This document discusses strain and strain rate imaging techniques used to quantify regional myocardial function. It describes various methods to measure strain, including tissue Doppler, 2D speckle tracking, and cardiac MRI. It outlines normal values and patterns of strain in healthy individuals and how strain is altered in various cardiac diseases, such as coronary artery disease, heart failure, cardiomyopathies, and congenital heart disease. Strain imaging can identify myocardial scar, viability, dysfunction, and response to treatments.

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