strain imaging speckle

1. STRAIN and STRAIN RATE

2.  Echocardiographic strain imaging= deformation imaging
 quantify regional myocardial function .

3. Deformation parameters can be estimated by
multiple methods
 Doppler-derived Deformation imaging
 Echo-cardiographic Acoustic Speckle Tracking 2D
Strain ( including velocity vector imaging)
 Echocardiographic Acoustic Speckle Tracking 3D
Strain
 Sono-micrometry
 Tagged MRI

4. STRAIN
 Sarcomeric unidirectional shortening results in
multi-directional change in size and shape of
the tissue = myocardial deformation .

5. • Strain - fractional change in length of a
myocardial segment relative to its baseline
length, and it is expressed as a percentage.
• Shear strain is change in the angle between two line
segments.
• It’s is distortion of tissue & analogous to differental
contraction of epi & endocardium.
 myocardial wall =3D object
 strain along 3 planes (x-, y-, and z-axes)= known as
normal strains, and 6 shear strains.
 simplified linear strain or deformation model by
echocardiography.

6.  4 principal types of strain or deformation
 Longitudinal
 radial
 Circumferential
 rotational

11. STRAIN RATE -speed at which the deformation
occurs and is expressed as per second (s-1).

12.  STRAIN RATE ANALYSIS
 BULL’S EYE REPRESENTATION
 STRAIN RATE CURVES .

14. Strain By TDI
 indirect computation of myocardial deformation
 velocity gradients along the myocardial tissue
 viability and deformation (strain) of the myocardium.
 Strain rate (strain per unit of time)
ε = V1 − V2/L,
ε = strain rate, V1 = velocity at point 1, V2 = velocity at
point 2, and L = length, usually set at 10 mm.
 TDI strain rate data could be integrated over time to
determine strain.
 direction of myocardial contractility needs to be aligned in
parallel with the direction of the ultrasound beam.
 reliable only in the apical imaging planes
 unpredictable in PLAX and SAX planes.
 Drawback of -Doppler angle of incidence.

15.  e velocity of the endocardium is normally higher
than that of the epicardium= tissue velocity gradient.
 akinetic but viable or nontransmurally infarcted
myocardium, - myocardial velocity gradient persists,
but there is no velocity gradient in scarred or
transmurally infarcted myocardium.

17. Strain By Speckle Tracking
 Speckle-tracking echocardiography (STE)
 alternative technique t
 analyzes motion by tracking natural acoustic
reflections and interference patterns within an
ultrasonic window
 post-processing computer algorithm
 uses the routine gray scale digital images of the
myocardium contain unique speckle patterns
 user-defined region of interest is placed on the
myocardial wall.
 Within this region of interest, the image-processing
algorithm automatically subdivides regions into blocks
of pixels tracking stable patterns of speckles.

18.  Subsequent frames are then automatically analyzed by
searching for the new location of the speckle patterns
within each of the blocks using correlation criteria and the
sum of absolute differences
 The location shift of these acoustic markers from frame to
frame representing tissue movement provides the spatial
and temporal data used to calculate velocity vectors
 Temporal alterations in these stable speckle patterns are
identified as moving farther apart or closer together and
create a series of regional strain vectors.

19.  The potential to track the speckles in any direction within
a 2D image allows the calculation of myocardial
velocities, displacement, strain and strain rate in any
given direction.
 multidirectional tracking ability
 angle independency
 depend significantly on good image quality and proper
image geometry

21.  physiological factors -age, gender, loading conditions
 technical factors -orientation of the imaging planes,
quality of the gray-scale images
 significant inter-vendor differences
 no universally accepted normal values are available for
the different myocardial deformation parameters.

22. TDI vs STE

23.  Among all the strain parameters, longitudinal strain is
more reproducible than the radial and circumferential
strain and rotation
 global strain has much better reproducibility than the
segmental strain.
 negative longitudinally and circumferentially (negative LS
and CS)
 positive radially (positive RS).
 normal GLS -16 to 18% or more (i.e. more negative).
 circumferential strain - greater than the longitudinal
strain with average values in excess of -20%.
 radial strain -+40 to +60%.
 Peak systolic SR varies between −1 to 1.4/sec.
 Radial Strain rate 3.1-4.1 sec-1
 The apical rotation is normally much greater than the
basal rotation which is limited by the tethering effect of

24. MYOCARDIAL ARCHITECTURE
 outer layer of oblique fibers
 middle layer of circumferential fibers
 inner layer of longitudinal and oblique fibers.

25.  subendocardial fibres -longitudinal strain
 mid-myocardial and subepicardial fibres -circumferential
and radial strain and rotation.
 most of the cardiac pathologies involve the
subendocardial layers first- longitudinal strain is usually
the earliest to get compromised.
 radial and circumferential strain remain preserved or
may even be accentuated during the early stages to
compensate for the loss of the longitudinal function.

26.  As the disease becomes more extensive and more
transmural, the radial and circumferential strain also
get progressively impaired.
 conditions that affect the heart from the outside-
constrictive pericarditis, circumferential strain and
rotation may get compromised earlier than the
longitudinal strain.

27. Coronary artery disease
 regional dysfunction
 extent of the ischemic area and differentiate
between transmural and non-transmural scar.

28.  POST SYSTOLIC SHORTENING- segment continues
shortening after the aortic valve closure( AVC), often
after a short relaxation giving one or two peaks a
systolic and a post systolic, or a single peak after AVC .
 A small amount of post systolic shortening may be
present in up to 1/3 of normal segments but not more
than 3%.
 Pathological strain = reduced systolic strain, and higher
post systolic strain (in magnitude), as well as later peak
PSS.

29.  longer persistence of the PSS after an ischemic event
was= severe coronary obstruction.
 PSS = inhomogeneity of force development, due to
differences in activation, load or contractility, and not as
specific marker of ischemia
 PSS at rest can be a sign of ischemia, myocardial scar, or
other conditions.
 PSS which occurs during stress echocardiography=
ischemia, so it can improve the accuracy of detecting CAD
during a dobutamine stress test.

32. Pattern of post-systolic shortening occurring after aortic
valve closure (AVC) during coronary occlusion and
reperfusion in a patient with coronary disease

33. CORONARY ARTERY DISEASE
ACUTE MI –
 systolic thinning, decreases systolic deformation, and
increases post-systolic thickening ( PST). = directly
related to perfusion .
 acute total vessel occlusion- systolic deformation is
totally ablated and replaced by systolic lengthening (
paradoxical strain).
 Reperfusion restores deformation to near normal, but
some early systolic lengthening and PST remains present
in the early phase as a result of stunning.

34.  LS - significantly reduced in the infarcted segments
proportional to the area of the infarcted region.
 subendocardial infarcts - LS are attenuated +
preservation of CS and RS
 transmural MI - CS and RS are also impaired.
 segmental RS cutoff of 16.5% and CS <11.1%
differentiated non-transmural and transmural
infarction
 rotational mechanics are also impaired (LV TWIST
and untwisting rate)

35. Preserved radial thickening in the
noninfarct region and dyskinesis in the
infarct region

36. Chronic Ischemia
 without infarction - LS may show impairment at rest
or during exercise stress.
 peak SR of −0.83/sec and early diastolic SR of
0.96/sec predicts
 peak basal and mid segmental strain cutoff value of
−17.9% = three vessel or left main CAD

37. Ischemic CMP and Viability
 identifying viability and myocardial contractile
reserve.
 A radial peak strain cutoff value of 17.2% = viable
myocardium
 LS value of −10.2% following the reperfusion
therapy after MI = nonviable myocardium

38. STRAIN IMAGING TO IDENTIFY
SCAR
 mean longitudinal strain
 without scarring −10.4 ± 5.2%
 0.6 ± 4.9% in segments with transmural scarring
 A strain cutoff value of −4.5% -viable myocardium
from segments with transmural scarring

39. Stress Echocardiography
 tissue velocity derived strains and STE LS
 Reduced Doppler derived peak LS, CS and RS
 CS showing the greatest reduction.
 STE-LS - reduced accuracy for LCx and RCA
territories( dependence of the STE on gray scale image
quality.)

40.  Assessment of diastolic strains during stress -useful
in identifying the ischemic regions.
 LV radial strains measured during the first 1/3 of
diastole at baseline, and after 5–10 minutes of
exercise = significant coronary stenosis.
 strain imaging diastolic index ratio of 0.74
predicted significant CADs
 Speckle strain -viability and LV myocardial
contractile reserve.
 Reduced CS and reduced torsion differentiate
transmural MI from nontransmural MI.

41. LV functional dispersion and
dyssynchrony
 Strain imaging = asynchronous LV deformation (e.g., by
measuring the time to peak strain).
 abnormalities in synchronicity= standard deviation of
the time to peak regional shortening= high risk for
arrhythmias.

43. HFpEF vs HFrEF
 Decreased LS but preserved apical rotational
mechanics =HFpEF,
 patterns of CS and RS could be variable
 systolic dysfunction = LV torsion and peak untwisting
rate are also reduced.

44. Longitudinal Strain by Speckle Tracking
Imaging in a Normal Subject and a Heart
Failure Patient

45. DILATED CARDIOMYOPATHY
 impairment of all the three directional strains (LS, CS
and RS).
 rotational mechanics - significant reduction at both base
and apex
 decrease in apical twist and untwisting velocity
 some -clockwise rotation at LV apex and
counterclockwise at LV base (reverse of normal pattern).

46. DYSSYNCHRONY
 LBBB - early septal radial thickening, followed by
delayed posterior and lateral wall thickening.
 speckle tracking radial strain – dyssynchrony
 time difference in peak anteroseptum to posterior wall
strain ≥130 ms=EF response to CRT

47.  Speckle tracking radial strain and transverse strain
were associated with response to CRT
 longitudinal and circumferential strain appeared less
sensitive in detecting important dyssynchrony.

48. LEFT- In a normal subject demonstrating synchronous peak
radial strain curves
RIGHT- In a heart failure patient with left bundle branch block
(LBBB) early anteroseptal peak strain followed by late
posterior wall peak strain

49. (A)tracking transverse (Trans.) strain using the apical 4-chamber view in a
normal subject demonstrating synchronous peak transverse strain curves
(B) Heart failure patient with LBBB showing early septal peak strain
followed by late lateral wall peak strain

50. STRESS CARDIOMYOPATHY
 Reduction in various LV strains that extend beyond any
single coronary artery territory
 Peak systolic strain and SRs are reduced in the apical
and basal regions

52. PERICARDIAL DISEASES AND
RESTRICTIVE CARDIOMYOPATHY
 The pericardium has = LV TWISTS deformation:
 congenital absence of pericardium = marked
impairment in LV torsion while the LS, CS and RS are
preserved.
 constrictive pericarditis -significant reduction in CS, RS
, apical twist while the LS is relatively preserved.
 restrictive CMP- significant attenuation of LS while CS,
RS and LV torsion are relatively unaffected until late
stages and these help maintain the LV-EF.
 continued progression of the disease process -
involvement of CS, RS and torsional mechanics

53. VALVULAR HEART DISEASE
 Identification of subclinical LV myocardial
dysfunction
 Impaired LS = first sign of myocardial dysfunction
 multidirectional strain and SR impairment occur with
increasing severity and chronicity.
 twist mechanics - relatively preserved in AS, AR and
MR, including peak systolic twist, systolic twist
velocity and untwisting velocity.
 LS, CS, RS-improve after surgical intervention in AS.
 AR -initial decline in CS and RS, which improves
over next 3–6 months.

54. Preoperative Systolic Strain Rate Predicts
Postoperative Left Ventricular Dysfunction in
Patients With Chronic Aortic Regurgitation
LEFT - normal
subject);
MIDDLE, pre-Ssr
2.06 per second, pre-
EF 58%, post-EF 65%;
RIGHT - pre-Ssr 1.50
per second, pre-EF
56%, post-EF 38%.
Although patients with AR
had similar preoperative EF,
intrinsic myocardial
dysfunction, as assessed by
Ssr, influenced postoperative
EF.

55. HYPERTENSION
 longitudinal strains are impaired
 CS, RS and LV torsional mechanics are preserved.

56. ATHLETE’S HEART
 pathological LVH - depressed LS and RS
 endurance athletes -enhanced strain values.

57. HYPERTROPHIC CARDIOMYOPATHY
 reduction in the LS
 relative preservation of the CS.
 apical variant -reduction in apical strain values relative to
the strain values in the basal segments with loss of the
normal apical to base gradient

58.  GLS and EF - global LV function, but both do it in a
different way.
 They follow a linear fit of EF=3|GLS| in most situations,
GLS and EF may diverge depending on the underlying
pathology.
 In hypertrophic pathology, GLS is frequently reduced
while EF is still normal.

59. AMYLOIDOSIS
 A higher EF/GLS ratio was found to differentiate
cardiac amyloidosis from other pathologies with
increased LV wall thickness, such as hypertrophic
cardiomyopathy.
 A relative “apical sparing” pattern of longitudinal strain
should raise the clinical suspicion for cardiac amyloid
in the differential diagnosis of LV hypertrophy.

61. CONGENITAL HEART DISEASE
 Objective and quantitative evaluation of RV mechanics is
= biventricular repair.
 Objective evaluation of the dominant ventricle function -
Fontan’s repair
 multidirectional strains -surgical selection

62.  morphological RV supports the systemic circulation-
apical twist is impaired.
 Loss of the apical twist -myocardial dysfunction.
 TOF - reduced LS in septal and lateral walls.
 ASD - reduced systolic LV TWIST due to reduced LV
filling

63. HEART TRANSPLANT AND
REJECTION
 normal transplanted hearts there is usually an
impaired apical twist mechanism while the LV-EF and
other multidirectional strains remain relatively
unaffected=denervation in the early weeks after
 rejection -reduced LS.
 a cutoff in LS of −11.4%, LS could predict cellular
rejection

64. CHEMOTHERAPY
 early subclinical LV dysfunction
 reduction in LV global LS by 10%

65. SUBCLINICAL CARDIAC INVOLVEMENT IN
SYSTEMIC
DISEASES
 type 1 diabetes mellitus - increased torsion,
suggesting the presence of subclinical microvascular
disease
 Impaired LV longitudinal and circumferential shortening
=Cushing’s disease

66. Right Ventricular Deformation
 RV has complex geometry with mainly
longitudinal/circumferential fibre orientation in the
free wall
 minimal radial function due to thin walls.
 Longitudinal deformation of the RV free wall =
systolic function
 RV free wall longitudinal strain is 5-10% more than
the LV free wall
 Abase-to-apex gradient is also seen but is not a
consistent finding.

67. Right Ventricle STE
 Peak systolic strains at the basal free wall of > 25% and
SR of more than 4/sec =RVEF more than 50%.
 RV dysfunction = peak systolic strain and SR are
significantly reduced
 less influenced by motion of translation
 n inverse relationship has been noted in RV systolic
pressure and RV LS.

68. LEFT ATRIAL STRAINS

69.  A total of 12 equidistance region (6 in 4C and 6 in
2C), with reference point of QRS onset
 positive peak atrial longitudinal strain (PALS) -atrial
reservoir function.
 atrial contractile function-total of 15 equidistance
regions (6 in 4C, 6 in 2C and 3 in inferoposterior wall
in apical long axis view) and timed with the “p” wave
=contractile functional strain is always negative.
 conduit functional strain -second positive peak
corresponding to early diastole (just beyond the T
wave).

70.  Normal values of PALS using the 12 segment model and
the QRS reference point is 32.2–53.2%.
The average values of positive and negative peak strains
23.2 ± 6.7% and −14.6 ± 3.5% in 15 segment model using
the p wave as reference point.

71.  Reduced PALS
1. Atrial septal device occlusion
sinus rhythm who have undergone catheter
ablation or cardioversion
LV diastolic dysfunction.
 Increased PALS is -MR.
 Peak atrial positive strain -inverse correlation with
invasively determined LVEDP, as well as with LA
volumes, Doppler mitral inflow indices and pulmonary
vein Doppler data.

72. TWIST
 subtracting basal rotation from the apical rotation
 twist deformation of the left ventricle =movement of two
orthogonally oriented muscular bands of a helical
myocardial structure with consequent clockwise rotation
of the base and counterclockwise rotation of the apex.

73.  As viewed from apex
 apical region = counterclockwise rotation during systole (8 – 12
degrees)
 basal region = clockwise rotation (5–8 degrees).
 counterclockwise apical rotation -positive value (+10 degrees)
 clockwise basal rotation = negative value (−6 degrees). The
LV TWIST is therefore 10 − (−6) = 16 degrees.
 Torsion = Twist/Length (base to apex) degrees/cm
(normal = 1.5 – 2 degrees/cm)

74. Rotational Strain Imaging From a Normal Subject

76. 
dilated cardiomyopathy (CMP), aortic stenosis,
hypertrophic CMP and ischemia=twist is increased,
while the untwist rate is decreased.

77. LEFT- synchronous time-to-peak strain curves = homogeneous coloring
at end-systole (arrow)
RIGHT- heart failure patient with LBBB= dyssynchronous time to peak
strain curves = heterogeneous coloring at end-systole, with early peak
strain in septal segments and delayed peak strain in posterior lateral
segments (arrow)

78. Patient A -latest mechanical activation in the midposterior
segment (red arrow).
Patient B - echanical activation in the midlateral segment (red
arrow).
Patient C -broad site of latest mechanical activation

79. THANK
YOU