Strain Rate Echocardiography Research Articles

Atrial strain rate echocardiography can predict success or failure of cardioversion for atrial fibrillation: A combined transthoracic tissue Doppler and transoesophageal imaging study

The purpose of this study was to assess the feasibility of measuring left atrial dysfunction with tissue Doppler imaging derived strain rate and to explore its role in predicting the maintenance of sinus rhythm after cardioversion for atrial fibrillation. Strain rate (SR) and tissue Doppler imaging (TDI) were performed with offline analysis of the basal left atrial wall (LA). SR detected a systolic (Ssr) and early diastolic (Esr) deformation induced by ventricular motion. LA dimensions and volume were measured. Left atrial appendage emptying (LAA_EV) and filling (LAA_FV) velocities were also obtained by transesophageal echocardiography. 27 healthy age-matched controls and 42 patients with AF before cardioversion were studied. Patients were grouped into (1): those who remained in sinus rhythm (group S, n=12) and (2) those who either failed cardioversion or reverted to AF within 4 weeks (group F, n=30). LA dimensions were significantly larger and atrial Esr was significantly lower in group F than group S (all p<0.01). LAA_EV and LAA_FV were not different between groups S and F. Multivariate regression analysis showed that a lower Esr and larger transverse LA diameter (LADtr) were independent predictors of failure of cardioversion (HR, 95% CI: 0.36, 0.14-0.88 and 2.85, 1.33-6.10, respectively). Esr combined with LADtr improved the sensitivity and specificity for predicting successful cardioversion. SR can be measured in the basal LA wall in atrial fibrillation and the magnitude of the early diastolic SR could predict the success of cardioversion and the likelihood of maintenance of sinus rhythm.

Strain and Strain Rate Echocardiography

Myocardial function is eventually determined by the shortening and lengthening of myocardium, i.e., myocardial deformation or strain. The exact and direct measure of myocardial deformation has been dependent on the in vitro analysis of myocardial length. This is not an ideal physiological approach due to the change of the surrounding environment, and the process is rather tedious. Thus, this in vitro approach is primarily a research tool. Thanks to recently developed imaging techniques, regional myocardial deformation can now be measured. Using the myocardial tagging technique, one can measure myocardial strain with high accuracy. Currently, this is used as the clinical standard for the noninvasive evaluation of regional function.1 However, due to cost and long time needed for off-line analysis, myocardial tagging by MRI is not routinely utilized for clinical purposes. In 1998 and then in 2000, Heidelm2 and Urheim,3 et al., reported that based on myocardial velocities by tissue Doppler imaging (TOI), the rate of myocardial deformation (strain rate or myocardial velocity gradient) can be calculated. In validation studies, Doppler-derived strain accurately reflected regional myocardial shortening and lengthening when compared to measurements by sonometric crystals. Since then, strain rate imaging (SRI) has been examined in animal and clinical studies for the assessment of cardiac function.

Strain And Strain Rate Echocardiography

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Echocardiographic Strain Imaging for Myocardial Viability

Echocardiographic strain imaging was introduced by Heimdal et al in 19981 as a means to calculate myocardial regional function from tissue Doppler velocity data.2,3 Strain imaging is a variation of the previous concept of tissue Doppler myocardial velocity gradient, which calculates regional thickening independent of passive whole heart motion.4,5 Because routine clinical evaluation of regional function is usually by visual wall-motion assessment, strain imaging has great promise to improve objective quantification of regional function. Strain imaging calculates deformation, which translates clinically to percent shortening in the longitudinal dimension (assessed from apical views) or percent thickening in the radial dimension (assessed from parasternal views).1,6,7 Theoretically, it has the important advantage of differentiating active myocardial motion from passive translational or tethering movements that other echocardiographic-Doppler approaches cannot differentiate. Indeed, there have been literally hundreds of publications over the last 10 years detailing a wide range of experimental and potential clinical applications of strain imaging; however, currently, few centers have adopted strain imaging in their routine clinical practice, preferring visual “eyeball” assessment, even though this is inherently subjective and requires a high level of experience and training.8 An important question remains: Is it now time for strain imaging to be adopted in a widespread clinical sense? Articles pp 3892 and 3901 Two important articles are contained in this issue of Circulation that address the application of strain imaging as a tool to assess myocardial viability: an animal study of experimental ischemia and infarction by Lyseggen et al9 and a clinical study using dobutamine echocardiography with outcome data after revascularization by Hanekom et al.10 The article by Lyseggen et al illustrates the additive value of strain imaging in an elegant open-chest animal model of coronary occlusion and reperfusion. Echocardiographic strain imaging was performed along with simultaneous dimensional …

254 Comparison of resting and exercise strain rate echocardiography parameters of patients with and without left ventricular associated with diastolic dysfunction

254 Comparison of resting and exercise strain rate echocardiography parameters of patients with and without left ventricular associated with diastolic dysfunction

Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism: An experimental strain rate echocardiographic study

Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR ( P < .0001), end-systolic strain ( P < .0001), and peak SRs of myocardial early and late filling waves ( P < .0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.

Differentiation of Systolic and Diastolic Heart Failure using Strain and Strain Rate Echocardiography

Background and Objectives:Diastolic heart failure (DHF) is defined as clinical evidences of heart failure, with a normal ejection fraction (EF) and abnormal diastolic function. However, the distinction between DHF and SHF is often difficult. Strain (S) and strain rate (SR) echocardiography can measure the regional myocardial function as a magnitude and rate of deformation. The hypothesis“myocardial velocity (Vel), S & SR can provide additional information for differentiation DHF from SHF”was assessed. Subjects and Methods: 30 patients with symptomatic HF and low EF (SHF group) and 27 with symptomatic HF, and normal EF and diastolic dysfunction (DHF group) were enrolled. 37 age-and sex-matched control subjects were recruited. Conventional echo and regional indices (Vel, S and SR), measured at the mid septum and posterior wall, were obtained. Results:Almost all clinical and echo indices of control were different between the two HF groups. The EF, LV mass, S’ and DT in DHF were greater than those with SHF. The LA size, diastolic dysfunction grades; E, A, E/A, E’, A’ and E/E’, were not different between the two HF groups. In the regional indices, the peak S (long axis: 12.0±5.4 vs. 17.6±5.9%, radial axis: 26.4±12.7 vs. 46.0±16.7%) and systolic Vel (long axis: 2.6±0.8 vs. 3.6±0.9 cm/s, radial axis: 2.1 (1.2 vs. 3.7±1.4 cm/s) with SHF were significantly lower than those with DHF. However, the SR of the two groups was not different. The best cutoff values of peak S were 13.7% (long axis) and 32.9% (radial axis), and the systolic Vel were 3.0 cm/s (long axis) and 2.8 cm/s (radial axis). Conclusion:The peak S and systolic Vel may be useful indices for differentiating DHF from SHF. A similarly decreased SR in the two HF groups suggests that DHF has decreased myocardial contractility, despite the normal EF. (Korean Circulation J 2004; 34(11):1090-1098)

Tissue Doppler, strain, and strain rate echocardiography for the assessment of left and right systolic ventricular function

Tissue Doppler (TDE), strain, and strain rate echocardiography are emerging real time ultrasound techniques that provide a measure of wall motion. They offer an objective means to quantify global and...

Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block

ObjectivesWe studied the effects of cardiac resynchronization therapy (CRT) on regional myocardial strain distribution, as determined by echocardiographic strain rate (SR) imaging. BackgroundDilated hearts with left bundle branch block (LBBB) have an abnormal redistribution of myocardial fiber strain. The effects of CRT on such abnormal strain patterns are unknown. MethodsWe studied 18 patients (12 males and 6 females; mean age 65 ± 11 years [range 33 to 76 years]) with symptomatic systolic heart failure and LBBB. Doppler myocardial imaging studies were performed to acquire regional longitudinal systolic velocity (cm/s), systolic SR (s−1), and systolic strain (%) data from the basal and mid-segments of the septum and lateral wall before and after CRT. By convention, negative SR and strain values indicate longitudinal shortening. ResultsBefore CRT, mid-septal peak SR and peak strain were lower than in the mid-lateral wall (peak SR: −0.79 ± 0.5 [septum] vs. −1.35 ± 0.8 [lateral wall], p < 0.05; peak strain: −7 ± 5 [septum] vs. −11 ± 5 [lateral wall], p < 0.05). This relationship was reversed during CRT (peak SR: −1.35 ± 0.8 [septum] vs. −0.93 ± 0.6 [lateral wall], p < 0.05; peak strain: −11 ± 6 [septum] vs. −7 ± 6 [lateral wall], p < 0.05). Cardiac resynchronization therapy reversed the septal–lateral difference in mid-segmental peak strain from −46 ± 94 ms (LBBB) to 17 ± 92 ms (CRT; p < 0.05). ConclusionsLeft bundle branch block can lead to a significant redistribution of abnormal myocardial fiber strains. These abnormal changes in the extent and timing of septal–lateral strain relationships can be reversed by CRT. The noninvasive identification of specific abnormal but reversible strain patterns should help to improve patient selection for CRT.

Decreased left ventricular longitudinal contraction in normotensive and normoalbuminuric patients with Type II diabetes mellitus: a Doppler tissue tracking and strain rate echocardiography study

Type II diabetes mellitus is associated with congestive heart failure with preserved ejection fraction. This group of patients has been assumed to have isolated diastolic dysfunction; however, the longitudinal systolic contraction of the left ventricle has not been studied previously. The objective of the present study was to investigate the longitudinal contraction of the left ventricle in normotensive Type II diabetes mellitus patients with normal ejection fraction. We examined 32 normotensive patients with Type II diabetes mellitus with ejection fraction >0.55 and fractional shortening >0.25. Exclusion criteria were angina pectoris, cardiac valve disease, albuminuria, retinopathy or neuropathy. Normal subjects (n =32) served as controls. A 16 segment model of motion amplitude assessed left ventricular longitudinal contraction and the average of the segments was calculated as the tissue tracking score index. Peak systolic velocity and strain rate was also obtained in each segment. Patients with Type II diabetes mellitus had a significantly lower tissue tracking score index compared with normal subjects (5.8+/-1.6 mm compared with 7.7+/-1.1 mm; P <0.001). Mean peak systolic velocity was also significantly lower (4.3+/-1.5 cm/s compared with 5.4+/-1.0 cm/s; P <0.001), as well as peak systolic strain rate (-1.2+/-0.3 s(-1) compared with -1.6+/-0.4 s(-1); P <0.001). Patients with Type II diabetes mellitus and preserved diastolic function had a significantly lower tissue tracking score index compared with normal subjects (6.6+/-1.5 mm; P <0.001), but patients with diastolic dysfunction had an even more profound decrease in tissue tracking score index compared with patients without diastolic dysfunction (4.9+/-0.9 mm; P <0.01). In conclusion, the longitudinal systolic contraction was significantly decreased in normotensive patients with Type II diabetes mellitus with normal ejection fraction, which was most profound in patients with concomitant diastolic dysfunction.

2644 Altered myocardial energy transport can be detected functionally by echocardiographic strain rate analysis of energetically demanding cardiac phases

2644 Altered myocardial energy transport can be detected functionally by echocardiographic strain rate analysis of energetically demanding cardiac phases

Strain and strain rate echocardiography.

Strain and strain rate echocardiography is an emerging technique for assessing myocardial systolic and diastolic function. It is envisioned that this modality could change the quantitative assessment of regional wall motion and improve the accuracy and reproducibility of test readings. Myocardial strain and strain rate can detect inducible ischemia and at earlier stages than visual estimation of wall motion or wall thickening parameters. Changes in systolic strain rate and strain have potential to discriminate between different myocardial viability states. Measurement of diastolic rate of deformation can differentiate physiologic from pathologic hypertrophy, and restrictive from constrictive cardiomyopathy. This article reviews basic principles and current experimental and clinical applications of strain and strain rate echocardiography.

Strain and Strain Rate Echocardiography

Strain and Strain Rate Echocardiography

Strain-rate echocardiography: A new quantitative tool for measurement of regional myocardial function during experimentally altered myocardial energetics Peter C. Anagnostopoulos, Marek Belohlavek, Petras Dzeja, James B. Seward. Mayo Clinic, Rochester, MN

Strain-rate echocardiography: A new quantitative tool for measurement of regional myocardial function during experimentally altered myocardial energetics Peter C. Anagnostopoulos, Marek Belohlavek, Petras Dzeja, James B. Seward. Mayo Clinic, Rochester, MN