameters in patients and controls showed that there was a significant positive correlation between septal-lateral delay and each of LVEDD and LV mass in the hypertensive group.

Similarly, there was a significant negative correlation between septal-posterior delay and each of septal wall thickness and posterior wall thickness in hypertensive patients.

In addition, there was a significant positive correlation between all-segmental maximum difference and each of LVEDD and LV mass in the hypertensive group; however, there was a significant negative correlation with each of septal wall thickness and LV mass in the control group.

Finally, there was a significant positive correlation between dyssynchrony index and each of LVEDD and LV mass in the hypertensive group, but there was a significant negative correlation with septal wall thickness in the control group.

With regard to the correlation between LV mass and dyssynchrony parameters, these findings are in agreement with Yang et al. [12] who studied LV dyssynchrony in 42 hypertensive patients without congestive heart failure. They found that dyssynchrony assessed with T-P max was significantly related to LV mass [12].


  Conclusion Top


Patients with systemic hypertension and normal systolic function may demonstrate LV dyssynchrony by TSI. The severity of dyssynchrony is significantly related to LV mass, septal wall thickness, posterior wall thickness, and LVEDD. Systolic dyssynchrony may identify hypertensive patients at risk for the development of congestive heart failure who may benefit from more intensive hypertension control at an earlier stage in their disease process.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.Kearney PM, Whelton M, Reynolds K, et al. Worldwide prevalence of hypertension: a systematic review. J Hypertens 2004; 22 :11-19.  Back to cited text no. 1
    
2. Chockalingam A, Campbell NR, Fodor JG. Worldwide epidemic of hypertension. Can J Cardiol 2006; 22 :553-555.  Back to cited text no. 2
    
3. Sherif F. Mechanical dyssynchrony in congestive heart failure diagnostic and therapeutic implications. J Am Coll Cardiol 2008; 51 :18-22.  Back to cited text no. 3
    
4. Ghio S, Constantin C, Klersy C, et al. Interventricular and intraventricular dyssynchrony are common in heart failure patients, regardless of QRS duration. Eur Heart J 2004; 25 :571-578.  Back to cited text no. 4
    
5. J Rickard. Cardiac resynchronization therapy. Topol & Griffin′s. Manual of cardiovascular medicine. Philadelphia: 2013. 920-930  Back to cited text no. 5
    
6. Kearney LG, Bryan Wai1, Michelle Ord, et al. Validation of rapid automated tissue synchronization imaging for the assessment of cardiac dyssynchrony in sinus and non-sinus rhythm. EP Europace 2011; 13 :270-276.  Back to cited text no. 6
    
7. Lang RM, Bierig M, Devereux RB, et al.members of the Chamber Quantification Writing Group: Recommendations for chamber quantification: a report from the American Society of Echocardiography′s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005; 18 :1440-1463.  Back to cited text no. 7
    
8. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57 :450-458.  Back to cited text no. 8
    
9. Yu CM, Zhang Q, Fung JW, et al. A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging. J Am Coll Cardiol 2005; 45 :677-684.  Back to cited text no. 9
    
10.Yu CM, Lin H, Zhang Q, et al. High prevalence of left ventricular systolic and diastolic dyssynchrony in patients with congestive heart failure and normal QRS duration. Heart 2003; 89 :54-60.  Back to cited text no. 10
    
11.CM Yu, Zhang Q, Yip GWD, et al. Diastolic and systolic asynchrony in patients with diastolic heart failure. J Am Coll Cardiol 2007; 49 :97-105.  Back to cited text no. 11
    
12.Yang B, Chettiveettil D, Jones F, et al. Left ventricular dyssynchrony in hypertensive patients without congestive heart failure. Clin Cardiol 2008; 31 :597-601.  Back to cited text no. 12
    
13.Bae BS, Kim KJ, Park JG, et al. Improvement in left ventricular systolic dyssynchrony in hypertensive patients after treatment of hypertension. Korean Circ J 2011; 41 :16-22.  Back to cited text no. 13
    
14.Yu CM, Zhang Q, Fung JW, et al. A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging. J Am Coll Cardiol 2005; 45 :677-684.  Back to cited text no. 14
    
15.Wang J, Kurrelmeyer KM, Torre-Amione G, et al. Systolic and diastolic dyssynchrony in patients with diastolic heart failure and the effect of medical therapy. J Am Coll Cardiol 2007; 49 :88-96.  Back to cited text no. 15
    
16.August P, Oparil S. Hypertension in women. J Clin Endocrinol Metab 1999; 84 :1862-1866.  Back to cited text no. 16
    
17.Izzo JL, Jr, AH Gradman. Mechanisms and management of hypertensive heart disease: from left ventricular hypertrophy to heart failure. Med Clin N Am 2004; 88 :1257-1271.  Back to cited text no. 17
    
18.Kýrýs A, Karaman K, Kýrýs¸ G¨, et al. Left ventricular dyssynchrony and its effects on cardiac function in patients with newly diagnosed hypertension. Echocardiography 2012; 29 :914-922.  Back to cited text no. 18
    
19.Schuster P, Matre K, Faerestrand S. Assessment of regional timing of left ventricular systolic longitudinal movement by Doppler tissue synchronization imaging in structurally normal hearts. Eur J Echocardiogr 2005; 6 :336-343.  Back to cited text no. 19
    


    Figures

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    Tables

  [Table 1], [Table 2], [Table 3]


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