Principles and Practical Aspects of Strain Echocardiography

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Principles and Practical Aspects of Strain Echocardiography Dai-Yin Lu, Monica Mukherjee, Theodore Abraham

INTRODUCTION Assessment of regional and global ventricular function has long relied on visual assessment. However, this approach is subjective and variable leading to significant interobserver variability in interpretation. The heart is a mechanical organ and undergoes cyclic deformation in systole and diastole. This cyclic deformation can be measured and for decades was restricted to those undergoing open-heart surgery when metal beads were sown onto particular locations on the left ventricle (LV); deformation was then assessed via fluoroscopy. Approximately 20 years ago, magnetic resonance methods were introduced that allowed noninvasive assessment of deformation. Later, tissue Doppler-based methodology was used to track tissue motion by echocardiography. Further refinement of these techniques enabled echo-based assessment of regional deformation via determination of strain.

PRINCIPLES OF STRAIN IMAGING Strain is a measure of tissue deformation. Strain is defined as a change in length of an object relative to its original length (i.e., reduction to half its original length is 50% strain; Fig. 6.1). Strain rate (SR) is the rate at which this deformation (length change) occurs. Although myocardial deformation is a three-dimensional phenomenon, echo-based interrogation techniques have generally been limited to interrogating one or more of three imaging planes—longitudinal, circumferential, and radial (Fig. 6.2). More recently, 3D strain has been introduced. Strain and SR allow a clinician to determine regional and global myocardial function at the same level as a muscle physiologist by providing parameters similar to shortening fraction and shortening velocity, respectively.1 Echo-based techniques measure deformation by two primary methods—tissue Doppler and speckle-based. In tissue Doppler imaging (TDI), SR is the difference in velocity between two points along the myocardial wall (velocity gradient) normalized to the distance between the two points (Fig. 6.3). A similar velocity gradient exists between the endocardium and the epicardium, because the endocardium moves faster. This concept is used to derive myocardial velocity gradient (radial SR). This velocity gradient depicts the rate of change of myocardial wall thickness during systole and diastole. Thus SR measures the rate at which the two points of interest move toward or away from each other. Integration of SR yields strain, the normalized change in length between these two points (Fig. 6.4). In speckle-tracking methodology, the system tracks unique acoustic patterns within the myocardium termed speckles. These speckles can be tracked over time, and speckle displacement can be used to calculate tissue velocity and strain (Fig. 6.5). This method is relatively angle-independent, because it is not based on the Doppler principle. Because speckle tracking can be automated, this technique lends itself to semiautomated measurements of strain. One such method allows the generation of bull’s-eye plots of longitudinal segmental strain (Fig. 6.6 and Video 6.1 ). Another similar technique uses arrows to display the direction and amplitude of motion at various points in the heart (velocity vector imaging). Speckle tracking imaging can use preexisting B-mode images; however, it is performed at much lower frame rates (40–90 frames per second) and may not be as accurate in timing mechanical events as Doppler-based imaging (100–250 frames per second).

Commonly measured strain parameters include systolic and diastolic SRs, and systolic strain (Fig. 6.7). Peak systolic SR is the parameter that comes closest to measuring local contractile function in clinical cardiology. It is relatively volume independent and is less pressure independent than strain. In contrast, peak systolic strain is volume dependent and does not reflect contractile function as well as SR.

TWIST AND TORSION Myocardium are three-dimensional continuous fibers that change direction from subendocardial right-handed helix to a subepicardial lefthanded helix.2 The fibers arranged in counter-direction generate sliding or shear deformation during contraction.3 When viewed from apex to base, the apex rotates counterclockwise during systole, while base rotates in clockwise (Fig. 6.8). Twist is the apex-to-base difference in rotation, which is expressed in degrees. Torsion refers to the normalized twist, where the twist angle is divided by the distance between LV base and apex, which is expressed in degrees per centimeter. The systolic twist and diastolic untwist can be influenced by age, change of preload or afterload, diastolic dysfunction, cardiomyopathy, and valvular heart disease.4

REGIONAL AND GLOBAL FUNCTION Left Ventricle Circumferential and radial strain values are obtained in standard parasternal short axis view at mitral valve, papillary muscle, and apex level. Longitudinal strain is calculated from apical two-, three-, and four-chamber views, with basal, mid, and apical segments in each of the six walls. Timing of aortic valve closure (AVC) is used to define end-systole in a cardiac cycle. To avoid underestimation, it is important to get a circular LV images when performing circumferential and radial strain analyses, and avoid foreshortened apical chamber views in longitudinal strain STRAIN −20%

SHORTENING

LENGTHENING

STRAIN +20%

Resting Dimension

FIG. 6.1  Strain is a dimensionless index defined as change in length normalized to the original length. This reduction in length of the myocardial segment by 20% would indicate a strain of −20%. Conversely, a lengthening of a myocardial segment by 20% would yield a strain of +20%. Strain rate is the rate at which these length changes occur.

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analysis. Global longitudinal strain (GLS), calculated as the average from all segments, is commonly used as a measure of global LV function. Fig. 6.9 shows typical segmental speckle-tracking strain in a healthy normal heart. Timing of end systole needs to be defined clearly to identify postsystolic shortening from systolic shortening. Normal GLS value is reported between 18% and 25% in healthy participants.5 However, there is intervendor variability.

Longitudinal Strain SHORTENING −18 to 20% Circumferential Strain SHORTENING −18 to 20%

Right Ventricle

Radial Strain LENGTHENING +30 to 50%

DIASTOLE

SYSTOLE

FIG. 6.2  Myocardial deformation is a three-dimensional phenomenon. However,

echocardiographic interrogation of strain occurs along three primary directions—longitudinal (apex to base), circumferential (along the short axis curvature), and radial (endocardial to epicardial). There is systolic shortening and diastolic lengthening in the longitudinal and circumferential directions. There is systolic thickening and diastolic thinning in the radial direction.

The RV wall is thinner than the LV myocardium, and these two ventricles have different shapes. DTI has been validated in quantification of RV myocardial deformation in healthy individuals. RV longitudinal velocities demonstrate a typical base-to-apex gradient with higher velocities at the base (Fig. 6.10A). The deformation properties within the LV are more homogeneous. Conversely, the SR and strain values are less homogeneously distributed in the right ventricle and show a reverse base-to-apex gradient, with the highest values in the apical segments and outflow tract (see Fig. 6.10B).6 This reverse pattern can be explained by the complex geometry of the thin-walled, crescent-shaped right ventricle, and the less homogeneous distribution of regional wall stress. DTI-derived and speckle tracking-derived strain and SR can be used to evaluate RV dynamics, and both were found to be feasible and generally comparable.7 Strain and SR correlate well with radionuclide RV EF. Systolic velocity and strain best correlated with invasively determined right ventricular stroke volume and change in right ventricular function after vasodilator infusion (Fig. 6.11).8 SRs and strain quantitate regional right ventricular systolic function in children and adults with various conditions.9,10

Left Atrium

FIG. 6.3  Tissue velocity–based strain imaging measures tissue velocities along to

locations in the long axis direction. The difference in peak velocities normalized to the distance between them yields myocardial velocity gradient or strain rate.

Under normal conditions, the left atrium (LA) is a low-pressure, highly expandable chamber, but in the presence of acute and chronic injury, the left atrial wall stretches and stiffens.11,12 LA volume is not a specific marker for LA function, as it reflects the chronic effect of LV filling pressure but may also be increased in patients with atrial arrhythmias or in athletes whose LV filling pressure is actually normal. Assessment of LA strain with two-dimensional (2D) speckle tracking and Doppler-based strain provide additional information on LA mechanics. Components of atrial function include reservoir, conduit, and active booster contraction. The LA strain and SR demonstrate atrial physiology and closely follow LV dynamics during the cardiac cycle. LA reservoir function is displayed by “total” strain, and contractile function is presented by the negative strain following the beginning of the “P” wave. There are two different ways to define the reference (zero) point: One is to define the onset of P wave as baseline, and then the first negative peak strain corresponds to atrial contractile function, peak positive strain as conduit function, and the total sum represents reservoir function. The other is to set the peak of QRS complex as baseline, and then

STRAIN RATE

INTEGRATION

STRAIN

FIG. 6.4  In tissue velocity-based strain imaging, a region of interest is placed in a particular location on the myocardium. This measures strain rate at that location. Integration of strain rate deals strain.

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DIASTOLE

Diastolic position of “speckle”

SYSTOLE

Displacement of speckle

FIG. 6.5 Two-dimensional strain imaging uses speckle tracking methodology. A

speckle is a particular acoustic pattern that can be computationally identified within the myocardium. For strain estimation, a speckle is identified at end diastole (yellow box) and tracked until end systole (blue box). The distance traveled by the speckle is displacement, which is used to calculate strain, the temporal derivative of which in turn yields strain rate.

peak positive longitudinal strain represents atrial reservoir function, and strains during early and late ventricular diastole equal to conduit and 6 atrial contractile function (Fig. 6.12).13,14 Global strain and SR are calculated by averaging values observed in all LA segments,15,16 either with a 15-segment model (six segments in the apical four-chamber view, six in the two-chamber view, and three in the three-chambers views)17 or a 12-segment (six segments in the four-chamber view and six more in the two-chamber views) model.18 LA deformation assessment has an established role in assessing LA performance and LV diastolic function. For patients with atrial fibrillation, those who have higher atrial strain and SR appear to have a greater likelihood of staying in sinus rhythm after cardioversion (Fig. 6.13).19

CORONARY ARTERY DISEASE AND ISCHEMIC CARDIOMYOPATHY Strain and SR appear to be sensitive indicators for subclinical diseases, including diabetic or nonischemic cardiomyopathy, myocardial ischemia, arterial hypertension, and valvular heart disease. They are also useful in evaluation of myocardial damage after infarction, as well as outcome after revascularization.20–28 Myocardial ischemia is associated with reduction in peak systolic strain and often accompanied by postsystolic shortening. Infarct or severe ischemia is associated with systolic lengthening. These changes in strain and SR are dynamic (i.e., rapid reduction in ischemia and immediate return to normal upon restoration of blood flow; Fig. 6.14). Bull’s-eye plots of 2D strain (speckletracking method) are not time-consuming, semiautomated, and easy to generate and interpret. Some examples of regional ischemia are shown in Fig. 6.15 and Video 6.2 . Another important application of strain imaging is to combine with low-dose dobutamine stress echocardiography to assess myocardial viability. Augmentation of strain and SR after dobutamine infusion helps identify viable muscle. Postsystolic shortening occurs in the presence of active myocardial contraction and hence reflects viable myocardium. However, it should not be used as the only parameter indicating viability, since postsystolic shortening may be also present in myocardium with transmural necrosis or scar.

NONISCHEMIC CARDIOMYOPATHY

FIG. 6.6  A representative example of two-dimensional strain output. Segmental

strain rate tracings are provided for each apical view: four-chamber (upper left), twochamber (upper right), and apical long (lower left). Peak strain values are converted into a color code depicted as a bull’s-eye plot (lower right).

In the presence of overt cardiomyopathy demonstrated by conventional echocardiography, strain imaging is generally not needed. Nevertheless, it can be of great help when diseases are in early stages or to predict prognosis. GLS appears to have superior prognostic value to left ventricular ejection fraction (LVEF) for predicting major adverse cardiac events.29 Strain mapping depicts a global reduction in GLS, with the typical preservation of function noted in the basal inferior and inferolateral segments (Fig. 6.16)

FIG. 6.7  Representative tracings of strain rate (left panel) and strain (right panel). Commonly measured parameters include peak systolic strain rate (SRs), early and late diastolic strain rates (SRe and SRa, respectively), and peak systolic strain (S).

Principles and Practical Aspects of Strain Echocardiography

Systolic position of “speckle”

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COUNTER-CLOCK CLOCK

A

B

FIG. 6.8  A, Subepicardial fibers wrap around the left ventricle (LV) in a left-handed helix (yellow arrows), and subendocardial fibers wrap around the LV in a right-handed helix (green arrows). B, The outer epicardial layer (red arrows) in LV base rotates in a clockwise direction, whereas the inner endocardium (blue arrows) rotates in an opposite direction. For the apex, the epicardial layer rotates in a counterclockwise direction, and the endocardium rotates in clockwise rotation. The overall LV rotational direction is dominated by the epicardial rotation because the epicardial layer has a larger radius. (A adapted from Partho P, Sengupta A, Tajik J, et al: Twist mechanics of the left ventricle: principles and application. JACC Cardiovasc Imaging. 2008;1(3):366–367.)

FIG. 6.9  Representative strain tracings from three apical views—four-chamber (upper left), two-chamber (upper right), and apical long-axis (lower left), and the resulting

“bull’s-eye” plot (lower right). In this example, segmental strain values are all normal and represented by shades of red in the bull’s-eye plot. Global longitudinal strain was −20% (normal range).

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B

FIG. 6.10  (A) RV lateral free wall velocities and (B) longitudinal strain assessed using color DTI in a normal subject. Note the base-to-apex gradient in velocities and apex-tobase gradient in longitudinal strain. Yellow tracing = basal; green tracing = apical.

Abnormal RV function

Normal RV function 10

10

TVI (cm/s)

5 0

RV Apex

5

TVI (cm/s)

5 0 5 10

10 25

25

Displacement (mm)

Displacement (mm)

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15 5

5

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Strain rate (1/s)

3

3

2

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2 5

RV free wall

Strain (%)

Strain rate (1/s)

2 5

Strain (%)

5

5

15

15

0.1 s

25

0.1 s

25

FIG. 6.11  Strain appears superior to other Doppler-based indices such as the index of myocardial performance and tissue Doppler-based isovolumic acceleration. Representa-

tive traces from the basal RV free wall illustrating tissue velocity (TVI), tissue displacement, strain rate, and strain from a normal subject (left), and a subject with abnormal RV function (right). (From Urheim S, Cauduro S, Frantz R, et al: Relation of tissue displacement and strain to invasively determined right ventricular stroke volume. Am J Cardiol. 2005;96(8):1173–1178.)

Strain (%)

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ε Total

εpos

0

ε neg

−20

P

A

QRS

T

Strain (%)

60

εE

εS

εA

0 −20

B

QRS

T

P

FIG. 6.12  Speckle tracking-derived left atrial (LA) global longitudinal strain can be demonstrated with triggering on the (A) starting of the P wave or (B) peak of the QRS wave.

εS = peak positive strain, εE = strain during early diastole, and εA = strain during late diastole. (Right panel from Hoit BD: Left atrial size and function: role in prognosis. J Am Coll Cardiol. 2014;63(6):493–505.)

Principles and Practical Aspects of Strain Echocardiography

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60 Positive

Negative

Positive

5.0

80

4.5

70

4.0 3.5 3.0 2.5 2.0

1.80 Sens: 92.3 Spec: 78.6

1.5

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Negative

60 50 40 30 22.0 Sens: 76.9 Spec: 85.7

20 10

1.0

0

0.5

MSR

AFR

MSR

AFR

FIG. 6.13  A cutoff value of 1.8 s−1 for atrial inferior wall peak systolic strain rate was associated with sinus rhythm maintenance, with a sensitivity of 92% and specificity of

79% (left panel). For atrial septal peak systolic strain, a cutoff value of 22% was associated with a sensitivity of 77%, specificity of 86% (right panel). MSR, Maintenance of sinus rhythm; AFR, recurrence of atrial fibrillation. (From Di Salvo G, Caso P, Lo Piccolo R, et al: Atrial myocardial deformation properties predict maintenance of sinus rhythm after external cardioversion of recent-onset lone atrial fibrillation: a color Doppler myocardial imaging and transthoracic and transesophageal echocardiographic study. Circulation. 2005;112(3):387–395.)

accurately (0.96 positive and 0.94 negative predictive value, respectively) between patients with HCM and physiologic hypertrophy in athletes (Fig 6.18).35 Furthermore, strain analysis may offer prognostic stratification. A GLS cutoff value of 15% measured at rest is an independent indicator of cardiac events and symptomatic exacerbation in patients with HCM.36

Chemotherapy-Related Cardiotoxicity

FIG. 6.14  A 78-year-old woman undergoing coronary angioplasty with serial

posterior wall regional strain (%) averaged for mean heart cycle. During the ischemia period, peak strain value was clearly decreased in systole, with the appearance of postsystolic thickening phenomenon. After reperfusion there was an increase in myocardial systolic thickening caused by reactive hyperkinesia. (Modified from Jamal F, Kukulski T, D’hooge J, et al: Abnormal postsystolic thickening in acutely ischemic myocardium during coronary angioplasty: a velocity, strain, and strain rate Doppler myocardial imaging study. J Am Soc Echocardiogr. 1999;12(11):994–996.)

Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is characterized by scattered regions of fiber disarray within the hypertrophic areas.30,31 Regional analysis differentiates abnormal hypertrophic regions of cardiac muscle in which there was no systolic shortening from adjacent normal regions.32–34 The thickest segments of myocardium are usually associated with greatest reduction or even absence of deformation (Fig. 6.17). In a study with patients having familial nonobstructive HCM, average longitudinal strain was reduced in affected individuals compared with healthy controls, despite apparently normal systolic function. In addition, there was no significant difference in the values obtained by TDI versus 2D strain echocardiography.32 An early diastolic SR ≤7 s−1 differentiated

Chemotherapy-related cardiotoxicity is usually defined as a reduction of LVEF greater than 5% in symptomatic or 10% in asymptomatic patients from baseline to an LVEF <55%.37 However, reduction in LVEF is not a sensitive parameter, since it appears late in the disease process, after significant cardiotoxicity has already developed. Myocardial deformation indexes have been applied to detect early-stage myocardial injury in patients receiving chemotherapy. The myocardial deformation parameters decreased rapidly, as early as 2 hours after the first dose of anthracyclines.38 In a recent systemic review, 13 publications with 384 patients demonstrated consistently that reduction in myocardial deformation occurred earlier than reduction in LVEF, despite the heterogeneity of patient age, cancer type, strain methodology, and timing of follow-up, and GLS being the most consistent parameter. Furthermore, a 10% to 15% early reduction in GLS by speckle tracking during chemotherapy appears to be the most useful parameter for the prediction of cardiotoxicity, with a drop in LVEF or heart failure.39 The Expert Consensus Statement from the American Society of Echocardiography and the European Association of Cardiovascular Imaging suggested that a relative percentage reduction of GLS <8% from baseline might not be meaningful, whereas a >15% reduction from baseline is likely to be abnormal.40 Because of intervendor variability, it is important that similar equipment and protocol for calculating strain should be used when patients undergo serial evaluations.

Other Cardiomyopathies Duchenne muscular dystrophy (DMD) is one of the most common X-linked recessive neuromuscular disorders. Boys with DMD lose independent ambulation by the age of 12 and die of respiratory failure or cardiomyopathy in their late teens or early 20s. A report in 2006 showed that radial strain was significantly lower in asymptomatic boys with DMD, when conventional echocardiography failed to show any abnormality.41 Friedreich ataxia (FRDA) is an inherited neurodegenerative disorder associated with cardiomyopathy and impaired glucose tolerance. SR offers a means of further characterizing the myocardial abnormalities in patients with FRDA. Early diastolic myocardial velocity gradient appear to relate most closely to the genetic abnormality and the consequential reduction in frataxin protein (Fig. 6.19).42

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anterior septal, anterior and anterolateral walls (arrows), and in the circumflex territory (right panel), demonstrating reduced strain and dyskinesis in the inferolateral region (arrows).

FIG. 6.16  Representative two-dimensional strain polar color plot in a patient with

nonischemic cardiomyopathy demonstrating reduced strain globally with preserved systolic function, normal strain, in the basal infer-septum, inferior and infero-lateral walls.

FIG. 6.17  In apical hypertrophic cardiomyopathy, the thickest segments in the apex (asterisk) are usually associated with greatest reduction or even absence of deformation.

Principles and Practical Aspects of Strain Echocardiography

FIG. 6.15  Representative two-dimensional strain polar color plots demonstrating ischemia in the left anterior descending territory (left panel) evidenced by low strain in the

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FIG. 6.18  An early diastolic (yellow dots) strain rate ≦7 s−1 differentiated between

patients with HCM and physiologic hypertrophy in athletes. (Modified from Palka P, Lange A, Fleming AD, et al: Differences in myocardial velocity gradient measured throughout the cardiac cycle in patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension. J Am Coll Cardiol. 1997;30[3]:760–768.)

FIG. 6.19  In patients with Friedreich ataxia (FRDA), the systole and early dia-

stolic strain rate were reduced compared with control subjects. In contrast, the late diastolic strain rate is higher in patients with FRDA than in control subjects. (Modified from Dutka DP, Donnelly E, Przemyslaw P, et al: Echocardiographic characterization of cardiomyopathy in Friedreich’s ataxia with tissue Doppler echocardiographically derived myocardial velocity gradients. Circulation. , 2000;102(11):1276–1282.)

of myocardial dysfunction than LVEF.43,44 Cardiac resynchronization therapy (CRT) is a catheter-based therapy for patients with heart failure and left ventricular dyssynchrony. Several large clinical trials have established the benefits of CRT on hospitalization or survival in patients with severe LV dysfunction and a QRS duration wider than 120 ms.45–47 However, about one-third of patients selected based on electrocardiogram criteria do not respond to CRT. Measurement of regional electromechanical activities with TDI information helps identify mechanical dyssynchrony and is useful in selecting patients who might get more benefit from CRT.48,49 Strain analyses by speckle tracking or TDI were used to detect and define intraventricular dyssynchrony, and they were demonstrated as reliable markers in predicting responders to CRT.50–52 Use of the strain delay index with longitudinal strain by speckle tracking has a strong value for predicting response to cardiac resynchronization therapy in both ischemic and nonischemic patients.48 Another important issue for CRT efficacy is to find optimal lead position in the left ventricular free wall. Several series have demonstrated that an LV lead position, coinciding with the regions of latest mechanical activation, yields superior outcomes compared with discordant positions.53

VALVULAR HEART DISEASE The timing for surgical intervention in asymptomatic or mild symptomatic moderate to severe valvular heart disease is largely based on symptoms, lesion severity, and negative LV volumetric remodeling or functional decline. Reduction in LVEF indicates impairment of contractility. However, it is often a late consequence of myocardial injury and sometimes not fully reversible after surgery. Subclinical myocardial dysfunction may be a potential guide for the timing of surgical intervention.54 Recent studies have suggested that strain imaging provides additional clinical value in aortic and mitral valve diseases.55–57 In patients with severe aortic stenosis, impaired LV strain and SR were noted, although LVEF was preserved. After aortic valve replacement, a significant improvement in these parameters was observed. These subtle changes in LV contractility can be detected by 2D speckle tracking imaging.58 Another report on percutaneous aortic valve replacement showed improvements of strain and SR in TDI.59 In patients with mitral stenosis who underwent percutaneous mitral balloon valvotomy (PMBV), GLS is a powerful predictor of long-term outcome after successful PMBV and provides incremental prognostic value over traditional parameters.60 In patients with asymptomatic mitral regurgitation, strain and SR help identify subclinical LV dysfunction and correlate with contractile reserve with exercise; strain and SR are significantly greater in patients with adequate contractile reserve.26 However, these results were largely based on observational studies, and prospective randomized control trials are needed before routine use of strain imaging can be recommended regarding to timing of surgery.

INFILTRATIVE DISEASE Amyloidosis

FIG. 6.20  The systolic strain rate in a patient with cardiac amyloidosis (right panel, arrow) is –0.4 s−1, which is marked smaller in the absolute value compared with an ­age-matched control (left panel, arrow).

DILATED CARDIOMYOPATHY AND DYSSYNCHRONY ANALYSIS Mechanical dyssynchrony is discoordinate ventricular contraction resulting from either an electrical condition delay or abnormal ventricular contraction. It has been reported as a more sensitive marker

Cardiac amyloidosis (CA) (see Chapter 24) is a manifestation of amyloidosis. As extracellular misfolding fibrillar proteins deposit in heart muscle, LV wall becomes thickened with the presentation of restrictive cardiomyopathy, followed by overt heart failure or sudden death.61 Patients with amyloidosis had severe diastolic dysfunction, and myocardial deformation was significantly decreased (Fig. 6.20).62 When compared with conventional mitral inflow spectral Doppler velocities (E wave and A wave), strain imaging of the right and LVs are more insightful and sensitive for the early identification of cardiac amyloidosis.63,64 A specific pattern of longitudinal strain characterized by worse longitudinal strain in the mid- and basal ventricle with relative sparing of the apex63 is typical for amyloid cardiomyopathy, which may help distinguish from hypertensive cardiomyopathy or hypertrophic cardiomyopathy (Fig. 6.21).65,66

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Principles and Practical Aspects of Strain Echocardiography FIG. 6.21  Two-dimensional speckle-tracking longitudinal strain (“bull’s-eye plot”) demonstrates reduced strain at the base and mid-levels, with apical sparing in patients with cardiac amyloidosis (cherry on sundae pattern).

Suggested Readings Mirea, O., Duchenne, J., & Voigt, J. U. (2016). Recent advances in echocardiography: strain and strain rate imaging. F1000Res, 5. pii: F1000 Faculty Rev-787. Opdahl, A., Helle-Valle, T., Skulstad, H., & Smiseth, O. A. (2015). Strain, strain rate, torsion, and twist: echocardiographic evaluation. Current Cardiology Reports, 17(3), 568.

Smiseth, O. A., Torp, H., Opdahl, A., et al. (2016). Myocardial strain imaging: how useful is it in clinical decision making? European Heart Journal, 37(15), 1196–1207. Voigt, J. U., & Flachskampf, F. A. (2004). Strain and strain rate. New and clinically relevant echo parameters of regional myocardial function. Z Kardiol, 93(4), 249–258. A complete reference list can be found online at ExpertConsult.com.

63.e1 References

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D., et al. (2014). Use of myocardial strain imaging by echocardiography for the early detection of cardiotoxicity in patients during and after cancer chemotherapy: a systematic review. Journal of the American College of Cardiology, 63(25 Pt A), 2751–2768. 40. Plana, J. C., Galderisi, M., Barac, A., et al. (2014). Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Journal of the American Society of Echocardiography, 27(9), 911–939. 41. Giatrakos, N., Kinali, M., Stephens, D., et al. (2006). Cardiac tissue velocities and strain rate in the early detection of myocardial dysfunction of asymptomatic boys with Duchenne’s muscular dystrophy: relationship to clinical outcome. Heart, 92(6), 840–842. 42. Dutka, D. P., Donnelly, J. E., Palka, P., et al. (2000). Echocardiographic characterization of cardiomyopathy in Friedreich’s ataxia with tissue Doppler echocardiographically derived myocardial velocity gradients. Circulation, 102(11), 1276–1282. 43. Becker, M., Kramann, R., Franke, A., et al. (2007). Impact of left ventricular lead position in cardiac resynchronization therapy on left ventricular remodelling. A circumferential strain analysis based on 2D echocardiography. European Heart Journal, 28(10), 1211–1220. 44. Yu, C. M., Gorcsan, J., 3rd, Bleeker, G. B., et al. (2007). Usefulness of tissue Doppler velocity and strain dyssynchrony for predicting left ventricular reverse remodeling response after cardiac resynchronization therapy. The American Journal of Cardiology, 100(8), 1263–1270. 45. Goldenberg, I., Kutyifa, V., Klein, H. U., et al. (2014). Survival with cardiac-resynchronization therapy in mild heart failure. The New England Journal of Medicine, 370(18), 1694–1701. 46. Bristow, M. R., Saxon, L. A., Boehmer, J., et al. (2004). 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6

Principles and Practical Aspects of Strain Echocardiography

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