(Circulation. 2000;102:655.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Differentiation Between Restrictive Cardiomyopathy and Constrictive Pericarditis by Early Diastolic Doppler Myocardial Velocity Gradient at the Posterior Wall
aw Palka, MDFrom the Departments of Cardiology at the Royal Hospital for Sick Children, Edinburgh (P.P., A.L.), and Hammersmith Hospital, DuCane Road, London (J.E.D., P.N.), UK.
Correspondence to Dr P. Palka, Department of Echocardiography, The Prince Charles Hospital, Rode Road, Brisbane Q4032, Australia. E-mail ppalka{at}hotmail.com
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—The differential diagnosis between restrictive cardiomyopathy (RCM) and constrictive pericarditis (CP) is challenging and, despite combined information from different diagnostic tests, surgical exploration is often necessary.
Methods and Results—A group of 55 subjects (mean age, 63±11 years; 36 men and 19 women) were enrolled in the study; 15 had RCM, 10 had CP, and 30 were age-matched, normal controls. The diagnosis of RCM was supported by a biopsy; in the CP group, the diagnosis was confirmed either surgically or at autopsy. All patients underwent a transthoracic echocardiogram that included the assessment of Doppler myocardial velocity gradient (MVG), as measured from the left ventricular posterior wall during the predetermined phases of the cardiac cycle. MVG was lower (P<0.01) in RCM patients compared with both CP patients and normal controls during ventricular ejection (2.8±1.2 versus 4.4±1.0 and 4.7±0.8 s-1, respectively) and rapid ventricular filling (1.9±0.8 versus 8.7±1.7 and 3.7±1.4 s-1, respectively). Additionally, during isovolumic relaxation, MVG was positive in RCM patients and negative in both CP patients and normal controls (0.7±0.4 versus -1.0±0.6 and -0.4±0.3 s-1, respectively; P<0.01). During atrial contraction, MVG was similarly low (P<0.01) in both RCM and CP patients compared with normal controls (1.6±1.7 and 1.7±1.8 versus 3.8±0.9 s-1, respectively).
Conclusions—Doppler myocardial imaging–derived MVG, as measured from the left ventricular posterior wall in early diastole during both isovolumic relaxation and rapid ventricular filling, allows for the discrimination of RCM from CP.
Key Words: cardiomyopathy • pericarditis • imaging
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Several echocardiographic parameters have been proposed as ways to differentiate restrictive cardiomyopathy (RCM) from constrictive pericarditis (CP).1 These parameters are based on conventional M-mode,2 3 2D images,4 and Doppler blood-flow patterns.5 6 7 8 9 The respiratory variation in transmitral velocity blood flow is the most frequently used parameter to differentiate RCM from CP.5 6 However, respiratory variation can also be observed in patients with chronic obstructive airway disease.10 Also, a considerable percentage of CP patients do not demonstrate respiratory variation in their blood-flow velocities.6 Oh et al11 proposed that in this group of patients, additional echocardiographic tests to reduce preload may help unmask or enhance respiratory variation on transmitral Doppler flow. Nevertheless, in some cases, the diagnosis remains equivocal, and other diagnostic tests and/or surgical exploration are required.1 12 13
Doppler myocardial imaging (DMI) is an echocardiographic technique that has the potential to enhance the diagnostic information available from Doppler blood-flow indices.14 15 16 17 18 19 Pulsed-wave DMI can be used to quantify longitudinal mitral annular motion, which can be useful in the distinction between RCM and CP.14 Little data exist on the potential role of the myocardial velocity gradient (MVG) in distinguishing RCM from CP. MVG was introduced as a new index of myocardial contraction and relaxation that quantifies the spatial distribution of intramural velocities across the myocardium.20 21 22 23 24 Recent studies have shown that MVG is relatively independent of the translational motion of the heart25 and/or preload alterations.26 In this study, MVG calculation at the left ventricular (LV) posterior wall was used to quantify myocardial contraction and relaxation in RCM and CP patients to establish whether it can be used in defining these groups.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
A group of 55 subjects (aged 63±11 years; 36 men and 19 women) was enrolled in this study; subjects consisted of 15 RCM patients, 10 CP patients, and 30 age-matched, normal controls (Table 1
). Subjects were recruited from the
Departments of Cardiology and Rheumatology at the
following institutions: Victoria Hospital, Kirkcaldy; Western General
Hospital and Royal Infirmary, Edinburgh; and Hammersmith Hospital,
London, UK. The study group was formed prospectively and in a
nonselective manner from all referrals of patients with unexplained
right-sided heart failure between January 1994 and December 1998. The
diagnosis of RCM or CP was based on clinical assessment and the results
of the following diagnostic tests: echocardiogram, cardiac
catheterization, MRI, and/or CT scan. All 15 patients
with RCM underwent a biopsy, which confirmed amyloidosis in 12
patients. In patients with CP, the diagnosis was confirmed at surgery
(n=8) or autopsy (n=2). In 4 patients, CP was described as idiopathic;
it was described as postpericardiotomy in 4, as postradiotherapy in 1,
and as neoplastic pericardial infiltration in 1. All 15 RCM and 7 of
the 10 CP patients had no evidence of coronary artery disease.
The remaining 3 CP patients who had previous open heart surgery due to
coronary artery disease had not had a myocardial infarction
and/or reversible ischemia on the inferoposterior LV wall.
Pericardial thickness (>4 mm) or pericardial calcification was
shown in 4 of the 5 CP patients in whom a CT scan and/or an MRI
was performed.
|
Protocol
Each subject underwent a standard
echocardiographic and DMI study of the LV posterior
wall using an Acuson ultrasound scanner (XP/10, Aspen).
Standard echocardiography consisted of M-mode, 2D, and Doppler blood-flow measurements. The parameters measured at end-diastole were interventricular septum, LV posterior wall, and LV diameter; at end-systole, we measured the left atrium. The M-mode of the LV posterior wall was digitized, and then the normalized peak rates of wall thickening and thinning were analyzed.27
LV ejection fraction was measured with a modified, biplane version Simpson’s method. Standard methods were used to record pulsed-wave Doppler transmitral velocity, which was used to measure the following: peak E- and A-wave velocities, E/A ratio, E-wave deceleration time, and isovolumic relaxation time. Both transmitral and hepatic venous flow velocities were recorded with simultaneously acquired respiratory tracing using a nasal respiratory probe.6 11 Good quality pulsed-wave Doppler hepatic vein waveforms were obtained in 13 of the 15 patients with RCM and 9 of the 10 patients with CP. All measurements were averaged over 3 cardiac cycles in patients with sinus rhythm and over 5 cycles for those in atrial fibrillation.
Doppler Myocardial Imaging
The system used in this study has been previously
described.20 28 M-mode DMI images of the LV posterior wall
were obtained at end-expiration and were digitally downloaded to the
image capture system for MVG off-line analysis. Peak MVG values
were determined in systole during early ventricular
ejection (VE), in early diastole during isovolumic
relaxation (IR) and rapid ventricular filling (RVF), and in
late diastole during atrial contraction (AC). These phases
were defined using the combined information derived from M-mode images
taken at the tips of mitral valve leaflets with visible valve openings
and the simultaneously recorded ECG and
phonocardiogram.17 20 28 To obtain M-mode DMI images, the
echocardiographic examination was extended by 2 to 3
minutes. Another 5 to 10 minutes were used for off-line
analysis of images. None of the patients was excluded from the
study on the basis of DMI image quality.
Doppler MVG was defined as the slope of linear regression of the myocardial velocity estimates along each M-mode scan line throughout the thickness of the myocardium.20 21 22 23 24 25 26 28 Myocardial velocity estimates were calculated automatically in each pixel of each M-mode scan. Positive or negative MVG indicated a faster motion of either a subendocardial or a subepicardial layer, respectively. To calculate peak MVG in the predefined phases of the cardiac cycle, a plot graph of MVG changes over time was drawn using computer software.
Interobserver and intraobserver variability for MVG were assessed in our previous work.20 28 Both interobserver and intraobserver variability were low, at 0.1±0.2 and 0.2±0.2 s-1, respectively.
Statistics
Data are expressed as mean±SD. ANOVA with Scheffe’s F
adjustment for multiple comparisons was used to assess the differences
between each group. The degree of respiratory variation in peak E-wave
velocity was calculated as follows: {[(peak E-wave in
expiration)-(peak E-wave in inspiration)]/(peak E-wave in
expiration)}x100%.11
Multivariate regression analysis was
performed to evaluate the relation between the MVG and other
echocardiographic variables. Linear regression
analysis was performed to present the relationship between
VE-MVG and LV posterior wall thickness in RCM patients.
P<0.05 was considered significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Standard Echocardiography
The RCM group had a greater LV wall thickness (44%) and a smaller LV diameter (-10%) compared with age-matched normal controls (Table 2
). The pericardium was
calcified/thickened in 6 CP patients, and interventricular
septal motion with a "respiratory bounce" was seen in 8 CP
patients. When compared with normal subjects, RCM and CP patients had
greater left atrial diameters (28% and 31%, respectively), higher
peak E-waves (75% and 63%), higher E/A ratios (110% and 149%),
shorter E-wave decelerations (-46% and -44%), and shorter
isovolumetric relaxation times (-40% and -47%).
|
In the CP group, the mean peak E-wave was 0.96±0.27 m/s in expiration and 0.69±0.18 m/s in inspiration; the mean respiratory variation in this group was 38±17% (range, 10% to 68%). In 8 of the 10 CP patients, respiratory variations were >25%, and the peak E-wave decreased from 1.06±0.20 m/s (range, 0.77 to 1.41 m/s) in expiration to 0.74±0.16 m/s (range, 0.50 to 1.00 m/s) in inspiration. In the remaining 2 CP patients, respiratory variations in the peak E-wave were <25% (10% and 15%).
In hepatic venous flow by pulsed-wave Doppler, a constriction pattern with a >25% decrease in diastolic forward flow and/or prominent late diastolic flow reversal after the onset of expiration was observed in 8 CP patients (7 of 8 with a concomitant characteristic pattern of transmitral inflow and one with an inconclusive pattern of transmitral inflow). The diagnosis of CP as based on combined information from all Doppler blood-flow recordings was inconclusive in 1 of the 10 CP patients studied.
Digitized M-Mode
No differences existed between the RCM and CP groups in the
measurement of the peak rate of systolic wall thickening and
diastolic wall thinning. However, the peak rate of wall
thinning was lower in the RCM group than in normal subjects
(-31%).
MVG
VE-MVG was lower in the RCM group when compared with both the CP
group (-36%) and normal controls (-40%). In all groups, VE-MVG was
positive, indicating that during the LV posterior wall thickening, the
subendocardium was moving faster than the subepicardium (Table 3 and Figure 1). For all groups, the IR-MVG was
relatively low compared with either the VE-MVG or RVF-MVG. IR-MVG
differed between the RCM group and both the CP group and normal
controls. The absolute value of IR-MVG was 75% higher for RCM patients
and 150% higher for CP patients than in normal controls. During the
IR, the analyzed myocardium was coded as blue,
indicating that the movement was away from the center of the LV. In the
RCM group, IR-MVG was positive, indicating that the subendocardium was
moving faster than the subepicardium. Conversely, in both CP patients
and normal controls, the IR-MVG was negative, indicating that outward
movement was mainly due to subepicardial motion. The RVF-MVG was lower
in RCM patients compared with both CP patients (-78%) and normal
controls (-49%); RVF-MVG was higher in CP patients than in normal
controls (135%). In all groups, RVF-MVG was positive, indicating that
the LV posterior wall was thinning and the subendocardium was moving
faster than the subepicardium. AC-MVG was lower in both the RCM and CP
groups compared with normal controls (-68% and -55%, respectively);
AC-MVG was positive, indicating that the LV posterior wall was thinning
due to a faster motion of the subendocardium rather than the
subepicardium.
|
|
,
patients with atrial fibrillation. *P<0.01 compared
with CP or normal subjects; 
P<0.01 compared with
normal subjects, by ANOVA.
Examples of MVG analysis in RCM and CP patients (with and
without marked respiratory variation on transmitral Doppler blood
flow) are shown in Figure 2. Figure 3 shows the differences in early
diastolic MVG changes in the study groups.
|
|
Multivariate Regression Analysis of
MVG
Systole
In RCM patients, VE-MVG was dependent on LV posterior wall
thickness but was independent of other
echocardiographic and clinical variables. Figure 4A shows a correlation between LV
posterior wall thickness and VE-MVG (for RCM group,
r=-0.75; P<0.001).
|
Diastole
All diastolic MVGs (IR-MVG, RVF-MVG, and AC-MVG) were
independent of other echocardiographic variables,
including transmitral Doppler blood-flow indices, LV dimension, and
the degree of LV posterior wall thickness (Figures 4B
through
4D). Also, IR-MVG and RVF-MVG were independent of age, heart rate, and
systolic blood pressure. Figure 5
shows a relation between the transmitral peak E-wave, E-wave
deceleration time, and RVF-MVG.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The results of this study indicate that the assessment of myocardial contraction and relaxation using Doppler MVG at the LV posterior wall may be helpful in distinguishing RCM from CP.
Although in CP patients there is an increase in ventricular interaction29 and a dissociation of intrathoracic-intracardiac pressure changes with respiration,5 6 30 both CP and RCM may have similar clinical manifestations, which are related to decreased LV compliance.31 However, the mechanism leading to the decrease in chamber compliance is different. In CP, decreased ventricular compliance is due to an increase in pericardial restraint, which is related to the pathological process of pericardial scarring and/or calcification.32 Conversely, in RCM, the LV wall is resistant to stretch due to myocardial or endocardial disease.33 In this study, Doppler MVG was used to quantify structural/functional myocardial status by following the hypothesis that DMI has the potential to quantify changes in the intrinsic mechanical elastic properties of the myocardium.19 Garcia et al14 conducted the first pulsed-wave DMI study to measure mitral annulus longitudinal velocities to differentiate RCM from CP. Although pulsed-wave DMI records myocardial motion as reflected by annulus motion, it has some important limitations, including the angulation of the ultrasound beam and the potential effect of LV contractile function and cavity size/shape on mitral annulus velocities.14 A different approach was undertaken to quantify color DMI images by our group and others.16 17 18 19 20 21 22 23 24 25 26 28
Findings
Conventional echocardiographic assessment allowed
us to establish the correct diagnosis in all RCM and CP
patients.1 2 3 4 5 6 The evaluation of respiratory variations of
Doppler blood-flow velocities alone were inconclusive in 2 patients
for transmitral velocity pattern and in 2 patients for hepatic vein
flow. For the entire study group, the information from both transmitral
and hepatic vein Doppler blood flow assisted the diagnosis of CP in
all but one patient. This is in agreement with Oh et al,6
who found that characteristic respiratory variations of Doppler
blood-flow velocities are present in 
88% of CP patients.
Our results from digitized M-mode images are in agreement with previously published data.2 Although the peak rate of wall thinning was reduced in RCM patients compared with normal subjects, the data did not allow for a clear distinction between RCM and CP.
Both VE-MVG and RVF-MVG were reduced in RCM patients compared with both
CP patients and normal subjects. Although VE-MVG was reduced by 36% in
RCM patients compared with CP patients, an overlap in MVG measurements
still occurred; this overlap did not allow for a clear-cut distinction
between RCM and CP. In addition, this reduction of VE-MVG in RCM was
dependent on LV hypertrophy. The most striking difference
between RCM patients and both CP patients and normal controls was
observed during RVF; at this time, no overlap between the study groups
occurred. In RCM patients, the RVF-MVG was 78% lower than that
measured in CP patients and 50% lower than that in normal controls.
Also, IR-MVG differed between RCM patients and both CP patients and
normal subjects. The absolute value of IR-MVG was 75% higher in RCM
patients and 150% higher in CP patients compared with normal subjects.
Both IR-MVG and RVF-MVG were independent of the degree of LV
hypertrophy. Thus, even in the absence of LV
hypertrophy in RCM patients, RVF-MVG was lower in the RCM
group than in the CP group.
Low VE-MVG and RVF-MVG in the RCM group indicate a pathological uniform distribution of transmyocardial velocities between the endocardium and epicardium. We believe that the observed clear reduction in both VE-MVG and RVF-MVG in the RCM group results from fibrotic and/or infiltrative processes involving the subendocardium and/or myocardium.33 34 This process of structural and functional myocardial changes is typical for RCM rather than CP.
High IR-MVG and RVF-MVG in CP patients may be explained by the increased dissociation of intrathoracic-intracardiac pressure changes during end-respiration.
In all study subjects, the LV posterior wall was thickening during VE and thinning during RVF; in both these time periods, wall thickening and thinning was generated by a faster movement of the subendocardial layer. The situation was different in early diastole during IR. In all study groups, the IR period was coded blue, indicating that the wall movement was away from the center of the LV. We found that during this time period, MVG was positive in RCM patients, indicating that the LV posterior wall was thinning due to faster subendocardial velocities. In both CP patients and normal subjects, the IR period was also coded blue, but the MVG was negative, which indicates a faster movement of the subepicardial layer, causing wall thickening. Although this was observed in all study patients, the magnitude of IR-MVG was relatively low compared with other analyzed periods; therefore, a study in a larger patient population is needed to fully investigate this observation.
AC-MVG was reduced by >50% in both the RCM group and CP group. Thus, the analysis of MVG in late diastole was not helpful in differentiating RCM from CP. We speculate that the increase in LV end-diastolic pressure, which is well documented in both RCM and CP,29 34 reduces late diastolic blood inflow to the LV,35 which will reduce AC-MVG.
Table 4 summarizes our results in light
of already published data on the role of MVG in the differentiation of
myocardial/pericardial disorders.
|
Limitations
In this study, we do not have a patient in whom the
diagnosis of CP or RCM was not made by standard
echocardiography alone. However, a standard
echocardiographic study is technically demanding and
involves complex measurements taken from several acoustic windows. No
single conventional echocardiographic
parameter could have been used to make the diagnosis. The
measurement of MVG, taken as a single diagnostic index,
allowed for the differentiation of CP from RCM in all patients. The DMI
study was technically simple, and it was not time consuming. We did not
routinely perform preload reduction to unmask Doppler respiratory
variation.10 However, a recent study by Shimizu et
at26 showed that MVG is relatively independent of loading
conditions. Therefore, we can assume that MVG measurements should be
similar to those obtained with preload reduction.
Our study group consisted of 6 subjects (24%) in atrial fibrillation, and the influence of missing atrial function might be an important underscoring factor for blood-flow recordings or MVG calculation. However, MVG did not differ between patients in sinus rhythm and those in atrial fibrillation. Therefore, we assume that MVG can be of clinical value in the differentiation of CP from RCM in patients in both sinus rhythm and atrial fibrillation.
RCM patients had a lower New York Heart Association class than CP patients, which suggests that the latter group had a higher left atrial pressure. This could lead to an earlier mitral valve opening and/or an increase in RVF-MVG in CP patients. However, in this study, invasive measurements of LV diastolic function were not performed to verify this hypothesis. Although our patients had no evidence of LV posterior wall ischemia, some data suggest that ischemia may reduce MVG, as was observed in the RCM group in this study.22 We did not include patients with combined constrictive/restrictive disease12 31 36 ; however, we believe that in this group of patients, MVG would also be reduced after myocardial infiltration.
Conclusions
This study confirmed the hypothesis that direct evaluation of
structural/functional myocardial status by DMI-derived MVG calculation
at the LV posterior wall is helpful in distinguishing restrictive from
constrictive physiology. It seems that the measurement of early
diastolic MVG is an accurate
echocardiographic parameter that
differentiates patients with RCM from those with CP.
Received December 2, 1999; revision received February 18, 2000; accepted March 2, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Vaitkus PT, Kussmaul WG. Constrictive pericarditis versus restrictive cardiomyopathy: a reappraisal and update of diagnostic criteria. Am Heart J. 1991;122:1431–1441.[Medline] [Order article via Infotrieve]
2.
Morgan JM, Raposo L, Clague JC, et al.
Restrictive cardiomyopathy and constrictive
pericarditis: non-invasive distinction by digitised M mode
echocardiography. Br Heart J. 1989;61:29–37.
3. Engel PJ, Fowler NO, Tei C, et al. M-mode echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1985;6:471–474.[Abstract]
4. Pandian NG, Skorton DJ, Kieso RA, et al. Diagnosis of constrictive pericarditis by two-dimensional echocardiography: studies in an experimental model and in patients. J Am Coll Cardiol. 1984;4:1164–1173.[Abstract]
5.
Hatle LK, Appleton CP, Popp RL. Differentiation of
constrictive pericarditis and restrictive
cardiomyopathy by Doppler
echocardiography. Circulation. 1989;79:357–370.
6. Oh JK, Hatle LK, Seward JB, et al. Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1994;23:154–162.[Abstract]
7. Schiavone WA, Calafiore PA, Saleedo EE. Transesophageal Doppler echocardiographic demonstration of pulmonary venous flow velocity in restrictive cardiomyopathy and constrictive pericarditis. Am J Cardiol. 1989;63:1286–1288.[Medline] [Order article via Infotrieve]
8. Klein AL, Cohen GI, Pietrolungo JF, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol. 1993;22:1935–1943.[Abstract]
9. Von Bibra H, Schober K, Jenni R, et al. Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein. Am J Cardiol. 1989;63:483–488.[Medline] [Order article via Infotrieve]
10.
Boonyaratavej S, Oh JK, Tajik AJ, et al. Comparison of
mitral inflow and superior vena cava Doppler velocities in chronic
obstructive pulmonary disease and constrictive pericarditis.
J Am Coll Cardiol. 1998;32:2043–2048.
11.
Oh JK, Tajik AJ, Appleton CP, et al. Preload reduction
to unmask the characteristic Doppler features of constrictive
pericarditis. Circulation. 1997;95:796–799.
12.
Schoenfeld MH, Supple EW, Dec GW, et al. Restrictive
cardiomyopathy versus constrictive pericarditis:
role of endomyocardial biopsy in avoiding
unnecessary thoracotomy. Circulation. 1987;75:1012–1017.
13.
Sechtem U, Tscholskoff D, Higgins CB. Magnetic
resonance imaging of the abnormal pericardium. Am J
Radiol. 1986;147:245–252.
14. Garcia MJ, Rodriguez L, Ares M, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol. 1996;27:108–114.[Abstract]
15. Derumeaux G, Ovize M, Loufoua J, et al. Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion. Circulation. 1998;19:1970–1976.
16. Miyatake K, Yamagishi M, Tanaka N, et al. New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies. J Am Coll Cardiol. 1995;25:717–724.[Abstract]
17.
Zamorano J, Wallbridge DR, Ge J, et al. Non-invasive
assessment of cardiac physiology by tissue Doppler
echocardiography: a comparison with invasive
haemodynamics. Eur Heart J. 1997;18:330–339.
18. Gorcsan J, Gulati VK, Mandarino WA, et al. Color-coded measures of myocardial velocity throughout the cardiac cycle by tissue Doppler imaging to quantify regional left ventricular function. Am Heart J. 1996;131:1203–1213.[Medline] [Order article via Infotrieve]
19.
Gorcsan J, Strum DP, Mandarino WA, et al. Quantitative
assessment of alterations in regional left ventricular
contractility with color-coded tissue Doppler
echocardiography: comparison with sonomicrometry
and pressure-volume relations. Circulation. 1997;95:2423–2433.
20. Palka P, Lange A, Fleming AD, et al. Differences in myocardial velocity gradient measured throughout the cardiac cycle in hypetrophic cardiomyopathy, athletes and hypertensive hearts. J Am Coll Cardiol. 1997;30:760–768.[Abstract]
21. Gorcsan J, Deswal A, Mankad S, et al. Quantification of the myocardial response to low-dose dobutamine using tissue Doppler echocardiographic measures of velocity and velocity gradient. Am J Cardiol. 1998;81:615–623.[Medline] [Order article via Infotrieve]
22.
Tsutsui H, Uematsu M, Shimizu H, et al. Comparative
usefulness of myocardial velocity gradient in detecting
ischemic myocardium by a dobutamine
challenge. J Am Coll Cardiol. 1998;31:89–93.
23. Pellerin D, Berdeaux A, Cohen L, et al. Comparison of 2 myocardial velocity gradient assessment methods during dobutamine infusion with Doppler myocardial imaging. J Am Soc Echocardiogr. 1999;12:22–31.[Medline] [Order article via Infotrieve]
24. Uematsu M, Miyatake K, Tanaka N, et al. Myocardial velocity gradient as a new indicator of regional left ventricular contraction: detection by a two-dimensional tissue Doppler imaging technique. J Am Coll Cardiol. 1995;26:217–223.[Abstract]
25. Uematsu M, Nakatani S, Yamagishi M, et al. Usefulness of myocardial velocity gradient derived from two-dimensional tissue Doppler imaging as an indicator of regional myocardial contraction independent of translational motion assessed in atrial septal defect. Am J Cardiol. 1997;79:237–241.[Medline] [Order article via Infotrieve]
26.
Shimizu Y, Uematsu M, Shimizu H, et al. Peak negative
myocardial velocity gradient in early diastole as a
noninvasive indicator of left ventricular
diastolic function: comparison with transmitral flow
velocity indices. J Am Coll Cardiol. 1998;32:1418–1425.
27.
St. John Sutton MG, Reichek N, Kastor JA, et al.
Computerized M-mode echocardiographic analysis
of left ventricular dysfunction in cardiac amyloid.
Circulation. 1982;66:790–799.
28. Palka P, Lange A, Wright RA, et al. Myocardial velocity gradient measured throughout the cardiac cycle in dilated cardiomyopathy hearts-a potential new parameter of systolic and diastolic myocardial function by Doppler myocardial imaging. Eur J Ultrasound. 1997;5:141–154.
29. Meaney E, Shabetai R, Bhargava V, et al. Cardiac amyloidosis, constrictive pericarditis and restrictive cardiomyopathy. Am J Cardiol. 1976;38:547–556.[Medline] [Order article via Infotrieve]
30.
Hurrell DG, Nishimura RA, Higano ST, et al. Value of
dynamic respiratory changes in left and right ventricular
pressures for the diagnosis of constrictive pericarditis.
Circulation. 1996;93:2007–2013.
31. Kern MJ, Lorell BH, Grossman W. Cardiac amyloidosis masquerading as constrictive pericarditis. Cathet Cardiovasc Diagn. 1982;8:629–634.[Medline] [Order article via Infotrieve]
32. Hirschman JV. Pericardial constriction. Am Heart J. 1978;96:110–122.[Medline] [Order article via Infotrieve]
33.
Benotti JR, Grossman W, Cohn PF. Clinical profile of
restrictive cardiomyopathy. Circulation. 1980;61:1206–1212.
34. Katritsis D, Wilmshurst PT, Wendon JA, et al. Primary restrictive cardiomyopathy: clinical and pathological characteristics. J Am Coll Cardiol. 1991;18:1230–1235.[Abstract]
35. Appleton CP, Hatle LK, Popp RL. Demonstration of restrictive physiology by Doppler echocardiography. J Am Coll Cardiol. 1988;11:757–768.[Abstract]
36. Daubert JP, Gaede J, Cohen WJ. A fatal case of constrictive pericarditis due to marked, selective pericardial accumulation of amyloid. Am J Med. 1993;94:335–340.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  M. Schwefer, R. Aschenbach, J. Heidemann, C. Mey, and H. Lapp Constrictive pericarditis, still a diagnostic challenge: comprehensive review of clinical management Eur. J. Cardiothorac. Surg., September 1, 2009; 36(3): 502 - 510. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. P. Abraham and H.-Y. Liang Stress echocardiography diastole to the rescue. J. Am. Coll. Cardiol., February 24, 2009; 53(8): 706 - 708. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Soler-Soler and J. Sagristà-Sauleda CHAPTER 19 Pericardial Disease ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. P. Abraham, V. L. Dimaano, and H.-Y. Liang Role of Tissue Doppler and Strain Echocardiography in Current Clinical Practice Circulation, November 27, 2007; 116(22): 2597 - 2609. [Full Text] [PDF]
|
|
|
|
|
|
J. N. Kirkpatrick, M. A. Vannan, J. Narula, and R. M. Lang Echocardiography in Heart Failure: Applications, Utility, and New Horizons J. Am. Coll. Cardiol., July 31, 2007; 50(5): 381 - 396. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Palka, A. Lange, J. Atherton, W. J. Stafford, and D. J. Burstow Biventricular diastolic behaviour in patients with hypertrophic and hereditary hemochromatosis cardiomyopathies Eur J Echocardiogr, October 1, 2004; 5(5): 356 - 366. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D Pellerin, R Sharma, P Elliott, and C Veyrat Tissue Doppler, strain, and strain rate echocardiography for the assessment of left and right systolic ventricular function Heart, November 1, 2003; 89(90003): iii9 - 17. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. D. Hoit Management of Effusive and Constrictive Pericardial Heart Disease Circulation, June 25, 2002; 105(25): 2939 - 2942. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||