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European Journal of Echocardiography 2004 5(5):356-366; doi:10.1016/j.euje.2004.01.003
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Copyright © 2004, The European Society of Cardiology

Biventricular diastolic behaviour in patients with hypertrophic and hereditary hemochromatosis cardiomyopathies

Przemyslaw Palkaa,*, Aleksandra Langea, John Athertonb, Wayne J. Stafforda and Darryl J. Burstowc

aSt Andrew's Heart Institute, Brisbane, Australia
bDepartment of Cardiology, Royal Brisbane Hospital, Brisbane, Australia
cDepartment of Echocardiography, Prince Charles Hospital, Brisbane, Australia

Received 27 May 2003; received in revised form 24 December 2003; accepted after revision 5 January 2004.

* Corresponding author. St Andrew's Heart Institute, St Andrew's Place; Level 5, Suite 335, 33 North Street, Brisbane, Qld 4000, Australia. Tel.: +61-7-3834-4353; fax: +61-7-3831-6663. drpalka{at}sawmh.com.au


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Aim: To define biventricular diastolic behaviour in patients with cardiomyopathies with predominant diastolic left ventricular (LV) dysfunction.

Methods and results: Doppler tissue echocardiography and both mitral and tricuspid Doppler inflow profiles were investigated in hypertrophic (n = 17), hereditary hemochromatosis (n = 12) cardiomyopathies and age-matched normals (n = 31). The cardiomyopathy group had both lower early diastolic mitral lateral annular (El), cm/s (13.9±6.5) and medial (Em) (10.0±4.5) velocities compared with normals (19.5±5.5, 15.9±3.4, p<0.01, respectively). In the cardiomyopathy group, late isovolumic relaxation myocardial velocity gradient (IVR-MVG) (s–1) was positive compared with negative in normals (1.3±1.3 vs. –0.7±1.4, p<0.01, respectively). In both the cardiomyopathy group and in normals the onset of the tricuspid E-wave preceded the onset of the mitral E-wave. However, the onset of early diastolic tricuspid annular (Et) motion preceded the onset of El (ms) only in normals, but not in the cardiomyopathies (43±26 vs. –8±44, p<0.01, respectively). In the cardiomyopathy group there was a positive correlation between the onset of Et and abnormally positive late IVR-MVG (r = 0.51, p = 0.002).

Conclusions: Biventricular early diastolic behaviour is abnormal in the selected group of cardiomyopathy patients. The delay in the Et (early diastolic longitudinal right ventricular relaxation) may have a negative effect on LV diastolic function.

Keywords: Cardiomyopathies; Doppler echocardiography; Diastolic dysfunction

Nomenclature
ElEarly diastolic mitral annulus velocity
EmEarly diastolic medial (septal) annulus velocity
EtEarly diastolic tricuspid annulus velocity
HCMHypertrophic cardiomyopathy
HHCHereditary hemochromatosis cardiomyopathy
IVRIsovolumic relaxation
LVLeft ventricle, left ventricular
MVGMyocardial velocity gradient
RVRight ventricle, right ventricular
RVFRapid ventricular filling


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Recent studies have shown that cardiac resynchronization therapy is a promising new therapeutic approach in patients with severe heart failure due to left ventricular (LV) systolic dysfunction and intra-ventricular conduction delay.1–3 Either simultaneous1,2 or sequential with individualized interventricular delay programming3 biventricular stimulation improved both patients' symptoms and LV systolic performance. In addition, previous studies have shown the importance of atrio-ventricular adjustment to optimize hemodynamic response in patients with heart failure.4,5 However, little data exist on diastolic biventricular mechanical behaviour6 and it is unknown whether ‘similar’ diastolic resynchronization therapy may bring any benefit in patients with symptoms of predominant diastolic heart failure. It has been suggested that in some patients with predominant systolic LV dysfunction the right ventricle (RV) is dilated such that LV filling is impeded by the surrounding RV and pericardium.7 Diastolic biventricular interaction may thereby contribute to increased symptoms due to raised intracavitary filling pressures (secondary to increased external force) and impaired ability to augment stroke volume.8 A similar effect of RV volume related ventricular interaction on LV diastolic behaviour can also be observed in patients with constrictive pericarditis9 and in patients with pulmonary embolism.10 However, potential mechanical asynchrony between RV relaxation and LV diastolic behaviour in patients with diastolic dysfunction is unknown. Therefore, the aim of this study was (i) to determine whether biventricular diastolic mechanical behaviour is abnormal in a selected group of cardiomyopathies with predominant diastolic dysfunction (hypertrophic—HCM, and hereditary hemochromatosis—HHC), and (ii) whether there are links between potentially abnormal RV relaxation and LV diastolic function. For the purpose of this study, combined information derived from conventional echocardiographic studies of mitral and tricuspid Doppler inflow profiles and Doppler tissue echocardiography of both longitudinal mitral and tricuspid annular velocities11,12 and circumferential LV velocities13–17 were studied.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Our study group consisted of 60 subjects; including patients with HCM (n = 17), patients with HHC (n = 12), and 31 age-matched normal subjects. Patients with impaired LV systolic function (LV ejection fraction ≤50%), left or right bundle branch blocks, resting LV outflow tract obstruction (≥10 mmHg), atrial fibrillation, systemic or pulmonary hypertension, clinical evidence of coronary artery disease, and/or significant (grade≥2) valvular disease were not included into the study. The study group was formed prospectively between 1999 and 2001 at the Prince Charles Hospital, Brisbane, Australia. The study was approved by The Prince Charles Hospital Research Ethics committee and prior to the examination written consent was obtained from all subjects. The diagnosis of HCM was based on the presence of unexplained LV hypertrophy.18 In all HHC patients the initial diagnosis was based on an elevated transferrin saturation and serum ferritin level.19 Ten HHC patients were Cys282Tyr homozygotes, while 2 were compound heterozygotes (Cys282Tyr/His63Asp). Age-matched healthy normals were selected from the local community. Each subject underwent a standard echocardiographic assessment (M-mode, 2-dimensional, Doppler blood-flow measurements) Table 1 and Doppler tissue echocardiographic study using an Acuson ultrasound scanner (Sequoia, California, USA) with a variable frequency transducer (2.5–4.0 MHz). All echocardiographic measurements were averaged over 3 cardiac cycles. Two-dimensional, 4-chamber apical view was used to record lateral mitral, septal (medial) and lateral tricuspid annular velocities.20 Peak annular velocities were measured in both early diastole (mitral lateral—El, mitral medial—Em; tricuspid—Et) and in late diastole. Using parasternal color M-mode Doppler tissue echocardiography, LV posterior wall myocardial velocity gradient (MVG) was analyzed.21 MVG was measured in early diastole during IVR, in rapid ventricular filling (RVF), and in late diastole during atrial contraction. IVR period was divided into first half (early IVR) and second half (late IVR).22 Additionally, timings between the onset of electrocardiographic Q-wave and (1) mitral and tricuspid inflow velocity (the onset and the peak of E-wave and A-wave), (2) annulus velocities (the onset and the peak of the El, Em, Et, and late diastolic-lateral mitral, septal (medial) and lateral tricuspid velocities, and (3) MVG (the peak during early IVR, late IVR, RVF and atrial contraction) were measured (Fig. 1).23 To present and to illustrate our complex data, consecutive diastolic events observed on either left or right side of the heart were added together to form one cycle. The events separated by less than 15 ms apart were combined and constituted the first diastolic sequence. Next diastolic sequences (from 2 to 9) were created in a similar fashion starting from the following consecutive diastolic event when the time was longer than 15 ms between two consecutive events.


Figure 1
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  		Figure 1 Schematic diagram of timings measured from the onset of electrocardiographic Q-wave and Doppler mitral or tricuspid inflow velocities, Doppler tissue echocardiography derived mitral or medial or tricuspid annulus velocity and LV myocardial velocity gradient. PCG, phonocardiogram; ECG, electrocardiogram; El,m,t, early diastolic mitral/medial/tricuspid annulus velocity; RVF, rapid ventricular filling; AC, atrial contraction.

 


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  		Table 1 Clinical and conventional echocardiographic data of study subjects

 
Statistical analysis
All data are expressed as mean value ± SD for continuous variables and as frequency number (%) for dichotomous variables. ANOVA with Scheffe's F adjustment for multiple comparisons was used to assess the differences between HCM, HHC, and age-matched normals. Unpaired and paired t-tests were used when appropriate. Univariate and multivariate logistic regressions were used to assess potential relationships of LV hypertrophy, LV dimensions, LV volumes and other echocardiographic measurements including Doppler tissue echocardiographic indexes. In addition, possible relationships between echocardiographic measurements derived from RV and LV were examined. A value of p<0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The cardiomyopathy group had lower El, and Em velocities compared with normal subjects (Table 2). Both El and Em velocities were similarly low in the HCM and HHC subgroups. Although Et velocities were lower in the cardiomyopathy group compared with normal subjects, only in the HHC subgroup Et velocities were significantly reduced. All late diastolic annulus velocities were similar in the cardiomyopathy group compared with normal subjects. In the cardiomyopathy group as well as in both subgroups (HCM, HHC) late IVR-MVG (s–1) was positive (1.3±1.3, 1.0±1.6, 1.6±0.9, respectively) compared with negative in normal subjects (–0.7±1.4), p<0.01. MVGs measured during both RVF and atrial contractions were lower only in HCM but not in HHC subgroup compared with normal subjects. In both cardiomyopathy subgroups and in normal subjects 9 consecutive sequences were defined (Table 3). The differences between cardiomyopathies and normal subjects in annular motion and MVG peak values were present only in early diastolic sequences (1–5), but not in late diastolic sequences (6–9). In the cardiomyopathy group, the onsets of Et, Em, and El were all noted later (sequence 3) than in normal subject (sequences 1 and 2). Also, in the cardiomyopathy group, the peak of Et, and El were found in sequences 5 and 4 compared with 4 and 5 in the normal subjects group. As a consequence, the peak of tricuspid E-wave was delayed in the cardiomyopathy group and noted in sequence 5 compared with sequence 4 in normal subjects group. Both subgroups HCM and HHC had similar sequences and their timing events (Table 4). In both the cardiomyopathy group and in normal subjects the onset of the tricuspid E-wave preceded the onset of the mitral E-wave (ms) by 40±33, and 54±29, respectively (p = NS). Similarly, in both cardiomyopathy subgroups (HCM, HHC) the onset of the tricuspid E-wave preceded the onset of the mitral E-wave (ms) by 41±37, and 40±28, respectively (p = NS). However, the onset of Et preceded the onset of El (ms) only in normal subjects (43±26) but not in the cardiomyopathy group and both subgroups HHC and HHC (–8±44, –12±53, –3±28, respectively, p<0.01 compared with normal subjects). In parallel, the peak Et and the peak of the tricuspid E-wave preceded the peak El and the peak of the mitral E-wave only in normal subjects. In normal subjects, the difference in time (ms) between the peak Et and the peak El was 20±22, and the timing difference between the peak of the tricuspid E-wave and the peak of the mitral E-wave was 30±23. In the cardiomyopathy group, and both subgroups HCM and HHC, the situation was opposite. The timing difference (ms) between the peak Et and the peak El was –19±44 for the whole group, –21±52 for HCM, and –15±31 for HHC. The differences between peak tricuspid E-wave and peak mitral E-wave were –12±26 (whole cardiomyopathy group), –13±31 (only HCM), and –11±17 (only HHC), p<0.01 compared with normal subjects. The timing differences in late diastolic tricuspid and mitral annulus velocities or tricuspid and mitral A-wave were similar for the cardiomyopathy group and normal subjects. Multivariate logistic regression analysis showed that, apart from the peak Em velocity in HCM patients, other Doppler tissue echocardiographic indices (peak values and timings) were independent of the degree of LV hypertrophy or LV dimension/volume. Among the echo-derived measurements obtained either from RV and LV, a significant relationship was present only between the time of the onset of Et and late IVR-MVG. In the cardiomyopathy group there was a positive correlation between the onset of Et and abnormally positive late IVR-MVG (r = 0.51, p = 0.002). In contrast, in normal subjects this correlation was weaker but negative (r = –0.36, p = 0.025, Fig. 2). Fig. 3 shows schematically the differences in consecutive early diastolic sequences (from 1 to 5) and the differences in Doppler echocardiographic indices in the cardiomyopathy and in normal subject groups.


Figure 2
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  		Figure 2 Relation between the onset of Et and IVR-MVG (a) cardiomyopathies, (b) normal subjects. Filled circles, HCM; empty circles, HHC. Thin solid lines indicate regression line and thin dotted lines indicate the 95% predictive interval.

 


Figure 3
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  		Figure 3 Schematic diagram of consecutive early diastolic timing events and their sequences (from 1 to 5) in normal subjects (a) and in the studied group of cardiomyopathy patients (b). Red arrows, blood flow through the right heart; orange arrows, blood flow through the left heart; grey arrows, atrio-ventricular annular velocities; green (horizontal) arrows, circumferential LV myocardial velocities; blue arrows show abnormally positive late IVR-MVG (related to the subendo- rather than the subepicardial motion) and the delay in Et velocities in the cardiomyopathy group. 5*, peak El, Em velocities were before the peak of mitral E-wave (difference 19 ± 17 ms, p<0.01). P, pressure; ECG, electrocardiogram; PCG, phonocardiogram; for other abbreviations see text.

 


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  		Table 2 Doppler tissue echocardiographic data of study subjects

 


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  		Table 3 Diastolic timing sequences of blood inflow velocities (mitral and tricuspid), annulus velocities (lateral, medial and tricuspid) and LV myocardial velocity gradient (MVG) in patients with cardiomyopathies and in normal subjects

 


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  		Table 4 Diastolic timing sequences of blood inflow velocities (mitral and tricuspid), annulus velocities (lateral, medial and tricuspid) and LV myocardial velocity gradient (MVG) in patients with HCM and HHC

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
In HCM, due to the presence of myocardial fibers disarray and fibrosis LV diastolic dysfunction is a common feature even at an early stage of disease progression.24–28 Also, in HHC iron-catalyzed myocardial injury leads to diastolic dysfunction affecting predominantly LV subepicardial layers.29,30 It has been shown that in patients with severe LV systolic dysfunction Doppler tissue echocardiography can be used to select optimum interventricular delay during cardiac systolic resynchronization during biventricular pacing.3 In order to understand whether cardiac diastolic resynchronization therapy may also be of help in the treatment of diastolic dysfunction, consecutive sequences of diastolic events relating to both RV and LV diastole and mechanical biventricular diastolic asynchrony in the selected group of cardiomyopathies with predominantly diastolic dysfunction (HCM and HHC patients) have been defined.

Findings in the current study
In agreement with previous studies by others in HCM, we found that in HHC, similar to HCM, LV early diastolic abnormalities can be demonstrated as shown by a reduction in longitudinal El and Em velocities.17,28,30 The most likely explanation is that in the studied group of cardiomyopathies active longitudinal LV relaxation is impaired. In addition, we have found that the onset of El, Em and Et, and the peak of Et were delayed in time. In normal subjects, the mitral lateral and medial annular motion (El and Em velocities) commenced before the opening of the mitral valve in late IVR and their peak motion was observed before the peak of the mitral E-wave (difference 19 ± 17 ms, p<0.01). In contrast, in the cardiomyopathy group the onset of El and Em were simultaneous with the onset of mitral early diastolic velocity (E-wave) and also the peak of Em was simultaneous with the peak of E-wave. In addition, only in normal subjects, did the onset and the peak of Et and the peak of tricuspid E-wave precede parallel diastolic events in the LV (the onset and the peak of El and the peak of mitral E-wave). In HCM and HHC patients, these events were parallel except for the peak of Et which appeared after the peak of El. In addition in cardiomyopathy group, but not in normal subjects, the onset of tricuspid E-wave preceded Et, which emphasized abnormal RV relaxation and suggests presence of passive RV filling. Both, HCM and HHC had abnormally positive circumferential LV late IVR-MVG. In our previous work, we postulated that this parameter may be used as a new marker of abnormal diastolic performance.21,22,30 The presence of positive late IVR-MVG indicates a decrease or even a lack of LV wall circumferential subepicardial motion during the late IVR phase. During IVR phase, the mitral and aortic valves are closed. Therefore the abnormally positive IVR-MVG is directly related to active LV circumferential wall thinning rather than physiological thickening. In contrast to HHC patients, MVG was significantly reduced during RVF and in late diastole during an atrial contraction in the HCM patients. These abnormalities may be explained by the presence of both abnormal myocardial relaxation26 and an increase in passive LV stiffness in HCM patients.6 As previously discussed, the LV damage begins from the subepicardial layers in HHC. However, as LV subepicardial layers extend and wrap around the RV, this may explain why HHC patients have reduced RV longitudinal motion as reflected in this study by significantly lower Et. This is further illustrated by the presence of a positive correlation between abnormally positive late IVR-MVG and the delay in Et. Conceptually this means that the pathological circumferential LV wall thinning due to subendocardial motion (rather than physiological thickening due to subepicardial motion) during late IVR may have a negative impact on early diastolic longitudinal RV relaxation (Fig. 4). Until now, a possible link between LV changes during IVR (late IVR-MVG) and RV active relaxation was unknown. We speculate that the described abnormalities in RV relaxation, as a rebound effect, may have an independent effect on LV early diastolic behaviour and contribute to LV diastolic dysfunction.


Figure 4
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  		Figure 4 Schematic diagrams show anatomical (dots) and functional link between subepicardial left ventricular (LV) myocardial fibers and right ventricular (RV) myocardial fibers in early diastole during LV isovolumic relaxation (IVR) period in healthy normals (a) and in patients with cardiomyopathy (b). Horizontal arrows indicate direction of subepicardial circumferential LV velocities (positive late IVR myocardial velocity gradient (MVG)); cross horizontal arrows indicate lack of these velocities. Vertical arrow indicates direction of longitudinal RV velocities (early diastolic tricuspid annulus velocities (Et)); cross vertical arrow indicates lack of these velocities during IVR period. The onset of Et was "shift" from IVR period to LV filling phase. RA, right atrium; LA, left atrium.

 
Limitations
Pre-load dependent changes may potentially have affected Doppler tissue echocardiographic measurements. However, this potential influence will be less pronounced in patients with abnormal myocardial relaxation as compared to healthy myocardium.31 Both blood pressure and heart rate can potentially influence echo/Doppler measurements. However, in our study there were no significant differences in these measurements. Previous reports showed that Doppler tissue echocardiographic indices are age-related,32,33 and therefore the group of normal subjects was carefully age-matched. We did not use hemodynamic data to analyze LV/RV diastolic parameters. However, previous study by others34 showed a relatively flat dynamic LV diastolic pressure/volume relationship in HCM patients. They concluded that not only right-heart loading but also other maneuvers to reduce biventricular diastolic interaction might hold the promise of substantial benefit to this group of patients. Because electrical asynchrony may affect mechanical biventricular diastolic behaviour, patients with conduction abnormalities were excluded from the current study. Prior attempts to assess biventricular behaviour have met with limited success, thwarted by the low temporal resolution of angiographic, nuclear, or magnetic resonance imaging systems. In order to minimize potential errors in timing measurements, we have tried to obtain as high as possible temporal resolution of Doppler echocardiographic images (between 2 and 8 ms). Although our study group of cardiomyopathies was carefully selected (e.g. patients with conduction abnormalities or pulmonary hypertension were excluded), we did not examine other cardiomyopathies or hypertensive patients.35


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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