Left Ventricular Torsion by Two-Dimensional Speckle Tracking Echocardiography in Patients with Diastolic Dysfunction and Normal Ejection Fraction

doi:10.1016/j.echo.2008.04.002

Journal of the American Society of Echocardiography

Volume 21, Issue 10, October 2008, Pages 1129-1137

https://doi.org/10.1016/j.echo.2008.04.002 Get rights and content

Background

Left ventricular torsion (LVtor) and subsequent untwisting play an important role in diastolic filling. There is, however, limited information about how LVtor and untwisting are related to the severity of diastolic dysfunction. The aim of this study was to assess LVtor and untwisting in the progressive severity of diastolic dysfunction.

Methods

We studied 148 subjects (116 with diastolic dysfunction, 32 healthy controls). Apical and basal short-axis rotations were measured by 2-dimensional speckle tracking echocardiography. LVtor was defined as the instantaneous net difference of the basal and apical rotation. Patients were divided into 3 groups according to diastolic dysfunction grade and their underlying disease, such as hypertension, hypertrophic cardiomyopathy, and amyloidosis.

Results

Age, gender, and ejection fraction were similar in the 3 groups and control. Mitral annulus early diastolic velocity was reduced by design in all 3 groups. Peak LVtor was significantly greater in mild diastolic dysfunction (n = 45; 29.7 ± 9.0 degrees) compared with control (n = 32: 15.6 ± 4.0 degrees) and then normalized in moderate (n = 49; 19.3 ± 4.8 degrees) and severe diastolic dysfunction (n = 22; 17.3 ± 9.3 degrees). The twisting and untwisting rates were significantly higher in mild diastolic dysfunction group.

Conclusion

Systolic torsion and diastolic untwisting are significantly increased in patients with mild diastolic dysfunction. In patients with advanced diastolic dysfunction with increased filling pressure, they are normalized or reduced. Whether increased LVtor is a compensatory mechanism for reduced myocardial relaxation or a consequence of reduced filling in the early stage of diastolic dysfunction requires further investigation. Analysis of LVtor with speckle tracking echocardiography should be further explored to elucidate the role of torsion in patients with diastolic dysfunction.

Section snippets

Study Populations

We prospectively examined 116 patients with different grades of diastolic dysfunction and normal ejection fraction (EF) who were undergoing transthoracic echocardiography for an evaluation of dyspnea from December of 2006 to May of 2007. The patients were stratified by the grades of diastolic dysfunction (grades 1-3) using pulsed-wave Doppler of the mitral inflow and TDI of the mitral annulus as described: grade 1 (abnormal relaxation: ratio of transmitral early diastolic to late diastolic

Patients and Their Clinical Characteristics

The 116 patients were divided into 3 groups on the basis of grading the diastolic dysfunction according to the mitral inflow and TDI of the mitral annulus: grade 1 = 45 patients with mild diastolic dysfunction, grade 2 = 49 patients with moderate diastolic dysfunction, and grade 3 = 22 patients with severe diastolic dysfunction. The demographic data of these 3 groups and 32 healthy controls are shown in Table 1. No significant intergroup differences were present in mean age and sex distribution.

Discussion

Our study demonstrated that peak LVtor is increased in patients with mild or early-stage diastolic dysfunction, mainly because of more vigorous and increased LV apical rotation. Diastolic untwisting is also increased, and the time from the peak systolic torsion to MVO was lengthened in this group. Wang et al²⁰ recently demonstrated that LVtor and diastolic untwisting in patients with diastolic heart failure were not significantly different from those of healthy controls despite abnormal

Conclusions

Noninvasive assessment of LVtor and untwisting was feasible in patients with various grades of diastolic dysfunction and healthy controls using 2-D STE. Systolic torsion was increased, and diastolic untwisting was also increased and lengthened in patients with an early stage of diastolic dysfunction (grade 1). We showed that hypertorsion and hyperuntwisting are characteristic of early asymptomatic diastolic dysfunction with normal EF. Thus, we propose that hypertorsion and hyperuntwisting may

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Reduced Exercise Capacity in Diabetes Mellitus Is Not Associated with Impaired Deformation or Twist
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Citation Excerpt :
Exercise leads to an increase in HR and reduction in LV filling time. Effective LV untwisting via rapid apical uncoiling is essential to increase the diastolic intraventricular pressure gradient and thereby enhance LV filling to the apex without raising left atrial pressure.15,32 This physiology is eloquently illustrated in a recent paper from Kosmala et al.,33 who describe an association with VO2 peak and LV untwist rate in participants with heart failure with preserved ejection fraction, although untwist measurements were not measured after peak exercise.
Exercise capacity is frequently reduced in people with diabetes mellitus (DM) and may be due to subclinical cardiac dysfunction. Speckle-tracking echocardiography is now widely available; however, the clinical utility and significance of left ventricular (LV) strain and twist parameters remain uncertain. We hypothesized that LV strain and twist would be reduced in DM subjects during exercise.
Adults with type 1 or type 2 DM and age- and sex-matched controls performed cardiopulmonary exercise testing (VO₂ peak) and supine bicycle exercise echocardiography. Detailed echocardiographic assessment of biventricular function was performed at baseline and repeated during incremental exercise to maximal intensity.
Of the 60 participants completing the study protocol, 51 (34 DM, 17 controls; mean age, 42 ± 13 years; 69% male; DM duration, 16 ± 10 years) had sufficient image quality to assess LV deformation and twist mechanics at rest. Of these, 38 (25 DM, 13 controls) were able to be assessed immediately after exercise. Baseline LV systolic and diastolic function using standard echocardiography measurements were similar between groups. Resting LV global longitudinal strain, twist, twist rate and untwist rate, and the corresponding peak exercise and reserve measures did not differ significantly. As compared with the control subjects, exercise capacity was reduced in the DM cohort (VO₂ peak 33 ± 10 vs 41 ± 12 mL/minute/kg; P = .02); however, no correlation was observed between VO₂ peak and LV twist reserve (R = 0.28, P = .09), LV twist rate reserve (R = 0.14, P = .39), or LV untwist rate reserve (R = 0.24, P = .14).
Despite reduced VO₂ peak, LV twist mechanics at rest and after maximal intensity exercise did not differ significantly in a cohort of asymptomatic DM subjects with normal resting LV systolic and diastolic function compared with age- and sex-matched controls. This would suggest that exercise capacity can be reduced in the absence of subclinical cardiac dysfunction and that noncardiac factors should be considered as alternative explanations.
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In hypertrophic cardiomyopathy (HCM), macroscopic and microscopic alterations in myocardial structure (myocardial hypertrophy, fiber disarray, increased loose connective tissue, and fibrosis) and abnormalities of the coronary microvasculature interfere with both myocyte force generation and myocardial relaxation. The mutations related to HCM result in the production of abnormal myocardial sarcomeric proteins that have altered contraction and relaxation characteristics. These include changes in the affinity between the various contractile proteins, changes in the sensitivity to Ca⁺², the efficiency of energy utilization (from ATP), and its expenditure. During stress, ischemia-induced diastolic dysfunction occurs at higher heart rates, reducing the diastolic filling period, resulting in increased intracavitary pressures aggravating subendocardial ischemia further. This is compounded by reduced left ventricular (LV) diastolic distensibility during exercise. Dyspnea is a common symptom, predominantly related to the presence of diastolic dysfunction and LV outflow tract (LVOT) obstruction. Worsening dyspnea may be precipitated by either the acute onset of atrial fibrillation or more insidiously by the development of LV systolic dysfunction. Echocardiography is the imaging modality of choice for the assessment of diastolic function in HCM, although accurate classification of diastolic function grade presents a challenge due to the compounding effects of LVOT obstruction and mitral regurgitation. Myocardial mechanics (assessment of strain rate, apical reverse rotation, and left atrial phasic volumes) may aid in diastolic functional assessment and be correlated with symptoms. Medical and invasive (septal reduction) therapy of LVOT obstruction may also improve diastolic function in patients with obstructive HCM.
Left Ventricular Diastolic Function: Understanding Pathophysiology, Diagnosis, and Prognosis With Echocardiography
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Left ventricular diastolic function plays an important role in determining left ventricular filling and stroke volume. Abnormal diastolic function has been recognized in many cardiovascular diseases and is associated with worse outcomes, including total mortality and hospitalizations due to heart failure. Using echocardiography, it is possible to diagnose the presence of diastolic dysfunction and the pathophysiologic mechanisms involved as they affect left ventricular and left atrial structure and function. This review addresses the role of echocardiography in understanding the pathophysiology of diastolic dysfunction, its diagnosis, and utility in predicting outcomes.
Intervendor Discordance of Fetal and Neonatal Myocardial Tissue Doppler and Speckle-Tracking Measurements
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Fetal and neonatal studies report a wide range of cardiac parameters derived by pulsed-wave Doppler tissue imaging (DTI) and two-dimensional speckle-tracking echocardiographic (STE) imaging. The use of different ultrasound systems and their vendor-specific software compromises the ability to compare echocardiographic findings among various studies. The aim of this study was to evaluate intervendor reproducibility as well as intra- and interobserver repeatability of DTI and STE measurements in normal-term fetuses and neonates.
A prospective study was conducted of term fetuses (n = 196) from uncomplicated pregnancies assessed days before the onset of labor and a few hours after birth. Fetal and neonatal DTI and STE parameters were obtained and analyzed using vendor-specific software on three ultrasound systems: Toshiba Aplio MX versus GE Vivid E9 and GE Vivid E9 versus Philips EPIQ. A reproducibility study in fetuses and neonates (n = 118) was performed by systematic scanning with head-to-head comparison.
DTI reproducibility showed moderate to good correlation, with good agreement for fetuses and neonates on Toshiba versus GE (intraclass correlation coefficient [ICC] = 0.4–0.8). Correlation of DTI measurements on GE versus Philips was poor to moderate for fetuses (ICC = 0.1–0.6) and moderate to good for neonates (ICC = 0.5–0.8), with wider limits of agreement. Fetal and neonatal STE parameters revealed very poor correlation (ICC = 0.1–0.3) and agreement among ultrasound vendors. Intra- and interobserver repeatability demonstrated good to excellent correlation of all fetal and neonatal DTI and STE measurements, with good agreement irrespective of the ultrasound platform used.
These findings demonstrate reliable assessment of fetal and neonatal DTI and STE measurements when performed on the same ultrasound platform, whereas ultrasound machines and software from different vendors give significantly divergent estimates of DTI and STE parameters in fetuses and neonates. These intervendor discrepancies have significant clinical and research implications and should be considered when interpreting and comparing study findings, establishing reference standards, or performing systematic reviews.
Western Diet-Fed, Aortic-Banded Ossabaw Swine: A Preclinical Model of Cardio-Metabolic Heart Failure
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The development of new treatments for heart failure lack animal models that encompass the increasingly heterogeneous disease profile of this patient population. This report provides evidence supporting the hypothesis that Western Diet−fed, aortic-banded Ossabaw swine display an integrated physiological, morphological, and genetic phenotype evocative of cardio-metabolic heart failure. This new preclinical animal model displays a distinctive constellation of findings that are conceivably useful to extending the understanding of how pre-existing cardio-metabolic syndrome can contribute to developing HF.
Concomitant systolic and diastolic alterations during chronic hypertension in pig
2019, Journal of Molecular and Cellular Cardiology
The mechanical and cellular relationships between systole and diastole during left ventricular (LV) dysfunction remain to be established. LV contraction-relaxation coupling was examined during LV hypertrophy induced by chronic hypertension. Chronically instrumented pigs received angiotensin II infusion for4weeks to induce chronic hypertension (133 ± 7 mmHg vs 98 ± 5 mmHg for mean arterial pressure at Day 28 vs 0, respectively) and LV hypertrophy. LV function was investigated with the instrumentation and echocardiography for LV twist-untwist assessment before and after dobutamine infusion. The cellular mechanisms were investigated by exploring the intracellular Ca²⁺ handling. At Day 28, pigs exhibited LV hypertrophy with LV diastolic dysfunction (impaired LV isovolumic relaxation, increased LV end-diastolic pressure, decreased and delayed LV untwisting rate) and LV systolic dysfunction (impaired LV isovolumic contraction and twist) although LV ejection fraction was preserved. Isolated cardiomyocytes exhibited altered shortening and lengthening. Interestingly, contraction-relaxation coupling remained preserved both in vivo and in vitro during LV hypertrophy. LV systolic and diastolic dysfunctions were associated to post-translational remodeling and dysfunction of the type 2 cardiac ryanodine receptor/Ca²⁺ release channel (RyR2), i.e., PKA hyperphosphorylation of RyR2, depletion of calstabin 2 (FKBP12.6), RyR2 leak and hypersensitivity of RyR2 to cytosolic Ca²⁺ during both contraction and relaxation phases. In conclusion, LV contraction-relaxation coupling remained preserved during chronic hypertension despite LV systolic and diastolic dysfunctions. This implies that LV diastolic dysfunction is accompanied by LV systolic dysfunction. At the cellular level, this is linked to sarcoplasmic reticulum Ca²⁺ leak through PKA-mediated RyR2 hyperphosphorylation and depletion of its stabilizing partner.

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: Sung-Ji Park, MD, PhD, is supported by the Division of Cardiology, Department of Internal Medicine, GyeongSang National University College of Medicine, Jinju, South Korea.

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Left Ventricular Torsion by Two-Dimensional Speckle Tracking Echocardiography in Patients with Diastolic Dysfunction and Normal Ejection Fraction

Background

Methods

Results

Conclusion

Section snippets

Study Populations

Patients and Their Clinical Characteristics

Discussion

Conclusions

Am J Cardiol

J Am Soc Echocardiogr

J Am Coll Cardiol

J Am Soc Echocardiogr

J Am Soc Echocardiogr

J Am Coll Cardiol

J Am Soc Echocardiogr

J Am Soc Echocardiogr

J Am Coll Cardiol

Am Heart J

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Soc Echocardiogr

Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase

Am J Physiol