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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 1  |  Page : 136-144

Assessment of right ventricular response to exercise using vector velocity imaging in hypertrophic cardiomyopathy


Department of Cardiology, Faculty of Medicine, Menoufiya University, Menoufiya, Egypt

Date of Submission28-Nov-2013
Date of Acceptance06-Jan-2014
Date of Web Publication20-May-2014

Correspondence Address:
Maged M. Khalifa
BSc, Karram Towers, Mahmoudia Canal Street, Moharram Bek, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.132787

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  Abstract 

Objective
The objective of this study was to assess right ventricular (RV) deformation response to exercise in hypertrophic cardiomyopathy (HCM) and its relationship with left ventricular (LV) function using vector velocity imaging (VVI).
Background
RV adaptive mechanisms to exercise in HCM are poorly understood. VVI is achieved through the combination of speckle tracking, mitral annulus motion, tissue-blood border detection, and the periodicity of the cardiac cycle using R-R intervals. It can measure different parameters of deformation and dyssynchrony of the regional myocardium.
Patients and methods
Resting and exercise echocardiography was performed in 40 HCM patients and 33 healthy control individuals. Longitudinal peak systolic strain (εsys ) and strain rate (SR sys , SR e , SR a ) of RV segments from the apical four-chamber view were used to evaluate RV functional reserve (stress-rest/rest). Similar parameters were quantified in LV wall segments. Intra-V dyssynchrony was defined as SD of TTP (measured from regional strain curves for each segment as time from the beginning of the Q wave to time to peak åsys ).
Results
In HCM and immediately after exertion, RV åsys and SR sys were significantly lower and RV dyssynchrony was greater compared with those in the control participants. A significant correlation was evident between exercise capacity and RV TTP-SD and RV SR sys . RV functional systolic reserve showed a direct relationship with LV systolic functional reserve. However, using multivariate regression analysis, LV SR sys , and LV, TTP-SD is the only predictor of exercise capacity, whereas the RV functional reserve did not alter the outcome. Exercise stress-induced RV dysfunction in HCM is associated with exercise intolerance and strongly related to LV deformation abnormalities as evaluated by VVI.
Conclusion
Although exercise-induced RV dysfunction assessed during stress was statistically associated with exercise capacity, it was found that the LV systolic SR and systolic dyssynchrony at rest are major determinants of exercise tolerance in HCM.

Keywords: Exercise, hypertrophic cardiomyopathy, right ventricle, vector velocity imaging


How to cite this article:
Badran HM, Ahmed NF, Ibrahim WA, Khalifa MM. Assessment of right ventricular response to exercise using vector velocity imaging in hypertrophic cardiomyopathy. Menoufia Med J 2014;27:136-44

How to cite this URL:
Badran HM, Ahmed NF, Ibrahim WA, Khalifa MM. Assessment of right ventricular response to exercise using vector velocity imaging in hypertrophic cardiomyopathy. Menoufia Med J [serial online] 2014 [cited 2020 Feb 28];27:136-44. Available from: http://www.mmj.eg.net/text.asp?2014/27/1/136/132787


  Introduction Top


Hypertrophic cardiomyopathy (HCM) is a primary cardiac disorder that results from genetic defects in sarcomeric proteins of the cardiac myocyte. The disorder is considered to be inherited in an autosomal dominant manner with variable penetrance and expressivity [1].

HCM has a complex set of symptoms and potentially devastating consequences. The clinical presentation and course varies widely; some patients are completely asymptomatic, whereas others experience sudden cardiac death, especially among adolescent children, in whom HCM is the leading cause of sudden cardiac death during exertion [2].

The right ventricle (RV) plays a critical role in normal and abnormal hemodynamics and the onset of RV dysfunction can adversely affect the left ventricular (LV) function and might lead to heart failure [3].

It is reasonable that the RV may participate to the disease because of an extension of the myopathic process and/or because RV and LV share structurally hypertrophied interventricular septum [4-6]. Exercise echocardiographic (EE) assessment of LV regional and global function has been well established in the diagnosis and risk stratification of many disease entities including HCM.

Previous studies showed increased RV wall thickness and RV diastolic dysfunction in a large proportion of patients affected by HCM using MRI, 2-dimensional (2D) echocardiography, and biplane RV angiography [7],[8],[9].

However, RV function is not commonly assessed during EE because of the challenges posed by its complex geometry and kinematics, and observation or measurement of RV wall motion during exercise, using the previously mentioned techniques, is difficult because of the lack of trackable landmarks in the RV wall [3].

Recently, 2D strain measurements from grayscale images have been introduced on the basis of speckle tracking. Speckle tracking is a method in which ultrasound speckles within the image are tracked and strain is determined from the displacement of speckles in relation to each other, therefore providing an angle-independent parameter of myocardial function [7],[10].

A new feature-tracking echocardiographic method using vector velocity imaging (VVI) is achieved through the combination of speckle tracking, mitral annulus motion, tissue-blood border detection, and the periodicity of the cardiac cycle using R-R intervals. It can measure the myocardial strain, strain rate (SR), and velocity of the regional myocardium [8].


  Objectives Top


To assess the effect of exercise on RV deformational mechanics using 2D strain VVI and to report its relation to LV dynamics in patients with HCM.


  Patients and methods Top


Study population

Between September 2011 and November 2012, we prospectively included 40 HCM patients, mean age 41 ± 19 years, who were referred to our echocardiographic laboratories for risk stratification. They were examined in a single center (Yacoub Research Unit, Menoufiya University, Egypt). The diagnosis of HCM was made on the basis of conventional echocardiographic demonstration of a nondilated, hypertrophic LV (≥15 mm) in the absence of other cardiac or systemic diseases capable of producing the magnitude of hypertrophy evident [11].

The HCM group was compared with 33 age-matched and sex-matched healthy individuals without detectable cardiovascular risk factors or receiving any medication. They were volunteers recruited from among hospital staff, medical and nursing students, and members of the local community. The entire population studied was enrolled after their informed consent and approval of the Ethics Committee of Menoufiya University Hospitals was obtained.

Exclusion criteria

The following patients were excluded from the study: patients with left ventricular outflow obstruction (LVOTO ≥30 mmHg at rest), and patients who had more than moderate tricuspid regurge (a resting peak TR velocity >3.0 m/s), ejection fraction (EF) less than 50%, previous myectomy or alcohol septal ablation, ICD, diabetes mellitus, evidence of coronary artery disease, atrial fibrillation, lung disease, and exercise-limiting diseases [9].

Procedure

All patients and control participants were subjected to 12-lead ECG, conventional echocardiographic examination, 2D-strain imaging using VVI, and the Bruce protocol treadmill exercise test.

Conventional echocardiography

Echocardiographic images were obtained in the parasternal long, short-axis, apical two-chamber and four-chamber views using standard transducer positions. The Esaote Mylab Gold ultrasound system (Esaote S.p.A, Florence, Italy) equipped with a 5 MHz phased-array transducer was utilized. All echocardiographic measurements were obtained at rest and within 1 min after treadmill exercise. LV end-diastolic diameter, end-systolic diameter (ESD), septum, posterior wall thickness, EF%, and left atrial (LA) diameter and volume were measured in accordance with the recommendations of the American Society of Echocardiography [12]. Continuous-wave Doppler was used to diagnose resting obstruction, and estimation of pulmonary artery pressure was performed from tricuspid regurge velocity (Bernoulli equation).

Peak early (E) and late (A) transmitral (Em and Am ) and transtricuspid (Et and At ) filling velocities were measured from mitral and tricuspid inflow velocities. Peak systolic (Sa ), early diastolic (Ea ), and atrial diastolic (Aa ) velocity were obtained by placing a tissue Doppler sample volume at the RVFW and lateral mitral annulus in the apical four-chamber view. The Em /Eam and Et /Eat ratio were calculated.

Analysis of right ventricular and left ventricular deformation

Strain measurement was performed on the basis of the VVI: The VVI is based on the concept that tissue moves from one frame to the next, and multiple speckle tracking algorithms ultimately identify the tissue displacement at every point. Practically, a single endocardial border tracing leads to automatic tracking of the entire cardiac cycle, allowing analysis of velocity vector mechanics, including the velocity, displacement, strain, and SR. The global longitudinal myocardial deformation was evaluated from standard 2D-images at frame rate (70 ± 20 F/s) and adjusted depending on the heart rate. RV and LV images were recorded and processed. Tracking and subsequent strain calculations were performed using the software package Esaote-X-Strain software (ESAOTE, Italy) on the basis of a previously validated algorithm [13] Scanning was performed longitudinally from the apex to acquire the best apical views. Peak systolic strain (åsys ), systolic strain rate (SR sys ), early and atrial diastolic strain rate (SR e and SR a ) in the basal, mid, and apical segments of RV septal and RV free wall, and LV septal, lateral, anterior, and inferior wall segments were measured and averaged (in three cardiac cycles) to calculate the global longitudinal deformation [Figure 1].
Figure 1:

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To estimate mechanical dyssynchrony, the index of myocardial systolic activation was calculated, from regional strain curves for each ventricular segment, as time from the beginning of the Q wave of ECG to the peak longitudinal systolic strain time to peak (TTP). RV and LV electromechanical delay was measured in six RV and 12 LV segments, respectively [14],[15]. Intra-V dyssynchrony was defined as the standard deviation of the averaged time-to-peak-strain (TTP-SD) [16],[17]. The stress echocardiographic images were acquired immediately at peak exercise (within one minute) and focused on analysis of RV and LV deformation.

Exercise testing

A standard multistage symptoms limiting exercise test was performed on a motorized treadmill (MyFormula, RAM model 770M; Esaote S.p.A., Baar, Switzerland) according to the Bruce protocol [6],[18]. The exercise testing began with participants walking slowly for 3 min at 1.7 m/h at a 10% grade; speed and grade were then increased every 3 min until exhaustion. Patients were asked to hold β-blockers and calcium channel blockers (if any) at least 24 h before the stress testing. The exercise test was interrupted promptly when age-related maximum heart rate was reached or severe hypertension (systolic blood pressure ≥?250 mmHg), or significant ventricular arrhythmia developed. Each participant was informed that he/she could stop voluntarily by indicating whether he/she had any symptoms such as chest pain, intolerable fatigue, dizziness, breathlessness, etc.

The ECG, heart rate, and blood pressure were recorded during the last minute of each stage of exercise and after exercise [19]. The ECG was monitored continuously and the 12 leads were displayed continuously on the monitor throughout the exercise. Exercise capacity was determined by:

  1. metabolic equivalent (METS) (1 MET = 3.5 ml/kg/min of oxygen consumption) and was estimated on the basis of the protocol, speed, and grade achieved [20].
  2. Duration of exercise (exercise treadmill time).
  3. Rate pressure product (RPP) is a measure of myocardial oxygen uptake during clinical exercise testing. It is estimated by the product of maximal achieved heart rate and systolic blood pressure.


Statistical analyses

Categorical data were shown as frequencies and percentages, and comparisons were made using χ΂-tests or Fisher exact tests as appropriate. Continuous data were expressed as mean ± SD. They were correlated by Spearman's test and compared between groups using one-way analysis of variance or unpaired Student's t-test, as indicated. Linear regression analysis was used to identify independent predictors of RPP, METS, exercise treadmill time in patients presenting with HCM. Variables introduced into the model were patients' age, body surface area, NYHA class, LA volume, ESD, end diastolic diameter, EF%, left ventricular mass index, resting LVOT gradient, degree of MR, E/Ea , resting and exercise global € sys , SR sys , SR e , SR a , TTP-SD, magnitude of change in each value (Δ), and percent of change (Δ/rest value). A P value of 0.05 or less was set a priori and considered statistically significant. All statistical analyses were carried out using the statistical software package IBM-SPSS, New York, USA version 20.


  Results Top


Clinical characteristics

The clinical, echocardiographic, and baseline characteristics of the 40 patients with HCM, 72.5% men, and the 33 control participants are shown in [Table 1]. The population studied was well matched for age, sex, and BMI. At baseline, HCM patients had larger LA volume, smaller ESD, greater LV and RV wall thickness, left ventricular mass index, DT, and higher Em /Eam and Et /Eat ratios compared with the control participants (P < 0.001) [Table 1].
Table 1: Clinical and conventional echocardiographic criteria of the study population

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Hemodynamics during exercise

The level of exercise achieved was maximal in all control participants and in 22 (55%) HCM patients (P < 0.001). More symptoms developed in HCM patients than in the control participants during exercise. The mean exercise duration and METS were lower compared with those in the control participants (P < 0.001). Eight (20%) HCM patients had low exercise capacity (METS <7). Meanwhile, during exercise, the heart rate increased significantly (P < 0.0001) in patients and control participants, but the peak RPP, METs, and exercise duration were significantly lower in HCM patients compared with control participants (P < 0.001) [Table 2].
Table 2: Hemodynamics during exercise

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Right ventricular deformation analysis

From the apical four-chamber view of RV, all studies at both baseline and peak stress were feasible for VVI analysis. In the control group, there was a significant increase in longitudinal RV åsys , SR sys , SR e, and SR a during peak stress and their corresponding Δ of change and the functional reserve estimated as the Δ/rest value (P < 0.0001). In the HCM group, the RV deformation variables were significantly lower at rest (P < 0.0001). Exercise-induced reduction in global RV åsys developed in 20 (50%) HCM patients. Although there was a mild increase in the systolic functional reserve at peak stress, it remained significantly lower in comparison with the control participants (12 vs. 16% for åsys ; P<0.004 and 19 vs. 67% for SR sys ; P < 0.001) [Table 3]. Furthermore, the diastolic functional reserve was considerably smaller in the HCM group compared with the control participants (18.8 vs. 76% for SR e ; P<0.02 and 24 vs. 49% for SR a ; P < 0.007) [Figure 1].
Table 3: Changes in right ventricular deformation during exercise

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Right ventricular velocity during exercise

Longitudinal systolic velocity of the RV basal lateral wall (Sta ) showed a significant increase at peak stress (6.4 ± 4.1 to 6.7 ± 3.8 cm/s; P<0.05) and a negative change (-4.4 ± 49%) in HCM versus an increase by 11.2 ± 34% in the control group during exercise. Augmented early diastolic velocity (Eta ) during exercise was significantly less in HCM patients (at rest: vs. 4.6 ± 3.1 to 5.1 ± 4.0; P < 0.05) compared with the control participants (7.5 ± 1.5 to 9.2 ± 2.9; P < 0.001).

Right ventricular electromechanical heterogeneity

TTP-SD between the RV segments was marked in HCM at rest and amplified at peak stress (66.5 ± 46, 73.9 ± 33 ms) compared with the control participants (35.9 ± 9, 28.4 ± 12 ms) (P<0.01). If TTP-SD more than 54 ms (mean + 2SD of age-matched controls) was defined as intra-RV dyssynchrony, upon stress, the prevalence of systolic dyssynchrony increased modestly from 22 (55%) to 26 (65%) in HCM (P < 0.001) during exercise [Table 3], [Figure 2] and [Figure 3].
Figure 2:

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Figure 3:

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Left ventricular deformation

Absolute values of LV åsys and SR sys were significantly smaller in HCM patients compared with the control participants at the segmental and global levels both at rest and at peak exercise (P < 0.001) [Table 4]. There was even a reduction in the LV global strain by -23.5 ± 28% during peak exercise versus an increase by 17.7 ± 6% of εsys in the control participants at peak exercise (P < 0.001).
Table 4: Changes in left ventricular deformation during exercise

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Among our patients, 32 (80%) of HCM patients showed a decrease in their εsys at peak stress. Furthermore, exercise SR sys was significantly reduced in HCM by -15 ± 24%, but augmented by 40 ± 9% in healthy participants (P < 0.0001). In HCM patients, SR e was significantly lower at rest in comparison with the control participants and showed greater reduction at peak exercise (P < 0.001). There was a reduction in SR e by -10 ± 31% in HCM patients versus an increase by 23 ± 7% in the control participants (P < 0.001). Although SR a was significantly lower at peak exercise in the HCM group (P < 0.001), Δ of changes in late diastole did not differ between groups.

Left ventricular dyssynchrony

TTP-SD between the LV segments was marked in HCM at rest and amplified at peak stress (52 ± 28, 60 ± 37 ms) compared with the control participants (28 ± 17.5, 20.9 ± 12 ms) (P < 0.0001) [Table 4]. If TTP-SD of more than 44 ms (mean+2 SD of age-matched controls) was defined as LV dyssynchrony, upon stress, the prevalence of systolic dyssynchrony increased markedly from 14 (35%) to 25 (62.5%) in HCM patients (P < 0.0001), but the contraction become more homogeneous in the control participants at peak stress.{Table 4}

Relation of exercise capacity to right ventricular deformation

In the HCM group, a significant direct correlation was observed between RPP and RV SR sys at peak stress (r = 0.34; P < 0.03), SR a (r = 0.32; P < 0.04) and an inverse relation to intra-RV dyssynchrony (TTP-SD) (r = -0.32; P < 0.04) [Figure 4],[Figure 5] and [Figure 6]. Duration of exercise was correlated directly to SR a (r = 0.31; P < 0.05) and related inversely to RV TTP-SD (r = -0.38; P < 0.01). Again, METs showed a significant inverse relation to RV (TTP-SD) (r = -0.39; P < 0.01).
Figure 4:

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Figure 5:

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Figure 6:

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Relation of right ventricular strain to left ventricular strain during exercise

RV εsys during peak exercise showed a direct correlation to LV function as expressed by LV εsys (r = 0.42; P < 0.0007). Furthermore, the RV functional systolic reserve (%εsys ) showed a direct relationship with the LV systolic functional reserve (LV εsys ) (r = 0.32; P<0.04) [Figure 7].
Figure 7:

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Multivariate analysis

We constructed a multivariate logistic regression model to define the independent predictors of exercise capacity as measured by RPP and the total exercise time. Variables introduced into the model were those variables that were statistically significant in bivariate analysis. From all RV and LV deformation variables, only LV Global SR sys (β = 0.327; P = 0.038) and LV dyssynchrony (TTP-SD) (β = 0.401; P = 0.011) were independent predictors of exercise capacity in HCM patients, whereas RV functions at rest and exercise failed to change the outcome.


  Discussion Top


In the present study, RV longitudinal deformation showed a blunted increase during peak exercise in HCM. Exercise stress-induced RV dysfunction is strongly related to changes in LV deformation as evaluated by VVI. Despite the strong relation of exercise capacity to RV function, LV systolic strain rate and dyssynchrony remain the central determinants in this population.

Measurement of longitudinal strain (rate) in the RV can be considered a reliable measure for global RV myocardial function and EF, even more than in the LV, as 80% of the total stroke volume is generated by longitudinal shortening [21].

Since 1979, EE has been used extensively to evaluate stress-induced LV wall motion abnormalities [22]. However, only a few studies have evaluated RV function during EE [14],[15]. Recently, in patients with adult congenital heart disease, the systemic RV function evaluated using M-mode and tissue Doppler velocity showed its role as a determinant of exercise capacity during EE [23]. Bangalore et al. [24] reported the prognostic value of visual RV wall motion analysis independent of LV ischemia in EE.

Exercise capacity in hypertrophic cardiomyopathy

Exercise intolerance is the most common symptom in patients with HCM [11],[24]. The majority of patients are incapable of increasing their oxygen consumption (VO 2 ) during exercise as a result of an inability to increase systolic volume [6]; LV outflow tract obstruction, mitral regurgitation, prolonged isovolumetric relaxation, and an increased stiffness of the LV chamber are the commonly considered underlying pathophysiologic mechanisms [6],[18],[25]. Nevertheless, information on the changes in RV mechanics during exercise that could be part of exercise intolerance is not available.

In this study, we excluded the presence of resting LVOTO as earlier studies had recognized its strong association with functional limitation and one of the most important restraining factors [11],[26],[27]. In the present study, HCM patients showed a reduction in exercise capacity as estimated by RPP, duration of exercise, and maximal metabolic equivalent compared with the controls. Exercise capacity was correlated directly to the RV systolic strain rate and atrial diastolic strain rate and correlated inversely to intra-RV dyssynchrony. The reduction of RPP in the HCM group cannot be attributed to lower peak exercise heart rate or abnormal BP response to exercise that occurred only in ∼18% of our patients. However, the lack of stroke volume augmentation resulting from abnormal RV adaptation and LV dysfunction might be another possible mechanism behind reduced cardiac output in affected individuals. Earlier studies have reported that SV is the major determinant of peak exercise capacity in HCM whereas HR augmentation does not appear to be a major determinant, especially in the upright position [28].

Right ventricular systolic functional reserve

In the control group, there was a significant positive augmentation in RV longitudinal velocity (systolic and diastolic) and the new regional RV deformation parameters (strain and SR) of RV wall segments at peak exercise. Yang et al. [29] tested RV function in 73 normal participants using VVI. They assessed the radial, circumferential and longitudinal strain, SR, velocity, and displacement of RV. They found that the longitudinal velocity and SR showed a significant increase in magnitude at peak stress, whereas the strain did not. They speculated that a parameter calculated with a time interval (velocity, SR) is more sensitive to stress-induced RV regional changes than a parameter with no bearing on time (displacement, strain). This is in agreement with our figures, where the change in RV SR during exercise was correlated strongly with exercise capacity at a time the strain changes failed to do that.

The current study provides new insights into altered adaptation of the RV during exercise in HCM. RV longitudinal deformation showed a lower baseline value as well as a blunted increase during exercise stress compared with healthy controls.

Although depressed RV function is a well-known independent predictor of poor outcome in different disease entities [30], its role in determining exercise capacity is challenging. Witte et al. [31], using only conventional measurements of RV function at rest in patients with chronic heart failure, reported a lack of correlation with exercise capacity. However, Di Salvo et al. [32] realized that RV EF, determined by radionuclide ventriculography, was related independently to exercise capacity in patients with advanced heart failure. In the present study, we searched for the relation between RV function and exercise tolerance in HCM patients. We found that only LV systolic deformation parameters (SR and dyssynchrony) were independent predictors of exercise capacity in HCM patients, and the overall influence of RV function on exercise capacity was not significant.

Right ventricular diastolic function during exercise

In accordance with previous studies, we ascertained significantly lower early and atrial SR and diastolic myocardial velocities at rest that aggravated during peak stress in comparison with the control participants [33],[34]. The reliability of noninvasive estimation of RV filling pressure with the use of the early tricuspid inflow (E) and early diastolic myocardial velocity (Eta ), known as the E/Eta ratio, was confirmed by Nageh et al. [35], who realized that an RV E/Eta ratio of more than 6 had a high accuracy in predicting mean right atrial pressure over 10 mmHg.

In our study, the elevated RVEDP as estimated by Et /Eat , confirming a pattern of impaired RV filling despite no correlation, was detected between this ratio and exercise capacity in HCM patients. In accordance with our findings, Rubis' et al. [36] investigated RV dynamics during exercise in heart failure patients using tissue Doppler-based longitudinal velocity and strain. They could not predict exercise capacity using Et /Eat . Similarly, there were no correlations between the diastolic parameters and VO 2 peak at rest but modest correlations were noted only at peak stress.

Right ventricular dyssynchrony

The heterogeneity of RV regional function is assessed by calculating the standard deviation from six-segmental TTP derived from regional strain curves at rest and at peak exercise. In the control group, exercise yielded more uniform contraction of the RV wall segments whereas in HCM patients, reduced RV deformation at peak stress was associated with RV dyssynchrony and reduced exercise tolerance.

RV dyssynchrony has recently been reported as an index of mechanical dysfunction and observed to be associated with reduced myocardial performance [37]. In addition, RV regional systolic function is linked to dyssynchrony in patients with pulmonary hypertension as evaluated by real-time 3D echocardiography [38].

Left ventricular dysfunction as a predictor of outcome

In the current study, LV systolic SR and dyssynchrony at rest is an independent predictor of exercise capacity in HCM. Our results are consistent with the previous work linking LV deformation with outcome in different diseases, for example degenerative MR [39], dilated cardiomyopathy [40], and heart failure irrespective of the EF or QRS interval [41], suggesting that earlier identification of LV dysfunction during exercise could aid decision making.


  Conclusion Top


The present study investigated the changes in RV deformational mechanics by means of a novel utilization of VVI during an exercise stress test in HCM patients. This study advances previous findings into the role of RV and LV adaptation to exercise in HCM. Although exercise-induced RV dysfunction assessed during stress was statistically associated with exercise capacity, it was found that the LV systolic strain rate and, to a greater extent, systolic dyssynchrony at rest are major determinants of exercise tolerance in HCM patients. Larger studies in HCM patients with more different phenotypes are necessary to determine the prognostic role of exercise-induced changes in RV function.


  Acknowledgements Top


Conflicts of interest

None declared.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
 
 
    Tables

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



 

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Abstract
Introduction
Objectives
Patients and methods
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