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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 30  |  Issue : 3  |  Page : 823-831

Assessment of right atrium function in hypertrophic cardiomyopathy by speckle-tracking echocardiography


Department of Cardiovascular Disease, Menoufia University Hospitals, Menoufia University, Shebin El Kom, Egypt

Date of Submission14-Aug-2016
Date of Acceptance09-Oct-2016
Date of Web Publication15-Nov-2017

Correspondence Address:
Hatem A Mohamed
Department of Cardiovascular Disease, Menoufia University Hospitals, Menoufia University, Shebin El Kom, 32511
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.218263

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  Abstract 


Objective
We sought to evaluate the regional and global longitudinal strain/strain rate (SR) profiles in the right atrial (RA) wall to quantify RA function in hypertrophic cardiomyopathy.
Background
According to previous studies on the deformational properties of the left atrium, the systolic strain and SRs represent the atrial reservoir function and the early and late diastolic SRs show the conduit and booster functions, respectively.
Patients and methods
Speckle-tracking echocardiography of the RA, right ventricle, and left ventricle was acquired from apical four-chamber view in 118 hypertrophic cardiomyopathic patients and 33 healthy individuals; all had normal left ventricular systolic function. Subendocardium was traced to obtain atrial volumes, ejection fraction, velocities, and strain (ε)/SR measurements.
Results
Hypertrophic cardiomyopathic patients had significantly lower global and regional peak RA reservoir function (εsys, SRsys) and conduit function (SRe) compared with the controls: global εsys52.9 ± 27.9 versus 77.8 ± 31.3, SRsys2.4 ± 0.84 versus 3 ± 1.2, SRe− 2.2 ± 0.70 versus − 3.99 ± 0.73, respectively (P 0.001). RA contractile function (SRa) did not differ between the groups studied. RA ejection fraction was significantly reduced in the hypertrophic cardiomyopathy group compared with the control group (56 ± 16.7 vs. 68.9 ± 9.3, respectively, P 0.0001).
Conclusion
RA reservoir and conduit function as measured by strain/SR were significantly impaired, whereas contractile function showed no difference between the groups studied.

Keywords: hypertrophic cardiomyopathy, right atrium, speckle tracking, strain–strain rate


How to cite this article:
Badran HM, Sultan GM, Ahmed NF, Mohamed HA. Assessment of right atrium function in hypertrophic cardiomyopathy by speckle-tracking echocardiography. Menoufia Med J 2017;30:823-31

How to cite this URL:
Badran HM, Sultan GM, Ahmed NF, Mohamed HA. Assessment of right atrium function in hypertrophic cardiomyopathy by speckle-tracking echocardiography. Menoufia Med J [serial online] 2017 [cited 2019 Nov 22];30:823-31. Available from: http://www.mmj.eg.net/text.asp?2017/30/3/823/218263


  Introduction Top


Hypertrophic cardiomyopathy (HCM) is a hereditary cardiac disease with an autosomal dominant pattern of inheritance and incomplete penetrance [1] with a prevalence of 0.2% in the general population according to the echocardiographic criteria

[2].

The right atrium (RA) plays multiple roles in the cardiac cycle: acting as a reservoir for the systemic venous return when the tricuspid valve is closed, as a passive conduit when the tricuspid opens, and, finally, acting as an active conduit when it contracts [3].

The reservoir phase of the RA is a dynamic rather than a static phase of the cardiac cycle and RA deformation is dependent on pulmonary pressures exerted on the right ventricle (RV) and therefore backwards on the RA. Speckle-tracking echocardiography (STE) is a novel non-Doppler-based method for the angle-independent and objective quantification of myocardial deformation from standard bidimensional datasets that can potentially explore the RA deformation at each phase of the cardiac cycles [4].

Two-dimensional (2D) STE has recently been shown to be a feasible technique for the assessment of myocardial RA deformation dynamics with a good reproducibility. However, to date, no echocardiographic research has focused on mechanical assessment of RA function per se in HCM [5]. In this study, we sought to determine for the first time RA function and dimension in HCM by standard echocardiography and by 2D STE. We aimed to assess the feasibility of measuring the regional longitudinal strain and strain rate (SR) profiles in the RA wall to quantify the RA function in patients with HCM.


  Materials and Methods Top


Study population

Between October 2014 and March 2016, we prospectively included 118 HCM patients ranged in age from 20 to 60 years who were referred to our echocardiographic laboratories for risk stratification. They were examined in a single center (Yacoub Research Unite, Menoufiya University, Egypt and as a part of the BA-HCM National Program). The diagnosis of HCM was made on the basis of conventional echocardiographic demonstration of a nondilated, hypertrophic left ventricular (LV) (≥15 mm) in the absence of other cardiac or systemic diseases capable of producing the magnitude of hypertrophy evident [6],[7]. We included patients with sinus rhythm and normal ejection fraction (EF% >55%).

Patients with other known causes of LV hypertrophy (e.g., hypertension), patients with diabetes mellitus, anemia, pericardial disease, evidence of coronary artery disease, or pulmonary disease, significant arrhythmia, for example, atrial fibrillation, and inadequate or poor image quality were excluded.

Also, we studied 33 age-matched and sex-matched healthy individuals without detectable cardiovascular risk factor or receiving any medication. Volunteer controls were all selected from departments of adult cardiology among the individuals investigated for work eligibility. All study participants were enrolled in the study after their informed consent and approval of the Ethics Committee of Menoufiya University Hospitals were obtained.

Full medical history including any symptoms suggesting cardiac problems and family history of sudden death or hypertrophic cardiomyopathy (HCM) was obtained. All participants underwent a complete physical examination, ECG, and standard echocardiography according to the recommendation of the American Society of Echocardiography [7].

Conventional echocardiographic

Echocardiographic exams were performed in the left lateral decubitus, in the parasternal long, short-axis, and apical two-chamber and four-chamber views using standard transducer positions. Esaote Mylab Gold 30 ultrasound system (Esaote S.p.a, Florence, Italy) equipped with a multifrequency 2.5–3.5 MHz phased-array transducer was utilized [8]. LV end diastolic diameter, LV end-systolic diameter, and also septal and posterior wall thickness, maximal wall thickness (MWT), LV mass and mass index, fractional shortening (FS), EF%, left atrial diameter and volume, RA diameter, RV diameter, and RV thickness free wall were measured.

Pulsed-wave Doppler imaging

Color flow mapping and continuous-wave Doppler were used to define resting LV outflow tract obstruction; pulmonary artery pressure (PAP) was estimated from tricuspid regurge velocity (Bernoulli equation).

Deformation analysis using 2D strain analysis

Border tracking of the LV, RV, and RA was traced manually from the digitalized 2D video clips recorded during breath holding and with good quality of the ECG signal. All views were acquired and stored for off-line analysis using XStrain software (Arlington, VA) with a frame rate between 40 and 80 fps. The 'Zoom/RES' feature on the echocardiographic machine was used to improve the accuracy of atrial measurements [9].

RA strain measurement

For RA assessment, care was taken to obtain a true apical four-chamber view using standard anatomic landmarks in each view and not foreshorten the RA, allowing for a more reliable delineation of the atrial endocardial border. A circular region of interest was traced on the endocardial cavity interface of the apical four-chamber view at end diastole (RA minimum cavity area) using a point-and-click approach. An image-processing algorithm automatically subdivides the atrial wall into 12 segments distributed in the septum, lateral RA wall, and RA roof. Six graphs from these segments were displayed and averaged to calculate the global RA function.

The longitudinal strain curves were generated using the software for each atrial segment. All measurements were taken from the onset of the QRS complex, as described previously for the LA and RA [5],[10],[11]. RA peak systolisc strain (εsys) and RA systolic strain rate (SRsys) were measured as a positive curve at RV systole (representing reservoir function), whereas early diastolic strain rate (SRe) (representing conduit function) and late atrial diastolic strain rate (SRa) (representing contractile function) were shown as a negative curve during ventricular diastole [Figure 1].
Figure 1: RA strain and strain rate using variable valve timing. (a) Curved M-mode of RA longitudinal strain. (b) Tracing of the RA endocardial border in an apical four-chamber view showing velocity vectors. (c) RA strain and (d) strain rate versus time curves in septal and lateral segments. RA, right atrium; SRa, atrial diastolic strain rate; SRe, early diastolic strain rate; SRsys, peak systolic strain rate.

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Time–volume curves were extracted from RA wall tracking (tracing of the RA endocardial border in an apical four-chamber view) that provided automatically indexed maximum and minimum RA volume and automatically calculated right artrium ejection fraction (RAEF%) [Figure 2].
Figure 2: Upper panel shows The time–volume curve of RA generate RAEF% and the lower panel shows the RA strain curves of all segments. EF%, ejection fraction; RA, right atrium.

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LV and RV strain measurement

For LV and RV deformation assessment, the same parameters were used to measure global strain and strain rate of LV and RV from apical four-chamber and two-chamber views. To reduce random noise, each sample was obtained by averaging three consecutive heart cycles [Figure 3] and [Figure 4].
Figure 3: LV strain and strain rate using VVI. (a) Curved M-mode of LV longitudinal strain. (b) Tracing of the LV endocardial border in an apical four-chamber view showing velocity vectors. (c) LV strain and (d) strain rate versus time curves in septal and lateral walls. LV, left ventricle.

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Figure 4: RV strain and strain rate using VVI. (a) Curved M-mode of RV longitudinal strain. (b) Tracing of the RV endocardial border in an apical four-chamber view showing velocity vectors. (c) RV Strain segments and (d) strain rate versus time curves in septal and lateral segments. RV, right ventricle.

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Statistical analyses

Data were presented as number (%) or mean + SD. The distribution of qualitative variables was analyzed using the c2-test or Fisher's exact test. Quantitative variables were correlated using Pearson's correlation coefficient 'r'. All tests were two tailed and a P value of 0.05 or less was considered statistically significant. To identify significant independent predictors of global RA strain and SR, variables that were statistically significant in univariate analysis were introduced into a multivariate regression model; the overall fitness of the model was evaluated with the calculation of the coefficient R+SE. Receiver operating characteristic (ROC) curve analysis was carried out to select optimal cut-off values of RA deformation measurements [12]. The analysis was carried out using the statistical software package IBM SPSS statistics for Windows, version 22.0 (IBM Corp., Armonk, New York, USA).


  Results Top


A total of 118 HCM patients (48 women) were analyzed and compared with 33 (eight women) age-matched and sex-matched healthy individuals.

Clinical characteristics of the study population

There were no differences between the HCM and the control group in age, sex, BSA, heart rate, or diastolic blood pressure, but systolic blood pressure was significantly higher in the HCM group. Of 118 HCM, 48 (40.7% women) and 70 (67.8%) were symptomatic [~65% were New York Heart Association (NYHA) class II, 31% were class III, and 4% were class IV], and nine (8%) had a history of syncope. 40 (34%) patients had the familial type (on the basis of a prospective evaluation of relatives) and 16 (14%) patients had a positive family history of premature sudden death. 91 (~77%) patients had asymmetric septal hypertrophy, 23 (20%) patients had concentric LVH, and three (~3%) patients had apical HCM. 27 (23%) patients patients had extreme LVH (MWT 30 mm or more), 27 (23%) patients had LV outflow tract obstruction 30 mmHg or more, 57 (48%) patients had LA volume index more than 30 m/m2, 13 (11%) patients had severe tricuspid regurge, and 30 (25%) patients had PAP more than 30 mmHg [Table 1].
Table 1: Clinical characteristics of the study population

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Conventional echocardiographic analysis

There was a significant difference among the HCM and control groups in LA dimension, LA volume, LV EF%, FS%, septal thickness (SPT) and LV posterior wall thickness, S/PW ratio, MWT, LV mass, and LV mass index, and RV thickness; these were significantly greater in the HCM group (P 0.0001). Rest LVOT gradient and PAP were also significantly greater in the HCM group (P 0.05). LV end-systolic diameter, LV end diastolic diameter, and RAEF were significantly reduced in the HCM group (P 0.0001) [Table 2].
Table 2: Conventional echocardiography of the groups studied

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LV deformation analysis

In HCM, despite the slightly higher LV EF, 2D strain analysis detected significantly lower global peak LV εsys, SRsys, and SRe in comparison with the control group (P 0.0001). However, LV global SRa did not differ between the HCM and the control group [Table 3].
Table 3: LV deformation in the groups studied

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RV deformation analysis

In HCM, 2D strain analysis detected lower global peak RV εsys, RV SRsys, and RV SRe of the (P 0.0001) in comparison with the control group, whereas RV global SRa did not differ from that of the control group [Table 4].
Table 4: RV deformation in the groups studied

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RA deformation analysis [Table 5]
Table 5: RA deformation in the groups studied

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Compared with the control group, HCM patients had lower reservoir function as measured by peak RA εsys and SRsys and lower conduit function as expressed by SRe(P 0.0001). In HCM, global RA εsys% was 52.9 ± 27.9 versus 77.8 ± 31.3 (P 0.0001). Global RA SRsys was 2.4 ± 0.84 versus 3 ± 1.2 in the control group, (P 0.001). Global RA SRe was significantly reduced (−2.2 ± 0.70 vs. −3.99 ± 0.73, respectively, P 0.0001). However, the difference between RA contractile function, as expressed by SRa, remained and did not reach statistical significance between the groups studied. Furthermore, RAEF as measured from the time–volume curve was significantly reduced in the HCM group compared with the control group (56 ± 16.7 vs. 68.9 ± 9.3, respectively, P 0.0001) [Table 5].

To explore the cut-off point that discriminates RA dysfunction, we constructed ROC curves for RA єsys, SRsys, SRe, and SRa in HCM [Figure 5]a, [Figure 5]b, [Figure 5]c, [Figure 5]d. For RA reservoir function, an RA εsysa value of 66.6 or lower has a 70% sensitivity and a 60% specificity to denote a patient and an SRsysa value of 2.67 or lower has a 60% sensitivity and a 66.6% specificity to denote a patient. For conduit function, an SRea value of − 2.758 or lower has a 100% sensitivity and an 85% specificity to denote a patient. In addition, for contractile function, there was no suitable cut-off point for RA SRa as shown in the ROC analysis section.
Figure 5: (a) (RA εsys) ROC curve of global RA deformation parameters has been plotted for differentiating HCM patients with RA dysfunction. (b). RA SRsys ROC curve of global RA deformation parameters has been plotted for differentiating HCM patients with RA dysfunction. (c). RA SRe ROC curve of global RA deformation parameters has been plotted for differentiating HCM patients with RA dysfunction. (d) (RA SRa) ROC curve of global RA deformation parameters has been plotted for differentiating HCM patients with RA dysfunction. εsys, peak systolic strain; HCM, hypertrophic cardiomyopathy; RA, right atrium; ROC, receiver operating characteristic; SRa, atrial diastolic strain rate; SRe, early diastolic strain rate; SRsys, peak systolic strain rate.

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Univariate relations of RA 2D strain indexes

When considering the relation of RA mechanics to the severity of hypertrophic cardiomyopathy, the RA reservoir function was inversely correlated to NYHA functional class (P 0.02) [Figure 6], RA systolic (P 0.0001), and diastolic (P 0.003) volumes, and directly correlated to RA ejection fraction (P 0.0001). SRe was inversely correlated to MWT (P 0.001), age (P 0.0001), NYHA functional class (P 0.003), RA systolic (P 0.0001) and diastolic (P 0.001) volumes, and LV SPT (P 0.004) and directly correlated to RA ejection fraction (P 0.0001) [Table 6] and [Table 7]).
Figure 6: Relationship of RA reservoir function with NYHA functional class. NYHA, New York Heart Association; RA, right atrium.

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Table 6: Relationship of RA deformation with clinical and other echocardiographic parameters

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Table 7: Relationship of RA mechanics with RV and LV deformation parameters

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Interestingly, RA contractile function as derived from SRa was inversely correlated to RA systolic and diastolic volumes (P 0.0001) and directly correlated to LV outflow tract obstruction (P 0.001) and RAEF% (P 0.0001). However, the PAP and severity of tricuspid regurge did not affect RA mechanics in this HCM study population.

In HCM, the deformation variables estimated by RA εsys and SR were concordant with those derived by longitudinal peak RA velocities (P 0.001). RA reservoir function as derived by global strain and SRsys was directly correlated to global LV (P 0.001) and PV systolic (P 0.0001) functions (as reflected by εsys), global LV and RV diastolic function (P 0.0001) (as reflected by SRe), and RAEF% (P 0.0001) [Table 7]. In addition, RA conduit function as measured by SRe showed a positive correlation with LV systolic function (P 0.002) and LV diastolic function (P 0.003). This RA conduit function was also correlated to RV systolic function (εsys) (P 0.005) and RV diastolic function (RV SRe) (P 0.001).

However, the RA contractile function as measured by SRa was only correlated to RV systolic function RV εsys(P 0.02), RV SRsys(P 0.03), and RV diastolic function RV SRe(P 0.01).

Multivariate analysis

RAEF (β coefficient 0.071 ± 0.019, P 0.0001) and RV global SRe dia (β coefficient 0.901 ± 0.363, P 0.013) were independent predictors of impaired RA reservoir function. MWT (β coefficient − 0.701 ± 0.245, P 0.004) and RV thickness (β coefficient − 0.492 ± 0.224, P 0.028) were independent predictors of impaired SRe.


  Discussion Top


The present study is the first attempt to assess the RA mechanical properties in patients with HCM. Most studies, even the latest, used speckle-tracking modality to study LV functional and mechanical remodeling in HCM [13],[14] and only a limited number of studies have investigated RV structure and mechanics in patients with HCM [8],[15]. Also, left atrium (LA) mechanics was studied in patients with HCM by speckle tracking [16].

In the current study, we showed that RA mechanics completely followed RV function and LV function and severity of the disease; thus, they were markedly reduced in comparison with the healthy controls. The three components of the atrial functions, the reservoir function, conduit function, and booster pump function, were investigated. Our work showed a predominant reduction in RA reservoir and conduit function in HCM patients in comparison with the normal individuals, whereas the contractile function was unaltered in this patient subset with preserved LV EF.

When a cardiac chamber is exposed to chronic pressure and/or volume overload and its diastolic properties begin to change, the Frank–Starling mechanism starts working to counterbalance the increase in pressure, resulting in a progressive augmentation in chamber size and performance. This behavior, which might be limited by the degree of diastolic dysfunction, has been clearly documented in various pathophysiological conditions in both the LV and the LA [17],[18],[19],[20].

RA reservoir and conduit function were predominantly deteriorated. According to the previous studies on the deformational properties of the LA and the few studies carried out to date on the RA function, the systolic strain and strain rates represent the atrial reservoir function and the early and late diastolic strain rates show the conduit and booster functions, respectively [10],[21],[22].

In the present study, HCM patients had lower global and regional RA strain and SRsys(reservoir function) and SRe(conduit function) compared with the controls. RA contractile function as expressed by SR measured during late diastole remained the same and did not differ between the groups studied. RAEF was significantly reduced in the HCM group compared with the control group.

In our cohort, quantification of longitudinal myocardial RA deformation during reservoir phase showed a significant reduction in HCM that was strongly related to RAEF%, global LV εsys, LV SRe, and global RV εsys, RV SRe. Meanwhile, RA reservoir was inversely correlated to the severity of LV cardiomyopathy. LA diameter and volume, RA volumes, could exacerbate the deterioration of reservoir function in HCM patients.

Furthermore, in this study, evidence of impaired RA conduit function in HCM patients was strongly related to the severity of LV cardiomyopathy and LV mechanics for example, MWT, age, functional class, and SPT. RA conduit function as measured by SRe was strongly related to LV systolic function (εsys) and LV diastolic function (LV SRe). This RA conduit function was also correlated to RV systolic function (εsys) and RV diastolic function (RV SRe). RA contractile function SRa was inversely correlated to RA systolic and diastolic volumes and directly correlated to LV outflow tract obstruction and RAEF% and RV systolic and diastolic function.

The mechanics of the RA are complex. In 1628, Harvey [23] was the first to identify the atrium as a 'receptacle and store-house', noting that the RA was 'the first to live, and the last to die'.

In an elegant computer model, Suga [24] found that increased atrial compliance markedly improved cardiac performance and concluded that a 'flexible atrium' (increased receptacle capabilities) would markedly improve the cardiac output. This means that, as the atrium fills during the reservoir phase, the atrial myocardium (like the ventricle) stores elastic energy that is released when the tricuspid valve opens to aid early ventricular filling [23],[24],[25],[26],[27],[28],[29],[30].

In a previous study in our center, Badran et al. [16], studied LA deformation in 108 HCM patients in comparison with 33 healthy individuals; all had normal LV systolic function. Left atrial reservoir (LA εsys, SRsys) and conduit (early diastolic SRe) function were significantly reduced in the HCM group compared with the controls (P 0.0001), whereas contractile function was preserved among HCM patients. Left atrial deformation was considerably influenced by LV mechanics, global LV SRsys, and LV SPT, (P 0.0001) are independent predictors for global LA strain, and only LV end-systolic diameter is an independent predictor for SRsys(β coefficient 0.033; 95% confidence interval: 0.015–0.083, P 0.03). For atrial conduit function, LA EF (β coefficient 5.27; 95% confidence interval: 3.24–7.45, P 0.001) is an independent predictor of SRe.

Similar to our study, D'Ascenzi et al. [31] studied patients with LVH. one hundred top-level athletes were recruited from professional sports team and were compared with 78 normal individuals matched for age and sex. Athletes during an off-training period or during prolonged forced rest resulting from injuries were excluded. Peak atrial longitudinal strain and peak atrial contraction strain values were significantly lower in athletes in comparison with the controls (40.92 ± 9.86 vs. 48.00 ± 12.68%, P 0.001; 13.05 ± 4.84 vs. 15.99 ± 5.74%, P 0.001, respectively). The same research group reported that RA area, volume, and volume index were significantly greater in athletes than in the controls (P 0.001). This increase was associated with greater RV and inferior vena cava diameters (P 0.001).

Also, Ojaghi Haghighi et al. [32], studied thirty patients with a diagnosis of heart failure and the control group included 32 healthy adults matched for age and sex. The RA deformation indices were significantly compromised in the heart failure patients versus the normal individuals (RAεsys: 68.5 ± 53.9 vs. 189.3 ± 61.2, P 0.0001; RA SRsys: 2.9 ± 1.9 vs. 5.3 ± 1.5, P 0.0001).

Padeletti et al. [4], reported that RA global strain significantly correlated with pulmonary pressure and showed that RA global strain and strain rate could predict pulmonary artery hypertension in patients with heart failure.

Clinical implications

This study provides further insight into the influence of HCM on mechanical function. Our figures and cut-off values show that RA deformation indices could be considered both diagnostic and prognostic adjuncts, which facilitate unmasking of incipient myocardial dysfunction in HCM. Serial measurement of RA strain/SR to detect the onset of RA contractile dysfunction and impaired RA compliance, known to take place in more advanced disease, is recommended. These indices may prove to be useful in treatment decision-making.

The RA is a dynamic structure. Ideally, the RA should transfer a high volume of blood rapidly to the ventricle at low pressure to prevent peripheral edema and hepatic congestion [21]; the significance of these findings and their possible application will require further study.

Study limitation

The speckle-tracking method is influenced by image quality, and in particular, clinical conditions; they can present limitations because of the physiological growth of the myocardial chambers, which prevents, sometimes, the perfect framing of the image in the echocardiographic window. The resolution of 2D imaging may be a problem in some patients and inadequate border recognition of the RA may be another factor limiting assessment of myocardial strain.


  Conclusion Top


Our study showed that RA mechanics, strain and strain rate during systole (reservoir function) and strain rate during early diastole (conduit function), in HCM patients were impaired compared with healthy controls. The impairment is more extensive in the patients with more impaired ventricular function and severity of the disease. Further longitudinal analyses are needed to compare these findings with other methods and to investigate the effects of cardiac changes on the patients' outcomes and the clinical utility of these results in management strategy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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