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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3715_Библиотеки_им_академика_М_И_Перельмана
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8 Imaging Studies andHaemodynamics inChronic Constrictive Pericarditis
a
b
c
Fig. 8.6 Preoperative echo images in a patient with chronic constrictive pericarditis. (a) Pulse
wave Doppler signals at the mitral valve showing increased respiratory variations. (b) Pulse wave
Doppler signals at the tricuspid valve showing increased respiratory variations. (c and d) Doppler
signals using Tissue Doppler Imaging (TDI) in apical 4-chamber view with sample volume placed
at the medial and lateral annulus of mitral valve respectively showing annulus reversus. (e) Mitral
valve inow e/a>1.5
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d
e
Fig. 8.6 (continued)
(e) Mitral and tricuspid inow pattern and mitral annular tissue Doppler
velocities
Diagnosis of constrictive pericarditis on echocardiogram to a large extent relies
on Doppler evaluation. Mitral E/A ratio is usually >0.8in constrictive pericarditis
due to abnormal early rapid lling and high E velocities in both ventricles [120–
126]. The inspiratory decline in mitral and tricuspid E-wave velocities are typically,
≥25% and≥40% respectively when compared with that during expiration [85–92].
The formula ([peak E
expiration
−peak E
inspiration
]/peak E
)×100 is used to calcu-
expiration
late the percentage of respiratory variations for the peak E-wave velocity across
both the mitral and tricuspid valve [85]. The mitral valve E-wave respiratory variations result in positive values, while tricuspid valve E-wave respiratory variations
result in negative values. This is explained by the discordant lling of ventricles
[85]. Since signicant respiratory variations are absent even in 30% to 50% of
patients with denite post operative diagnosis of constrictive pericarditis, the demonstration of mitral and tricuspid respiratory variations ≥25% and≥40% respectively is not considered essential for the diagnosis [120–126]. Usually respiratory
variations are poor in patients with elevated lling pressures or reduced preload [1,
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ab
cd
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8 Imaging Studies andHaemodynamics inChronic Constrictive Pericarditis
g
Fig. 8.7 Postoperative echo images of the same patient with chronic constrictive pericarditis
showing (a) Normal sized inferior caval vein (ICV). (b) Apical 4-chamber view (2D image) showing normal chamber geometry. (c) Pulse wave Doppler signals at the mitral valve showing normal
respiratory variations. (d) Pulse wave Doppler signals at the tricuspid valve showing normal respiratory variations. (e and f) Doppler signals using Tissue Doppler Imaging (TDI) in apical 4- chamber
view with sample volume placed at the medial and lateral annulus of mitral valve respectively
showing normalization of annulus reversus. (g) Mitral valve inow e/a normal
ef
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a
c
g
b
d
h
i
j
k
Fig. 8.8 (a) Preoperative echocardiographic images in a patient with chronic constrictive pericarditis. Apical four chamber view showing normal valvular, left and right ventricular morphology,
(b) Apical ve chamber view showing normal valvular, left and right ventricular morphology, (c)
M-mode echocardiogram showing normal left ventricle with attened interventricular septum, (d)
Colour ow Doppler echocardiogram showing normal ow across the mitral valve, (e) Colour ow
Doppler echocardiogram showing normal ow across the tricuspid valve, (f) Hepatic vein ow
Doppler showing increased respiratory variations, (g) Inferior caval venous imaging showing
dilated and non-collapsing inferior caval vein, (h) Pulse wave Doppler signals at the tricuspid valve
showing increased respiratory variations, (i) Pulse wave Doppler signals at the mitral valve showing increased respiratory variations, (j, k) Doppler signals using tissue Doppler imaging in apical
four chamber view with sample volume placed at the medial and lateral annulus respectively showing annulus reversus. Mitral valve inow e/a>1.5
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8 Imaging Studies andHaemodynamics inChronic Constrictive Pericarditis
a
c
b
d
Fig. 8.9 (a) Preoperative echocardiographic images in a patient with chronic constrictive pericarditis. Apical four chamber view showing normal valvular, left and right ventricular morphology,
(b) Apical ve chamber view showing normal valvular, left and right ventricular morphology, (c)
M-mode echocardiogram showing normal left ventricle with attened interventricular septum, (d)
Colour ow Doppler echocardiogram showing normal ow across the mitral valve, (e) Colour ow
Doppler echocardiogram showing normal ow across the tricuspid valve, (f) Hepatic vein ow
Doppler showing increased respiratory variations, (g) Inferior caval venous imaging showing
dilated and non-collapsing inferior caval vein, (h) Pulse wave Doppler signals at the tricuspid
valves showing increased respiratory variations, (i) Pulse wave Doppler signals at the mitral valve
showing increased respiratory variations, (j, k) Doppler signals using tissue Doppler imaging in
apical four chamber view with sample volume placed at the medial and lateral annulus respectively
showing annulus reversus. Mitral valve inow e/a>1.5
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i
j
k
Fig. 8.9 (continued)
138–144]. Similar to variations in mitral and tricuspid inow velocities, respiratory
variations are present in pulmonary venous ow.
Interpretation of respiratory variation in Doppler velocities are further difcult in
presence of atrial brillation. Patients with advanced disease typically show
increased early diastolic lling velocity (E) followed by rapid deceleration, leading
to a short lling period with mitral E wave typically being <160msec. There is a
distinctive pattern of transvalvular ow on Doppler echocardiography. Since all
Doppler-derived variables are load-dependent and, with increasing preload, a respiratory variation in peak transmitral ow (E>25%) may not occur in about 50% of
patients with chronic constrictive pericarditis, the search for new variables and algorithms continues.
Tissue Doppler imaging evaluates the myocardial wall velocities and provides
additional diagnostic information. The sensitivity and specicity of tissue Doppler
in diagnosing constrictive pericarditis are 88.8% and 94.8% respectively [47–49,
93, 95, 117, 138–144, 161, 168, 191–203]. However the effect of pericardiectomy
on mitral and tricuspid annular velocities are not well established because of limited
studies and restricted observations [47–49, 93, 95, 117, 138–144, 161, 168,
191–203].
Normally the e’ velocity of the lateral mitral annulus is higher than that of the
medial mitral annulus. In constrictive pericarditis, although the mechanoelastic
properties of the myocardium are preserved, the lateral expansion is restricted.
Therefore the longitudinal mitral annular velocities remain normal or may be even
exaggerated [95, 96, 160, 203].
The mitral annulus descends towards the apex during systole. However the apex
of the heart appears stationary in relation to the echo transducer. This downward
annular displacement of mitral valve is proportional to the shortening of myocardial
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8 Imaging Studies andHaemodynamics inChronic Constrictive Pericarditis
bres in longitudinal plane. Therefore it has a good linear correlation with global
left ventricular function [26, 27, 85, 89–91, 203]. Tissue Doppler imaging (TDI) is
used to measure mitral or tricuspid annular motion in the long axis which in turn
reects ventricular systolic and diastolic motion [2, 3, 47–49, 62–69, 89, 138–144,
161, 174, 175, 191–203]. In constrictive pericarditis, early diastolic septal velocity
(medial e’) is preserved or even increased as explained earlier. Normally early diastolic lateral mitral annular velocity (mitral lateral e’) is higher than medial e’. This
relation is reversed in chronic constrictive pericarditis [2, 3, 47–49, 62–69, 89, 138–
144, 161, 174, 175, 191–203]. This mitral annular velocity pattern is relatively spe-
cic for constrictive pericarditis in patients with heart failure, since e’ velocity is
usually reduced in patients with myocardial disease whether left ventricular ejection
fraction is preserved or reduced [2, 3, 47–49, 62–69, 89, 138–144, 161, 174, 175,
191–203].
Another notable feature of constrictive pericarditis is reversal of the normal relationship of mitral lateral e’ and medial e’ velocities. Mitral lateral e’ velocity is
lower than medial e’ velocity and therefore the lateral/medial e’ ratio is inverted.
This is termed as “annulus reversus” [160, 161]. This is due to the tethering of the
adjacent brotic and scarred pericardium, which restricts the lateral mitral annulus
motion in constrictive pericarditis. In patients with preserved mitral e’ velocities (>
8cm/sec) and a low E/e’ ratio (< 8cm/sec) with high left ventricular lling pressures, “annulus reversus” is an indication of constrictive pericarditis [62–66, 93–96,
160, 161, 191–203, 240]. A cut-off value of e’ velocity≥8cm/sec for diagnosis of
constrictive pericarditis was associated with 95% sensitivity and 96% specicity
[62–66].
The postoperative changes in mitral annular velocities were evaluated and correlated with changes in clinical symptoms using tissue Doppler imaging in a prospective study of 54 patients undergoing pericardiectomy for chronic constrictive
pericarditis by Chowdhury etal. They concluded that patients with congestive heart
failure and normal left ventricular ejection fraction, preserved or increased mitral
medial e’ velocity with annulus reversus was diagnostic of constrictive pericarditis.
Although tissue Doppler imaging was useful in diagnostic evaluation, it was not
helpful in postoperative evaluation of chronic constrictive pericarditis [25].
Several investigators have demonstrated normal or increased mitral medial annular early diastolic velocity (e’≥ 9cm/sec) in constrictive pericarditis [2, 93–96,
120–126]. Medial mitral annular e’≥ 9cm/sec when combined with respiratory
shift is diagnostic of constrictive pericarditis with high sensitivity and specicity
≥90% respectively [160, 191–203]. However in the presence of associated myocar-
dial disease, segmental non-uniform myocardial velocities, or extensive annular
calcication, e’ should be used with caution [191–203].
Studies have shown that in normal circumstances E/e’ ratio correlates well with
left ventricular lling pressure. E/e’<8 suggests normal and E/e’ >15 suggests
increased left ventricular lling pressure [62–66]. Concept of annulus paradoxus
was introduced by Ha etal., which describes the paradoxical behaviour of the mitral
annular motion velocity in constrictive pericarditis. They demonstrated an inverse
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Table 8.1 Diagnostic sensitivity and specicity of the echocardiographic parameters in
constrictive pericarditis (The Mayo Clinic Criterions) [232]
Sensitivity
S.No. Echocardiographic features
1 Septal shift 93 69 92 74
2 Inspiratory change in mitral velocity 84 73 92 55
3 Medial e’≥9cm/sec 83 81 94 57
4 Medial e’/ lateral e’>0.91 75 85 95 50
5 Hepatic vein diastolic reversal velocity/
forward
6 1and 3 80 92 97 56
7 1 with 3 or 5 87 91 97 65
8 1 with 3 and 5 64 97 99 42
Abbreviations: PPV positive predictive value, NPV negative predictive value
(%)
76 88 96 49
Specicity
(%) PPV% NPV%
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relationship between E/e’ and left ventricular lling pressure. This is explained by
the exaggerated longitudinal motion of mitral annulus in cases of constrictive pericarditis leading to an increase in e’, despite high lling pressures (Figs.8.8 and 8.9)
[64–66]. A combination of echocardiographic variables as enunciated in Table8.1
by Mayo Clinic Group has yielded higher sensitivity and specicity [232].
Left ventricle contains a right-handed helical arrangement of bres in the subendocardial region that gradually changes into a left-handed geometry in this subepicardial region [28, 135]. Despite the change in orientations of myobres, all
layers of the left ventricular wall operate synergistically. The bres in the subendocardial region is responsible for longitudinal shortening, while the bres in the
subepicardial region causes radial shortening and torsion [36, 37, 109, 191–
202, 214].
During systole, the apex moves counterclockwise and the base moves clockwise resulting in a wringing motion of the left ventricle. In 2006, Sengupta and
associates demonstrated that helical orientation of the myobres is the reason for
this particular motion [192, 193]. This torsional motion during systole results in
storage of potential energy. This stored energy is utilised for diastolic recoil. This
results in ventricular suction and early diastolic lling [135, 192–196]. The stiffness of the pericardial layers modulates the extent of circumferential and longitudinal expansion of the left ventricle during early diastolic recoil and untwisting
[52, 53, 107].
Translational motion can result in overestimation and tethering and causes
underestimation in measurement of myocardial velocities. This limitation can overcome by Strain (E) and strain rate imaging which measure the actual extent of myocardial deformation (stretching or contraction). Strain can be measured utilizing
either tissue Doppler imaging or by 2D echocardiographic speckle tracking derived
parameters. Sengupta etal. employed speckle tracking echocardiography, an angleindependent technique and found close correlation with measurements obtained via
MRI and sonomicrometry [193–197, 202].
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8 Imaging Studies andHaemodynamics inChronic Constrictive Pericarditis
(f) Speckle tracking echocardiography
Recent studies have shown that Doppler tissue imaging-derived myocardial
velocity gradient of the posterior left ventricular (LV) wall is relatively independent
of the translational motion of the heart and/or preload alterations and can distinguish chronic constrictive pericarditis from restrictive cardiomyopathy. They had
shown that myocardial velocity gradient was lower in patients with restrictive cardiomyopathy compared with both chronic constrictive pericarditis and normal [50,
52, 147–153, 202].
Strain is an index without dimension and reects deformation of myocardium
during cardiac cycle relative to its initial length. When all points within a moving
object have the same velocity, the object would be described as having displacement. On the other hand, if different points within an object are moving at different
velocities, then the object will exhibit deformation. This is dened as Langranian
strain. Since myocardial deformation is caused by contraction, strain can be used as
a measure of the contractile function of myocardium. By convention, a positive
value for strain indicates lengthening and, a negative value indicates shortening.
Strain allows differentiation of active versus passive movement within a myocardial
segment. Strain rate is the rate of change in length, calculated as the difference
between two velocities normalized to distance between them; it is expressed in seconds [193–197].
At lower left ventricular volumes, the pericardium expands, but after a certain
volume further circumferential expansion is resisted by the increasing stiffness of
the left ventricular wall. Normal pattern of circumferential and longitudinal diastolic recoil is altered by loss of compliance of the pericardial layers.
Garcia and associates suggested that in chronic constrictive pericarditis the lling and expansion of left ventricle is more affected in the circumferential plane
rather than in the longitudinal direction. Additionally, in chronic constrictive pericarditis the scarring and inammation from pericardial layers might extend into the
myocardial wall which also affect the circumferential recoil of the left ventricle.
They investigated longitudinal, circumferential and radial mechanics of the left ventricle simultaneously in patients with chronic constrictive pericarditis and restrictive
cardiomyopathy. They demonstrated for the rst time in the literature that restrictive
cardiomyopathy was characterized by abnormal longitudinal left ventricular
mechanics with relative sparing of the left ventricular rotation, while patients with
chronic constrictive pericarditis had relatively preserved longitudinal left ventricular mechanics and a markedly abnormal circumferential deformation, torsion and
untwisting velocity [47].
In echocardiography, the term strain describes lengthening, shortening, or thickening, otherwise called as regional deformation [2, 36, 37, 116, 117, 133–135,
151–154]. The four principal types of myocardial strain are longitudinal, radial,
circumferential, and rotational. The myocardial deformation occurs along these
strain vectors in a three dimensional space. However for the ease of it, most studies
have been done using individual strain assessments.
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Patients with constrictive pericarditis had higher global longitudinal scale than in
those with restrictive cardiomyopathy [−18.5% (−20.1 to −15.2) vs −11.6% (−14.6
to −9.3); p<0.001]. Both techniques were found to have similar diagnostic value
(area under the curve, 0.84 vs 0.88 for cardiac magnetic resonance imaging and
echocardiography, respectively) [3, 93]. Patients with restrictive cardiomyopathy
had marginally lower circumferential ε [−23.9 (−28.3 to −20.2) vs −19.3 (−23.3 to
−16.0)%, p=0.07] [89, 93].
Several studies have evaluated left ventricular mechanics of patients with constrictive pericarditis quantitatively. However, only limited studies have assessed
change before and after pericardiectomy. No studies have compared outcomes in
terms of changes in myocardial mechanics after pericardiectomy performed via
median sternotomy versus modied anterolateral thoracotomy. Similarly speckletracking derived myocardial mechanics and their relationship following surgery are
also not well studied. Following total or radical pericardiectomy, the constrictive
pericardial layer which prevented undue cardiac displacement was lost, and heart
starts to swing vigorously [2, 36, 37, 116, 117, 133–135, 151–154].
Negishi and colleagues investigated 83 post-pericardiectomy patients using twodimensional speckle tracking echocardiography. After pericardiectomy, septal displacement decreased (−20.3 ± 5.0% vs −17.7 ± 4.6%, p = 0.032), but lateral
displacement increased (−14.7±5.8% vs −15.2±3.4%, p=0.51). Patients with
constrictive pericarditis had lower absolute values of global longitudinal strain
(−20.1 ± 1.9 vs −16.2 ± 3.3%, p < 0.01) and global circumferential strain
(−20.7± 5.1 vs −14.7 ± 5.0%, p < 0.01), with no signicant difference in global
radial strain (50.4±16.2 vs40.8±18.8%, p=0.07), compared with controls. After
pericardiectomy, there were signicant improvement of global circumferential
strain (GCS) (−13.5±5.7 vs −17.6±5.5, p<0.01) and SLRD (−0.8±3.3% vs
2.1±3.0, p<0.01) values with no signicant changes in global longitudinal strain
(GLS) (−15.6 ± 3.9% vs −15.8 ±3.2, p =0.88) and global radial strain (GRS)
(37.4±18.9% vs 39.1±16.5%, p=0.73) [136].
In a study conducted at All India Institute of Medical Sciences, New Delhi, myocardial mechanics in patients undergoing pericardiectomy were assessed using
speckle tracking to evaluate the effectiveness of pericardiectomy. The study revealed
(i) signicant increase in global circumferential strain from preoperative value of
24.43±3.17 to 28.77±2.55 and further improvement to 30.08±2.61 on 6month
follow-up, (ii) slight increase in global longitudinal strain from preoperative value
of 19.63±2.98 to 21.66±2.61 and on 6month follow-up to 22.31±2.62, and (iii)
increase in global radial strain from preoperative value of 46.28±7.39 to postoperative of 54.24±5.53 with no signicant improvement on 6month follow- up [204].
This is in accordance with the study conducted by Negishi and associates who demonstrated an increase of global circumferential strain among 83 patients with constrictive pericarditis undergoing pericardiectomy 13.5±5.7 to 17.6±5.5, p<0.01);
with no signicant difference in global longitudinal strain and global radial strain
[136, 204].
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