Halfdan Ihlen

New Noninvasive Method for Assessment of Left Ventricular Rotation: Speckle Tracking Echocardiography

Background— Left ventricular (LV) torsion is due to oppositely directed apical and basal rotation and has been proposed as a sensitive marker of LV function. In the present study, we introduce and validate speckle tracking echocardiography (STE) as a method for assessment of LV rotation and torsion. Methods and Results— Apical and basal rotation by STE was measured from short-axis images by automatic frame-to-frame tracking of gray-scale speckle patterns. Rotation was calculated as the average angular displacement of 9 regions relative to the center of a best-fit circle through the same regions. As reference methods we used sonomicrometry in anesthetized dogs during baseline, dobutamine infusion, and apical ischemia, and magnetic resonance imaging (MRI) tagging in healthy humans. In dogs, the mean peak apical rotation was −3.7±1.2° (±SD) and −4.1±1.2°, and basal rotation was 1.9±1.5° and 2.0±1.2° by sonomicrometry and STE, respectively. Rotations by both methods increased (P<0.001) during dobutamine infusion. Apical rotation by both methods decreased during left anterior descending coronary artery occlusion (P<0.007), whereas basal rotation was unchanged. In healthy humans, apical rotation was −11.6±3.8° and −10.9±3.3°, and basal rotation was 4.8±1.7° and 4.6±1.3° by MRI tagging and STE, respectively. Torsion measurement by STE showed good correlation and agreement with sonomicrometry (r=0.94, P<0.001) and MRI (r=0.85, P<0.001). Conclusions— The present study demonstrates that regional LV rotation and torsion can be measured accurately by STE, suggesting a new echocardiographic approach for quantification of LV systolic function.

Determination of cardiac output by Doppler echocardiography.

Cardiac output determined by Doppler echocardiography was compared with that determined by thermodilution at rest and during dobutamine infusion in 10 patients (group A) and by the Fick method at rest in 11 patients (group B). All patients had angina pectoris without valvular heart disease. Maximum spatial blood velocity and cross sectional aortic area were estimated by the Doppler technique and echocardiography. Cardiac output was calculated by multiplying blood velocity by aortic area at various levels in the ascending aorta. The best correlation of cardiac output between the invasive and non-invasive methods was obtained when maximum velocity in the aortic root and the aortic orifice area were used in the calculations. Cardiac output was considerably overestimated when area measurements in the aortic root were used.

Regional myocardial systolic function during acute myocardial ischemia assessed by strain Doppler echocardiography

OBJECTIVES We sought to evaluate if echocardiographic strain measurements could detect acute myocardial ischemia, and to compare this new method with myocardial velocity measurements and wall motion score index. BACKGROUND Tissue Doppler echocardiography (TDE) is a promising method for assessing regional myocardial function. However, myocardial velocities measured by tissue Doppler echocardiography (TDE) vary throughout the left ventricle (LV) because of tethering effects from adjacent tissue. Strain Doppler echocardiography (SDE) is a new tool for measuring regional myocardial deformation excluding the effect of adjacent myocardial tissue. METHODS Seventeen patients undergoing angioplasty of the left anterior descending coronary artery (LAD) were studied. Left ventricular longitudinal wall motion was assessed by TDE and SDE from the apical four-chamber view before, during and after angioplasty from multiple myocardial segments simultaneously. RESULTS Systolic strain values were uniformly distributed in the different nonischemic LV segments, whereas systolic velocities decreased from basis to apex. During LAD occlusion, strain measurement showed expansion in the apical septal segment in 16 of 17 patients (7.5 +/- 6.5% vs. -17.7 +/- 7.2%, p < 0.001) and reduced compression in the mid-septal segment (p < 0.05) compared with baseline. Segments not supplied by LAD remained unchanged. Tissue Doppler echocardiography showed reduced velocities in all septal segments (p < 0.05) during angioplasty even though LAD does not supply the basal septal segment. Negative systolic velocities were present in 11 of 17 patients. Wall motion score index increased during ischemia (1.3 +/- 0.4, p < 0.05). CONCLUSIONS The new SDE approach might be a more accurate marker than TDE for detecting systolic regional myocardial dysfunction induced by LAD occlusion.

Quantification of left ventricular systolic function by tissue Doppler echocardiography: added value of measuring pre- and postejection velocities in ischemic myocardium.

Background—Tissue Doppler imaging (TDI) is a potentially powerful method for diagnosing myocardial ischemia. This study was designed to investigate how velocity patterns in ischemic myocardium relates to regional function, and to determine whether timing of velocity measurements relative to ejection and isovolumic phases may increase the diagnostic power of TDI. Methods and Results—In 17 open-chest anesthetized dogs we measured pressures by micromanometers, myocardial longitudinal segment lengths by sonomicrometry, and velocities by TDI. Myocardial longitudinal strain rate was calculated as velocity divided by distance to the left ventricle apex. Moderate ischemia (left anterior descending coronary artery stenosis) caused parallel reductions in regional systolic shortening by sonomicrometry (P <0.05) and in peak systolic velocities by TDI (P <0.05). Severe ischemia (left anterior descending coronary artery occlusion), however, induced systolic lengthening by sonomicrometry (P <0.001), whereas peak TDI velocity during ejection remained positive (P <0.05). When velocities during isovolumic contraction (IVC) and isovolumic relaxation (IVR) were included, TDI correlated well with sonomicrometry; ie, systolic lengthening occurred predominantly during IVC and was evident as negative velocities (r =0.70, P <0.001), and postsystolic shortening during IVR (r =0.72, P <0.001) as positive velocities. In nonischemic myocardium peak systolic strain rates were more uniform than velocities. Conclusion—The present results indicate that peak ejection velocity is an inappropriate measure of function in severely ischemic myocardium. Dyskinetic myocardium deforms predominantly during the isovolumic phases, and therefore IVC and IVR velocities are better markers of function. When isovolumic as well as ejection velocities are measured, TDI has excellent ability to quantify regional myocardial dysfunction. Longitudinal strain rates are more uniform than velocities and may further improve the diagnostic power of TDI.

Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.

BackgroundColor M-mode Doppler echocardiography has been suggested as a new noninvasive technique for assessing left ventricular diastolic function. The present study investigated intraventricular filling pattern by color M-mode Doppler in patients during percutaneous transluminal coronary angioplasty (PTCA). In a dog model of myocardial ischemia, the color M-mode flow pattern was related to indices of global and regional myocardial function. Methods and ResultsFrom color M-mode images, the time difference (TD) between occurrence of peak velocity in the apical region and at the mitral tip was determined in 20 patients and eight anesthetized dogs during coronary occlusions. During PTCA, the timing of peak velocity was progressively delayed from mitral valve to apex. Consistent with this, the dog model showed delayed apical filling during coronary occlusion; TD increased from 18±4 to 71±9 milliseconds (P<.01). In the ischemic region, systolic shortening (sonomicrometry) decreased from 20±3% to -5±2% (P<.01). The one-third filling fraction decreased from 59±5% to 31±6% (P<.01) and correlated with TD (r=.85, p>.01). The time constant of isovolumic relaxation (T) increased slightly and correlated with TD (r=.81, p>.01). Pacing tachycardia, caval constriction, and volume loading were performed to mimic the ischemia-induced changes in heart rate, stroke volume, and intracavitary filling pressure, respectively. There were no significant changes in TD or during these interventions. ConclusionsColor M-mode Doppler echocardiography showed a marked delay of apical peak filling velocity during PTCA. The experimental data suggest that this reflects retarded filling of the ischemic ventricle. Thus, color M-mode Doppler may provide a useful method for assessing diastolic dysfunction.

Left atrial volumes assessed by three- and two-dimensional echocardiography compared to MRI estimates

Objectives: The aim of the present study was to establish the accuracy and reproducibility of left atrial volume measurements by three-dimensional (3D) echocardiography compared to 2D biplane and monoplane measurements. Background: No echocardiographic technique is generally accepted as optimal for estimation of left atrial size. Methods: Left atrial volumes of 18 unselected cardiac patients were obtained with magnetic resonance imaging (MRI) (volumes 145 ± 58 ml). These volumes were compared with those obtained with different echocardiographic methods: a multiplane 3D method based on 90 images acquired by apical probe rotation, a simplified 3D method using only the three standard apical views, and 2D biplane and monoplane methods based on area-length, disc summation and spherical formulas. Results: The echocardiographic methods significantly underestimated maximum left atrial volumes as obtained by MRI by 14–37% (p < 0.001). Accuracy, expressed as 1 SD of individual estimates around this systematic underestimation, was 25 to 27% for all methods, except for the 2D 2-chamber monoplane method (37%). Interobserver coefficient of variation was between 14 and 20% for all methods (n.s.). Conclusion: All echocardiographic methods significantly underestimated left atrial volumes as obtained by MRI. A minor non-significant improvement in individual echocardiographic estimates by the 3D methods was obtained at the cost of more time consumption. In unselected patients ultrasound image quality precludes significant improvement of left atrial volume measurements by the applied 3D methods.

Postsystolic Shortening in Ischemic Myocardium Active Contraction or Passive Recoil

Background—Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE). Methods and Results—In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4±1.2% to 5.9±0.9% (P <0.05), whereas postsystolic shortening increased from 1.1±0.3% to 4.2±0.7% (P <0.05). In hypokinetic and akinetic segments, LV pressure–segment length and LV stress–segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2±1.0% (P <0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (r =0.83, P <0.01). Conclusions—Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.

Global longitudinal strain measured by two-dimensional speckle tracking echocardiography is closely related to myocardial infarct size in chronic ischaemic heart disease

2D-STE (two-dimensional speckle tracking echocardiography) is a novel echocardiographic modality that enables angle-independent assessment of myocardial deformation indices. In the present study, we tested whether peak systolic epsilon(parallel) (longitudinal strain) values measured by 2D-STE could identify areas of MI (myocardial infarction) as determined by CE MRI (contrast-enhanced magnetic resonance imaging). Conventional echocardiographic apical long-axis recordings were performed in 38 patients, 9 months after a first MI. Peak systolic epsilon(parallel) measured by 2D-STE in 16 left ventricle segments was compared with segmental infarct mass and transmurality assessed by CE MRI. Segmental values were averaged to global and territorial values for assessment of global function and myocardial function in the coronary distribution areas. CE MRI identified transmural infarction in 27 patients, and a mean infarct size of 36+/-25 g. Peak systolic epsilon( parallel) correlated with the infarct mass at the global level (r=0.84, P<0.001). A strain value of -15% identified infarction with 83% sensitivity and 93% specificity at the global level and 76% and 95% at the territorial level, and a strain value of -13% identified transmural infarction with 80% sensitivity and 83% specificity at the segmental level. Global infarct mass correlates with the wall motion score index (r=0.70, P<0.001), and left ventricular ejection fraction measured by MRI or echocardiography (r=-0.71 and -0.58, both P<0.001). In chronic infarction, peak systolic epsilon(parallel) measured by 2D-STE correlates with the infarct mass assessed by CE MRI at a global level, and separates infarcted from non-infarcted tissue. Global strain is an excellent predictor of myocardial infarct size in chronic ischaemic heart disease.

Noninvasive Separation of Large, Medium, and Small Myocardial Infarcts in Survivors of Reperfused ST-Elevation Myocardial Infarction A Comprehensive Tissue Doppler and Speckle-Tracking Echocardiography Study

Background—The objective of the study was to evaluate the ability of established and new parameters of global systolic left ventricle function to estimate myocardial infarct size. Increasing infarct extent is associated with impaired prognosis in chronic ischemic heart disease. Systolic myocardial deformation is a complex 3D process that is mainly influenced by the amount and transmural distribution of viable myocardium. Speckle-tracking echocardiography (2D-STE) enables deformation assessment along the 3 main cardiac axes independent of insonation angle. Methods and Results—Global longitudinal, circumferential, and radial strain and left ventricle twist by 2D-STE, global longitudinal strain rate and strain by tissue Doppler imaging, and left ventricle ejection fraction and wall motion score index were assessed in 40 patients 8.5±5.4 months after a first myocardial infarct and compared with global myocardial infarct mass assessed by contrast-enhanced MRI. Longitudinal and circumferential strain by 2D-STE and longitudinal strain and strain rate by tissue Doppler imaging significantly separated medium-sized infarcts from small or large infarcts at the global level (P<0.05). All deformation indices correlated significantly with global infarct mass (P<0.01). Circumferential and longitudinal strains by 2D-STE demonstrated the best ability to identify medium-sized global myocardial infarcts. Conclusions—Circumferential and longitudinal strains by 2D-STE correlate with myocardial infarct mass and significantly differentiate among large, medium, and small myocardial infarcts.

Intracavitary filling pattern in the failing left ventricle assessed by color M-mode doppler echocardiography

OBJECTIVES The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade. BACKGROUND Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle. METHODS In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling. RESULTS There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution. CONCLUSIONS Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.