Evaluating myocardial contractile function by echocardiography has traditionally centered on volume-based assessments such as ejection fraction and regional evaluations of wall motion and visual estimation of regional thickening. However, these conventional methods present challenges related to reproducibility, standardization, and a high sensitivity to loading conditions. These limitations have spurred interest in more objective and reproducible techniques for assessing myocardial contractile function, leading to the development of deformation imaging techniques, including myocardial strain. Speckle-tracking echocardiography (STE) has emerged as a valuable tool in the evaluation of myocardial strain, particularly longitudinal strain. This technique uses ultrasound to generate interference, reflection, and scattering as the ultrasound beam passes through myocardial tissue, creating acoustic markers called “speckles” on a standard B-mode echocardiographic image ( Fig. 7.1 ). Regional myocardial function can be assessed by tracking the movement of these speckles throughout the cardiac cycle.
The key components of speckle-tracking analysis used to assess myocardial deformation. (A) to (C) The three principal directions of myocardial strain in which a standard echocardiogram of the left ventricle (LV) shows acoustic “speckles” that result from the interaction between the ultrasound beam and myocardial tissue. These speckles are the foundation of strain calculation.
(A) Longitudinal strain, tracking speckle movement in the long axis of the LV.
(B) Radial strain, showing myocardial thickening (inward motion) during ventricular systole.
(C) Circumferential strain, representing myocardial shortening around the circumference of the LV.
(D) Depiction of the process of “block matching,” an important part of the speckle-tracking technique in which the speckle pattern within a region of interest is identified in one frame and tracked across successive frames. The search regions (dotted blocks) are analyzed to find the optimal matching region. The displacement of the matching block determines tissue motion. This method, repeated across multiple regions of interest, allows estimation of regional myocardial deformation throughout the cardiac cycle.
(Modified and reproduced from Badano LP, Visentin S, Palermo C, et al. Echocardiographic techniques of deformation imaging in the evaluation of maternal cardiovascular system in patients with complicated pregnancies. Biomed Res Int . 2017;1:1–10.)
An organ’s gross and/or histologic structure dictates its function. In the heart, differences in cavitary pressure between the pulmonary and systemic circulations drive several structural distinctions between the ventricles. The left ventricle (LV), with its thick walls and conical shape, propels blood into the high-pressure systemic circulation. In contrast, the right ventricle (RV), characterized by thin walls and a crescent shape, directs blood into the low-resistance pulmonary circulation. Despite the dynamic nature of the circulation, the RV is adept at maintaining low pressure, even under conditions of varying volume. At both the cellular and tissue levels, the ventricles adapt to meet the physiological demands of the entire body, continuing to develop into adulthood to fulfill the heart’s function. The myocardial architecture of the ventricles supports these distinct roles. In the RV, the majority of muscle fibers are transverse fibers with a smaller proportion of subendocardial longitudinal fibers. The LV, on the other hand, comprises endocardial and epicardial fibers arranged in a helical structure with circumferential fibers located at the mid-wall creating a more complex myocardial architecture. The structural organization of myocardial muscle fibers in the ventricles and atria underscores the heart’s mechanical efficiency ( Fig. 7.2 ). Each myocardial bundle spirals around the heart chambers in a helical arrangement, enabling coordinated contraction and relaxation. This intricate fiber architecture highlights the heart’s evolutionary optimization for mechanical efficiency and forms the foundation for advanced imaging and therapeutic strategies. Insights into myocardial fiber orientation are critical for interpreting strain imaging and identifying pathologies such as ischemia, cardiomyopathies, and arrhythmias. Given these distinct structural differences and functional roles, STE offers a noninvasive method for assessing the unique strain patterns of both ventricles.
(A) Helical fiber arrangement . The heart’s muscle fibers are organized in a double-helical structure that facilitates the coordinated rotation of the base and apex during systole, optimizing blood ejection and diastolic filling. Subepicardial fibers adopt a left-handed spiral, and subendocardial fibers form a right-handed spiral. This arrangement creates a chiral fiber system that enables twisting (systole) and untwisting (diastole) motions, enhancing torsional mechanics. Circumferential fibers in the mid-myocardial layer contribute to radial thickening and support efficient ventricular pumping. (Reproduced from Nakatani S. Left ventricular rotation and twist: why should we learn? J Cardiovasc Ultrasound . 2011;19(1):1–6.)
(B) Anatomic fiber structure . Anatomically, the myocardial fibers spiral continuously from the apex to the base. This configuration ensures uniform contraction, generating torsion for effective ejection of blood into the aorta and pulmonary artery. The twisting motion also optimizes diastolic filling.
(C) Atrial muscle fibers . Atrial muscle fibers also exhibit a helical arrangement, supporting atrial contraction and reservoir functions. This structure plays a critical role in atrial efficiency, particularly in the context of arrhythmias such as atrial fibrillation. (Reproduced from Opdahl A, Helle-Valle T, Skulstad H, Smiseth OA. Strain, strain rate, torsion, and twist: echocardiographic evaluation. Curr Cardiol Rep . 2015;17(3):568.)
(D) Fiber interaction and functional implications . The complex organization of fibers supports torsional mechanics, allowing for coordinated clockwise rotation of the base of the heart and counterclockwise rotation of the apex during systole. This interaction ensures energy-efficient contractions and optimal blood ejection.
The right atrium (RA) and left atrium (LA) also exhibit distinct myocardial functions. Emerging evidence suggests that the LA serves a far more dynamic role than simply acting as a conduit for left ventricular filling. Embryologically, most of the left atrial myocardium evolves from the primitive pulmonary vein (PV), and the RA is formed from the primitive RA and the sinus venosus that contributes to their smooth-walled endocardium. , This structural development makes both the LA and RA more susceptible to volume overloading due to mitral regurgitation (MR) or tricuspid regurgitation (TR), respectively, because of the thinner myocardial fibers oriented primarily in the longitudinal direction. , In addition, these thinner fibers allow the aria to expand more easily when exposed to increased volume stress. Echocardiographically, the strain patterns of the LA and RA differ from those of the ventricles. Whereas the LV and RV exhibit longitudinal, circumferential, and radial strain, the atria show primarily longitudinal strain because of their simpler myocardial structure. These differences in strain patterns reflect the embryologic and structural distinctions between the chambers and their corresponding roles in cardiac physiology (see Fig. 7.2C ).
Strain imaging provides a comprehensive, noninvasive tool for assessing the unique functional roles of the atria and ventricles, offering crucial insights into both normal and pathological myocardial mechanics. This advanced imaging modality is particularly valuable in detecting subtle, early changes in myocardial function that may not yet manifest in traditional measures such as ejection fraction or atrial volumes. By identifying these early changes, strain imaging plays a pivotal role in diagnosing arrhythmias such as atrial fibrillation (AF) at a stage when structural or functional alterations in the atrial myocardium are just beginning to develop. For example, reduced atrial strain can indicate impaired atrial compliance and/or contractile function, which often precede the onset of AF. , Similarly, strain imaging can detect early ventricular abnormalities, including regional strain impairments, that may signal ischemia, cardiomyopathy, or even subclinical fibrosis. These capabilities make strain imaging an indispensable tool in modern cardiology and cardiac surgery, enabling earlier interventions that can improve patient outcomes and prevent the progression of disease.
Left Ventricular Strain
Historically, the assessment of left ventricular systolic function in AF has been challenging because of beat-to-beat variations. However, research has demonstrated that using the index beat to measure left ventricular global longitudinal strain (LV-GLS) in patients with AF is as accurate as averaging multiple cardiac cycles. Thus LV-GLS derived from the index beat serves as a definitive parameter for evaluating systolic function, even in patients with an irregular rhythm caused by AF. , Beyond its role in defining heart failure at earlier stages, LV-GLS also has significant predictive value in identifying patients at risk of developing AF. Studies suggest that impaired LV-GLS may reflect subtle myocardial changes such as fibrosis or remodeling, which are precursors to the onset or progression of AF. , Moreover, a reduction in the LV-GLS in AF patients with preserved left ventricular ejection fractions (LVEF) often indicates underlying subclinical dysfunction, emphasizing the utility of LV-GLS as a sensitive biomarker.
During ventricular systole, the ventricular myocardium shortens longitudinally and circumferentially while thickening radially. These changes reverse during diastole. As mentioned, strain measures the percentage change in myocardial fiber length from diastole to systole and is expressed as a negative percentage. , Specifically, longitudinal strain quantifies the shortening of myocardial fibers along the long axis of the heart. It is calculated using the following formula:
in which L 0 is the diastolic (resting) fiber length and L 1 is the systolic (shortened) fiber length. For example, if the myocardial fibers shorten from 2 cm at end-diastole to 1.6 cm at end-systole, the strain value would be
This formula highlights the relationship between fiber shortening and myocardial performance, with negative values reflecting contraction. Longitudinal and circumferential strain values are typically negative because the fibers shorten during systole, but radial thickening produces positive strain values caused by fiber expansion. , For example, a 20% shortening corresponds to a strain value of minus 20% (–20%). Importantly, more negative strain values indicate better myocardial contraction and function ( Fig. 7.3 ).
The term “strain” fundamentally means “deformation.” In the context of ventricular function, it provides a quantitative measure of how much the myocardial fibers stretch or contract during the cardiac cycle. Ventricular strain is defined as the percentage change in myocardial fiber length between the end-diastole (resting phase) and end-systole (contractile phase).
Left upper panel, The state of myocardial fibers at their longest, corresponding to the heart’s relaxation phase or end-diastole.
Right upper panel, The state of myocardial fibers after shortening, corresponding to the heart’s contraction phase or ventricular systole
Lower panel, Strain is calculated using a formula in which L 0 represents the diastolic fiber length, and L 1 represents the systolic fiber length. Because the fibers shorten during contraction, L 1 is less than L 0 , making strain a negative percentage , which reflects the reduction in fiber length during ventricular systole.
Myocardial Fiber Orientation and Mechanics
Understanding myocardial fiber orientation is fundamental to interpreting strain. As mentioned, subepicardial fiber contraction rotates the LV base clockwise and the apex counterclockwise, and subendocardial contraction produces the opposite effect. , , This interplay results in torsion, a twisting motion that enhances ventricular ejection during systole and facilitates diastolic filling ( Figs. 7.2A , 7.4 , and 7.5 ). The torsional mechanics are critical for efficient cardiac performance, with subepicardial fibers dominating because of their larger radius of rotation. Clinically, evaluating the balance between subepicardial and subendocardial function is essential for diagnosing and managing conditions such as myocardial ischemia, heart failure, and valvular diseases.
Left panel, Left ventricular longitudinal strain represents the shortening of the long axis of the left ventricle (LV) during systole. This strain reflects the downward movement of the base toward the apex during contraction. In addition to longitudinal strain, the LV undergoes a rotational or torsional motion around its long axis during systole. When viewed from the apex, the apex rotates counterclockwise, and the base rotates clockwise. This opposing rotation creates a wringing or twisting motion of the LV, which enhances the efficiency of blood ejection during systole. During diastole, the LV untwists, generating an active suction force that promotes its early diastolic filling.
Right panel, Left ventricular circumferential strain represents the reduction in the circumference of the left ventricular cross-section during contraction. This strain is a key indicator of the LV’s ability to reduce its diameter and effectively eject blood. Radial strain, on the other hand, measures the thickening of the left ventricular wall along its radius during contraction. These two types of strain work in harmony to ensure efficient myocardial function and are complementary with longitudinal strain in maintaining overall cardiac performance. Radial strain predominantly reflects the contractility of the mid-myocardial fibers, whereas circumferential strain highlights the role of the subendocardial and subepicardial fiber layers in ventricular contraction.
(Modified from Kislitsina ON, Thomas JD, Crawford E, et al. Predictors of left ventricular dysfunction after surgery for degenerative mitral regurgitation. Ann Thor Surg. 2020;109:669–677.)
(A) The helical arrangement of myocardial fibers within the left ventricle (LV). The transition of the myocardial fibers begins with a right-handed spiral pattern in the epicardium and gradually shifts to an orthogonal left-handed spiral in the subendocardium. This unique architecture supports the efficient torsional mechanics required for ventricular contraction and relaxation.
(B) This is a cross-sectional view of the LV showing the orientation of myocardial fibers at different layers of the left ventricular wall. The subendocardium has longitudinal fibers that run from the base to the apex of the LV. They are responsible for longitudinal strain and are sensitive to early ischemia and other pathological processes. The mid-myocardial layer has circumferential fibers arranged around the circumference of the left ventricular cavity that contribute to circumferential strain, which plays a critical role in overall systolic function. The subepicardium has fibers that are arranged obliquely in a helical configuration that provide rotational and torsional motion. They ensure efficient cavitary blood ejection during systole and facilitate ventricular filling during diastole. This unique fiber architecture allows for the synchronized contraction and relaxation of the heart, which is critical for its efficient function as a pump. RV, Right ventricle.
(Modified from Luis SA, Chan J, Pellikka PA. Echocardiographic assessment of left ventricular systolic function: an overview of contemporary techniques, including speckle-tracking echocardiography. Mayo Clin Proc . 2019;94(1):125–138; used with permission of Mayo Foundation for Medical Education and Research. All rights reserved.)
Longitudinal Strain: A Sensitive Marker
Longitudinal strain is often the first strain parameter to show impairment in early cardiac dysfunction. This is primarily because the subendocardial fibers, which are most vulnerable to ischemia, fibrosis, and increased wall stress, contribute predominantly to longitudinal contraction. Longitudinal strain is less affected by loading conditions (e.g., preload and afterload) compared with traditional measures of left ventricular function such as LVEF, making it a sensitive and reliable marker of intrinsic myocardial function. It is particularly valuable for the early detection of cardiotoxicity in patients undergoing chemotherapy and predicting outcomes in heart failure and ischemic heart disease. , , The normal range for LV-GLS is generally accepted to be −18% to −22%, with less negative values (e.g., −16%) indicating abnormal function. Although vendor variability and hemodynamic factors such as heart rate and blood pressure can influence strain values, LV-GLS remains a robust and reproducible metric for determining left ventricular systolic function.
Atrial Fibrillation and Left Ventricular Strain
AF significantly impacts left ventricular function because of the loss of atrial compliance and booster function, which impairs left ventricular filling and compromises hemodynamics. Rapid ventricular rates resulting from AF can further exacerbate left ventricular dysfunction by promoting ventricular cardiomyopathy. Even with optimal ventricular rate control, the absence of the atrial compliance and booster pump functions may impair left ventricular systolic performance. Several studies confirm that AF independently affects LV-GLS, even after adjusting for factors such as blood pressure, heart rate, diabetes, left atrial volume index, and left ventricular mass index. , Compared with age-matched and LVEF-matched control participants without AF, AF patients consistently demonstrate impaired LV-GLS, underscoring its role as a major determinant of LV systolic function.
Global and Regional Strain Analysis
Left ventricular strain analysis includes both global longitudinal strain (LV-GLS) and regional (segmental) strain assessments, which are critical for evaluating myocardial function. Using the 16-, 17-, or 18-segment models recommended by the American Society of Echocardiography, left ventricular segmental strain provides an in-depth assessment of left ventricular performance. Whereas LV-GLS provides an overall measurement of left ventricular function, regional (segmental) strain analysis allows for the identification of localized dysfunction such as ischemia, fibrosis, or mechanical dyssynchrony, all of which are often associated with regional ischemia within specific coronary artery territories.
Global Longitudinal Strain
For LV-GLS analysis, two-dimensional grayscale images are acquired from standard echocardiographic views, including the parasternal long axis and apical four-, three-, and two-chamber views ( Figs. 7.6 and 7.7 ). LV- GLS is computed using advanced speckle-tracking software that automatically constructs strain curves by analyzing myocardial deformation across cardiac cycles. The short-axis views of the apical, midlevel, and basal portions of the LV are then stacked to create a “bullseye map” to show the global longitudinal strain distribution across the entire left ventricular myocardium ( Fig. 7.8 ). , Left ventricular strain imaging, including longitudinal, circumferential, and radial motion, has shown unparalleled sensitivity in detecting subclinical left ventricular dysfunction, often preceding detectable changes in the LVEF by other means, which leads to earlier treatment in asymptomatic patients.
(A–C) The echocardiographic views used to evaluate left ventricular global longitudinal strain (LV-GLS). Each panel corresponds to a standard imaging plane. (A) The “two-chamber view” shows the anterior and inferior walls of the left ventricle (LV). Strain values are calculated for specific myocardial segments along the left ventricular long axis. (B) The “four-chamber view” displays the septal and lateral walls of both the LV and the adjacent right ventricle (RV). This view is crucial for measuring strain in the septal and LV lateral wall segments. (C) The “three-chamber view” highlights the left ventricular posterior and septal walls. Each myocardial segment is color coded with strain values to provide a quantitative assessment of regional left ventricular function.
(D–F) The three cross-sectional levels of the LV. (D) The left ventricular apex is divided into four myocardial segments representing the most distal part of the LV. (B) The cross-section of the LV at the mid-ventricular level is divided into six segments and passes through both papillary muscles. (C) The base of the LV also includes six segments and is aligned in the plane of the mitral valve.
LV-GLS represents the average strain across all 17 left ventricular segments, capturing the overall deformation of the LV during systole. LV-GLS is particularly valuable for early detection of left ventricular dysfunction, even when the left ventricular ejection fraction appears to be normal. Left ventricular segmental strain provides for the functional analysis of individual myocardial segments, thus identifying regional dysfunction in the LV.
(Modified from Kislitsina ON, Thomas JD, Crawford E, et al. Predictors of left ventricular dysfunction after surgery for degenerative mitral regurgitation. Ann Thor Surg. 2020;109:669–677.)
Longitudinal echocardiographic views of the left ventricle in the three standard planes. Each echocardiographic image demonstrates myocardial deformation as determined by speckle-tracking echocardiography.
(A) The three-chamber view shows the anterior, posterior, and septal left ventricular walls.
(B) The four-chamber view highlights the left ventricular septal and lateral walls.
(C) The two-chamber view focuses on the left ventricular anterior and inferior walls.
(D) Bullseye maps provide a visual representation of left ventricular strain across all of its 17 standard segments, divided into apex, mid-ventricle, and basal levels. The color-coded myocardial segments and associated strain values indicate regional left ventricular function. Left bullseye map : Normal left ventricular segments are represented by red hues , indicating strong contraction, and segments with impaired strain are shown in lighter shades and abnormal strain values. Right bullseye map : This map is based not on the strength of left ventricular segmental contraction but rather on the time it takes each segment to reach its peak strain value. The blue segments show areas of delayed contraction suggesting mechanical dyssynchrony, which is often seen in such conditions as left bundle branch block or cardiomyopathies.
Left ventricular strain across its three primary segments: the apex, mid-ventricle, and base, illustrating how the left ventricle (LV) is functionally divided for global and segmental strain analysis.
Left panel, The left ventricular apical plane is the narrowest portion of the LV and represents only the most distal region of the LV involved in contraction and relaxation during the cardiac cycle. The mid-ventricular plane contributes to overall left ventricular function by coordinating strain dynamics with the apex and base. The basal plane is the section of the LV and is located near the level of the mitral valve plane. It plays a critical role in tethering the ventricular wall to ensure synchronized myocardial function.
Right panel, The bullseye map is a two-dimensional representation of left ventricular strain data divided into 17 myocardial segments. Each segment corresponds to specific regions of the apex, mid-ventricle, and base, helping clinicians assess regional strain patterns and detect functional abnormalities.
(Modified from Kislitsina ON, Thomas JD, Crawford E, et al. Predictors of left ventricular dysfunction after surgery for degenerative mitral regurgitation. Ann Thor Surg. 2020;109:669–677.)
Left Ventricular Regional (Segmental) Strain
An analysis of left ventricular segmental strain is particularly valuable for identifying localized areas of myocardial dysfunction in diseases such as ischemic cardiomyopathy, mitral valve (MV) prolapse, and degenerative MR (DMR). , For example, we have recently shown that in DMR, preoperative left ventricular segmental strain analysis can identify hypocontractility in the left ventricular wall segments subjacent to papillary muscles that is predictive of the late recurrence of MR after successful MV repair. Our study found that for every 1% decrease in strain in the critical subpapillary left ventricular segments, there is a 6.2% increase the odds of developing late moderate-to-severe MR (odds ratio, 1.062). The early detection of left ventricular segmental strain abnormalities in patients with DMR and subsequent earlier MV repair can preclude the development of AF and irreversible left atrial remodeling ( Fig. 7.9 ).
Upper panels, Left ventricular segments 1 and 6 (purple) are located in the basal anterior and basal anterolateral regions and are subjacent to the anterolateral papillary muscle. We recently documented that abnormal preoperative strain in these left ventricular segments correlates with late recurrent mitral regurgitation (MR) after mitral valve (MV) repair for degenerative mitral regurgitation (DMR). We also found that abnormal preoperative strain in left ventricular segments 7, 11, and 12 (orange), which are subjacent to the posteromedial papillary muscle in the mid-anterior, mid-anterolateral, and mid-inferolateral regions, is also predictive of late recurrent MR in these patients.
Lower panels, The identification of these critical subpapillary left ventricular segments in our study is consistent with the current literature that associates segments 7, 12, 11, and 10 with the posteromedial papillary muscle and segments 1, 6, 5, and 4 with the anterolateral papillary muscle. The purple segments and orange segments are the ones we found to be predictive of late recurrent MR in DMR patients undergoing MV repair. These findings suggest that reinforcement of the anterior MV commissure during MV repair for DMR may be helpful in preventing long-term late recurrent MR. LV, Left ventricle.
Restoration of atrial function after conversion from AF to normal sinus rhythm is impacted by patient comorbidities and the duration of AF. The recovery of atrial function is usually rapid in patients after isolated coronary artery bypass grafting (CABG) with a concomitant Maze procedure or after the Maze procedure alone. However, in patients with long-standing DMR, both global and regional atrial dysfunction are often worsened by preexisting conditions. , The replacement of healthy atrial tissue with fibrotic tissue leads to irreversible remodeling of the LA, placing these patients at a higher risk for recurrent AF and stroke (see Chapter 8 ). Therefore the early detection of left ventricular segmental strain abnormalities is critical because it can help identify changes in the LA before AF develops. This underscores the importance of left ventricular segmental strain analysis not only in ischemic heart disease but also in valvular and arrhythmic conditions. Regional left ventricular strain abnormalities reflecting early mechanical dysfunction may be particularly important in guiding the timing of MV repair in asymptomatic patients. Early detection of left ventricular segmental changes allows clinicians to intervene before AF or irreversible remodeling occurs.
In summary, global and regional left ventricular strain imaging enhances diagnostic precision, aids in risk stratification, and provides a foundation for personalized treatment strategies. By combining LV-GLS and left ventricular segmental strain analysis, clinicians can assess both diffuse and localized myocardial dysfunction, offering a comprehensive view of left ventricular performance and guiding earlier, more targeted surgical interventions. The integration of regional and global strain data allows clinicians to assess both diffuse and focal myocardial dysfunction comprehensively, making strain imaging a cornerstone of modern cardiac diagnostics. Emerging techniques, such as myocardial work analysis, integrate strain with pressure-volume loops to provide an even more detailed evaluation of myocardial function.
Right Ventricular Strain
The RV plays a pivotal role in maintaining hemodynamic balance, particularly as it adapts to variations in preload and afterload from the pulmonary circulation. Unlike the LV, the RV is more sensitive to changes in afterload because of its thin wall and unique geometry. This sensitivity makes the RV prone to dysfunction in conditions such as pulmonary hypertension, TR, and chronic volume or pressure overload. , These hemodynamic disturbances can trigger right atrial dilatation, ultimately predisposing patients to AF. TR and volume overload increase RV diastolic volume, stretching the myocardium and transiently enhancing contraction via the Frank-Starling mechanism. However, chronic volume overload eventually leads to right ventricular dilatation and impaired systolic function. Pulmonary hypertension increases right ventricular systolic pressure, which can result in right ventricular hypertrophy and strain on the free wall.
In the past, right ventricular function was determined primarily by tricuspid annular plane systolic excursion (TAPSE) measured on standard echocardiography and by tissue Doppler imaging. The main limitations of those two techniques for assessing RV function is that they are both angle dependent. Speckle-tracking analysis is not angle-dependent and therefore has become the most important and accurate tool for the assessment of right ventricular function. ,
Right ventricular global longitudinal strain (RV-GLS) is calculated as the average value of the longitudinal strain in the right ventricular free wall and the right ventricular septum ( Fig. 7.10 ). Normal ranges for RV-GLS are −20% to −25%. Right ventricular fractional area change (RV-FAC) is calculated from the end-diastolic and end-systolic areas of the RV (see Fig. 7.10B ) as follows, in which FAC is the right ventricular fractional area change, EDA is the end-diastolic area of the RV, and ESA is the end-systolic area of the RV:
(A) Four-chamber echocardiographic view with speckle-tracking echocardiography of the right ventricle (RV) outlined in green . The view simultaneously highlights the left ventricle (LV), left atrium (LA), and right atrium (RA), offering a comprehensive evaluation of all cardiac chambers.
(B) Right ventricular fractional area change (RV-FAC) measures the percentage difference in the RV area between end-diastole (orange) and end-systole (green). A reduced RV-FAC indicates impaired right ventricular contraction and function.
(C) Right ventricular global longitudinal strain (RV-GLS) is calculated as the average strain value of the right ventricular free-wall and the right ventricular septal segments. The strain curve illustrates the deformation of the right ventricular myocardium throughout the cardiac cycle. Specific annotations identify the septal and free-wall strain, along with the averaged global strain value. RV-GLS is a sensitive marker for right ventricular systolic function and is particularly valuable in conditions such as pulmonary hypertension and heart failure.
Unlike ejection fraction, RV-FAC reflects area change and has a normal threshold of greater than 35%. RV-FAC is particularly valuable for assessing right ventricular performance in conditions such as pulmonary hypertension, valvular heart disease, and heart failure. Its prognostic capability extends to predicting outcomes such as mortality after pulmonary embolectomy and the progression of heart failure.
Right ventricular free-wall strain (RV-FWS) measures the percentage change in the length of the RV free-wall during systole, providing a regional assessment of right ventricular function. The normal range for RV-FWS in healthy individuals is approximately −29%, with negative values indicating myocardial shortening and contraction. As shown in Fig. 7.11 , strain analysis allows for the visualization of segmental strain and highlights regional abnormalities in the right ventricular free-wall. ,
(A) The apical four-chamber view shows strain measurements in the right ventricular free-wall (RV-FWS) and interventricular septum (IVS). Each segment’s longitudinal strain value is noted, with the basal (−17.4%), mid (−20.3%), and apical (−33.6%) segments illustrating varying degrees of deformation. The strain curve below tracks segmental deformation over time, with distinct curves for the free-wall and septum. These values are averaged to calculate the free-RV-FWS and the right ventricular global longitudinal strain (RV-GLS). Notably, the RV-FWS (−24.1%) is more sensitive to early right ventricular dysfunction than the septal strain (−18.9%), highlighting its utility in clinical evaluation.
(B) The three primary components of right ventricular deformation are illustrated: longitudinal strain (L1), circumferential strain (La), and radial strain (Lr). This diagram underscores the unique contributions of the right ventricular free wall and IVS to overall right ventricular function and highlights the mechanical interplay necessary for effective ventricular performance. RVEW , Right Ventricular Endocardial Wall.
(Modified from Cho EJ, Jiamsripong P, Calleja AM, et al. Right ventricular free wall circumferential strain reflects graded elevation in acute right ventricular afterload. Am J Physiol Heart Circ Physiol . 2009;296(2):H413–420.)
RV-FWS is considered a better indicator of right ventricular function than RV-GLS because it isolates deformation of the free wall, which is most sensitive to pressure and volume overload. In contrast, RV-GLS incorporates septal strain, which may be influenced by left ventricular function and interventricular interactions, thereby limiting its specificity for right ventricular performance.
In conditions such as pulmonary hypertension, significant TR, and RV pressure overload, RV-FWS detects early RV dysfunction even when conventional parameters like TAPSE and fractional area change (RV-FAC) remain normal. This is particularly relevant in patients with severe isolated TR, in whom RV-FWS can reveal subclinical impairment and guide the timing of interventions such as transcatheter tricuspid valve replacement. Severe functional TR, often associated with AF, contributes to right ventricular volume overload, right atrial dilatation, and AF progression. , As TR worsens, the increased preload stretches the RV, and the RV free-wall compensates by increasing contractility, which is reflected in RV-FWS measurements. However, prolonged overload eventually leads to reduced RV-FWS, right ventricular decompensation, and irreversible remodeling. Studies have shown that reduced RV-FWS is associated with worse outcomes in patients with significant TR, including higher rates of right heart failure, AF recurrence, and mortality. Our investigations have demonstrated that patients with DMR and paroxysmal AF (PAF) exhibit significantly worse RV-FWS than those without AF. This highlights the role of right ventricular dysfunction as both a consequence and contributor to atrial remodeling and AF. ,
Chronic volume or pressure overload of the RA caused by TR or pulmonary hypertension leads to right atrial stretch and fibrosis, promoting the development of AF. In turn, the AF usually exacerbates TR because of the loss of atrial function, further increasing right ventricular preload and perpetuating the cycle of right ventricular dysfunction. RV-FWS, as a load-sensitive yet highly reproducible parameter, is uniquely positioned to detect these dynamics early, enabling timely management to break this cycle.
In summary, right ventricular strain analysis, particularly RV-FWS, represents a paradigm shift in the ability to evaluate right ventricular function accurately. By isolating free-wall deformation, RV-FWS provides a more specific and sensitive measure of right ventricular performance than traditional parameters. It plays a critical role in the early detection of right ventricular dysfunction, guiding risk stratification and the timing of interventions in patients with such conditions as TR, pulmonary hypertension, and AF. As the role of the RV in systemic processes becomes clearer, right ventricular strain analysis will continue to shape clinical decision-making processes and improve outcomes.
Left Atrial Strain
The left atrium (LA) is a complex structure consisting of three distinct components, each originating from different embryologic sources: the anterior LA, the posterior (venous) LA, and the LA appendage (LAA). The LA plays an active and dynamic role throughout the cardiac cycle, coordinating closely with the LV (see Fig. 7.2C ).
The atria are far more than simply passive chambers positioned between their venous inlets and respective ventricles. Instead, they function in an interdependent relationship with the ventricles to optimize cardiac performance. Synchronized phasic changes within the atria are crucial to ensuring effective ventricular filling, whether on the left or right side of the heart. , Beyond their mechanical function, the atria also respond to stretching by releasing atrial natriuretic peptide, a hormone with potent diuretic, natriuretic, and vasorelaxant effects.
Unlike ventricular strain, which is typically expressed as a negative percentage because of myocardial shortening during systole, atrial strain is expressed as a positive percentage. This distinction arises from their primary role as capacitance chambers, deforming passively in response to intracavitary pressure and volume rather than through active muscle contraction. However, depending on the chosen methodology and reference points (e.g., R-R or P-P intervals), atrial strain values, particularly during the contractile or conduit phases, may sometimes be negative because of the tracking system’s coordinate setup or analysis of tissue displacement in opposing directions. When using the speckle-tracking method, the analysis examines changes in the position of points on the tissue, which can result in negative values. This is because the system tracks deformation relative to the initial position of the point during contraction and relaxation. In such cases, negative values may indicate that tissue deformation occurs in the opposite direction (e.g., a compressive effect during contraction phases). Negative values can also be associated with the chosen method for analyzing distal tissue deformation. For example, if tissue contraction or tissue displacement is measured in the opposite direction relative to its normal functional position (e.g., opposite in the context of volume increase), it can produce negative results ( Fig. 7.12 ).
(A) The reservoir, conduit, and contractile phases of left atrial function are highlighted on the strain curve to reflect its contribution during the different phases of the cardiac cycle. The images depict the speckle-tracking process used to record strain measurements and quantitatively evaluate LA deformation.
(B) The left atrial strain curve is further analyzed by two different gating methods. R-R gating (top panel) adjusts left atrial strain measurements to align with the R-R interval, and P-P gating (bottom panel) adjusts left atrial strain measurements to align with the P-P interval, emphasizing atrial mechanical function during the complete cardiac cycle. The definitions of (A), (B), and (C) in the R-R gating method and the P-P gating method remain consistent, but the timing of the measurements during the cardiac cycle is different.
(Modified from Sun BJ, Park JH. Echocardiographic measurement of left atrial strain- a key requirement in clinical practice. Circ J . 2021;86(1):6–13.)
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