Presentation: The video shows a flow convergence or PISA formation in the LV/LVOT.
#1: What is the cause of the flow convergence (PISA formation)?
Explanation: The flow convergence or PISA formation in
the LV/LVOT that is sometimes present is due to the flow acceleration of
blood out of the ventricle. Since the CFD maximum velocity is 50
cm/sec, any flow that exceeds that velocity will alias, thereby
producing a pseudo-flow convergence. If the LVOT is more perpendicular
to the scan line than what is present in this video, the flow may also
produce a fake flow convergence or PISA formation. A VSD in the septum
with a flow convergence or PISA formation can also be a cause, however,
one would expect to see a jet in the RV and, possibly, a defect in the
septum.
Presentation: A patient had a MVR (replacement) several years
ago and is asymptomatic but had this echo loop.
#1: What is the definition of endocarditis? #2: What is the diagnosis?
Explanation:
The definition of
endocarditis requires one of three following requirements being met:
(Duke
Criteria)
1 - Two major
criteria are present
2 - One major and
three minor criteria are met
3 - Five minor
criteria are met
Major Citeria
1. Positive Blood
Culture for Infective Endocarditis
2. Evidence of
Endocardial Involvement
oscillating
intracardiac mass on valve or supporting structures, in the path of
regurgitant jets, or on implanted material in the absence
of an alternative anatomic explanation, or
abscess, or
new partial
dehiscence of prosthetic valve
new heart
murmur
Minor Criteria
1. Predisposition:
Predisposing heart condition or intravenous drug use
2. Fever:
temperature > 38.0 ° C (100.4 ° F)
3. Vascular
Phonomena: major arterial emboli, septic pulmonary infarcts, mycotic
aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and
Janeway lesions
5.Microbiological
Evidence: positive blood culture but does not meet a major criterion
as noted above or serological evidence of active infection with
organism consistent with IE 6. Echocardiographic Findings:
consistent with IE but do not meet a major criterion as noted above
The patient does not
meet the above criteria so this mass is a thrombus.
Presentation: A patient present to the operating room with this loop.
#1: What is the definition of
tamponade?
#2: Does this patient have
tamponade?
#3: Is the patient compensating
for the left atrial compression?
Explanation:
The
definition of cardiac tamponade is the accumulation of
fluid/blood/effusion in the pericardial sac that causes decreased
filling of the heart.
With
the left atrial compression, the left atrium is inhibited from
filling so tamponade would be present. However, classically,
tamponade, when global, also exhibits collapse of the low pressure
areas (atria and right ventricle). In localized tamponade, the
affected area is located where the clot or tumor is located. In this
patient the left atrium is collapsed. One would expect that the right
ventricle and right atrium to be enlarged from decreased filling of
the left atrium. They are not enlarged. Also, decreased filling of
the left ventricle would exhibit a small ventricular cavity. It is
not decreased in size. Therefore, this echo indicates that flow is at
least getting through the left atrium to minimally fill the left
ventricle.
This
clot may be pleural in it's location. A small separation of the left
atrial wall and the pericardium can be seen in the video which would
indicated that the clot is in the pleural space. While pleural clots
causing left atrial compression are rare, it would be consistent with
what is seen in the RA, RV, and LV.
Presentation: A patient came to the OR with this echo loop.
#1: What is the type and severity of the valve
lesion in this loop? #2: What is the etiology of the valve lesion?
Explanation:
This loop shows severe aortic regurgitation. The
aortic regurgitant jet is > 65% of the LVOT diameter and has a
high turbulent pattern. The etiology of the aortic regurgitant jet is
an ascending aortic aneurysm. As the STJ dilates, the AV
leaflets are pulled apart and the AR jet is central in all views. The
STJ is effaced so the etiology of the ascending aortic aneurysm is
probably a connective tissue disorder such as Marfans or Cystic
Medial Necrosis,
Presentation:
A patient came to the OR with this echo loop. The loop
shows a pericardial effusion.
#1: What is the severity of the pericardial
effusion?
#2: Please discuss how pericardial effusions are
placed into the small, medium, or large category?
Explanation:
This effusion is a small pericardial effusion.
Pericardial effusions are classified as small, medium, or large and
are < 100ml, 100-500ml, or > 500ml respectively. Since we
can't easily measure the volume by echocardiography, small
pericardial effusions are typically behind the inferolateral wall
(posteriorly) of the heart. As the effusion enlarges, it fills
up the lateral and apical areas. A large effusion is global and
surrounds the heart. Typically, large effusions will be global
and the epicardial to pericardial distance will be more than 1 cm.
Presentation: A patient was having a total hip knee performed. Upon the last stitch being placed, the patient suddenly went hypotensive are required epinephrine to resuscitate the patient.
#1:
What is your diagnosis?
#2:
What therapy would you suggest for this patient?
Explanation:
The patient has a massive pulmonary embolism that is
occluding the right pulmonary artery. The view is the
midesophageal ascending aorta view with eh right pulmonary artery
roofing the ascending aorta.
Two main therapies exist -
thrombolytic therapy or surgical therapy. Surgical therapy is
reserved for patients who have a contraindication to thrombolytic
therapy or where thrombolytic/anticoagulation therapy is
ineffective. While thrombolytic therapy is perferred, sometimes
the patient's hemodynamic status is not conducive to waiting for
thrombolytic therapy. If the patient is somewhat
hemodynamically stable, operative embolectomy has a mortality rate
around 11%. If the patient is hemodynamically unstable with
moderate/severe right ventricular dilation/dysfunction, hemodynamic
collapse, with resuscitation, the mortality rate was 85%.
This
patient was hemodynamically unstable and had severe RV dysfunction
and required epinephrine infusion to maintain minimal perfusion.
We referred the patient to surgery for emergency embolectomy because
of the TKA operation would have lead to excessive bleeding from the
thrombolytics.
Presentation: A patient developed hypotension post CABG. This echo loop was obtained.
#1: What
is your diagnosis?
#2: Explain
the echocardiographic signs that you would expect with this
diagnosis?
Explanation:
The patient has a pericardial clot causing tamponade.
Signs
of tamponade depend upon the pericardial sac and the type of
pericardial fluid. In an intact pericardium, an acute rise in
volume can quickly cause tamponade without much volume.
However, in chronic effusions, tamponade may occur with several
liters of fluid in the pericardium where the pericardium has had time
to enlarge. In the patient with an intact pericardium, the pressure
in the pericardium rises and in transmitted to the lower pressure
chambers of the heart - the atria. The atria become collapsed
and the preload to the heart is decreased despite high filling
pressure to the atria (CVP). As the pressure increases more the right
ventricle is the first ventricle to be affected. If the
pressure exceeds the diastolic right ventricular pressure the RV
collapses during diastole (diastolic collapse) and eventually, with
more increased pericardial pressure the right ventricle fails to fill
during systole and diastole.
Post-op CABG patients do not have
an intact pericardium. Fluid or blood must collect around the heart
to affect the chambers. Fluid pressure is transmitter
throughout the chest, whereas, clots will push on adjacent structure
- their pressure is more localized and directed to nearby structures.
If a clot is by the left atrium, the left atrium will be affected
first. If the pressure exerted exceeds the atrial filling
pressure, the atria become collapsed. Similarly, the
ventricles become affected.
In this video the clot is
pushing on the right atrium and right ventricle, inhibiting the
filling of those chambers. Since the filling is compromised,
the ejection is compromised also. The left atrium and ventricle
are hypovolemic and the video shows a small left ventricular cavity
that is foreshortened. A clot also exists around the apex of
the heart.
Presentation: A patient presented with a cough and a new murmur.
#1: What is your diagnosis? #2: Explain the echocardiographic signs of your diagnosis? #3: Discuss the clinical presentation of this diagnosis?
Explanation: The loops show a left atrial myxoma (LAM). LAM are round or oval masses that may be undulating and appear with a ground glass texture. LAM are mobile and are attached to the left atrium, sometimes by a stalk. LAM can occur just about anywere in the atrium and TV/MV leaflets.
The clinical presentation is usually a CVA, TIA, palpitations, shortness of breath, dyspnea, ventricular failure, syncope, or chest pain. The LAM is usually benign but can be cancerous. Acute hemorrhage into the LAM has ocurred and cause acute occlusion of the MV. Atrial myxomas can be single or multiple, can occur in multiple locations in a single atrium or in both atria.
Presentation:
A patient with atrial fibrillation scheduled for a CABG
w/ECC had this loop of his right atrium.
#1: What is your differential diagnosis? #2: What is the most likely diagnosis? #3: Could you perform cardioversion on this
patient?
Explanation: The differential diagnosis for a right
atrial mass is thrombus, lipoma, artifact, myxoma, vegetation, and
tumor. A linear mass would make it more likely to be a thrombus, lipoma
or artifact. Myxomas, vegetations and tumors do not tend to be
linear. Since the patient is in atrial fibrillation, this most likely
represents a thrombus. Lipomas tend to be more echogenic whereas
thrombi tend to be more echo lucent (probably because they are made of
blood products sitting in a pool of blood). Atrifacts or pitfalls would
include right atrial pectinate muscles and shadowing from another
structure.
Cardioversion is used to convert patients in atrial fibrillation to
normal sinus rhythm. In patients with RA thrombi who are anticoagulated
and who do not have a right to left shunt, the risk of stroke or
pulmonary embolus is low. However, patients with RA spontaneous echo
contrast and RA thrombi tended to have recurrence of their atrial
fibrillation when compared to patients without SEC or RA thrombi.
Article sur les masses cavités droites
https://www.dropbox.com/s/j08au879cacf9b5/Echocardiography%20Volume%2027%20issue%209%202010%20%5Bdoi%2010.1111%252Fj.1540-8175.2010.01264.x%5D%20Marina%20Leitman%3B%20Ehud%20Rahanani%3B%20Ilan%20Wassermann%3B%20Simha%20Rosenblatt%20--%20Unusual%20Right-Sided%20Cardiac%20Masses.pdf?dl=0
Et le lien vers les vidéos de l'article:
http://onlinelibrary.wiley.com/doi/10.1111/j.1540-8175.2010.01264.x/suppinfo
Article sur les masses OD:
https://www.dropbox.com/s/edgwtcsz0hyc17x/Echocardiography%20Volume%2022%20issue%205%202005%20%5Bdoi%2010.1111%252Fj.1540-8175.2005.04049.x%5D%20Michael%20S.%20Chen%3B%20Jing-Ping%20Sun%3B%20Craig%20R.%20Asher%20--%20A%20Right%20Atrial%20Mass%20and%20a%20Pseudomass.pdf?dl=0
Article sur le CS et les thrombi intra-OD dans le cadre du traitement de la FA:
https://www.dropbox.com/s/97ryrfbgkyh3srp/Journal%20of%20the%20American%20Society%20of%20Echocardiography%20Volume%2014%20issue%202%202001%20%5Bdoi%2010.1067%252Fmje.2001.108668%5D%20Bashir%2C%20Mohammad%3B%20Asher%2C%20Craig%20R.%3B%20Garcia%2C%20Mario%20J.%3B%20Abdalla%2C%20Ib%20--%20Right%20Atrial%20Spontaneous%20.pdf?dl=0
Remarque:
Concernant la cardio-version en cas de thrombus OD, dans tous les articles que j'ai lu, les patients ont en bénéficié qu'après disparition des thrombi sous anticuoagulation.
Presentation: We did a PWD of a LA appendage and had a forward velocity of 17 cm/s and a negative velocity of 13-17 cm/sec.
#1: Discuss the normal and abnormal left atrial velocities and their significance?
Explanation:
If the velocity of the LAA is low, one would expect that
stasis and an environment for thrombus formation would be present.
Where you measure LAA velocity is important. The velocity is
higher 1 cm below the LAA orifice than 1 cm from the LAA apex.
The normal LAA velocity exceeds 50 cm/sec.
In patients with
atrial fibrillation, the LAA emptying velocity drops. One study
found that elderly patients with low LVEF (< 40%) and a LAA
velocity (LAAV) < 20 cm/sec were more likely to develop LAA
thrombi. A TTE will measure about the same velocities as TEE so the
modality is not important. One study showed that TTE measured
LAAV at 50 cm/sec were measured at 47 cm/sec.
Presentation: A patient for CABG had this video loop.
#1: What is your differential for this
abnormality? #2: What is the most likely cause of the
abnormality?
Explanation: This video loop shows something near the
orifice of the left atrial appendage. Our differential was thormbus,
artifact, or tumor (myoxoma).
It is very small and the LAA was
contracting normally as does the left atrium. Since there was no
stasis, and we felt the shadow was real, we felt that the shadow is
myxoma.
A thrombus can mimick a myxoma and vice versa.
Hemangiomas have
occurred in the left atrial appendage but are usually large. While this
mass was small, there was no associated signs of stasis, making thrombus
less likely.
Although very rare, LAA myxomas have been reported.
Presentation: A patient presents for a CABG with some RV abnormalities.
#1: What are the abnormalities of the right ventricle? #2: Name the differential diagnosis for each of the abnormalities. #3: Does this patient have diastolic dysfunction causing one of the abnormalities? #4: What is the most likely cause of the major abnormality?
Explanation: The abnormalities in this loop is right
ventricular enlargement (RVE) and a moderator band. The moderator band
is normal but is sometimes confused with a turmor, thrombus, or
artifact. A moderator band is a pitfall that can be overread and
misinterpreted.
The right ventricular enlargement, in this case is more interesting.
The differential diagnosis for right ventricular enlargement fall into
three main categories: increased afterload, increased preload, and
decreased contractility. The RV is not a pressure pump, per se, but can
hypertrophy in the presence of longstanding afterload conditions.
Acute increases in afterload will lead to RV dilation and decreased wall
motion. Chronic increased afterload leads to RV hypertrophy and normal
wall motion until the afterload is so high that the RV cannot
compensate and cause it to dilate and become hypokinetic. High afterload
would stent the interventricular septum (IVS) (D shaped IVS) or cause
it to bow towards the LV during systole as the RVSP increases.
Increased preload from chronic volume overload (ESRD, TR, PR) or a left
to right shunt (ASD) would lead to RV enlargement with normal wall
motion until pulmonary hypertension occurred. Then a mixed pattern
would occur. ASD and TR would cause RAE as would volume overload from
ESRD. The IVS would deviate towards the LV during diastole if the RVEDP
exceeded the LVEDP.
In decreased contractility, the wall motion would be decreased from a RV ischemia/infarction.
A patient with diastolic dysfunction where it affects the right
ventricle, causing it to dilate, would first cause left atrial
dilation. Since the left atrium is not dilated, it is very unlikely
that diastolic dysfunction is the underlying condition.
In this video, the IVS appears to not deviate during systole or diastole
so the RVSP must be higher than normal, otherwise the normal motion for
an IVS is to deviate slightly towards the RV. The wall motion of the
RV is normal so contractility is normal and the pulmonary artery
pressures are not so high that the RV function is affected. Since the
left side of the heart appears normal - this is probably a process that
is right sided only. Severe PR would cause the TV to close earlier in
the diastolic period than the MV which is not the case. We suspect that
there is moderate pumonary hypertension from pulmonary causes and other
findings will be trivial.
#1: What is wall motion of the anterolateral
wall?
#2: Is there diastolic dysfunction?
Explanation: The lateral wall cannot be
visualized so the wall motion cannot be directly interpreted.
However, indirect interpretation via mitral annular plane systolic
excursion (MAPSE) can be predictive of left ventricular ejection
fraction. If the MAPSE is < 12 mm the LVEF is most likely
less than 50%. However, Tissue Doppler appears to be more
accurate. MAPSE by M Mode does have correlation with diastolic
parameters such as Tissue Doppler peak systolic annular velocity in
healthy individuals but there is not effective concordance and cannot
be used in place of Tissue Doppler measurements. In this loop
the lateral wall cannot be interpreted, but, given that the septal
wall is hypokinetic, the apex is akinetic and the MAPSE appears less
than 12 mm, we could estimate that the ejection fraction is less than
50% and the lateral wall is most likely not normal. MAPSE does
not indicate the diastolic dysfunction of the left ventricle.
Mitral annular motion as a surrogate for left ventricular function: Correlation with brain natriuretic peptide levels
Results MAPSE < 12 mm determined by MME
has 90% sensitivity, 88% specificity & 89% accuracy for detection of
LVEF <50%, while these values were 94%, 93% & 94% respectively
for (Sm) < 8 cm/s determined by PWDTI. BNP level >75 pg/ml has 98%
sensitivity, 90% specificity & 97% accuracy for detection of LV Dys
either (S,D, or both). BNP levels were significantly higher in patients
with combined (S & D) Dys. Than those with only (S) Dys, the later
group had significantly higher BNP levels than those with only (D) Dys.
(1054.5 ± 202.3 pg/ml vs. 500 ± 39.9 pg/ml & 500 ± 39.9 pg/ml vs.
215.3 ± 100.9 pg/ml respectively, P < 0.001) & each were significantly higher than control group (12.3 ± 5.7 pg/ml, P < 0.001). Significant correlations (P < 0.001 for all) were found between BNP levels and Em (r =−0.82), Sm (r=−0.7), early transmitral (E) to Em ratio (r=0.61), MAPSE (r=−0.54), LVEF(r=−0.64) & LV end D dimension (r=0.63).
Conclusion
MME and PWDTI used for assessment of MAM are useful methods for
evaluation of LV function but parameters measured by PWDTI correlate
more strongly with plasma BNP levels than those measured by MME and
provide a simple, sensitive, accurate and reproducible tool for early
diagnosis of LV dysfunction.
Mitral annular plane systolic excursion (MAPSE) in shock: a valuable echocardiographic parameter in intensive care patients
Compared to survivors,
non-survivors had a significantly lower MAPSE (8 [IQR 7.5-11] versus 11 [IQR 8.9-13]
mm; p= 0.028). Other univariate predictors were age (p=0.033), hsTNT (p=0.014) and
Sequential Organ Failure Assessment (SOFA) scores (p=0.007). By multivariate analysis
MAPSE (OR 0.6 (95% CI 0.5- 0.9), p= 0.015) and SOFA score (OR 1.6 (95% CI 1.1- 2.3),
p= 0.018) were identified as independent predictors of mortality. Daily measurements
showed that MAPSE, as sole echocardiographic marker, was significantly lower in most
days in non-survivors (p<0.05 at day 1–2, 4–6).
Conclusions
MAPSE seemed to reflect LV systolic and diastolic function as well as myocardial injury
in critically ill patients with shock. The combination of MAPSE and SOFA added to
the predictive value for 28-day mortality.
Clinical implication of mitral annular plane systolic excursion for patients with cardiovascular disease
MAPSE and ejection fraction
The average normal value of MAPSE derived from previous
studies for the four annular regions (septal, anterior, lateral, and
posterior) ranged between 12 and 15 mm3,14
and a value of MAPSE <8 mm was associated with a depressed LV EF
(<50%) with a specificity of 82% and a sensitivity of 98%.3
A mean value for MAPSE of ≥10 mm was linked with preserved EF (≥55%) with a sensitivity of 90–92% and a specificity of 87%.16,19
In addition, a mean value for MAPSE of <7 mm could be used to detect
an EF <30% with a sensitivity of 92% and a specificity of 67% in
dilated cardiomyopathy patients with severe congestive heart failure.14
It is of note that the association between MAPSE and EF is only valid in case of normal or dilated left ventricles,20,21 while the correlation is rather poor in patients with LV hypertrophy.
Hypertensive heart disease
The impairment in the contractile function of LV longitudinal fibres may
substantially precede that of LV circumferential fibres in patients with
hypertension because of LV hypertrophy, geometry, and wall stress.5
This might explain the ‘early’ reduced longitudinal function (= MAPSE)
in contrast to the long time preserved circumferential and radial
function (= EF). Thus, reduced MAPSE can be used as a sensitive early
marker of LV systolic dysfunction in hypertensive patients.48
Coronary artery disease
Willenheimer et al.55
demonstrated that MAPSE was reduced in 88 out of 1350 consecutive
patients with visual evaluated normal LV regional wall motion and these
patients with reduced MAPSE had either prior myocardial infarction (60%)
or coronary artery disease without infarction (33%), or uncontrolled
hypertension (2%) while definitive evidence for cardiovascular diseases
was absent in only 4% patients with reduced MAPSE. This suggests that
decreased MAPSE, in the case of normal LV regional wall motion, could
serve as a echocardiographic functional sign for myocardial
abnormalities, predominantly indicating subendocardial dysfunction.55
Aortic stenosis
MAPSE could be used as a predictor of long-term prognosis
for patients receiving aortic valve replacement operation and MAPSE
>7 mm is linked with satisfactory functional improvement after aortic
valve replacement. In the clinical setting, it is sometimes difficult to
distinguish between moderate AS with low gradient and severe AS with low
gradient due to reduced stroke volume. A recent study found that MAPSE
was useful to distinguish between these two entities.57
In patients with an isolated low-gradient AS, a cut-off value of MAPSE
<9 mm had an excellent sensitivity (100%) and specificity (100%) to
distinguish between moderate and severe AS .
Implication for prognosis and therapy
MAPSE is of prognostic importance in the risk stratification for patients with atrial fibrillation,61 patients post-myocardial infarction,62 and patients with heart failure.15,63,64 Cardiac mortality was 44% in atrial fibrillation patients with an MAPSE <7 mm during 45 months follow-up.61 In post-myocardial infarction patients with MAPSE <8 mm, the combined mortality/hospitalization incidence was 43.8%.62 Sveälv et al.64
showed that 10 years survival was significantly better in heart failure
patients with highest MAPSE (>9 mm) than in heart failure patients
with the lowest MAPSE (<5 mm) (Figure 5). Interestingly, significant correlation was found between serum BNP levels and MAPSE (r = −0.54, P < 0.001).31
Limitation of MAPSE
Some of the
variations of MAPSE are due to cardiac size. Theoretically, this means
that the annular displacement should be normalized for heart size. This
is definitely necessary in children, where the variation in cardiac size
is great.
The interpretation of MAPSE should be carefully applied in
case of a mobile apex, such as large pericardial effusion. Also in
patients with paradox septal motion, because of severe right heart
dysfunction, septal MAPSE is not only reflecting LV function but rather
RV abnormalities. Thus in these patients, the lateral MAPSE should be
used. It is to be mentioned that MAPSE, as opposed to global
longitudinal systolic strain assessment, cannot detect regional areas of
dysfunction.
After cardiac surgery, septal MAPSE, together with RV function, might be more reduced compared with lateral MAPSE.
Sometimes
in patients with mitral valve disease, the mitral ring is extremely
calcified. In these patients, the direct MAPSE measurement at the mitral
ring is not possible and longitudinal functional assessment should be
done slightly more above in the myocardium.
Another
limitation of this parameter is that small localized abnormalities (i.e.
small areas of fibrosis) cannot be detected as it is only possible to
assess longitudinal function of the complete wall.
#1: What is this patients ejection fraction
(estimate please)?
#2: Is it accurate?
Explanation:
This scan is a M Mode scan of the left ventricle short
axis. The endocardial walls are easily visible so the ejection
fraction (> 50% in this case) is easily calculated.
The
ejection fraction from a M Mode scan of the LV SAX view is very
accurate in most cases except where remote wall motion abnormalities
are present.
However, even in the presence of remote wall
motion abnormalities, this calculation is fairly accurate because all
of the coronary arteries supplied myocardium are present in this view
and significant remote wall motion is unlikely.
About the only
serious wall motion abnormality that would make this scan inaccurate
would be a distal LAD lesion where the whole apex is akinetic or
dyskinetic thereby decreasing the ejection fraction signficantly.
Présentation:
Enregistrement de la coupe ETO suivante chez un patient.
Questions:
Décrivez la cinétique.
Quels sont les étiologies possibles à cette anomalie de la cinétique ?
Réponses:
La vidéo montre un dyskinésie septale, par ailleurs, la contraction reste bonne.
Les causes possibles sont la stimulation VD, le bloc de branche droit complet, le bloc de branche gauche complet, et certains troubles non spécifiques de la conduction.
Dans la stimulation VD et le BBGc, la contraction du septum inter-ventriculaire se fait en premier, avant la contraction du reste des parois, la dyskinésie se voit en télé-systole, lorsque le reste du VG se contracte alors que le septum entame sa relaxation.
Dans le BBDc, le VG se contracte contre le septum inter-ventriculaire créant une dyskinésie septale en proto-systole, puis le septum se contracte.
En cas de troubles non-spécifique de la conduction, la dyskinésie est soit proto-systolique ou télé-systolique selon l'atteinte anatomique.
Dans cette vidéo, la dyskinésie septale se fait en proto-systole, ce qui est en faveur d'un BBDc.
N.B: Dans l'article original, l'auteur parle aussi de l'insuffisance mitrale sévère comme étiologie possible de la dyskinésie par l'afflux brusque du sang, créant une dyskinésie en pré-systole. Je ne l'ai pas rajouté parce-que je ne suis pas d'accord.
Présentation:
L'image échographique suivante montre des colonnes charnues au niveau de l'atrium gauche.
Questions:
#1: Quels sont les caractéristiques des muscles pectinés de l'auricule gauche?
#2: Quels sont les caractéristiques du thrombus de l'auricule gauche?
#3: Quel est votre diagnostic ?
Réponses:
Les
muscles pectinés de l'auricule gauche se présente à l'échocardiographie
sous forme de colonnes, typiquement multiples et parallèles, souvent
orienté selon le petit axe de l'auricule.
A l'état normal,
l'auricule gauche n'est pas dilatée et il n'y a pas de contraste
spontanée eau niveau de l'oreillette gauche (OG). Il n'y a pas de signes
en faveur d'un ralentissement du flux sanguin atrial (rétrécissement
mitral, dysfonction VG, dilatation ou dysfonction atrial).
Le
thrombus de l'auricule gauche est souvent associée à un ralentissement
du flux sanguin atrial. L'auricule gauche est souvent dilatée, et l'OG
présente un contraste spontané. Une FA est fréquente.
Le thrombus
se localise au fond de l'auricule et croît en direction de son
abouchement jusqu'à ce qu'il rencontre une zone de haute vélocité où le
thrombus ne peut se former, c'est-à-dire l'abouchement de l'auricule
gauche ou un peu plus en distalité. Le thrombus apparaît généralement
homogène et peut être fixe.
La vidéo montre un auricule normal avec ses muscles pectinés.
