Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 31  |  Issue : 2  |  Page : 395-401

Right ventricular mechanics in patients with idiopathic dilated cardiomyopathy using strain imaging


1 Department of Cardiology, Menoufia University, Menoufia, Egypt
2 Department of Cardiology, Al Ahrar Teaching Hospital, Al Dakahlya, Egypt

Date of Submission06-Dec-2016
Date of Acceptance11-Mar-2017
Date of Web Publication27-Aug-2018

Correspondence Address:
Ehab E Mahdy
Department of Cardiology, Al Ahrar Teaching Hospital, Mit Ghamr, Al Dakahlya
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_671_16

Rights and Permissions
  Abstract 


Objectives
The aim of this study was to assess right ventricular (RV) mechanics in patients with idiopathic dilated cardiomyopathy (DCM) using two-dimensional (2D) strain imaging technique.
Background
Imaging using strain and strain rate (SR) was recently applied as a promising tool to analyze global and regional myocardial function in different disease entities, including DCM. 2D strain echo would be especially useful in assessing DCM as an accurate, time-sparing method.
Patients and methods
A total of 104 patients with documented DCM as proved by echocardiography were investigated using 2D echo, and 25 age-matched and sex-matched individuals served as control. Off-line 2D strain analysis was performed for the assessment of global and regional strain of the RV, including the RV free wall and the interventricular septum.
Results
RV deformation parameters showed loss of longitudinal systolic strain and SR base to apex gradient and significantly declined values in the DCM group. The averaged RV free wall segment systolic strain (−9.84 ± 6.73 vs. −30.86 ± 4.44%), systolic strain rate (SRsys) (−0.88 ± 0.47 vs. −1.75 ± 0.68 s−1), and early systolic strain rate (SRe) (0.67 ± 0.50 vs. 2.08 ± 1.08 s−1) were significantly reduced in the DCM group compared with the control group (P < 0.0001). These findings were also apparent in global RV deformation and gave similar significance (P < 0.0001) with the exception of late diastolic SR (P = NS). Intraventricular dyssynchrony was verified and showed a significant increase in time-to-peak standard deviation in the DCM group (75.71 ± 47.76 vs. 44.18 ± 26.72 ms, P < 0.002) compared with the control group.
Conclusion
In conclusion, our results suggest that the same cardiomyopathic pathology affects the RV as much as it affects the left ventricle with reduction in both RV systolic and diastolic functions. We have made an attempt to understand RV mechanics in different cardiac pathologies.

Keywords: two-dimensional strain, dilated cardiomyopathy, right ventricle


How to cite this article:
Badran HM, Ahmed NF, Mahdy EE. Right ventricular mechanics in patients with idiopathic dilated cardiomyopathy using strain imaging. Menoufia Med J 2018;31:395-401

How to cite this URL:
Badran HM, Ahmed NF, Mahdy EE. Right ventricular mechanics in patients with idiopathic dilated cardiomyopathy using strain imaging. Menoufia Med J [serial online] 2018 [cited 2018 Nov 21];31:395-401. Available from: http://www.mmj.eg.net/text.asp?2018/31/2/395/239765




  Introduction Top


Dilated cardiomyopathy (DCM) refers to a large group of myocardial disorders that are characterized by ventricular dilation and depressed myocardial contractility in the absence of abnormal loading conditions such as hypertension or valvular disease [1],[2].

In 1616, Sir William Harvey was the first to describe the importance of right ventricular (RV) function in his seminal treatise, De Motu Cordis: 'Thus, the right ventricle may be said to be made for the sake of transmitting blood through the lungs, not for nourishing them' [3],[4]. For many years that followed, emphasis in cardiology was placed on left ventricular (LV) physiology, overshadowing the study of the RV. In the first half of the 20th century, the study of RV function was limited to a small group of investigators who were intrigued by the hypothesis that human circulation could function adequately without RV contractile function [5].

For the past three decades, the LV anatomy and function has been extensively researched and studied. The RV has been ignored probably due to the technical difficulties in imaging as well as the poor understanding of its function and hemodynamics. Recent advances in medicine led to the better understanding of the role of the RV in various medical conditions [6].

The RV can be studied with many imaging and functional modalities such as cardiac MRI, as it is increasingly used as a standard tool in the evaluation of RV structure and function. MRI is the most accurate method for the assessment of RV volume. However, in clinical practice, echocardiography is the mainstay of evaluation of RV structure and function. Compared with other modalities, it offers the advantages of versatility and availability. Moreover, Doppler-derived indices of RV function, such as the myocardial performance index and tricuspid annular isovolumic acceleration, are emerging as promising parameters of RV function [7].

Strain imaging is a novel method that has been developed to quantify regional myocardial function. Myocardial strain imaging was initially obtained using tissue Doppler imaging. More recently, it is being obtained with myocardial speckle tracking using two-dimensional (2D) echocardiography [8].

The aim of this study was to assess RV mechanics in patients with idiopathic dilated cardiomyopathy (IDC) using 2D strain imaging technique.


  Patients and Methods Top


This was a single-center prospective study. We enrolled 104 patients with IDC on the basis of patients' clinical history, physical examination, 12-lead ECG, chest radiography, echocardiography, and coronary angiography according to the WHO criteria [2]; patients were recruited from Yacoub Research Unite, Menoufia University, Egypt, between January 2013 and May 2016.

The other limb of the study was the control group in which we studied 25 age-matched and sex-matched healthy individuals without a detectable cardiovascular risk factor or receiving any medication and with a normal 12-lead ECG. The study was approved by the Ethical Committee of Menoufia Faculty of Medicine. Informed consent was taken from each participant in the study.

The exclusion criteria included patients with the following:

  1. Systemic hypertension (>150/95 mmHg)
  2. Coronary artery disease (>50% in one or more major branches)
  3. Chronic excess alcohol (>40 g/day in women and >80 g/day in men for more than 5 years after 6-month abstinence
  4. Systemic disease known to cause DCM
  5. Pericardial diseases
  6. Congenital heart disease
  7. Cor pulmonale
  8. Rapid, sustained supraventricular tachycardia.


Echocardiography

Echocardiographic examinations were performed for all participants in the left lateral decubitus position in the parasternal long, short-axis, apical two-chamber and four-chamber views using standard transducer positions. Esaote Mylab Gold ultrasound system (Esaote S.p.A, Florence, Italy) equipped with a 5 MHz phased-array transducer was utilized. RV end-diastolic diameters (basal, mid, and longitudinal) and wall thickness, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), septum, posterior wall thickness, ejection fraction (EF%), and left atrial (LA) diameter and volume were evaluated.

Color flow mapping and continuous-wave Doppler was used to estimate pulmonary artery pressure (PAP) from tricuspid regurge velocity (simplified Bernoulli equation). The severity of mitral regurge and tricuspid regurge was graded according to the jet area method. Peak early (E) and late (A) transmitral (Em and Am) filling velocities were measured from mitral inflow velocities, and deceleration time was obtained. Peak systolic (Sa), early diastolic (E'), and atrial diastolic (A') velocities were obtained by placing a tissue Doppler Diagnostic Medical Imager (DMI) sample volume at the right ventricular free wall (RVFW) and lateral mitral annulus in the apical four-chamber view. The early mitral inflow velocity/early mitral annular velocity (Em/E'm) was calculated.

Quality, ECG signal and a frame rate (70 ± 20 frames/s), was adjusted depending on the heart rate and stored for off-line analysis using XStrain software (coMakeIT B.V., Stationsplein 62, 3743 KM Baarn., The Netherlands). Vector velocity imaging (VVI) is a dedicated software that derives longitudinal myocardial velocity, strain (ε), strain rate (SR), and displacement from the digitized 2D video clips.

Analysis of deformation

LV images were recorded and processed. Tracking and subsequent strain calculations were performed. Systolic strain (εsys), systolic strain rate (SRsys), early systolic strain rate (SRe), and atrial strain rate (SRa) in the basal, mid, and apical segments of septal, lateral, anterior, and inferior wall were measured. To reduce random noise, each sample was obtained by averaging more than one consecutive heart cycle (usually three), by averaging all previously collected data. LV Global εsys, SRsys, early diastolic strain rate (SRe dia), and diastolic atrial strain rate (SRa dia) were obtained.

RV images were recorded and processed. Tracking and subsequent strain calculations were performed. Longitudinal εsys, SRsys, SRe dia, and SRa dia in the basal, mid and apical segments of the RVFW and septum were obtained. Global RV deformation was calculated from RVFW and septal segments. To estimate LV and RV mechanical dyssynchrony, myocardial contraction time was measured from regional strain curves for each ventricular segment, as time from the beginning of Q wave of ECG to the time-to-peak systolic strain. LV and RV dyssynchrony was defined as the standard deviation of the averaged time-to-peak strain (TTP-SD).

Statistical analysis

Values were presented as means ± SD or as numbers and proportions, as appropriate. The relations between qualitative variables were evaluated using the χ2-test or Fisher's exact test, as indicated. Means were compared with Student's test. Quantitative variables were correlated with the use of coefficient of correlation r. We have used Sm lateral annulus less than 9.5 as an indicator of RV dysfunction and receiver operating characteristic analysis was performed to detect suitable cutoff points for RV εsys%, SRsys, SRe, and SRa to differentiate RV dysfunction in DCM. Variables that were statistically significant in univariate analysis were introduced in a logistic regression model to detect independent predictors of RV dysfunction. All tests were bilateral and a P value of 0.05 was the limit of statistical significance. Analysis was performed using IBM SPSS for Mac (version 24) software (IBM Corp. Released 2016. Armonk, NY).

IBM SPSS statistics is available in a base version and three editions:

  1. SPSS statistics base provides a range of statistical procedures suitable for many problems, including crosstabs, linear regression, Monte Carlo simulation, geospatial analytics, and the ability to extend built-in capabilities with Python, R, or Java code
  2. SPSS statistics standard includes techniques such as logistic and nonlinear regression and presentation quality custom tables to help business managers and analysts
  3. SPSS statistics professional addresses nonstandard analyses and issues such as data quality and automation with features such as automatic data preparation, decision trees, and forecasting
  4. SPSS statistics premium supports enterprise businesses needing advanced techniques such as structural equation modeling, sampling assessment and testing, and small sample and rare occurrence analysis.



  Results Top


Study groups consisted of 104 patients (37 ± 17 years) (39.5% female patients) and 25 controls (24 ± 14 years) (44.0% female participants). There were no differences between the IDC and control groups in sex, body surface area, and systolic or diastolic blood pressure. Age (P < 0.001) and heart rate (P < 0.003) in the DCM group were significantly higher than that in the control group. All (104) DCM patients (39.5% female patients) were symptomatic (~7% are New York Heart Association class I, 44% class II, 28% class III, and 21% class IV).

Conventional echocardiographic data

LA dimension, volume, LVESD, LVEDD, LV mass, left ventricular mass index (LVMI), mitral regurgitation severity, tricuspid regurgitation severity, PAP, RV longitudinal and mean diameters, and RVFW thickness were significantly greater, whereas LV EF%, fractional shortening%, Em inflow deceleration time, and E'm were significantly reduced in the DCM group (P < 0.0001). LV end-diastolic pressure as estimated using Em/E'm ratio was significantly elevated in comparison with the control group (P < 0.0001). There was no significant difference among the two groups in interventricular septum and left ventricular posterior wall thickness, Em inflow velocity, Am inflow velocity, mitral E/A, and RV basal and mid diameters [Table 1].
Table 1: Conventional echocardiographic measurements

Click here to view


Left ventricle global deformation analysis

In the DCM group, 2D strain analysis detected lower global and regional peak myocardial εsys, SRsys, SRa, and SRe (P < 0.0001) at the level of all analyzed segments in comparison with the control group.

Similarly, electromechanical delay was considerably prolonged in all LV segments compared with its corresponding segments in healthy individuals (P < 0.0001). Intraventricular dyssynchrony (TTP-SD) was significantly greater in the group DCM (84.79 ± 61.61) compared with the control group (29.24 ± 16.81) (P < 0.0001) [Table 2].
Table 2: Left ventricular global deformation parameters

Click here to view


Regional and global right ventricular deformation analysis

Both longitudinal εsys and SR values showed a base to apex gradient in the control group. RV deformation parameters showed loss of this gradient and a significant decline in the DCM group. The averaged RVFW segments εsys (−9.84 ± 6.73 vs. −30.86 ± 4.44%), SRsys (−0.88 ± 0.47 vs. −1.75 ± 0.68 s −1), and SRe (0.67 ± 0.50 vs. 2.08 ± 1.08 s −1) were significantly reduced in the DCM group compared with the control group (P < 0.0001 for each). These findings were also apparent in global RV deformation and gave similar significance (P < 0.0001) with the exception of SRa dia (P = NS) [Table 3].
Table 3: Right ventricular global and regional deformation

Click here to view


As regards electromechanical delay between RV segments, controls showed no significant difference compared with the DCM group at the level of different RV wall segments (P = NS). Intraventricular dyssynchrony was verified and showed a significant increase in TTP-SD in the DCM group (75.71 ± 47.76 vs. 44.18 ± 26.72 ms, P < 0.002) compared with the control group [Table 3].

Correlation between global right ventricular systolic strain% and right ventricular free wall systolic strain% and other echocardiographic parameters in the dilated cardiomyopathy group

Both global RV εsys% and RVFW εsys% were significantly correlated with indexed LA volume, LV EF%, fractional shortening%, LVESD, LVEDD, LVMI, mitral E/A, PAP, LV global εsys%, LV TTP-SD, and LV global SRe dia (P < 0.0001). Global RV εsys% rather than RVFW εsys% had a significant correlation with LA volume and LV global SRsys (P < 0.003) for both of them. There was no significant correlation between Eam, Em inflow deceleration time, Em/Eam, Am inflow velocity, LV global SRa dia and either global RV εsys% or RVFW εsys% (P = NS).

Assessment of right ventricular dysfunction in the dilated cardiomyopathy group

A Sm lateral tricuspid annulus of less than 9.5 cm/s was taken as a cutoff value of RV dysfunction that leads to recognition of two subgroups, one with RV dysfunction (n = 46) and another with no RV dysfunction (n = 58).

Comparison between dilated cardiomyopathy patients with and those without right ventricular dysfunction

In comparison with DCM patients with no RV dysfunction, DCM patients with RV dysfunction were directly related to decreased values of LV EF% (34.60 ± 9.68 vs. 28.50 ± 8.55) (P < 0.001), LV global εsys% (−6.87 ± 4.51 vs. 4.48 ± 3.25) (P < 0.003), LV global SRe dia (0.45 ± 0.32 vs. 0.33 ± 0.24) (P < 0.04), LV global late SR dia (0.39 ± 0.36 vs. 0.24 ± 0.14) (P < 0.008), εsys% global RV (−10.36 ± 6.05 vs. −7.15 ± 4.17) (P < 0.003), RV global SRsys (0.93 ± 0.44 vs. 0.69 ± 0.33) (P < 0.002), global RV SRe dia (0.73 ± 0.48 vs. 0.48 ± 0.27) (P < 0.002), RV global late SR dia (0.70 ± 0.39 vs. 0.41 ± 0.21) (P < 0.0001), early diastolic myocardial velocity lateral annulus (12.40 ± 4.01 vs. 8.29 ± 6.51) (P < 0.0001), late diastolic myocardial velocity latanulus (13.84 ± 5.38 vs. 7.64 ± 6.21) (P < 0.0001), mean displacement (3.92 ± 2.35 vs. 2.74 ± 2.05) (P < 0.009), and RV EF (29.92 ± 12.89 vs. 24.38 ± 12.97) (P < 0.03) [Table 4].
Table 4: Comparison between dilated cardiomyopathy patients with and those without RV dysfunction according to different echocardiographic parameters

Click here to view


However, RV dysfunction was directly related to increased values of indexed LA volume (34.03 ± 16.65 vs. 42.73 ± 18.48) (P < 0.015), LVESD (52.61 ± 12.97 vs. 58.63 ± 12.13) (P < 0.017), LVMI (174.91 ± 65.23 vs. 208.49 ± 80.26) (P < 0.023), RV longitudinal diameter (60.97 ± 13.19 vs. 66.37 ± 11.37) (P < 0.03), RV mean diameter (41.28 ± 8.58 vs. 44.94 ± 6.72) (P < 0.019), and RV thickness (6.17 ± 1.58 vs. 6.97 ± 1.31) (P < 0.007) [Table 4].

To explore the cutoff point that discriminates RV dysfunction, we constructed receiver operating characteristic curves for RV ∈sys, SRsys, SRe, and SRa in the DCM group. For global ∈sys% a cutoff value of −8.7% shows 63% sensitivity, 60.3% specificity, and area under the curve (AUC) of 0.653 [confidence interval (CI): 0.548–0.757, P < 0.008]. For global SRsys, a cutoff value of −0.76% shows 71.7% sensitivity and 60.3% specificity with AUC of 0.683 (CI: 0.580–0.787, P < 0.001) [Table 4].

For diastolic function, RV global SRe cutoff value of 0.53 shows 62.2% sensitivity, 60.3% specificity, and an AUC of 0.659 (CI: 0.555–0.764, P < 0.006). In addition, RV global SRa cutoff value of 0.58 shows 73.3% sensitivity, 60.3% specificity, and AUC of 0.731 (CI: 0.635–0.827, P < 0.0001) [Table 4].

Stepwise forward, multiple linear regression analyses that were performed in DCM patients showed that SRa dia global RV was an independent predictor of RV dysfunction (P < 0.01).


  Discussion Top


Current research in clinical cardiac mechanics is moving from LV short-axis and EF to long-axis function and from global to regional deformation abnormalities in different myocardial diseases. Measurement of longitudinal SR in the RV can be regarded as a reliable measure for (global) RV myocardial function and EF, even more than that in the LV, as 80% of total stroke volume is generated by longitudinal shortening [9].

This study with special focus on the RV provides new insights into mechanical alteration in the RV using feature tracking. Quantitative RV functional evaluation revealed a reduction in systolic and diastolic deformation, which is strongly correlated with LV function in DCM. The most important finding of this study was that RVFW mechanics was closely related to global RV deformation and gave the same clinical correlates. The former might consequently be used as an alternative measure of RV pump function.

Previous experimental and clinical studies indicate that the septum is the lion of RV function, and the fiber orientation and septal architecture and function are essential for RV ejection and suction for rapid filling [10].

In the present study, despite septal and myocardial dysfunction due to involvement by myopathic process, the RVFW still playing important role in overall RV performance. Both RVFW and global RV longitudinal deformation were firmly parallel and were directly related to LV systolic and diastolic function.

In previous reports analyzing the RV Doppler inflow, Lazzaret et al. [11] described slow deceleration of rapid filling wave and an increase in the lengthening of atrial contraction.

The present study verified RV myocardial diastolic dysfunction in DCM, as RV global εsys and regional 2D SRe and SRa peaks were significantly impaired; however, clinical evidence of RV failure does not exist.

Integration of the new evidence in basic science and evolution in imaging technology must be matched with a new understanding of cardiac mechanics to provide insights into disease that can lead to new therapy [12].

Many of the recent efforts to assess RV function have used tissue velocity (Doppler) signals to assess velocity at the tricuspid annulus [9],[10].

Researchers have demonstrated the ability of the diffusion tensor imaging (DTI) to characterize global and regional myocardial motion or deformation with high temporal resolution, but the angle dependency of Doppler, high noise-to-signal ratio, and interobserver variability are unavoidable limitations [13]. Conversely, the alternative method for motion estimation proposed here is based on 2D feature tracking using VVI processing, a novel approach that is inherently 2D and independent of both cardiac translation and interrogation angle as it tracks speckle patterns (acoustic markers) within serial B-mode sector scans [14].

RV global function as estimated by εsys determines the total amount of local deformation of RV wall segments, whereas SR reflects the rate of myocardial deformation, developed by estimating the spatial gradients in myocardial velocities. VVI echocardiography represents a simplified and angle-independent modality for the quantification of regional RV and LV myocardial deformation; longitudinal strain and SR are more sensitive in the assessment of subclinical systolic and diastolic dysfunction of the heart [12],[15].

To the best of our knowledge, this is one of the first studies to analyze RV regional deformation by the use of feature tracking VVI technology in patients affected by DCM.

The present study found an RV and LV myocardial systolic and diastolic dysfunction at global and regional level using VVI and that loss of base to apex gradient is concordant with LV EF.

Besides, our result highlights a systolic asynchronicity involving the RVFW and septum in DCM. The electromechanical delay between RV segments and prevalence of perceived stress scale (PSS) and diminished RV myocardial deformation might be explained on the grounds of a direct involvement of the RV wall by myopathic process.

However, the lower LV myocardial deformation indexes and its close correlation with RV dysfunction suggest ventricular interaction as further explanation of impairment in RV function in DCM. Ventricular interaction is an expression of close anatomic association between the two ventricles. this is strengthened and well scored in our study by the close relation between deterioration of RV deformation and the aggressiveness of LV dysfunction.

Interestingly, the present study sights the existence of extreme RV myocardial systolic nonuniformity and dyssynchrony in DCM as evidenced by increased values of RV TTP-SD, even in the absence of intraventricular conduction delay.

RV deformation was strongly related to intraventricular asynchrony, which is the most powerful predictor of sudden cardiac arrest [9].

Additional longitudinal studies using 2D strain analyses are warranted to advance our understanding of the natural history of RV myocardial deformation in DCM, the extent of reversibility of RV dysfunction with medical therapy, and the possible long-term impact of such changes on patient outcomes.


  Conclusion Top


In conclusion, our results suggest that the same cardiomyopathic pathology affects the RV as much as it affects the LV with reduction of both RV systolic and diastolic functions as well as global and RVFW function.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Yancys CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013; 62:e147–e239.  Back to cited text no. 1
    
2.
Richardson P, McKenna W, Bristow M, Maisch B, Mautner B, O'Connell J. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation 2006; 113:1807–1816.  Back to cited text no. 2
    
3.
Friedland G., Discovery of the function of the heart and circulation of blood. Cardiovasc J Afr 2009; 20:160.  Back to cited text no. 3
    
4.
Goldstein J. The right ventricle: what's right and what's wrong. Coron Artery Dis 2005; 16:1–3.  Back to cited text no. 4
    
5.
Lee FA. Hemodynamics of the right ventricle in normal and disease states. Cardiol Clin 1992; 10:59–67.  Back to cited text no. 5
    
6.
Vitarelli A, Terzano C. Do we have two hearts? New insights in right ventricular function supported by myocardial imaging echocardiography. Heart Fail Rev 2010; 15:39–61.  Back to cited text no. 6
    
7.
Haddad F, Hunt SA, Rosenthal DN, Daniel J. Murphy right ventricular function in cardiovascular disease, part i: anatomy, physiology, aging, and functional assessment of the right ventricle, Circulation 2008; 117:1436–1448.  Back to cited text no. 7
    
8.
Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr 1998; 11:1013–1019.  Back to cited text no. 8
    
9.
D'Andrea A, Caso P, Sarubbi B, D'Alto M, Giovanna Russo M, Scherillo M, et al. Right ventricular myocardial activation delay in adult patients with right bundle branch block late after repair of tetralogy of fallot. Eur J Echocardiogr 2004; 5:123–131.  Back to cited text no. 9
    
10.
Buckberg GD RESTORE Group. The ventricular septum: the lion of right ventricular function, and its impact on right ventricular restoration. Eur J Cardiothorac Surg 2006; 29 (Suppl 1):S272–S278.  Back to cited text no. 10
    
11.
Lazzaret F, Pellerin D, Fournier C, Witchitz S, Veyrat C. Right and left isovolumic ventricular relaxation time intervals compared in patients by means of asingle pulsed Doppler method. J Am Soc Echocardiogr 1997; 10:699–706.  Back to cited text no. 11
    
12.
Bussadori C, Moreo A, di Donato M, de Chiara B, Negura D, Dall'Aglio E, et al. A new 2D-based method for myocardial velocity strain and strain rate quantification in a normal adult and paediatric population: assessment of reference values. Cardiovasc Ultrasound 2009; 7:8.  Back to cited text no. 12
    
13.
D'Andrea A, de Corato G, Scarafile R, Romano S, Reigler L, Mita C, et al. Left atrial myocardial function in either physiological or pathological left ventricular hypertrophy: a two-dimensional speckle strain study. Br J Sports Med 2008; 42:696–702.  Back to cited text no. 13
    
14.
Purushottam B, Parameswaran AC, Figueredo VM. Dyssynchrony in obese subjects without a history of cardiac disease using velocity vector imaging. J Am Soc Echocardiogr 2011; 24:98–106.  Back to cited text no. 14
    
15.
Vannan MA, Pedrizzetti G, Li P, Gurudevan S, Houle H, Main J, et al. Effect of cardiac resynchronization therapy on longitudinal and circumferential left ventricular mechanics by velocity vector imaging: description and initial clinical application of a novel method using high-frame rate B-mode echocardiographic images. Echocardiography 2005; 22:826–830.  Back to cited text no. 15
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Patients and Methods
Results
Discussion
Conclusion
References
Article Tables

 Article Access Statistics
    Viewed136    
    Printed0    
    Emailed0    
    PDF Downloaded20    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]