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J Am Coll Cardiol Img, 2008; 1:787-800, doi:10.1016/j.jcmg.2008.09.002
© 2008 by the American College of Cardiology Foundation
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From Pictures to Practice Paradigms

Echocardiography in Hypertrophic Cardiomyopathy

The Role of Conventional and Emerging Technologies

Luis C. Afonso, MD, FACC*, Juan Bernal, MD*, Jeroen J. Bax, MD{dagger}, Theodore P. Abraham, MD, FACC{ddagger},*

* Division of Cardiology, Wayne State University, Detroit, Michigan
{dagger} Division of Cardiology, University of Leiden, the Netherlands
{ddagger} Division of Cardiology, Johns Hopkins University, Baltimore, Maryland


   Abstract
Top
 Abstract
General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
Hypertrophic cardiomyopathy is a relatively common inherited cardiomyopathy that is occasionally challenging to differentiate from hypertensive heart disease and athlete hearts on the basis of morphologic or functional abnormalities alone. Echocardiography has traditionally played a preeminent role in the diagnosis, formulation of management strategies, and the prognostication of this complex disease. In this review, we briefly profile the utility and pitfalls of established echocardiographic modalities and discuss the evolving role of novel echocardiographic imaging modalities such as tissue Doppler, Doppler-based strain, 2-dimensional strain (speckle tracking imaging), and 3-dimensional imaging in the assessment of hypertrophic cardiomyopathy.

Key Words: hypertrophic cardiomyopathy • strain imaging • tissue Doppler

Abbreviations and Acronyms
  {varepsilon} = systolic myocardial strain
  CMR = cardiac magnetic resonance
  HCM = hypertrophic cardiomyopathy
  LA = left atrial
  LV = left ventricular
  LVH = left ventricular hypertrophy
  LVOT = left ventricular outflow tract
  Sa = systolic mitral annular tissue velocity
  SAM = systolic anterior motion
  SR = strain rate
  SRI = tissue Doppler-based strain imaging (SRI)
  TDI = tissue Doppler imaging
  3D-E = 3 dimensional echocardiography

Hypertrophic cardiomyopathy (HCM) is a genetically heterogeneous disease resulting from sarcomeric protein mutations (1–6) and characterized by inappropriate myocardial hypertrophy (without identifiable etiology), interstitial fibrosis, myofiber disarray, disorganized myocardial architecture, and impaired left ventricular (LV) performance (7). This complex condition, typified by phenotypic and clinical diversity, tends to afflict patients of all ages.

Historically, 2-dimensional (2D), M-mode, and Doppler echocardiography have been key to the noninvasive diagnosis of HCM. Together, these fundamental modalities allow for a composite assessment of the morphology, structural abnormalities, and hemodynamic disturbances in HCM, some of which have profound prognostic value (8,9).

Although global systolic function is typically preserved or hyperdynamic in HCM (10), magnetic resonance myocardial tagging studies first demonstrated heterogeneity of myocardial deformation in HCM, reflecting regional variations in myofiber disarray and fibrosis characteristic of this condition (11,12).

Left ventricular contraction is characterized by complex 3-dimensional (3D) deformation of the myocardium, including longitudinal myofiber shortening, radial thickening, circumferential shortening and LV twist or torsion (i.e., basal clockwise rotation coupled with apical anticlockwise rotation when viewed from the apex). After ejection, recoil of torsional deformation results in untwisting coincident with isovolumic relaxation and generates the ventricular suction force that accompanies early diastolic relaxation (13). The myocardium is composed of a highly aligned continuum of muscle fibers whose orientation relative to the long axis of the ventricle depends on their transmural location. Although midmyocardial fibers maintain a predominantly circumferential orientation, the epicardial helical fibers course obliquely toward the apex whereas subendocardial helical fibers course obliquely to the base (14). This geometrical orientation of myofibers allows for maximal fiber strain homogeneity during ejection (15).

The evolution of newer ultrasound-based technologies such as tissue Doppler, strain imaging, speckle tracking-based LV torsion analysis, and 3D echocardiography (3D-E) has revolutionized the assessment of cardiac performance from mere assessment of ejection fraction to a more sophisticated appraisal of regional cardiac mechanics (16–19). Specifically, the complex deformations that constitute systolic contraction, including ventricular twist; longitudinal, circumferential, and radial displacement; velocities; strain; and strain rate can now be reliably quantified (20–25). These novel technologies have provided profound mechanistic insight into abnormalities of regional contractility and diastolic function and have enabled the noninvasive characterization of abnormal intramural myocardial mechanics emblematic of HCM. In addition, these advances have facilitated preclinical diagnosis (26,27), refined risk stratification (28–30), and furthered our understanding of existing therapies for HCM (31,32). In this review, we briefly discuss conventional echocardiographic techniques and elaborate on the evolving role of newer echo imaging modalities in the assessment of HCM.


   General Considerations
Top
 Abstract
 General Considerations
Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
Hypertrophic cardiomyopathy is characterized by asymmetric left ventricular hypertrophy, typically involving the septum, but almost any myocardial segment may be involved. Compared with nonapical variants, the apical hypertrophic phenotype has a reputation for being misdiagnosed or under-recognized on 2D echocardiography (33). Septal thickness >15 mm and a septal to posterior free wall ratio (interventricular septum/posterior wall ratio) >1.3 have been traditionally considered time-honored diagnostic criteria for the diagnosis of asymmetrical septal hypertrophy (34). It is important to recognize however, that asymmetric left ventricular hypertrophy (LVH) in itself is not pathognomonic of HCM but may be encountered in a variety of congenital or acquired conditions, including right ventricular hypertension, systemic hypertension, aortic stenosis, septal sarcomas, Fabry disease, Freidreich's ataxia, mucopolysaccharide or glycogen storage disorders, amyloidosis and, on occasion, mistakenly diagnosed as a result of technical challenges inherent with cross-sectional imaging (35).


   Systolic Anterior Motion (SAM)
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
Systolic anterior motion of the anterior mitral leaflet with or without a pressure gradient across the left ventricular outflow tract (LVOT), although not pathognomonic, is highly indicative of HCM, with a specificity approaching 98% (Fig. 1B) (36). Initially, believed to be due to a "Venturi" effect, it has now been demonstrated that hydrodynamic "drag" or the "pushing" force of flow might be the dominant operant mechanism, based on temporal observations of flow and dynamic cross-sectional analysis of mitral apparatus geometry (37). Of note, SAM may also be encountered in assorted conditions such as transposition of great vessels, hypercontractile states, after mitral valve repair, anomalous papillary muscle insertion, anteroapical infarction with hyperkinetic basal segments and, elderly women with LVH/sigmoid septum and hyperdynamic ventricular function (38).


Figure 1
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  		Figure 1 Characteristic Echocardiographic Features of Obstructive HCM

(A) Parasternal long-axis view depicting severe asymmetric septal hypertrophy and systolic anterior mitral valve motion (arrowhead); (B) M-mode across the mitral leaflets depicting prominent systolic anterior motion (thick arrows) of the anterior mitral leaflet (SAM); (C) M-mode tracing across the aortic valve demonstrating partial closure of aortic leaflets (arrowheads); and (D) accentuation of late-peaking dynamic left ventricular outflow tract obstruction after the Valsalva maneuver. Ao = aorta; HCEM = hypertrophic cardiomyopathy; IVS = interventricular septum; LA = left atrium; SAM = systolic anterior motion; PW = posterior wall ratio

 

   LVOT or Subaortic Obstruction
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
Resting LVOT obstruction, defined as a peak gradient >30 mm Hg, has prognostic significance and is a strong predictor of death (related to HCM) and progression to heart failure (39). Doppler interrogation across the LVOT in dynamic obstructive HCM results in a characteristic signal with a late-peaking dagger-shaped appearance (Fig. 1D) (40,41) A midsystolic decrease in LV ejection velocity is observed in some patients with severe obstruction, giving rise to the characteristic "lobster claw" Doppler tracing abnormality (42), and is caused by a truncation of LV longitudinal segmental shortening (43). Most individuals with HCM do not exhibit resting obstruction. In symptomatic individuals with resting gradients <30 mm Hg, attempts to provoke hemodynamic obstruction either by administering amyl nitrite, upright exercise, or the Valsalva maneuver should be pursued. Midsystolic notching, aortic valve preclosure (Fig. 1C), coarse systolic fluttering of the aortic valve, and fibrotic septal changes at the level of leaflet-septal contact are related echocardiographic features in obstructive HCM.


   Systolic Dysfunction
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
Systolic function typically is normal or supernormal in obstructive and nonobstructive variants of HCM when ejection fraction or fractional shortening (radial contractile function) is used as a metric. Ejection fraction usually is preserved (10) despite significant impairment of longitudinal contractile function, evidenced by attenuation in systolic annular velocities, strain and strain rate (44). With the use of strain imaging, it is now possible to spatially map and identify regional heterogeneity in contractile function, an important advance in our understanding of deranged myocardial mechanics in HCM.

Terminally in the disease process, myocardial fibrosis may result in progressive impairment of systolic function (end-stage HCM) (45). This transformation is characterized by myocardial thinning, systolic impairment, cavity dilation and variably attributed to fibrotic changes in the intercellular matrix, ischemia, infarction, and small vessel disease. Deterioration of systolic function has also been associated with increased mortality (up to 11% per year) and sudden cardiac death (45).


   Diastolic Dysfunction
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 
A reduction of chamber compliance (increased LV mass) and increased stiffness (myocardial fibrosis) coupled with a reduction of ventricular volume and suction play a role in the pathophysiology of diastolic dysfunction in patients with HCM. Likewise, regional asynchrony, post-systolic shortening, and heterogeneity of relaxation appear to be important underlying contributory mechanisms. Doppler echocardiography allows the characterization of diastolic abnormalities in HCM, mostly indicating impaired myocardial relaxation regardless of symptoms or the presence of LV outflow obstruction (46). Nishimura et al. (47) initially showed that conventional Doppler parameters such as mitral E velocity deceleration time and ratio of early to late diastolic filling do not accurately correlate with LV filling pressures in HCM. Subsequently, Doppler-derived diastolic function parameters such as the E/E' ratio (using lateral annular tissue Doppler velocities), color M-mode–derived flow propagation velocity (estimated by shifting the Nyquist baseline until a distinct color border is obtained and then measuring the slope of its most linear component past the valve leaflets), E/flow propagation velocity ratio, but not pulmonary venous velocity parameters, were shown to correlate reasonably well with invasive measurements of pre-A LV end-diastolic pressure (48). These parameters also reliably predict exercise tolerance (49) and reductions in filling pressure post-septal ablation or myectomy (50). However, the authors of a recent study of symptomatic patients with HCM found that E/E' (irrespective of whether medial and lateral annular velocities were used) overall correlated modestly with invasively derived mean left atrial pressure but was less accurate in precisely predicting LV filling pressure in individual patients (51). In this study, approximately 25% of patients with E/E' >15 had left atrial pressure measurements of <15 mm Hg, illustrating the relative lack of specificity of this ratio in determining filling pressure in the setting of HCM compared with its established utility in other populations (52).


   Left Atrial (LA) Enlargement in HCM
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
Novel Techniques
 Conclusions
 REFERENCES
 
LA volume is largely determined by the presence of diastolic dysfunction (severity and chronicity of LA pressure elevation), mitral regurgitation, and atrial myopathy. Although LA enlargement as assessed from linear dimensions was shown to independently predict long-term prognosis in patients with HCM (53) and post-myectomy survival in patients with obstructive HCM (54), it is important to recognize that linear dimensions, particularly anteroposterior measurements of the LA, may misrepresent true LA size, because this chamber frequently remodels asymmetrically (55). Volume determinations circumvent this inherent limitation and have been demonstrated to correlate better with cardiovascular outcomes. The American Society of Echocardiography recommends indexing LA volume (derived from biplane area length or method of disks) to body surface area for quantification of LA size (normal indexed LA volume = 22 ± 6 ml/m2) (56). LA volume has been found to be a long-term independent indicator of functional capacity (57) and an LA volume index of >34 ml/m2 has been shown to be predictive of a greater degree of LVH, severity of diastolic dysfunction, and adverse cardiovascular outcomes (58). Echocardiographic indices of left atrial filling and relaxation (atrial mechanical function) have also been shown to be impaired in HCM in contrast to other secondary forms of LVH, implicating a more generalized myopathic process, not necessarily restricted to the LV myocardium (atrial myopathy) (58).


   Novel Techniques
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
Conclusions
 REFERENCES
 
Tissue Doppler Imaging (TDI).   TDI, a relatively new echocardiographic modality developed for clinical use, measures high-amplitude, low-velocity signals of myocardial tissue motion (18). This Doppler-based technique allows real-time quantification of axial or longitudinal myocardial function. During the cardiac cycle, the apex remains stationary relative to the mitral annulus. Annular displacements toward the apex in systole and away from the apex in diastole represent surrogate measures of longitudinal ventricular contraction and relaxation, respectively.

TDI can be performed in pulse wave or color mode. In pulse wave interrogation, a sample volume is placed within the ventricular myocardium, immediately adjacent to the medial or lateral annulus to record systolic and diastolic myocardial velocities. Color TDI allows color coding of myocardial velocities superimposed on a 2D gray-scale or M-mode image. As the result of higher spatial resolution, multiple structures or segments can be visualized simultaneously in a single field of view.

Systolic myocardial velocity, a measure of longitudinal systolic function, has been shown to be attenuated in HCM, even in nonhypertrophied ventricular segments (59). Early diastolic mitral annular velocity is a pre-load–independent index for evaluating diastolic function. Early mitral annular velocities are reduced in patients with HCM compared with age-matched controls and relate to the magnitude of ventricular hypertrophy (49).

Useful diagnostic (26,60,61) as well prognostic (62) information has emerged from clinical studies assessing the role of TDI in patients with HCM. First, Nagueh et al. (26) investigated myocardial velocities in genotype-positive individuals with HCM in the absence or presence of LVH. Compared with normal controls, all individuals with HCM presented significantly reduced systolic tissue velocities (Sa) and early diastolic tissue velocities at both corners of the mitral annulus. Most importantly, mutation positive subjects without evidence of echocardiographic LVH were accurately identified by a Sa TDI velocity of <13 cm/s in the lateral mitral annulus with a sensitivity of 100% and a specificity of 93%. These investigators also reported on the utility of TDI to predict the development of manifest HCM in mutation positive subjects with reduced TD velocities on follow-up (27).

The use of TDI also can assist in differentiating between variants of LVH. Vinereanu et al. (19) used TDI to distinguish pathological from physiological LVH in a study comprising patients with HCM, patients with systemic hypertension, athletes, and normal subjects. Preserved peak systolic annular velocities help discriminate physiologic LVH from pathologic variants of LVH, whereas heterogeneity of systolic mitral annular velocities enable the differentiation of HCM (low velocities, high heterogeneity) from hypertensive LVH (low velocities, low heterogeneity) (19). The authors proposed a mean systolic annular motion Sa <9 cm/s for differentiating pathological LVH (HCM/hypertensive LVH) from physiological LVH (diagnostic accuracy of 92%).

A significant negative correlation also has been observed between TDI Sa (peak systolic), early diastolic mitral annular velocities, and LVOT peak gradient, underscoring the influence of LVOT obstruction on longitudinal myocardial performance (62). In a recent report of patients with established HCM, low lateral mitral annular systolic velocity (<4 cm/s) was found to have prognostic value and independently predicted death or hospitalization for worsening heart failure (63).

Tissue Doppler interrogation permits quantification of velocity vectors parallel to the ultrasound beam but being a Doppler-based technique, is limited by its inherent inability to appraise regions nonparallel to the ultrasound beam (angle-dependence). Consequently, the utility of pulsed wave TDI in the assessment of regional longitudinal myocardial velocities is restricted to the apical views (64). Although TDI provides an assessment of regional myocardial function, it measures absolute tissue velocities and not myocardial deformation (Figs. 2A and 2B) and is therefore influenced by cardiac translational motion and tethering (65,66). These limitations led to the development of more sophisticated echocardiographic techniques, including TDI-derived myocardial strain and strain rate imaging, which hinge on analysis of relative changes in tissue Doppler velocities obtained using TDI.


Figure 2
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  		Figure 2 Tissue Doppler Imaging (TDI) and TDI-Derived Strain Assessment in Patients With HCM

(A) Myocardial tissue Doppler velocity tracings from 4 representative regions of interest (ROIs) in a patient with HCM. Note significantly attenuated systolic and early diastolic velocities from disparate ROIs in the septum. (B) Tissue Doppler-derived longitudinal strain curves in the same areas shown in (A) and corresponding parametric color strain map. Note positive longitudinal strain (systolic lengthening) or "paradoxical strain" (blue and green tracings) in 2 of the 4 depicted ROIs (basal septum) and attenuated longitudinal strain elsewhere (yellow tracing). Note striking heterogeneity of strain tracings in contrast to tissue Doppler data. AVO = aortic valve opening, AVC = aortic valve closure; other abbreviations as in Figure 1.

 
The use of TDI-derived strain in the assessment of HCM.   Although TDI was initially advocated as a technique for assessing regional myocardial performance, its inability to discern myocardial contractility from passive motion led to the development of strain imaging. In contradistinction to TDI, which examines myocardial motion relative to the transducer, strain assesses myocardial motion relative to the adjacent myocardium (20).

Systolic myocardial strain ({varepsilon}) is a dimension-less quantity and a measure of tissue deformation. When the left ventricle contracts, the myocardium shortens longitudinally and circumferentially (negative strain) and lengthens or thickens in the radial direction (positive strain). Strain rate (SR) represents the local rate of myocardial deformation (67). Unlike tagged cardiac magnetic resonance (CMR), tissue Doppler-based strain imaging (SRI) allows for the accurate estimation of regional myocardial deformation with high spatial and temporal resolution. The discriminatory value of SRI over TDI for the assessment of regional myocardial function is widely recognized and was elegantly demonstrated in an experimental model of intracoronary alcohol septal ablation that compared TDI and SRI measurements before and after ablation therapy (32). In contrast to TDI, SRI after ablation accurately identified areas of discrete regional infarction, reiterating its superiority over TDI for the objective quantification of regional dysfunction.

TDI-derived strain was first used for the evaluation of HCM by Weidemann et al. (68) in a case report of a child with nonobstructive HCM. Tissue Doppler velocities were found to be normal in all the septal segments interrogated. However, systolic longitudinal {varepsilon} as well as SR were significantly decreased "more positive" ({varepsilon} –9%; SR = –0.9 s–1) in the mid septal region with no significant changes in the basal ({varepsilon} –19%; SR = –1.8 s–1) or apical ({varepsilon} –23%; SR = –1.6 s–1) regions when compared with normal values obtained from 30 healthy children. Subsequently, Yang et al. (69) reported the assessment of regional myocardial function in 31 adults with HCM diagnosed echocardiographically. Longitudinal strain {varepsilon} was estimated at the basal, mid, and apical segments of the septal and lateral walls. It was significantly reduced in the septal segments of patients with HCM compared with control patients. More importantly, within the septum, mid-septum {varepsilon} was significantly diminished and "less negative" compared with basal and apical segments (–1.3 ± 8.2% vs. –12.2 ± 8.7% and –17.3 ± 10.4%, respectively). In fact, in 54% of the patients with HCM, {varepsilon} had a positive value (paradoxical systolic expansion) (Fig. 2B). A significant correlation was observed between the extent of midseptal {varepsilon} abnormality and the well-accepted interventricular septum/posterior wall ratio, (r = 0.81, p < 0.01). Midseptal thickness was significantly greater in segments with positive interventricular septal {varepsilon} compared with those with negative {varepsilon}. This study, along with the case reported by Weidemann et al. (68), highlight the relevance of myocardial disarray and fibrosis on regional performance (rapidly and reproducibly detected by strain imaging), because the commonly affected midseptum typically shows the greatest degree of dysfunction.

Longitudinal deformation abnormalities in HCM often are focal or subsegmental and may be underestimated when conventional segmental techniques are used to estimate myocardial strain. Sengupta et al. (70) compared {varepsilon} values using a conventional technique to linear mapping in 20 healthy volunteers and 20 individuals with HCM. Fifteen of the HCM patients had asymmetrical septal hypertrophy, while 5 had generalized hypertrophy. With the conventional technique paradoxical strain (systolic lengthening) was encountered in 45% of the HCM patients presenting at least 1 segment of "positive" strain. In contrast, linear mapping detected "positive strain" in 80% of the population studied, remarkably enhancing the yield of this diagnostic tool. Additionally, linear mapping identified post-systolic thickening or additional longitudinal contraction reflecting spatial nonuniformity (regional dyssynergy) of myocardial function in 50% of patients with HCM. These data suggest that the heterogeneity of myocardial function in HCM ranges from focal subsegmental to larger segmental abnormalities and emphasize the need for careful spatial mapping to increase diagnostic yield. This effort, in our experience, can be facilitated by information gleaned from parametric color strain maps.

Further clinical applications of TDI strain imaging include its role in the accurate differentiation of HCM from asymmetrical hypertensive LVH. Kato et al. (44) studied 34 patients evaluated for LVH. All patients underwent echocardiography, diagnostic cardiac catheterization, as well as endomyocardial biopsy. Twenty patients were diagnosed with HCM on the basis of tissue pathology, used as the gold standard, and the remaining 14 patients had hypertensive LVH. These investigators reported that only septum/posterior wall thickness and epsilon systolic {varepsilon} were each able to discriminate HCM patients from hypertensive LVH. An epsilon ({varepsilon}) value of >–10.6% was found to have a sensitivity of 85%, specificity of 100%, and a predictive accuracy of 91.2% for the diagnosis of HCM. Finally, post-systolic shortening implying segmental or focal/subsegmental myocardial contraction occurring temporally after the completion of ejection (aortic valve closure), detected by strain imaging, is common and has been implicated in the etiology of diastolic dysfunction in HCM (70,71). Several established, as well as more recent, echocardiographic parameters of diagnostic value in HCM along with their respective diagnostic accuracies have been itemized in Table 1.


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  		Table 1 Echocardiographic Features of Diagnostic Value in Hypertrophic Cardiomyopathy
 
2D strain or speckle tracking imaging.   This rapidly expanding technology entails spatial and temporal tracking of adjacent naturally occurring acoustic markers or "speckles" from standard black and white echocardiographic images in 2 dimensions. Deformation is calculated on a frame-frame analysis of speckle displacement, yielding angle-independent parameters of myocardial contraction, namely longitudinal, and transverse strain and strain rate (long-axis images). Similarly, radial and circumferential strain or strain rate may be measured off the short-axis images (25). Transverse and radial strains represent systolic radial deformation or thickening (expressed positively), whereas longitudinal and circumferential strains represent percent systolic shortening (negative values). The use of 2D strain or speckle tracking imaging overcomes the limitation of TDI-derived strain when tissue deformation in areas nonparallel to the insonating ultrasound beam (angle-independence) are assessed and has been well validated against tagged CMR and sonomicrometry (72,73)

Leitman et al. (74) first reported on the feasibility of 2D strain and compared the newly developed software with standard myocardial velocities, longitudinal {varepsilon}, and SR derived from TDI in healthy volunteers and patients who experienced a previous myocardial infarction. Longitudinal strain ({varepsilon}) and SR were used as indexes of longitudinal myocardial deformation. These authors found that providing image quality and tracking of segments of interest was adequate, myocardial tissue velocities, 2D {varepsilon}, and SR did not significantly differ from those obtained by TDI, with the advantage of simplicity and accuracy. However, satisfactory tracking of infarcted segments remained suboptimal (80%) compared with 98% of normal segments. Interestingly, a base-apex gradient was described, with a progressive increase in longitudinal {varepsilon} values noted from basal to apical segments.

Subsequently, Serri et al. (25) applied 2D strain echocardiography to a subset of patients with familial nonobstructive HCM. Average longitudinal {varepsilon} was reduced in affected individuals compared with healthy controls (–15.1 ± 6.2% vs. –20.3 ± 5.6%), despite apparently normal systolic function (with the use of standard criteria). No significant difference in the values obtained by TDI versus 2D {varepsilon} was observed. Furthermore, transverse, circumferential, and radial strain were significantly reduced in affected individuals (23.3 ± 17% vs. 27.2 ± 14.9%, –16.8 ± 7.1% vs. –19.6 ± 5.2%, 25.2 ± 13.9% vs. 36.8 ± 17.2%, respectively). Although overall longitudinal {varepsilon} values were reduced in the HCM group, a base to apex gradient was still observed, as in the control group. Similarly, radial strain in the mid- and apical short-axis segments in HCM was significantly attenuated compared with patients with hypertensive LVH (30). The authors concluded that 2D {varepsilon} can be used to identify subclinical global systolic dysfunction in patients with HCM, with improved interobserver as well as intraobserver variability compared with TDI-derived strain (7.5% vs. 13.7% and 7.9% vs. 14.5%, respectively).

A recent study of patients with HCM and preserved systolic function demonstrated attenuated longitudinal strain, increased circumferential strain, and normal overall systolic LV twist or torsion (75). Similar observations were reported in a prior study (23) that used TDI to assess torsional deformation at rest and during submaximal exercise. In this study, despite preserved LV systolic twist and near normal untwisting velocities at rest, patients with HCM exhibited a profound reduction in the magnitude of untwisting velocity with exercise compared with normal subjects (23).

Because of its intrinsic ability to provide angle-independent strain data, 2D strain holds a unique advantage over tissue Doppler-derived strain, which is particularly relevant when one analyzes myocardial deformation in the apical LV segments. We recently reported 2 cases of apical HCM in which 2D strain imaging revealed paradoxical longitudinal strain (systolic lengthening) in the apical segments (+9.2% and +16% in Patients #1 and #2, respectively) (76). In contrast to previous reports (25,74), we observed attenuated longitudinal {varepsilon} values in the mid and distal segments of the LV, findings suggesting a loss of the normal base-apex gradient, in this particular phenotype of HCM (Fig. 3).


Figure 3
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  		Figure 3 Echocardiographic Diagnosis of Apical Hypertrophic Cardiomyopathy

(A) Contrast-enhanced images (Definity; Bristol-Myers Squibb Medical Imaging Inc., North Billerica, Massachusetts) of a patient with apical hypertrophic cardiomyopathy in end-diastole and (B) "ace of spades" appearance of the left ventricle cavity with apical cavity obliteration in end-systole. (C) Conventional apical 4-chamber view showing exuberant LVH (arrow) in apical HCM. (D) Two-dimensional strain (quad format) images of same patient showing paradoxical apical longitudinal strain (crimson segment and tracing) and corresponding perturbations in the color M-mode of the parametric strain map. Note loss of base-apex (strain) gradient.

 
For nonapical variants of HCM, the TDI–strain technique offers the flexibility of linear mapping and interrogation of focal areas within the myocardium (unlike 2D strain, which displays average segmental strain), improving diagnostic yield, and should be the preferred method for screening patients with subclinical disease or confirming clinically manifest HCM. As alluded to earlier in this work, segmental post-systolic contraction or shortening representing an additional wave of contraction after aortic valve closure is observed frequently in patients with HCM, ischemia, infarction, and in a small percentage of healthy individuals. This phenomenon can be recognized in strain traces when 2D strain or TDI-based strain imaging are used, and needs to be differentiated from electromechanical delay in contraction or dyssynchrony (70).

Three-dimensional echocardiography.   The use of 3D-E has provided insights into the mechanics of SAM and deformational geometry of the LV outflow tract (Fig. 4) (77). Data suggest that the medial segments of the mitral valve are predominantly involved in SAM, resulting in a narrow laterally located LVOT in patients with obstructive cardiomyopathy (78). Likewise, 3D-E facilitates the assessment of LVOT area after intervention for septal reduction (79) and after surgical myectomy (80), volumetric estimates of left atrial mechanical function (81), and accurate estimation of LV ejection fraction as well as LV mass in hypertrophied hearts (comparing favorably with CMR imaging) (82). Live 3D-E also improves recognition of location and extent of LV cavity obliteration (83) and may be used in conjunction with LV contrast opacification for this purpose (84).


Figure 4
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  		Figure 4 Three-Dimensional Echocardiography

Still frame of a parasternal long-axis view obtained using real-time 3-dimensional imaging, angulated to depict systolic anterior motion of the anterior mitral leaflet (SAM) in a patient with obstructive HCM. Abbreviations as in Figure 1.

 
Contrast echocardiography.   Contrast echocardiography currently is used to enhance endocardial definition, Doppler signals, and to evaluate myocardial perfusion. Although not systematically studied, a potential role for contrast enhancement in the diagnosis of apical HCM has been demonstrated (Figs. 3A and 3B) (33). Likewise, contrast-enhanced 3D-E may also be well suited for the diagnosis of this entity (84), eliminating the need for LV angiography or more expensive imaging modalities such as CMR. Finally, myocardial contrast echocardiography can help anticipate the location and delineate the extent of septal infarct (selective injection of contrast into septal perforators) before alcohol septal ablation (85).

Intraventricular dyssynchrony and prognosis.   Interventricular and intraventricular delay is commonly encountered in patients with HCM, despite the absence of conduction abnormalities on surface electrocardiogram, and appears to correlate to the degree of septal LVH and the presence of LV outflow obstruction (29). Significant temporal heterogeneity of LV contractility when speckle tracking imaging-based measurements of peak radial and circumferential strain are used has been reported in patients with HCM compared with hypertensive LVH and age-matched control patients (30). The prevalence and degree of LV dyssynchrony was significantly greater in patients with HCM compared with hypertensive LVH and age-matched control patients (but not significantly different between the latter entities) (30). The authors of another study of 123 patients with HCM assessed systolic intraventricular dyssynchrony by using tissue Doppler and identified a strong association between the degree of intraventricular dyssynchrony and extent of LVH. In this study, an intraventricular delay of >45 ms, predicted an increased risk for ventricular tachyarrhythmias and sudden cardiac death at 5-year follow-up (85.5% sensitivity; 90.4% specificity; positive predictive value: 66.9%; negative predictive value: 96.7%; test accuracy: 88.8%) (28).

Study limitations.   Despite the tremendous advances in imaging technologies, there remain limitations to the routine application of 3D-E (suboptimal spatial and temporal resolution) and 2D strain analysis ensuing from their inherent dependence on image quality. Another practical limitation is the variability in radial strain measurements resulting from adjusting endocardial border tracings and the width of the region of interest. Further refinements in 3D-E may allow speckle tracking in 3D, facilitating a more comprehensive assessment of regional LV mechanics. The drawbacks of TDI analysis include angle-dependence and its susceptibility to signal noise that can influence peak velocity measures and TDI-derived strain data. Notwithstanding these limitations, in our opinion, TDI and strain imaging, particularly longitudinal strain linear mapping, should be incorporated into the routine diagnostic assessment of suspected HCM and screening of family members. Demonstration of focal or segmental areas of paradoxical strain can provide incremental information and consolidate the diagnosis of suspected or equivocal HCM, assessed by conventional echo techniques (Table 1). Pending further refinements, an algorithm incorporating novel parameters is presented to assist the clinician with a practical approach to the diagnosis and risk stratification of HCM (Fig. 5).


Figure 5
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  		Figure 5 Proposed Algorithm for the Diagnosis and Risk Stratification of Patients With Suspected HCM

*Mean transverse LA diameter; **difference between the longest and shortest Q-Sm time intervals (beginning of Q-wave in ECG to onset of systolic annular motion by TDI) among 4 different LV basal myocardial segments. HCM = hypertorphic cardiomyopathy; IVS/PW = interventricular septum/posterior wall ratio; LA = left atrial; LAVI = left atrial volume index; LV = left ventricular; LVH = left ventricular hypertrophy; LVOT = left ventricular outflow tract; RT-3DE = real time-3 dimensional echocardiography; SAM = systolic anterior motion; TDI = tissue Doppler imaging; 2D-strain = 2 dimensional speckle tracking imaging.

 

   Conclusions
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
REFERENCES
 
At this time, tissue Doppler-derived strain and 2D strain or speckle tracking imaging represent robust and rapidly evolving technologies that have advanced our understanding of regional myocardial mechanics in HCM. Ongoing refinements and additional research will define the incremental role and clinical utility of these promising techniques, including the identification of preclinical disease in carriers of HCM mutations, improvement of diagnostic accuracy, risk stratification, planning therapeutic strategies, and monitoring treatment.

* Reprint requests and correspondence: Dr. Theodore P. Abraham, Johns Hopkins University, 600 North Wolfe Street, Carnegie 568, Baltimore, Maryland 21287 (Email: tabraha3{at}jhmi.edu).

Manuscript received May 30, 2008; revised manuscript received August 27, 2008, accepted September 5, 2008.


   REFERENCES
Top
 Abstract
 General Considerations
 Systolic Anterior Motion (SAM)
 LVOT or Subaortic Obstruction
 Systolic Dysfunction
 Diastolic Dysfunction
 Left Atrial (LA) Enlargement...
 Novel Techniques
 Conclusions
 REFERENCES
 

  1. Niimura H, Patton KK, McKenna WJ, et al. Sarcomere protein gene mutations in hypertrophic cardiomyopathy of the elderly Circulation 2002;105:446-451.[Abstract/Free Full Text]
  2. Arad M, Penas-Lado M, Monserrat L, et al. Gene mutations in apical hypertrophic cardiomyopathy Circulation 2005;112:2805-2811.[Abstract/Free Full Text]
  3. Niimura H, Bachinski LL, Sangwatanaroj S, et al. Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy N Engl J Med 1998;338:1248-1257.[Abstract/Free Full Text]
  4. Geisterfer-Lowrance AA, Kass S, Tanigawa G, et al. A molecular basis for familial hypertrophic cardiomyopathy: a beta cardiac myosin heavy chain gene missense mutation Cell 1990;62:999-1006.[CrossRef][Web of Science][Medline]
  5. Thierfelder L, Watkins H, MacRae C, et al. Alpha-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere Cell 1994;77:701-712.[CrossRef][Web of Science][Medline]
  6. Watkins H, Conner D, Thierfelder L, et al. Mutations in the cardiac myosin binding protein-C gene on chromosome 11 cause familial hypertrophic cardiomyopathy Nat Genet 1995;11:434-437.[CrossRef][Web of Science][Medline]
  7. Maron BJ. Hypertrophic cardiomyopathy: a systematic review JAMA 2002;287:1308-1320.[Abstract/Free Full Text]
  8. Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ. Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy N Engl J Med 2000;342:1778-1785.[Abstract/Free Full Text]
  9. Elliott PM, Poloniecki J, Dickie S, et al. Sudden death in hypertrophic cardiomyopathy: identification of high risk patients J Am Coll Cardiol 2000;36:2212-2218.[Abstract/Free Full Text]
  10. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation 1995;92:1680-1692.[Free Full Text]
  11. Maier SE, Fischer SE, McKinnon GC, Hess OM, Krayenbuehl HP, Boesiger P. Evaluation of left ventricular segmental wall motion in hypertrophic cardiomyopathy with myocardial tagging Circulation 1992;86:1919-1928.[Abstract/Free Full Text]
  12. Kramer CM, Reichek N, Ferrari VA, Theobald T, Dawson J, Axel L. Regional heterogeneity of function in hypertrophic cardiomyopathy Circulation 1994;90:186-194.[Abstract/Free Full Text]
  13. Notomi Y, Popovic ZB, Yamada H, et al. Ventricular untwisting: a temporal link between left ventricular relaxation and suction Am J Physiol Heart Circ Physiol 2008;294:H505-H513.[Abstract/Free Full Text]
  14. Streeter Jr. DD, Spotnitz HM, Patel DP, Ross Jr. J, Sonnenblick EH. Fiber orientation in the canine left ventricle during diastole and systole Circ Res 1969;24:339-347.[Abstract/Free Full Text]
  15. Rijcken J, Bovendeerd PH, Schoofs AJ, van Campen DH, Arts T. Optimization of cardiac fiber orientation for homogeneous fiber strain during ejection Ann Biomed Eng 1999;27:289-297.[CrossRef][Web of Science][Medline]
  16. Sutherland GR, Di Salvo G, Claus P, D'Hooge J, Bijnens B. Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function J Am Soc Echocardiogr 2004;17:788-802.[CrossRef][Web of Science][Medline]
  17. Helle-Valle T, Crosby J, Edvardsen T, et al. New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography Circulation 2005;112:3149-3156.[Abstract/Free Full Text]
  18. Ho CY, Solomon SD. A clinician's guide to tissue Doppler imaging Circulation 2006;113:e396-e398.[Free Full Text]
  19. Vinereanu D, Florescu N, Sculthorpe N, Tweddel AC, Stephens MR, Fraser AG. Differentiation between pathologic and physiologic left ventricular hypertrophy by tissue Doppler assessment of long-axis function in patients with hypertrophic cardiomyopathy or systemic hypertension and in athletes Am J Cardiol 2001;88:53-58.[CrossRef][Web of Science][Medline]
  20. Marwick TH. Measurement of strain and strain rate by echocardiography: ready for prime time? J Am Coll Cardiol 2006;47:1313-1327.[Abstract/Free Full Text]
  21. 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;20:234-243.[CrossRef][Web of Science][Medline]
  22. Yip G, Abraham T, Belohlavek M, Khandheria BK. Clinical applications of strain rate imaging J Am Soc Echocardiogr 2003;16:1334-1342.[CrossRef][Web of Science][Medline]
  23. Notomi Y, Martin-Miklovic MG, Oryszak SJ, et al. Enhanced ventricular untwisting during exercise: a mechanistic manifestation of elastic recoil described by Doppler tissue imaging Circulation 2006;113:2524-2533.[Abstract/Free Full Text]
  24. Notomi Y, Lysyansky P, Setser RM, et al. Measurement of ventricular torsion by two-dimensional ultrasound speckle tracking imaging J Am Coll Cardiol 2005;45:2034-2041.[Abstract/Free Full Text]
  25. Serri K, Reant P, Lafitte M, et al. Global and regional myocardial function quantification by two-dimensional strain: application in hypertrophic cardiomyopathy J Am Coll Cardiol 2006;47:1175-1181.[Abstract/Free Full Text]
  26. Nagueh SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy Circulation 2001;104:128-130.[Abstract/Free Full Text]
  27. Nagueh SF, McFalls J, Meyer D, et al. Tissue Doppler imaging predicts the development of hypertrophic cardiomyopathy in subjects with subclinical disease Circulation 2003;108:395-398.[Abstract/Free Full Text]
  28. D'Andrea A, Caso P, Severino S, et al. Prognostic value of intra-left ventricular electromechanical asynchrony in patients with hypertrophic cardiomyopathy Eur Heart J 2006;27:1311-1318.[Abstract/Free Full Text]
  29. D'Andrea A, Caso P, Severino S, et al. Association between intraventricular myocardial systolic dyssynchrony and ventricular arrhythmias in patients with hypertrophic cardiomyopathy Echocardiography 2005;22:571-578.[CrossRef][Medline]
  30. Nagakura T, Takeuchi M, Yoshitani H, et al. Hypertrophic cardiomyopathy is associated with more severe left ventricular dyssynchrony than is hypertensive left ventricular hypertrophy Echocardiography 2007;24:677-684.[Medline]
  31. Carasso S, Woo A, Yang H, et al. Myocardial mechanics explains the time course of benefit for septal ethanol ablation for hypertrophic cardiomyopathy J Am Soc Echocardiogr 2008;21:493-499.[Medline]
  32. Abraham TP, Nishimura RA, Holmes Jr. DR, Belohlavek M, Seward JB. Strain rate imaging for assessment of regional myocardial function: results from a clinical model of septal ablation Circulation 2002;105:1403-1406.[Abstract/Free Full Text]
  33. Soman P, Swinburn J, Callister M, Stephens NG, Senior R. Apical hypertrophic cardiomyopathy: bedside diagnosis by intravenous contrast echocardiography J Am Soc Echocardiogr 2001;14:311-313.[CrossRef][Web of Science][Medline]
  34. Maron BJ, Epstein SE. Hypertrophic cardiomyopathy. Recent observations regarding the specificity of three hallmarks of the disease: asymmetric septal hypertrophy, septal disorganization and systolic anterior motion of the anterior mitral leaflet. Am J Cardiol 1980;45:141-154.[CrossRef][Web of Science][Medline]
  35. In: Weyman AE, editor. Principles and Practice of Echocardiography. 2nd edition. New York, NY: Lea and Febiger; 1994.
  36. Maron BJ, Gottdiener JS, Perry LW. Specificity of systolic anterior motion of anterior mitral leaflet for hypertrophic cardiomyopathy. Prevalence in large population of patients with other cardiac diseases. Br Heart J 1981;45:206-212.[Abstract/Free Full Text]
  37. Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy J Am Coll Cardiol 2000;36:1344-1354.[Abstract/Free Full Text]
  38. Nagueh SF, Mahmarian JJ. Noninvasive cardiac imaging in patients with hypertrophic cardiomyopathy J Am Coll Cardiol 2006;48:2410-2422.[Abstract/Free Full Text]
  39. Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy N Engl J Med 2003;348:295-303.[Abstract/Free Full Text]
  40. Panza JA, Petrone RK, Fananapazir L, Maron BJ. Utility of continuous wave Doppler echocardiography in the noninvasive assessment of left ventricular outflow tract pressure gradient in patients with hypertrophic cardiomyopathy J Am Coll Cardiol 1992;19:91-99.[Abstract]
  41. Sasson Z, Yock PG, Hatle LK, Alderman EL, Popp RL. Doppler echocardiographic determination of the pressure gradient in hypertrophic cardiomyopathy J Am Coll Cardiol 1988;11:752-756.[Abstract]
  42. Sherrid MV, Gunsburg DZ, Pearle G. Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy—the lobster claw abnormality J Am Soc Echocardiogr 1997;10:707-712.[CrossRef][Web of Science][Medline]
  43. Barac I, Upadya S, Pilchik R, et al. Effect of obstruction on longitudinal left ventricular shortening in hypertrophic cardiomyopathy J Am Coll Cardiol 2007;49:1203-1211.[Abstract/Free Full Text]
  44. Kato TS, Noda A, Izawa H, et al. Discrimination of nonobstructive hypertrophic cardiomyopathy from hypertensive left ventricular hypertrophy on the basis of strain rate imaging by tissue Doppler ultrasonography Circulation 2004;110:3808-3814.[Abstract/Free Full Text]
  45. Harris KM, Spirito P, Maron MS, et al. Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy Circulation 2006;114:216-225.[Abstract/Free Full Text]
  46. Maron BJ, Spirito P, Green KJ, Wesley YE, Bonow RO, Arce J. Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy J Am Coll Cardiol 1987;10:733-742.[Abstract]
  47. Nishimura RA, Appleton CP, Redfield MM, Ilstrup DM, Holmes Jr. DR, Tajik AJ. Noninvasive Doppler echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: a simultaneous Doppler echocardiographic and cardiac catheterization study J Am Coll Cardiol 1996;28:1226-1233.[Abstract]
  48. Nagueh SF, Lakkis NM, Middleton KJ, Spencer 3rd WH, Zoghbi WA, Quinones MA. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy Circulation 1999;99:254-261.[Abstract/Free Full Text]
  49. Matsumura Y, Elliott PM, Virdee MS, Sorajja P, Doi Y, McKenna WJ. Left ventricular diastolic function assessed using Doppler tissue imaging in patients with hypertrophic cardiomyopathy: relation to symptoms and exercise capacity Heart 2002;87:247-251.[Abstract/Free Full Text]
  50. Sitges M, Shiota T, Lever HM, et al. Comparison of left ventricular diastolic function in obstructive hypertrophic cardiomyopathy in patients undergoing percutaneous septal alcohol ablation versus surgical myotomy/myectomy Am J Cardiol 2003;91:817-821.[CrossRef][Web of Science][Medline]
  51. Geske JB, Sorajja P, Nishimura RA, Ommen SR. Evaluation of left ventricular filling pressures by Doppler echocardiography in patients with hypertrophic cardiomyopathy: correlation with direct left atrial pressure measurement at cardiac catheterization Circulation 2007;116:2702-2708.[Abstract/Free Full Text]
  52. Nagueh SF, Middleton KJ, Kopelen HA, Zoghbi WA, Quinones MA. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures J Am Coll Cardiol 1997;30:1527-1533.[Abstract]
  53. Nistri S, Olivotto I, Betocchi S, et al. Prognostic significance of left atrial size in patients with hypertrophic cardiomyopathy (from the Italian Registry for Hypertrophic Cardiomyopathy) Am J Cardiol 2006;98:960-965.[CrossRef][Web of Science][Medline]
  54. Woo A, Williams WG, Choi R, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy Circulation 2005;111:2033-2041.[Abstract/Free Full Text]
  55. Lester SJ, Ryan EW, Schiller NB, Foster E. Best method in clinical practice and in research studies to determine left atrial size Am J Cardiol 1999;84:829-832.[CrossRef][Web of Science][Medline]
  56. Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology J Am Soc Echocardiogr 2005;18:1440-1463.[CrossRef][Web of Science][Medline]
  57. Sachdev V, Shizukuda Y, Brenneman CL, et al. Left atrial volumetric remodeling is predictive of functional capacity in nonobstructive hypertrophic cardiomyopathy Am Heart J 2005;149:730-736.[CrossRef][Medline]
  58. Yang H, Woo A, Monakier D, et al. Enlarged left atrial volume in hypertrophic cardiomyopathy: a marker for disease severity J Am Soc Echocardiogr 2005;18:1074-1082.[CrossRef][Web of Science][Medline]
  59. Cardim N, Oliveira AG, Longo S, et al. Doppler tissue imaging: regional myocardial function in hypertrophic cardiomyopathy and in athlete's heart J Am Soc Echocardiogr 2003;16:223-232.[CrossRef][Web of Science][Medline]
  60. Solomon SD, Wolff S, Watkins H, et al. Left ventricular hypertrophy and morphology in familial hypertrophic cardiomyopathy associated with mutations of the beta-myosin heavy chain gene J Am Coll Cardiol 1993;22:498-505.[Abstract]
  61. Ho CY, Sweitzer NK, McDonough B, et al. Assessment of diastolic function with Doppler tissue imaging to predict genotype in preclinical hypertrophic cardiomyopathy Circulation 2002;105:2992-2997.[Abstract/Free Full Text]
  62. Araujo AQ, Arteaga E, Ianni BM, et al. Relationship between outflow obstruction and left ventricular functional impairment in hypertrophic cardiomyopathy: a Doppler echocardiographic study Echocardiography 2006;23:734-740.[Medline]
  63. Bayrak F, Kahveci G, Mutlu B, Sonmez K, Degertekin M. Tissue Doppler imaging to predict clinical course of patients with hypertrophic cardiomyopathy Eur J Echocardiogr 2008;9:278-283.[Abstract/Free Full Text]
  64. Galiuto L, Ignone G, DeMaria AN. Contraction and relaxation velocities of the normal left ventricle using pulsed-wave tissue Doppler echocardiography Am J Cardiol 1998;81:609-614.[CrossRef][Web of Science][Medline]
  65. Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound J Am Soc Echocardiogr 1998;11:1013-1019.[CrossRef][Web of Science][Medline]
  66. Miyatake K, Yamagishi M, Tanaka N, et al. New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies J Am Coll Cardiol 1995;25:717-724.[Abstract]
  67. Gilman G, Khandheria BK, Hagen ME, Abraham TP, Seward JB, Belohlavek M. Strain rate and strain: a step-by-step approach to image and data acquisition J Am Soc Echocardiogr 2004;17:1011-1020.[CrossRef][Web of Science][Medline]
  68. Weidemann F, Mertens L, Gewillig M, Sutherland GR. Quantitation of localized abnormal deformation in asymmetric nonobstructive hypertrophic cardiomyopathy: a velocity, strain rate, and strain Doppler myocardial imaging study Pediatr Cardiol 2001;22:534-537.[CrossRef][Web of Science][Medline]
  69. Yang H, Sun JP, Lever HM, et al. Use of strain imaging in detecting segmental dysfunction in patients with hypertrophic cardiomyopathy J Am Soc Echocardiogr 2003;16:233-239.[CrossRef][Web of Science][Medline]
  70. Sengupta PP, Mehta V, Arora R, Mohan JC, Khandheria BK. Quantification of regional nonuniformity and paradoxical intramural mechanics in hypertrophic cardiomyopathy by high frame rate ultrasound myocardial strain mapping J Am Soc Echocardiogr 2005;18:737-742.[CrossRef][Web of Science][Medline]
  71. Ito T, Suwa M, Tonari S, Okuda N, Kitaura Y. Regional postsystolic shortening in patients with hypertrophic cardiomyopathy: its incidence and characteristics assessed by strain imaging J Am Soc Echocardiogr 2006;19:987-993.[CrossRef][Web of Science][Medline]
  72. Amundsen BH, Helle-Valle T, Edvardsen T, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging J Am Coll Cardiol 2006;47:789-793.[Abstract/Free Full Text]
  73. Korinek J, Wang J, Sengupta PP, et al. Two-dimensional strain—a Doppler-independent ultrasound method for quantitation of regional deformation: validation in vitro and in vivo J Am Soc Echocardiogr 2005;18:1247-1253.[CrossRef][Web of Science][Medline]
  74. Leitman M, Lysyansky P, Sidenko S, et al. Two-dimensional strain-a novel software for real-time quantitative echocardiographic assessment of myocardial function J Am Soc Echocardiogr 2004;17:1021-1029.[CrossRef][Web of Science][Medline]
  75. Carasso S, Yang H, Woo A, et al. Systolic myocardial mechanics in hypertrophic cardiomyopathy: novel concepts and implications for clinical status J Am Soc Echocardiogr 2008;21:675-683.[Medline]
  76. Reddy M, Thatai D, Bernal J, Pradhan J, Afonso L. Apical hypertrophic cardiomyopathy: potential utility of strain imaging Eur J Echocardiogr 2008;9:560-562.[Abstract/Free Full Text]
  77. Salustri A, Kofflard MJ, Roelandt JR, et al. Assessment of left ventricular outflow in hypertrophic cardiomyopathy using anyplane and paraplane analysis of three-dimensional echocardiography Am J Cardiol 1996;78:462-468.[CrossRef][Web of Science][Medline]
  78. Song JM, Fukuda S, Lever HM, et al. Asymmetry of systolic anterior motion of the mitral valve in patients with hypertrophic obstructive cardiomyopathy: a real-time three-dimensional echocardiographic study J Am Soc Echocardiogr 2006;19:1129-1135.[CrossRef][Medline]
  79. Sitges M, Qin JX, Lever HM, et al. Evaluation of left ventricular outflow tract area after septal reduction in obstructive hypertrophic cardiomyopathy: a real-time 3-dimensional echocardiographic study Am Heart J 2005;150:852-858.[CrossRef][Medline]
  80. Qin JX, Shiota T, Asher CR, et al. Usefulness of real-time three-dimensional echocardiography for evaluation of myectomy in patients with hypertrophic cardiomyopathy Am J Cardiol 2004;94:964-966.[Medline]
  81. Anwar AM, Soliman OI, Geleijnse ML, et al. Assessment of left atrial ejection force in hypertrophic cardiomyopathy using real-time three-dimensional echocardiography J Am Soc Echocardiogr 2007;20:744-748.[Medline]
  82. Oe H, Hozumi T, Arai K, et al. Comparison of accurate measurement of left ventricular mass in patients with hypertrophied hearts by real-time three-dimensional echocardiography versus magnetic resonance imaging Am J Cardiol 2005;95:1263-1267.[CrossRef][Web of Science][Medline]
  83. de Gregorio C, Recupero A, Grimaldi P, Coglitore S. Can transthoracic live 3-dimensional echocardiography improve the recognition of midventricular obliteration in hypertrophic obstructive cardiomyopathy? J Am Soc Echocardiogr 2006;19:1190.e1-1190.e4.
  84. Frans EE, Nanda NC, Patel V, et al. Live three-dimensional transthoracic contrast echocardiographic assessment of apical hypertrophic cardiomyopathy Echocardiography 2005;22:686-689.[CrossRef][Web of Science][Medline]
  85. Nagueh SF, Lakkis NM, He ZX, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy J Am Coll Cardiol 1998;32:225-229.[Abstract/Free Full Text]




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