Applied Echocardiography in Coronary Artery Disease Ravi R Kasliwal, Manish Bansal
INDEX
×
Chapter Notes

Save Clear


1Echocardiographic Techniques Used in the Evaluation of Patients with Coronary Artery Disease
  • Assessment of Left Ventricular Systolic Function
    Shantanu P Sengupta, Bijoy K Khandheria
  • Assessment of Left Ventricular Diastolic Function in Coronary Artery Disease
    SK Parashar
  • Echocardiographic Evaluation of the Right Atrium and Right Ventricle
    Anuj Mediratta, Francesco Maffessanti, Karima Addetia, Roberto M Lang
  • Pharmacologic Stress Echocardiography
    Srikanth Sola
  • Nonpharmacologic Stress Echocardiography
    Asrar Ahmed, Roxy Senior
  • Contrast Echocardiography
    Adrian Chong, Sudhir Wahi
  • Tissue Doppler Imaging and Acoustic Speckle Tracking: Technical Considerations
    Jagdish C Mohan, Vishwas Mohan
2

Assessment of Left Ventricular Systolic FunctionCHAPTER 1

Shantanu P Sengupta,
Bijoy K Khandheria
 
INTRODUCTION
The most important clinical application of echocardiography has been the evaluation of left ventricular (LV) size, volume, and function. The first signals from the human heart were demonstrated by Edler with the use of A-mode and M-mode.1 Edler noted that the echo from the posterior wall of the heart moved anteriorly about 1 cm, and that with aortic valve incompetence, the amplitude of motion of this echo increased. These moving signals from the LV posterior wall and from the posterior mitral annulus were correlated with LV function. He also noticed that when the movement of the heart was well, all parts had greater motion than when cardiac function was globally impaired. Subsequently, Harvey Feigenbaum tried to measure LV systolic function by using an index comprising of the anteroposterior dimension of the heart, measured from the chest wall to the posterior LV signal multiplied by the M-mode excursion of the posterolateral mitral annulus measured from the cardiac apex. This index did not work well in all cases, but it was soon appreciated that, in optimal cases, one could see a signal representing the interventricular septum also. Nonetheless, this index was useful in measuring the LV dimensions. The earlier instruments used did not give consistent information. Subsequent improvements in the echocardiography instrumentation helped in better and consistent signals from blood–endocardial interfaces. These echocardiographic instruments delineated anterior right ventricular wall thickness, right ventricular internal dimension, interventricular septum thickness, internal LV dimension, and posterior LV wall thickness.2 This helped in understanding the cardiac dimensions in real time for the first time noninvasively, which was a reflection of cardiac function.
This was followed by a collaborative study between Feigenbaum and Harold Dodge, which correlated LV volume by angiography with echocardiographic parameters for the first time.3 Successful attempts were made to use the change in the M-mode LV dimension from diastole to systole as an indication of stroke volume in normally shaped hearts; however, the method was not robust in dilated hearts or in presence of regional wall abnormalities.
Subsequently, M-mode echocardiography was used for estimation of LV volume, stroke volume, and wall thickness with good results in clinical situations.4,5 At the end of the M-mode era, the Indiana group developed the technique of M-mode scanning that gave a sense of the shape and function of the LV but failed to record the apex and provided no additional quantitative information. The quest for more consistent measurement of cardiac size and function was a major reason for development of two-dimensional (2D) echocardiography.
 
TWO-DIMENSIONAL ECHOCARDIOGRAPHY
The first B-mode images from the heart were developed from linear array transducers by Bom et al.6 The aggregate image on a display screen produced a 2D echocardiogram. Then a group of scientists from Indiana and others worked out systems for rocking a standard M-mode transducer over a 30-degree angular sector of a circular plane to create a narrow real-time 2D echocardiogram.7 The resulting sector scan was most useful for understanding heart valve disease and pericardial effusion, but the narrow field of view was not optimal for assessing global LV function. Initial studies using this device, however, provided the apical information which was missing in the M-mode scan. Being portable, it helped in assessing significance and complications of acute myocardial infarction.8 Over a period of time, development of this technology increased the angle of view to approximately 60 degrees. Subsequently, the bioengineering group at Duke University (Durham, NC, USA), and later the Varian Corporation (Palo Alto, CA, USA), developed electronic phased-array 2D echocardiographic imaging systems with a field of view of approximately 90 degrees that encompassed the majority of the heart in most patients when scanned from either the anterior chest wall or the cardiac apex.9,10 Once the entire LV could be recorded, more accurate quantitation of LV volume was possible using the dimensions and areas contained in these images in a variety of mathematic models. The simple M-mode anteroposterior LV dimension was a reasonably accurate estimate of LV function in patients with symmetric ventricles.4
Table 1.1   Left ventricular dimensions by 2D echocardiography in males and females
Male
Normal
Mildly dilated
Moderately dilated
Severely dilated
LV diastolic diameter/BSA, cm/m2
2.2–3.0
3.1–3.3
3.4–3.6
>3.6
LV systolic diameter/BSA, cm/m2
1.2–2.1
2.2–2.3
2.4–2.5
>2.5
Female
Normal
Mildly dilated
Moderately dilated
Severely dilated
LV diastolic diameter/BSA, cm/m2
2.3–3.1
3.1–3.3
3.4–3.6
>3.6
LV systolic diameter/BSA, cm/m2
1.3–2.1
2.2–2.3
2.4–2.6
>2.6
Abbreviations: BSA, body surface area; LV, left ventricular.
However, this simple dimension could significantly overestimate or underestimate volume in more irregular ventricles. Hence, the recent chamber guidelines advocate the use of direct 2D linear measurements for quantification of LV internal dimensions, and these values are indexed to body surface area (Table 1.1).11 Addition of the LV long-axis measurement improved accuracy, while addition of area measurements into the formulas for a variety of geometric figures and the ventricular contours in Simpson's rule calculations incrementally increased measurement accuracy.
The most common method for determining LV volumes currently is the Simpson rule or the “disk summation method”. This technique requires recording an apical 4- and 2-chamber view from which the endocardial border is outlined in end-diastole and end-systole. The ventricle is then mathematically divided along its long axis into a series of disks of equal height. Individual disk volume is calculated as height multiplied by disk area where height is assumed to be the total length of the LV long axis divided by the number of segments or disks. The surface area of each disk is determined by the diameter of the ventricle at that point. The ventricular volume is then represented by the sum of the volume of each of the disks which are equally spaced along the long axis of the ventricle (Figure 1.1). If the ventricle is symmetrically contracting, then either the 4- or 2-chamber view will reflect the true ventricular volume. However, in an asymmetrically contracting LV, both the views are needed to obtain accurate volume measurements. In any view, foreshortening of the ventricular apex will result in underestimation of the LV volumes and most often in overestimation of the ejection fraction. The biggest limitation of Simpson's formula is myocardial drop out, which causes difficulty in identifying the endocardial border. Also, many times, the LV apex cannot be easily identified. These can be minimized by the use of contrast to identify the endocardial borders (Figure 1.2).
zoom view
Figure 1.1: Two-dimensional measurements for volume calculations using the biplane method of disks (modified Simpson's rule), in the apical 4-chamber (A4C) and apical 2-chamber (A2C) views at end-diastole (LVEDV) and at end-systole (LVESV). Note the papillary muscles should be excluded from the cavity in the tracing.
Numerous studies have validated the accuracy of 2D volumes and ejection fraction measurements by comparison with a variety of reference standards. However, there are various limitations to this: (i) the acquisition and assumed position of short-axis images along the ventricular long axis were based on internal ventricular landmarks and, thus, might not correspond precisely to the placement assumed by the geometric models, (ii) the placement of the transducer was assumed to be over the LV apex, which was often not the case, resulting in foreshortening of the ventricle, (iii) apical views were assumed to be obtained by rotation around the ventricular long axis and separated by known degrees of rotation, which was not always true, and (iv) in any acquisition format, the majority of the ventricular surface was not recorded and, hence, spatial symmetry had to be assumed. The normal values of LV volumes and thresholds for classification into mild, moderate, and severe dilated LV are provided in Table 1.2.
 
Is Visual Assessment an Alternative?
There is a routine use of visual assessment of LV function in day-to-day practice, for example, by estimating the LV ejection fraction (LVEF) in 5% steps, such as 30–35% or just classifying the LV function as normal, mildly, moderately or severely impaired.5
zoom view
Figure 1.2: Contrast echocardiography helps in better delineation of endocardial border.
Table 1.2   Left ventricular volumes by 2D echocardiography in males and females11
Males
Normal
Mildly dilated
Moderately dilated
Severely dilated
LV diastolic volume/BSA, mL/m2
34–74
75–89
90–100
>100
LV systolic volume/BSA, mL/m2
11–31
32–38
39–45
>45
Female
Normal
Mildly dilated
Moderately dilated
Severely dilated
LV diastolic volume/BSA, mL/m2
29–61
62–70
71–80
>80
LV systolic volume/BSA, mL/m2
8–24
25–32
33–40
>40
Abbreviations: BSA, body surface area; LV, left ventricular.
This is not recommended in the guidelines but is routinely practiced due to time constraints and difficulties in tracing the endocardial borders on still frames. Although visual assessment of global LV systolic function has been reported to be reasonably accurate among experienced readers,12,13 there is still considerable observer variability.14 This does not allow the use of visual assessment for follow-up studies of LVEF and volumes. Furthermore, when compared with cardiac MRI, visual assessment has been shown to result in significant underestimation (8.4%) of LVEF.15 For these reasons, it is recommended to use quantitative analysis for accurate assessment of LV systolic function.
 
Strain Imaging
Strain imaging by speckle-tracking echocardiography (STE) has emerged in last decade as a quantitative imaging tool to evaluate regional and global myocardial function by analyzing the motion of speckles identified by 2D or three-dimensional (3D) sonograms. STE uses non-Doppler, angle-independent, objective quantification of myocardial deformation and LV systolic and diastolic dynamics.16,17 It tracks the displacement of the speckles during the cardiac cycle and generates longitudinal, radial and circumferential strain measurements, and LV twist and torsion.
Strain analysis by STE is principally based on the analysis of speckles during the cardiac cycle. Single speckles are merged in functional units (kernels), which are identifiable given the peculiar disposition of the speckles. Each kernel thus constitutes a sort of ultrasound fingerprint which can be tracked by software during the entire length of the cardiac cycle. The motion is analyzed by the system without using the Doppler signal. This then gives a calculation of displacement, rate of displacement (velocity), deformation (strain) and rate of deformation (strain rate) of the selected myocardial segments, and LV rotation. Assessment is obtained by averaging at least 3 consecutive heart cycles to reduce the noise, setting the frame rate of the routine 2D image acquisition between 60 and 110 frames per second.18 The STE derived measurements have been validated using sonomicrometry and tagged magnetic resonance imaging (MRI), showing high feasibility and reproducibility.19 Potential limitations of this technique are its strict dependence on the frame rate and on high-quality 2D images which are necessary for obtaining an optimal definition of the endocardial border.
 
Strain
Strain is the degree of deformation of the analyzed myocardial segment in relation to its initial dimensions expressed as a percentage. The strain equation (ε) is as follows:
zoom view
where L is the length of the object after deformation, and L0 is the basal length.
By convention, lengthening or thickening deformation is given a positive value, whereas a shortening or thinning deformation is given a negative value.
 
Strain Rate
The strain rate (ε') represents the rate of myocardial deformation expressed as seconds−1. Studies have shown that the strain rate is less dependent on LV load variations than strain. However, because the strain rate signal is noisier and less reproducible, clinical studies still use strain measurements.6
 
Longitudinal Strain
Longitudinal strain represents myocardial deformation directed from the base to the apex in the longitudinal direction. It is a reflection of subendocardial muscle fibers which are predominantly arranged longitudinally. During systole, ventricular myocardial fibers shorten with a translational movement from the base to the apex. Analysis of the longitudinal strain in 4-chamber, 2-chamber, and apical long-axis view helps us in identifying global and regional (17 segments) strain values of the LV (Figure 1.3). Global longitudinal strain has been validated recently as a quantitative parameter of global LV function.
 
Radial Strain
Radial strain represents myocardial deformation toward the center of the LV cavity and thus indicates the LV thickening and thinning motion during the cardiac cycle. Consequently, during systole, radial strain values are always positive curves. Radial strain values are obtained by STE analysis of both basal, mid and apical LV short-axis views.20
 
Circumferential Strain
Circumferential strain represents LV myocardial deformation along the circular perimeter observed on a short-axis view.20 Consequently, during systole, circumferential strain measurements are represented by negative curves. As for longitudinal strain, it is possible to obtain a global circumferential strain value.
 
Twist and Torsion
Earlier, the evaluation of LV twisting had been possible only through MRI. STE has now emerged as a new promising tool for LV twisting analysis.21 LV twisting is a component of the normal LV systolic contraction that arises from the reciprocal rotation of the LV apex and base during systole.22,23 STE helps in quantifying LV twist by analyzing the reciprocal rotation of the LV apex and base during systole. The LV twist is the net difference in mean rotation between the apical and basal levels. The LV torsion is defined as LV twisting normalized with the base-to-apex distance.24
Of all the components of the STE, longitudinal strain has now been standardized and is in clinical use. The major use of longitudinal strain is in coronary artery disease (CAD), assessing subclinical LV dysfunction in various conditions, cancer chemotherapy, various cardiomyopathies, constrictive pericarditis, and understanding LV function in valvular heart disease.
 
THREE-DIMENSIONAL ECHOCARDIOGRAPHY
Earlier acquisition of 3D echocardiography was based on the reconstruction of 2D images.25 The images were obtained along with the cardiac cycle and were positioned in their proper orientation relative to one another. The quality of the 3D images from the reconstruction methods are a function of the quality and number of images used in the reconstruction. The highest quality images are usually obtained using position-sensing devices because they allow each plane to be aligned independently to achieve optimal target definition. Quantitation of LV volume in 3D was shown to be accurate with a minimum of 8 intersecting, nonparallel 2D images.26 Although reconstruction methods are time consuming, important studies have used these approaches to demonstrate the improved accuracy of assessment of LV size and function compared with 2D echocardiography.27,28 In addition, this approach improved our understanding of the shape and spatial relationships of many cardiac structures, such as the mitral valve and its supporting structures.29
zoom view
Figure 1.3: Speckle-tracking echocardiographic analysis of myocardial deformation by longitudinal strain in 17 segments represented as bull's eye map.
Over the years, there has been an evolution in transducer technology to the development of the matrix–array 7transducer. This transducer has elements arranged in a grid, and after transmission of a single pulse can acquire data from many lines of sight simultaneously to reconstruct a volume of ultrasound data in real time. The earliest of these transducers was a sparse array with 256 elements which resulted in limitations in spatial and temporal resolution.28 Currently, these transducers have more than 3,000 elements and enable a 30- to 50-degree volume to be acquired and displayed in real time. Although this is sufficient for visualization of valves, masses, the LV and color Doppler jets, it is typically not a large enough volume. To display and quantify the adult LV, a series of component volumes of the heart are obtained over consecutive cardiac cycles and then combined to obtain a larger volume. Currently, with this approach, 4 or more images are fused resulting in maximal frame rates of 25 Hz.29 In addition, the matrix–array transducer can record multiple individual planes simultaneously (Figure 1.4A to D).
When this full-volume 3D ultrasound data set is initially displayed, only the outer boundaries of the pyramid can be visualized. This provides minimal or no information. To see the cardiac structures, the volume is then cropped in various planes to define the structures. The LV volume can be calculated from the 3D image in several ways.
For defining the LV volume, the endocardial border is traced either manually from selected planes or auto-matically by a border-tracking algorithm. Alternatively, the machine then automatically defines the LV volume both in systole and diastole from which LVEF is obtained.
Compared with single plane and 2D approaches, 3D echocardiography has been shown to represent and quantify LV volumes and function more accurately.30 Although the early 3D reconstruction methods provide important data, real-time 3D acquisition has proven more rapid and hence, practical, for clinical application.
The advantage of LV volume calculation with 3D echocardiography over 2D echocardiography is easily explained by the fact that more of the LV endocardial surface is incorporated into the 3D echocardiographic quantification, the position of the transducer over the cardiac apex can be better appreciated, intersecting planes are precisely aligned, and no assumptions of shape are required.
zoom view
Figure 1.4A to D: A triplane view obtained from apical transducer position with matrix–array transducer. Scan planes 0, 60, and 120 degrees (yellow, white, and green planes, respectively) (A) yield familiar apical 4-chamber, 2-chamber, and long-axis images (B to D). The frame shown is end-systolic.
8As the LV volumes calculated from 3D echocardiograms are more accurate, the LV stroke volume and ejection fraction derived from these volumes are also more accurate (Figure 1.5).30 This improved accuracy, which is helpful in patients with ventricles that are distorted in shape and in those with regional wall-motion abnormalities caused by CAD. Despite the advantages of 3D echocardiography, there are the following few limitations: (i) image quality is often poor, because despite parallel processing, the line density within the 3D volume is much lower than in a 2D image and more interpolation is necessary, (ii) when the 3D volume is acquired from a fixed point many of the targets within the volume will not be optimally aligned to produce strong echoes and, thus, may be either missing or poorly recorded, (iii) when the entire LV is reconstructed from multiple subvolumes, arrhythmias and respiration can cause movement of the heart between cycles and result in artifacts in the images (stitch artifacts), and (iv) although acquisition time for one volume is much less than for multiple planes, the analysis time to this point has limited general application, and the technique has been primarily used in research studies. It can be anticipated that over the time, 3D image quality will improve, as has been the case with 2D images.
 
ASSESSMENT OF REGIONAL MYOCARDIAL CONTRACTION
Since CAD typically affects the myocardium regionally, regional assessment of LV systolic function is of paramount importance in the evaluation of CAD. It not only helps in assessing the extent of myocardial damage, but more importantly, also provides information about the coronary artery involved in the disease process.
Regional LV systolic function is commonly assessed by dividing the LV into 17 segments, a scheme that is agreed to by the echocardiographic, nuclear and magnetic resonance communities. The LV is divided into 6 walls: anterior, anteroseptal, inferoseptal, inferior, inferolateral, and anterolateral. Each wall is divided into basal, mid and apical segments (except for the anteroseptal and the inferolateral walls which are divided only into basal and mid segments), and the apical cap represents the 17th segment (Figure 1.6). In the earlier schemes, apical cap was not recognized as a separate segment, resulting in a 16-segment model.
zoom view
Figure 1.5: Example of left ventricular volume assessment by 4D auto-learning vector quantization software. The endocardial border is automatically detected in three dimensions throughout the cardiac cycle.Abbreviations: 4D, four-dimensional (same as three-dimensional); CO, cardiac output; EF, ejection fraction; HR, heart rate; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; SV, stroke volume.
9
zoom view
Figure 1.6: Approach to left ventricular myocardial segmentation for regional function assessment. The 17-segment model is depicted here. Please note the anteroseptal and the inferolateral walls are divided into two segments (basal and mid) only.
Several echocardiographers continue to use the 16-segement model for LV segmentation, both because of their familiarity with the earlier model and also because of the arguments that the apical cap is beyond the LV cavity and does not really take part in the LV cavity shortening during systole.
Regardless of the model used, each myocardial segment is visually assessed for the extent of endocardial thickening and is classified as normokinetic, hypokinetic (reduced thickening), akinetic (negligible or no thickening at all), or dyskinetic (systolic thinning or stretching). When there is resting outpouching of a myocardial segment during diastole, it is termed as aneurysm. A semiquantitative wall-motion score can also be assigned to each myocardial segment from 1 (normal) to 4 (dyskinetic/aneurysmal), depending on the extent of endocardial thickening.11 The average of the scores of all analyzed segments provides wall-motion score index (WMSI), which is a semiquantitative measure of overall LV systolic function. Higher is the WMSI, worse is the LV systolic function. This method of regional LV systolic function assessment is obviously observer dependent and has changed little from the initial descriptions of wall-motion abnormalities by echocardiography.31
The 17-segment model can also be applied to longitudinal strain analysis by 2D STE which is depicted as bull's-eye imaging (See Figure 1.3). However, most STE software use 18-segment model to divide the LV, in which each myocardial wall (including the anteroseptal and the inferolateral walls) is divided into basal, mid and apical segments. Although STE-based regional function assessment still suffers considerable variability, STE would generally show lower longitudinal strain value in areas of ischemia/infarction (Figure 1.7A and B). Further improvements in these newer echocardiographic modalities providing novel insights into myocardial structure may dramatically change the way we assess LV regional systolic function.
Since the regional wall-motion abnormalities in CAD follow distribution of coronary vascular supply, the pattern of regional myocardial dysfunction helps identify the affected coronary artery (Videos 1.1 and 1.2). The anteroseptum, anterior wall, apex, and mid-segments of the inferoseptal and the anterolateral walls are generalized supplied by the left anterior descending coronary artery; posterolateral wall and the basal anterolateral segment are usually supplied by the left circumflex artery; and the inferior wall and the basal inferoseptal segment are supplied by the right coronary artery. However, variations are common in this segmental distribution, depending on whether it is a right-dominant system or is left-dominant and also because of the differences in the sizes of the three coronary arteries and their major branches. The atypical distribution of wall-motion abnormalities are also common in patients with previous coronary artery bypass surgery in whom dual sources of blood supply (i.e. native and grafts) alter the myocardial blood-supply pattern.
While regional wall-motion abnormalities are considered to be the sine qua non of CAD, it should be remembered that various noncoronary diseases may also produce regional LV systolic dysfunction. These include intra-ventricular conduction abnormalities (bundle-branch blocks, accessory pathways, paced ventricular rhythms, etc.), post-pericardiotomy state, constrictive pericarditis, right ventricular pressure and volume overload, systemic illnesses, such as sarcoidosis, hemochromatosis, etc., and even nonischemic dilated cardiomyopathy (Videos 1.3 and 1.4). However, there are several important clues that can help in differentiating true ischemic wall-motion abnormalities from those seen in the nonischemic conditions. Atypical distribution of the wall-motion abnormalities not conforming to any particular vascular territory, abnormal myocardial motion but preserved myocardial thickening and the wall-motion abnormalities confined only to a brief period of cardiac cycle generally favor nonischemic etiology as the underlying cause.10
zoom view
Figure 1.7A and B: (A) Strain echocardiography of a patient with inferior wall myocardial infarction because of right coronary obstruction. (B) Strain echocardiography due to left anterior descending artery occlusion causing anterior wall myocardial infarction.
 
FUTURE DIRECTIONS
With the advent of time and advances, future machines will see a reduction in the size of many of the components of the echocardiography machine. The future will undoubtedly see a new model of clinical cardiology care that incorporates the equivalent of an ultrasound stethoscope. In addition, as investigators continue to make advances in understanding the molecular and genetic controls over cardiac physiology and disease, they will look to noninvasive imaging with echocardiography to assist in these correlations. Thus, echocardiographic assessment of LV function will be crucial in assessing the results of pharmacologic, molecular, and genetic manipulations of the failing heart to determine whether observations at the bench can be translated to effective therapies in patients.32,33
 
SUMMARY
Comprehensive and precise assessment of LV systolic and diastolic function is important and one of the most common indications for performing echocardiography in cardiovascular practice. Echocardiography readily assesses LV systolic function; its advantages include that echocardiography is noninvasive, does not require radiation, is portable, rapid, readily available and in competent hands, can provide an accurate and comprehensive assessment of LV systolic and diastolic function. Assessment of LV systolic function is important for diagnosis, prognostication, planning the treatment modality, and for monitoring response to treatment. Echocardiography is widely used to provide vital parameters of LV function, such as ejection fraction, wall-motion score indices, LV volumes, and regional wall-motion assessment. This chapter focuses on the evolution of various echocardiographic methods used in the assessment of LV systolic function.
 
VIDEO LEGENDS
Video 1.1
Apical 4-chamber view in a patient with previous myocardial infarction. Left ventricular apex and distal parts of mid-inferoseptal and mid-anterolateral segments are akinetic, consistent with involvement of the left anterior descending coronary artery. Left ventricular apical thrombus is also present.
Video 1.2
Apical 2-chamber view in a patient with inferior wall myocardial infarction demonstrating akinesia of basal and mid-inferior wall.
Video 1.3
Typical septal bounce in a patient with chronic constrictive pericarditis. Marked thickening of the pericardium in the posterior region can also be easily appreciated.
Video 1.4
Apical 4-chamber view in a patient with nonischemic dilated cardiomyopathy. Although there is global left ventricular hypokinesia, basal and mid-inferoseptal segments are almost akinetic, giving an impression of regional involvement.
REFERENCES
  1. Edler I. The diagnostic use of ultrasound in heart disease. Acta Med Scand Suppl. 1955;308:32.
  1. Popp RL, Wolfe SB, Hirata T, et al. Estimation of right and left ventricular size by ultrasound. A study of the echoes from the interventricular septum. Am J Cardiol. 1969;24:523–30.
  1. Feigenbaum H, Popp RL, Wolfe SB, Troy BL, Pombo JF, Haine CL, et al. Ultrasound measurements of the left ventricle. A correlative study with angiocardiography. Arch Intern Med. 1972;129:461–7.
  1. Popp RL, Filly K, Brown OR, et al. Effect of transducer placement on echocardiographic measurement of left ventricular dimensions. Am J Cardiol. 1975;35:537–40.
  1. Popp RL. Echocardiographic evaluation of left ventricular function. N Engl J Med. 1977;296:856–8.
  1. Bom N, Hugenholtz PG, Kloster FE, Roelandt J, Popp RL, Pridie RB, et al. Evaluation of structure recognition with 11the multiscan echocardiograph. A cooperative study in 580 patients. Ultrasound Med Biol. 1974;1:243–52.
  1. Griffith JM, Henry WL. A sector scanner for real time two-dimensional echocardiography. Circulation. 1974;49:1147–52.
  1. Weyman AE, Peskoe SM, Williams ES, et al. Detection of left ventricular aneurysms by cross-sectional echocardiography. Circulation. 1976;54:936–44.
  1. Von Ramm OT, Thurstone FL. Thaumascan: Design considerations and performance characteristics. In: White D (Ed): Ultrasound in Medicine. Plenum Press;  New York, NY: 1975. pp 373–8.
  1. Tajik AJ, Seward JB, Hagler DJ, et al. Two-dimensional real-time ultrasonic imaging of the heart and great vessels. Technique, image orientation, structure identification, and validation. Mayo Clin Proc. 1978;53:271–303.
  1. Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1–39.
  1. Gudmundsson P, Rydberg E, Winter R, Willenheimer R. Visually estimated left ventricular ejection fraction by echocardiography is closely correlated with formal quantitative methods. Int J Cardiol. 2005;101:209–212.
  1. Jensen-Urstad K, Bouvier F, Hojer J, et al. Comparison of different echocardiographic methods with radionuclide imaging for measuring left ventricular ejection fraction during acute myocardial infarction treated by thrombolytic therapy. Am J Cardiol. 998;81:538–544.
  1. Blondheim DS, Beeri R, Feinberg MS, Vaturi M, Shimoni S, Fehske W, et al. Reliability of visual assessment of global and segmental left ventricular function: a multicenter study by the Israeli Echocardiography Research Group. J Am Soc Echocardiogr. 2010;23:258–64.
  1. Sievers B, Kirchberg S, Franken U, Puthenveettil BJ, Bakan A, Trappe HJ. Visual estimation versus quantitative assessment of left ventricular ejection fraction: A comparison by cardiovascular magnetic resonance imaging. Am Heart J. 2005;150:737–742.
  1. Perk G, Tunick PA, Kronzon I. Non-Doppler two-dimensional strain imaging by echocardiography—from technical considerations to clinical applications. J Am Soc Echocardiogr. 2007;20:234–43.
  1. Geyer H, Caracciolo G, Abe H, Wilansky S, Carerj S, Gentile F, et al. Assessment of myocardial mechanics using speckle tracking echocardiography: fundamentals and clinical applications. J Am Soc Echocardiogr. 2010;23:351–369; Erratum in: J Am Soc Echocardiogr. 2010;23:734.
  1. Serri K, Reant P, Lafitte M, Berhouet M, Le Bouffos V, Roudaut R, et al. Global and regional myocardial function quantification by two-dimensional strain: application in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2006;47:1175–81.
  1. Amundsen BH, Helle-Valle T, Edvardsen T, Torp H, Crosby J, Lyseggen E, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol. 2006;47:789–93.
  1. Saito K, Okura H, Watanabe N, Hayashida A, Obase K, Imai K, et al. Comprehensive evaluation of left ventricular strain using speckle tracking echocardiography in normal adults: comparison of three-dimensional and two-dimensional approaches. J Am Soc Echocardiogr. 2009;22:1025–30.
  1. Takeuchi M, Nakai H, Kokumai M, Nishikage T, Otani S, Lang RM. Age-related changes in left ventricular twist assessed by two-dimensional speckle-tracking imaging. J Am Soc Echocardiogr. 2006;19:1077–84.
  1. Buckberg G, Hoffman JI, Mahajan A, et al. Cardiac mechanics revisited: the relationship of cardiac architecture to ventricular function. Circulation. 2008;118:2571–87.
  1. Sengupta PP, Khandheria BK, Korinek J, Jahangir A, Yoshifuku S, Milosevic I, et al. Left ventricular isovolumic flow sequence during sinus and paced rhythms: new insights from use of high-resolution Doppler and ultrasonic digital particle imaging velocimetry. J Am Coll Cardiol. 2007;49:899–908.
  1. Rüssel IK, Götte MJ, Bronzwaer JG, Knaapen P, Paulus WJ, van Rossum AC. Left ventricular torsion: an expanding role in the analysis of myocardial dysfunction. JACC Cardiovasc Imaging. 2009;2:648–55.
  1. Dekker DL, Piziali RL, Dong E Jr. A system for ultrasonically imaging the human heart in three dimensions. Comput Biomed Res. 1974;7:544–53.
  1. King DL, Harrison MR, King DL Jr, Gopal AS, Martin RP, DeMaria AN. Improved reproducibility of left atrial and left ventricular measurements by guided three-dimensional echocardiography. J Am Coll Cardiol. 1992;20:1238–45.
  1. Levine RA, Handschumacher MD, Sanfilippo AJ, Hagege AA, Harrigan P, Marshall JE, et al. Three-dimensional echocardiographic reconstruction of the mitral valve, with implications for the diagnosis of mitral valve prolapse. Circulation. 1989;80:589–98.
  1. Snyder JE, Kisslo J, von Ramm O. Real-time orthogonal mode scanning of the heart. I. System design. J Am Coll Cardiol. 1986;7:1279–85.
  1. Corsi C, Lang RM, Veronesi F, Weinert L, Caiani EG, MacEneaney P, et al. Volumetric quantification of global and regional left ventricular function from real-time three-dimensional echocardiographic images. Circulation. 2005;112:1161–70.
  1. Fleming SM, Cumberledge B, Kiesewetter C, et al. Usefulness of real-time three-dimensional echocardiography for reliable measurement of cardiac output in patients with ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 2005;95:308–10.
  1. Heger JJ, Weyman AE, Wann LS, et al. Cross-sectional echocardiography in acute myocardial infarction: detection and localization of regional left ventricular asynergy. Circulation. 1979;60:531–8.
  1. Hataishi R, Rodrigues AC, Neilan TG, Morgan JG, Buys E, Shiva S, et al. Inhaled nitric oxide decreases infarction size and improves left ventricular function in a murine model of myocardial ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2006;291:H379–84.
  1. Neilan TG, Blake SL, Ichinose F, Raher MJ, Buys ES, Jassal DS, et al. Disruption of nitric oxide synthase 3 protects against the cardiac injury, dysfunction, and mortality induced by doxorubicin. Circulation. 2007;116:506–14.