Download Analysis of left ventricular diastolic function using magnetic

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Radiología. 2012;54(4):295---305
www.elsevier.es/rx
UPDATE IN RADIOLOGY
Analysis of left ventricular diastolic function using magnetic
resonance imaging夽
G.C. Fernández-Pérez a,∗ , R. Duarte b , M. Corral de la Calle a , J. Calatayud c ,
J. Sánchez González d
a
Servicio de Radiología, Complejo Asistencial de Ávila, Ávila, Spain
Servicio de Radiología, Centro Hospitalar de Vila Nova de Gaia/Espinho, Portugal
c
Servicio de Radiología, Hospital POVISA, Vigo, Pontevedra, Spain
d
Clinical Science, Philips Healthcare, Madrid, Spain
b
Received 28 October 2010; accepted 4 September 2011
KEYWORDS
Magnetic resonance;
Systolic function;
Diastolic function;
Transmitral flow
PALABRAS CLAVE
Resonancia
magnética;
Función sistólica;
Función diastólica;
Flujo transmitral
Abstract Heart failure is not always due to an alteration in systolic function, and a diastolic dysfunction could explain many cases of heart failure with a normal systolic function.
Diastolic function depends on the left ventricular filling capacity to ensure a normal stroke
volume. It is routinely measured with transthoracic echocardiography, as it is an easily accessible non-invasive test. The magnetic resonance imaging (MRI), using flow sequences, shows
good agreement with the echocardiography, analysing the diastolic function in a practical way,
by the flow into the mitral valve and pulmonary veins. In this sense, the analysis of diastolic
function should be added as part of a routine cardiac MR examination.
© 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
Análisis de la función diastólica del ventrículo izquierdo mediante resonancia
magnética
Resumen La insuficiencia cardíaca no siempre es debida a una alteración sistólica, y una disfunción diastólica puede explicar muchos casos de insuficiencia cardíaca con función sistólica
normal. La función diastólica depende de la capacidad de llenado del ventrículo izquierdo para
garantizar un volumen latido normal. Se mide rutinariamente con la ecocardiografía transtorácica, ya que se trata de una prueba no invasiva y de gran accesibilidad. La resonancia magnética
(RM), utilizando secuencias de flujo, muestra una buena concordancia con la ecocardiografía,
analizando la función diastólica de forma práctica, a través del flujo en la válvula mitral y las
venas pulmonares. En este sentido, el análisis de la función diastólica debería añadirse como
parte de un examen rutinario de RM cardíaca.
© 2010 SERAM. Publicado por Elsevier España, S.L. Todos los derechos reservados.
夽 Please cite this article as: Fernández-Pérez GC, et al. Análisis de la función diastólica del ventrículo izquierdo mediante resonancia
magnética. Radiología. 2012;54:295---305.
∗ Corresponding author.
E-mail address: [email protected] (G.C. Fernández-Pérez).
2173-5107/$ – see front matter © 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
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296
G.C. Fernández-Pérez et al.
Introduction
The heart function depends substantially on a pump mechanism where blood is received at low pressure during
diastole and is ejected at high pressure during systole. A
patient has congestive heart failure, which implies that
the cardiac output is low and the ejection fraction (EF) is
reduced.1 However, congestive heart failure is defined as
a ‘‘pathophysiology syndrome, originated by a heart disorder that causes the inability to fill or pump blood to the
appropriate levels, and if achieved, it is at the expense of a
chronic elevation of the ventricular filling pressure’’.2 This
definition not only takes into account anomalies of the pump
mechanism or expulsion of blood, but also of the ventricular filling. The left ventricular filling capacity, consequent to
the blood flow at low pressure, is a complex mechanism that
depends on multiple factors, which can be summarized into
three: ventricular relaxation following systole (isovolumic
relaxation); ventricular compliance (mid diastole) and pericardial constriction. Any anomalies in these mechanisms will
alter diastole resulting in diastolic dysfunction. Diagnosis of
congestive heart failure secondary to diastolic dysfunction
requires three criteria: (a) presence of signs and symptoms
of heart failure; (b) normal or slightly reduced EF of the left
atrium (EF ≥ 50%), and (c) increase in pressure of the diastolic filling. This diastolic dysfunction would explain how
almost 40% of all patients with common signs of congestive
heart failure have a practically normal EF.3---12
The purpose of this study is to review the pathophysiology
of diastolic dysfunction and the most common associated
causes, illustrating with examples how to analyze it and
measure it using MR.
Physiology aspects of the diastole
The ventricular diastole has 4 defined phases (Fig. 1):
Isovolumic relaxation
Rapid filling
Diastasis
Atrial systole
Aortic V. closure
Aortic V. opening
Aortic P.
AV V.closure
AV V. opening
Atrial P.
Ventricular P.
Ventricular
volume
Systole
Diastole
Figure 1 Phases of the cardiac cycle. Two complete cardiac
cycles are illustrated showing changes in the left cardiac cavities: left ventricular pressure (P) and volume, atrial pressure
and aortic pressure. The cardiac cycle is divided into systole
and diastole. The gray area represents the diastole in 4 zones:
isovolumic relaxation, rapid filling, diastasis and atrial systole.
Isovolumic relaxation: time when the ventricle relaxes
while the valves are closed. A rapid fall of intraventricular pressure occurs but volumes remain unchanged. It is
similar to a suction effect.
Rapid ventricular filling: intraventricular pressure falls
causing the mitral valve to open and rapid blood flow
and filling of the left ventricle (LV) occurs. Under normal
conditions, it participates in 80---90% of the ventricular filling.
Diastasis: subsequently to this rapid ventricular filling,
pressure between the atrium and the ventricle becomes
equal. The left atrium acts only as a passive channel, not
having a direct influence in the filling; consequently, there
is only blood passage through the pulmonary veins.
Late ventricular filling (atrial contraction): this phase
begins with an atrial contraction or atrial systole and
ends with the closure of the mitral valve. It participates
in approximately 10---20% of the ventricular filling. During
this phase, the ventricular filling not only depends on the
LV distension capacity but also on the resistance of
the pericardium.13---16
Ventricular relaxation is an active process that has an
influence on the isovolumic relaxation and on the rapid ventricular filling. Ventricular relaxation can be affected by
various factors such as myocardial fiber stiffness; anomalies in the transportation of intracellular calcium within the
myocardial fiber wall, essential in the contraction of
the LV fibers (myocardial ischemia disrupts this transportation); and anomalies in the atrioventricular (AV)
synchronization, as occurs in the AV block.17 Ventricular
compliance, unlike ventricular compliance, is a passive process that does not require energy and has an influence in
all diastolic phases. Factors that contribute to alter the
LV stiffness are myocardial infiltrative diseases (amyloidosis, hemochromatosis, etc.); diseases defined by the own
stiffness of the cavities, which cannot normally expand
or contract (dilated or hypertrophic cardiomyopathy); or
pericardium anomalies that do not allow LV expansion
(constrictive pericarditis or cardiac tamponade).4,9 Other
aspects that affect diastolic function are heart rate and
mitral valve anomalies. In tachycardia, the diastole is shortened in a way that the rapid ventricular filling stops, there
is no diastasis, and ventricular filling will practically depend
on the atrial contraction. Mitral stenosis, for its part, alters
significantly the rapid ventricular filling and diastasis.13---16
Entities that cause anomalies in the diastolic
function
Diastolic dysfunction can be secondary to multiple
heart or systemic diseases. The most frequent causes
are hypertension, myocardial ischemia and hypertrophic
cardiomyopathy.13---16
Hypertension is one of the factors that most influences
diastolic function and heart failure. The increase in systemic
vascular resistance sets a difficulty at emptying the LV, which
causes an increase in ventricular stiffness and consequently
hypertrophy. It has been described that there are anomalies of the diastolic function in up to 25% of asymptomatic
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Analysis of left ventricular diastolic function using magnetic resonance imaging
hypertensive patients without ventricular hypertrophy and
in 90% with hypertrophy.16
Diastolic dysfunction can also be found in patients with
coronary disease. In an acute myocardial infarction there are
anomalies of the myocardial metabolism, of ATP consumption and calcium transportation in the myocyte, all causing
a delay in contraction.13,14 The influence of other factors
that might be present in these patients such as the asynchronicity of the LV, dysfunction of the papillary muscles or
mitral valve failure will contribute, to a large extent, to a
greater abnormal diastolic function. In this sense, nearly 60%
of patients with acute myocardial infarction present with
diastolic dysfunction. There are also late complications, as
it occurs in cases of LV remodeling, which lead to an increase
in ventricular stiffness and consequently to a more abnormal
ventricular filling.13---15
Hypertrophic cardiomyopathy is the paradigm of diastolic
dysfunction caused by changes in the elastic properties of
the myocardium and ventricular stiffness secondary to the
increase of myocardial mass, to changes in myocytes, and
to LV interstitial fibrosis.17
Valve anomalies disrupt the diastolic function in various ways. In aortic or mitral valvular dysfunction, there
are anomalies in the heart chambers with dilation and LV
hypertrophy.
Pericardial diseases (constrictive pericarditis) as well as
systemic diseases (amyloidosis, sarcoidosis, Fabry disease,
hemochromatosis, etc.) also have an influence in the diastolic function due to the infiltration of the myocardium and
stiffness increase (restrictive myocardiopathies) (Table 1).
It is common to observe moderate anomalies to the diastolic function in older patients. This is a ‘‘physiological’’
finding since the older, the bigger the myocardial mass
becomes and there are changes in ventricular elasticity. Logically, other frequent factors also usually add up in this group
of age such as arterial hypertension, cardiac ischemia or
anomalies of the cardiac rhythm.13---15
Measurement of the diastolic function using
magnetic resonance
Transthoracic echocardiography is the common method to
perform routine analysis of the diastolic function (Fig. 2).
Pulsed Doppler of transmitral and pulmonary venous flow
as well as tissue Doppler of the mitral annulus is used.18---21
Similarly, magnetic resonance imaging (MRI) obtains velocity and flow curves through the mitral valve and pulmonary
veins, using velocity flow sequences or phase-contrast
sequences.18 It has been proved that MRI is reproducible and
accurate, with an excellent correlation with transthoracic
echocardiography.22---24
After obtaining the localizer at different planes, a
standard study is performed obtaining images in the cardiac
planes and in cine mode in order to calculate the LV systolic
function and anatomically locate the structures where measurements are going to be performed, such as the pulmonary
veins and the mitral annulus.19
In our hospital, transmitral flow velocity curves are
calculated with phase-contrast sequences using retrospective ECG gating (TR: 4.2---7 ms; TE: 2.5---3.2 ms; flip
angle: 15---30◦ ; slice thickness: 5---10 mm) in a breath hold,
Table 1
297
Causes of diastolic dysfunction.
Common causes (in order of frequency):
--- Ischemic heart disease
--- Hypertension
--- Age
--- Obesity
--- Aortic stenosis
Other causes:
--- Myocardial anomalies:
• Myocardial diseases:
◦ Infiltrative diseases: amyloidosis, sarcoidosis, fatty
infiltration, thyroid diseases, acromegaly, other
restrictive cardiomyopathies
◦ Non-infiltrative diseases: idiopathic myocardial
hypertrophy and myocardial hypertrophy
• Endocardial diseases: hypereosinophilic syndrome
• Metabolic storage disorders: glycogen storage
disease, hemochromatosis, Fabry disease
--- Pericardial diseases: constrictive pericarditis, cardiac
tamponade
acquiring 40---50 phases per cardiac cycle. Velocity encoding
is set at 90---120 cm/s for the mitral valve and 50---80 cm/s for
the pulmonary veins to prevent the aliasing.19,21,25 Additionally, another similar sequence is repeated, but the patient is
asked to perform Valsalva maneuvers during image acquisition, and to force breathing with closed lips. This sequence
allows calculating velocity curves reducing the pressure in
the right atrium since the Valsalva maneuver decreases the
ventricular preload. In normal subjects, this sequence will
show a proportional reduction of the ventricular filling velocity. Its usefulness will help to demonstrate, in some cases,
the degree of diastolic dysfunction, as it will be shown later
on.19
Sequences are acquired on the mitral valve and the pulmonary vein, preferably on the right superior pulmonary
vein, since it has a more constant morphology and caliber,
and perpendicular to the inflow (through-plane). Regarding
the mitral valve, sequences are planned parallel to the
mitral annulus, at leaflet level, at the moment of their
Figure 2 Normal echocardiogram. Transmitral flow velocities
are shown. The E wave is higher than A wave (E > A).
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298
G.C. Fernández-Pérez et al.
atrial contraction, which causes a reflux toward the
pulmonary veins, which lack valves (it would coincide with
the A wave of the transmitral flow). Other additional parameters can also be calculated such as the deceleration time
(DT) and isovolumic relaxation time (IVRT). The DT is calculated by drawing a vertical line from the peak of E wave
to the ‘‘baseline’’ of the graph (line 1) and a second line
from the peak of E wave following the downslope until
intercepting with the ‘‘baseline’’ (line 2). The DT is the
difference between time line 2 and time line 1. The IVRT
is calculated from the time when the aortic valve is closed,
shown by the systolic flow in the transmitral graph (reversed
flow) until the beginning of wave E (Fig. 5).
Patterns of diastolic dysfunction
With the graphs obtained of the transmitral flow and the
pulmonary veins we can assess anomalies in the diastolic
function that can be classified as follows (Fig. 6).19,21
Normal pattern (E > A)
In normal subjects, the transmitral flow graph shows a E
wave higher than A wave, due to the flow of ‘‘rapid filling’’
(immediately after the opening of the mitral valve). A wave
is lower because atrial contraction does not contribute much
to the filling. If velocity ratios are calculated, a patient with
normal diastolic function has an E/A ratio > 1 (E > A).
Type I: Abnormal LV relaxation pattern (E < A)
Figure 3 (A) Transmitral flow using MR imaging. Sequences
are planned (perpendicular to the flow) at the maximum opening of the mitral valves, in four-chamber sections and at the
vertical long axis of the LV (arrows). (B) Pulmonary venous flow
using MR. It is planned on the axial and coronal planes of the
localizer. It is recommended to perform it on the right superior
pulmonary vein (lines), approximately 1 cm to the ostium of this
vessel (arrows).
maximum opening or separation. In the pulmonary veins,
sequences are planned perpendicular to the right superior
pulmonary vein, approximately 1 cm to the ostium (Fig. 3).
Subsequently, data are analyzed at the workstation by
drawing a region of interest (ROI) in the mitral valve and
pulmonary vein orifices and spreading it to all images of
the cardiac cycle, using a semiautomated or manual system. Graphs of velocity---time (or flow---time) are obtained
by calculating the maximum velocity of E wave and A wave
at the mitral valve (Fig. 4). The E wave is equivalent to the
rapid ventricular filling, and A wave, to the flow deriving
from the atrial contraction. There are two positive peaks
in the curves of the pulmonary veins, which are S (systolic)
wave S and D (diastolic) wave, and one negative wave (AR
wave). S wave occurs during systole and it is due to the positive flow in the pulmonary veins, secondary to the relaxation
of the left atrium and to the movement of the mitral annulus by the longitudinal shortening of the LV during systole.
D wave occurs during ventricular filling and is related to the
rapid filling phase (in a practical way it is related to mitral
E wave). A wave, a negative wave, is produced by
During the first stages of the diastolic dysfunction, abnormal
relaxation of the LV fibers occurs that reduces the ventricular filling capacity at the first diastolic phase (early rapid
filling E wave). This problem is compensated by raising the
flow during atrial contraction, that is, the velocity of A wave
rises. In the graph, A wave is higher than E wave, with an
E/A ratio < 1 (E < A). In the graph of the pulmonary veins, a
decrease of D wave occurs. The DT and IVRT become more
prolonged because the ventricle needs more time to relax.
This pattern is most common in patients aged over
65 years. Anomalies in LV relaxation, secondary to loss of
elastic fibers in its wall, diminishes the ‘‘suction’’ capacity during the isovolumic phase, and, with that, the flow
through the mitral valve during the period of rapid filling.
The elongation of IVRT and DT translates into a decrease of
the AV pressure gradient. This pattern can be also observed
in patients with ventricular hypertrophy, hypertension and
ischemic heart disease (Fig. 7).
Type II: Pseudonormal pattern (E > A)
As the abnormal ventricular relaxation and rapid ventricular
filling progresses, pressure of the left atrium rises as a compensatory mechanism to fill the ventricle. This phenomenon
entails a rise of the transmitral pressure gradient (the difference between the left atrium and ventricle) and, with
that, an improvement of the rapid filling of the LV that will
achieve a rise of E wave in the transmitral graph (E > A). In
this phase, thus, a graph of transmitral flow will be obtained
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Analysis of left ventricular diastolic function using magnetic resonance imaging
299
Figure 4 (A) Analysis of transmitral flow in a normal subject. A ROI is drawn at the mitral opening or following the contour of
the endocardium. Practically the entire ventricular filling occurs during the first phase or ‘‘rapid filling’’ and therefore the E/A
ratio will be >1 (E > A). (B) Analysis of pulmonary venous flow in a normal subject. A ROI is drawn at the vessel area to obtain the
velocity---time or flow---time curve. The S wave occurs during ventricular systole and the D wave during diastole. The A wave has a
negative sense since it is due to atrial contraction.
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300
G.C. Fernández-Pérez et al.
similar to that of a normal patient (E > A), even though the
patient has a diastolic dysfunction. As a consequence, this
pattern is called ‘‘pseudonormal’’.
In order to differentiate between the normal pattern
and the ‘‘pseudonormal’’, the transmitral flow must be
measured using the Valsalva maneuver.26 Under normal circumstances, the Valsalva maneuver will cause a reduction
proportional to the velocity of E and A waves, since it
reduces the arrival of the blood through the vena cava to the
right cavities and, therefore, to the LV, but the E/A ratio is
maintained >1. However, in cases of ‘‘pseudonormal’’ dysfunction pattern, the Valsalva maneuver causes the E wave
to decrease more, which transforms the graph into a dysfunction pattern type I (E < A). Therefore, it is also very
useful to obtain curves of the pulmonary veins because they
help detect this ‘‘pseudonormal’’ phase when the D wave is
higher than the S wave (Fig. 8).
During this phase of diastolic dysfunction, patients may
report exertional dyspnea, secondary to increased atrial
pressure. A dilation of the left atrium can even be observed.
E
60
50
A
40
cm/s
30
20
IVRT
10
DT
0
–10
0
200
400
600
800
1000
–20
–30
Time (ms)
Figure 5 Transmitral velocity---time curve. The first negative
curve is due to the left ventricular (LV) outflow (systole). The
second curve, positive, represents the E wave, which is produced by the flow through the valve immediately after the
opening of the mitral valve (rapid ventricular filling). The last
curve is the A wave, which represents the late filling of the
LV by atrial contraction. The isovolumic relaxation time (IVRT)
is calculated from the moment when the aortic valve closes,
represented by the end of the systolic wave (first negative
wave), until the beginning of the E wave. DT (deceleration time)
is the time between the vertical intersection of the E wave with
the baseline, and the intersection of the downslope of wave E
with the baseline.
NORMAL
0.75 <E/A <1.5
cm/s
A
TYPE I
Relaxation
alteration
E/A <0.75
TD >240ms
Types III and IV: Restrictive reversible
and irreversible pattern (E ≫ A)
At this point in time, there is a serious change in ventricular elasticity and relaxation, which leads to a higher
pressure within the atrium. This rise of intra-atrial pressure
causes the early opening of the mitral valve and the IVRT is
TYPE II
Pseudonormal
0.75 <E/A <1.5
TD >140ms
TYPE III
Restrictive
reversible
E/A <1.5
TD >140ms
TYPE III
Restrictive
irreversible
E/A <1.5
TD >140ms
Time (ms)
cm/s E/A changes to <40%
E/A cambia <40%
E/A changes to <40%
DT increases
E/A changes to <40%
DT increases
E/A changes to <40%
Or no change in DT
o
Time (ms)
B
cm/s
S/D ≈ 1
C
S>> D
S<D
S<< D
S<< D
Time (ms)
Figure 6 Diagram of the transmitral flow (A), with Valsalva maneuvers (B) and pulmonary venous flow (C). In a normal subject
the E/A ratio is slightly higher than 1. When there is abnormal ventricular relaxation, the E/A ratio is <1 and the pulmonary venous
flow shows a decrease of the D wave without noticeable changes during the Valsalva maneuver. As the anomaly in ventricular
relaxation progresses, the filling pattern changes to a type similar to a normal curve, but with the Valsalva maneuver it changes to a
type I pattern (pseudonormal pattern). When the diastolic function becomes more abnormal affecting distension or ‘‘compliance’’
of the LV, the E/A ratio is >1.5 (restrictive pattern) and in the pulmonary flow graph a decrease of the systolic flow and a rise of
the diastolic D wave (S < D) can be observed. If variations occur with the Valsalva maneuver, the pattern is considered restrictive
reversible; otherwise, it would be irreversible.
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Analysis of left ventricular diastolic function using magnetic resonance imaging
301
If Valsalva maneuvers are used and a change in the
filing pattern is observed toward a type I or II of the diastolic dysfunction, it is said that the restrictive pattern is
reversible (Fig. 9). On the contrary, the restrictive pattern
is irreversible or grade IV, when the pattern persists despite
using Valsalva maneuvers.
The restrictive pattern is typical of restrictive cardiomyopathies (amyloidosis, sarcoidosis, hemochromatosis, etc.),
of dilated cardiomyopathies with depressed systolic function, and of constrictive pericarditis.
At his point, patients frequently show symptoms and signs
of congestive heart failure. The rise of intra-atrial pressure
will cause a significant increase in size of the left atrium.
A
Limitations
B
cm/s
50
40
30
20
10
0
–10
0
50
100 150 200 250 300 350 400 450 500 550 600
time (ms)
RR - interval; 632 ms (from heart rate)
Figure 7 Twenty-seven-year-old male, asymptomatic with
normal systolic function and asymmetric ventricular hypertrophy data at echocardiography. (A) Balanced sequence (SSFP)
in the vertical long axis plane of the left ventricle showing apical hypertrophic cardiomyopathy. (B) The analysis of transmitral
flow shows a diastolic dysfunction type I (revealing an abnormal
ventricular relaxation; E/A < 1).
significantly reduced. The transmitral gradient shows that
the filling is shortened and accelerated (peaked E wave).
This shortening is due to the sudden ‘‘stop’’ of the rapid
ventricular filling secondary to LV stiffness, which immediately reaches a high pressure that equals atrial pressure. In
other words, the DT is shortened.
Moreover, ventricular filling due to atrial contraction is
also affected since the ventricle cannot be more distended
due to its ‘‘stiffness’’. The LV does not have much capacity
to relax and distend its cavity. This pattern is known by having an E/A ratio > 1.5 (E ≫ A), and shortening of the DT and
IVRT.
The pulmonary venous flow pattern shows a decrease
of the S wave (S < D) due to the reduction of the pressure
gradient between the pulmonary veins and the left atrium
(translating the significant increase of pressure within the
atrium). The A wave is also wider because it needs more time
for contraction that the rigid ventricle is trying to distend a
little more.
The measurement of the diastolic function based on the calculation of velocity curves of transmitral and pulmonary vein
flow has limitations that are necessary to be aware of, since
it depends on compliance and relaxation of the LV, LV filling pressure, preload, valvular diseases, cardiac rhythm and
arrhythmia. The most important limitations occur in cases
of preload reduction (or rise of afterload) since it will cause
a decrease in E wave and can be confused with a type I dysfunction pattern. Moreover, an increase of pressure in the
right ventricle (RV), as it can occur in pulmonary thromboembolism or in RV infarction, can affect the curves and
lead to a pattern of abnormal LV relaxation (type I). In cases
of tachycardia, a shortening of the diastole can cause a rise
in E wave or even a fusion of both waves making it difficult to define the type of diastolic dysfunction pattern. In
patients with atrial fibrillation, a reliable curve cannot be
obtained since there is no atrial contraction and E wave will
not be drawn. Regarding valvular diseases, studies can also
be limited. In severe mitral insufficiency, atrial pressure is
very high and the regurgitation flow shortens the LV rapid
filling which leads to a restrictive type curve.
Other forms of measuring the diastolic
function
Tissue Doppler
Like in echocardiography, a ROI is placed at the mitral
annulus in the four-chamber plane. A curve with negative waves on the baseline is obtained, with a first wave
which will be called Ea or e′ , and a second wave Aa or
a′ .27 This measurement can also be obtained using MR imaging, with phase-contrast sequences, in a way similar to the
one obtained for the transmitral flow and pulmonary venous
flow. In this case, the ROI is placed at the myocardial muscle, normally using a short axis in the mid plane and at the
inferoseptal segment, in order to spread it along all images
of the cardiac cycle. It must be taken into account that
velocity must be set at around 30 cm/s.21 This measurement
reflects the degree of myocardial shortening and provides
information regarding the relaxation degree, which is not
affected by the aforementioned limitations of the transmitral flow measurements, mainly preload anomalies, atrial
fibrillation or tachycardia and valvular disease. In this sense,
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302
G.C. Fernández-Pérez et al.
Figure 8 Pseudonormal pattern. Patient with ischemic heart disease and ejection fraction of 55%. The analysis of the transmitral
flow reveals a E/A ratio > 1, suggesting a normal diastolic function (left image). However, when the analysis is performed using
the Valsalva maneuver the E/A ratio is <1. These findings are typical of a pseudonormal pattern (type II pattern of the diastolic
dysfunction).
Figure 9 (A) Patient with dilated cardiomyopathy with slightly depressed systolic function with EF of 43%. (B) The analysis of the
transmitral flow shows diastolic dysfunction with a restrictive pattern defined by an E > A ratio. (C) A slight variation in velocities
can be observed when the transmitral flow is analyzed using the Valsalva maneuver, showing that the restrictive pattern is reversible
(pattern type III). (D) The pattern of flow the pulmonary veins (red line) and the vena cava (green line) show a S wave < D since
the pressure gradient between the pulmonary veins (or vena cava) and the left atrium (or right atrium) is reduced due to increased
atrial pressure.
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Analysis of left ventricular diastolic function using magnetic resonance imaging
Velocity vs Time
303
Velocity vs Time
Annotation
Data
Venc adjustment
Slice position:
Comp. Contours. PC generated may not corres. to the anatomy
Annotation
Data
Venc adjustment
Slice position:
Comp. Contours. PC generated may not corres. to the anatomy
Velocity vs Time
Annotation
Data
Venc adjustment
Slice position:
Comp. Contours. PC generated may not corres. to the anatomy
Figure 10 Forty-eight-year-old male. (A) Graph of normal transmitral flow (E/A ratio > 1). (B) Graph of normal velocity flow in
the pulmonary vein. (C) Graph of mean velocity in the interventricular septum (tissue) shows e′ and a′ waves an E/e′ ratio of
5.3 (No. < 10).
it is a method of great help to distinguish a ‘‘pseudonormal’’
pattern. An E/e′ ratio < 10 is considered normal (Fig. 10).
process. Two projections are required, normally a long-axis
and a four-chamber projection.21,28---30
Size of the left atrium
Myocardial tagging
As already mentioned, as the diastolic dysfunction degree
increases, there is also an increase of the left atrial pressure
that leads to a size increase. Increased left atrial size indicates chronic diastolic dysfunction and, therefore, is a good
marker, not only of the time of diastolic dysfunction, but
also of its seriousness. However, it has its limitations, since it
can also be increased due to other processes, fundamentally
valvular diseases. Therefore, the possibility of diastolic dysfunction must be confirmed by using this method in absence
of valvular disease. The size of the left atrium can be measured using four-chamber planimetry at the end systolic
phase, just before the opening of the mitral valve, which
is when the atrium reaches its largest size. An area > 20 cm2
indicates increased atrial size, which becomes serious when
it exceeds 40 cm2 . Calculating the volume is a more complex
It is obtained using saturation bands, which allow visualization of the degree of myocardial deformation during the
cardiac cycle. It is measured using deformity or torsion
units. The torsion degree is known to be an important factor in ventricular function. This type of movement is due
to the endocardial oblique fibers that contribute to the
effectiveness of the myocardial contractility and relaxation.
However, measurements take a long time and require great
expertise, which has limited its routine use.31
Spectroscopy
Spectroscopy using 30P-MR imaging allows measurements of the myocardial phosphocreatine and adenosine
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304
G.C. Fernández-Pérez et al.
triphosphate (ATP). The PCr/ATP ratio shows the energy
state of the cardiac muscle. A decrease in the ratio indicates a state of high energy and can be a marker for diastolic
dysfunction in patients with arterial hypertension or left
ventricular hypertrophy. As with the previous method, it
requires long sequences and great expertise, reason for
which it is not used routinely.21
Conclusion
Diastolic dysfunction is a common cause for congestive heart
failure in the absence of valvular heart disease with normal
systolic function. It must be considered as a continuous process that begins with relaxation anomalies and evolves to an
irreversible restrictive status. Not all patients will progress
in such a linear way, since detection at early stages, as it may
occur in hypertensive patients, can facilitate its regression
with appropriate treatment. For this reason, it is conceptually important to determine the degree of severity of the
diastolic dysfunction, so it must be yet another parameter
of information when a MR cardiac study is performed. The
use of phase-contrast sequences to assess transmitral flow
and pulmonary venous flow is a simple method that requires
very little additional time, since it can be performed in a
single breath hold.
Authorship
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Responsible for the integrity of the study: GCFP and RD.
Conception of the study: GCFP, RD, JC and JSG.
Design of the study: GDFP, MCC and JSG.
Acquisition of data: GCFP, RD and JC.
Analysis and interpretation of data: GCFP, JSG, JC and
MCC.
Statistical analysis: GCFP, JC and JSG.
Bibliographic search: RD, GCFP and MCC.
Drafting of the paper: GCFP and MCC.
Critical review with intellectually relevant contributions: MCC, JC and RD.
Approval of the final version: GCFP, RD, MCC, JC and
JSG.
Conflicts of interest
The authors declare not having any conflict of interest.
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