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Background: To date, echocardiography has not gained acceptance as an alternative imaging modality for the detection of massive pulmonary embolism (MPE) or submassive pulmonary embolism (SMPE). The objective of this study was to explore the clinical utility of early systolic notching (ESN) of the right ventricular outflow tract (RVOT) pulsed-wave Doppler envelope in the detection of MPE or SMPE., Methods: Two hundred seventy-seven patients (mean age, 56 ± 16 years; 52% women), without known pulmonary hypertension, who underwent contrast computed tomographic angiography for suspected pulmonary embolism (PE) and underwent echocardiography were retrospectively studied. Extent of PE was categorized using standard criteria. ESN identified from pulsed-wave spectral Doppler interrogation of the RVOT was analyzed, as were other echocardiography parameters such as McConnell's sign, the "60/60" sign, and acceleration and deceleration times of the RVOT Doppler signal. Analysis was conducted using probability statistics and receiver operating characteristic curve analysis., Results: Of the 277 patients studied, 100 (44%) had MPE or SMPE, 87 (38%) had subsegmental PE, and 90 (39%) did not have PE. ESN was observed in 92% of patients with MPE or SMPE, 2% with subsegmental PE, and in no patients without PE. Interobserver assessment of early systolic notching demonstrated 97% agreement (κ = 0.93, P < .001). Compared with more widely recognized echocardiographic parameters, the area under the receiver operating characteristic curve (AUC) of 0.96 (95% CI, 0.92-0.98) for ESN was superior to that for McConnell's sign (AUC, 0.75; 95% CI, 0.68-0.80), the 60/60 sign (AUC, 0.74; 95% CI, 0.68-0.79), and RVOT acceleration time ≤ 87 msec (AUC, 0.84; 95% CI, 0.79-0.88), as well as other study Doppler variables, in patients with computed tomography-confirmed MPE or SMPE., Conclusions: The pulmonary Doppler flow pattern of ESN appears to be a promising noninvasive sign observed frequently in patients with MPE or SMPE. Future prospective study to ascertain diagnostic utility in a broader population is warranted., (Copyright © 2019 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

Background: Assessment of aortic regurgitation (AR) severity is often based on Doppler echocardiographic imaging. Hemodynamic responses to AR are influenced by the interplay among cardiovascular properties, including left ventricular (LV) and aortic tissue properties, that cannot be measured directly. The aim of this study was to investigate how both echocardiographic measures of AR severity and the hemodynamic consequences of AR are influenced by LV and aortic stiffness., Methods: AR was simulated using the CircAdapt computational model of the human cardiovascular system. Simulations were performed with normal LV and aortic stiffness, high LV stiffness, high aortic stiffness, and high LV and aortic stiffness. For each configuration of levels of stiffness, four AR severity grades were simulated by setting the effective regurgitant orifice area (ROA) of the aortic valve at 0, 0.05, 0.25, and 0.6 cm 2 , representing no, mild, moderate, and severe AR, respectively. The regurgitant volume, regurgitant fraction (RF), and pressure half-time (PHT) were computed for each simulation giving an AR severity score (mild, moderate, or severe). Mean left atrial pressure was also calculated., Results: Increasing ROA resulted in faster decay of diastolic flow velocity and larger regurgitant blood flow across the aortic valve. This caused shorter PHT and larger regurgitant volume and RF, all indicating higher AR severity. Increasing aortic stiffness resulted in a larger decline in diastolic aortic pressure, whereas increasing LV stiffness resulted in a larger rise in diastolic LV pressure. Hence, increasing LV and/or aortic stiffness led to faster decay of the transvalvular pressure gradient and, therefore, to faster decay of diastolic flow velocity across the aortic valve compared with normal stiffness with the same ROA. This faster decay led, on one hand, to a shorter PHT, indicating higher severity scores, and, on the other hand, to a lower RF, as less regurgitant blood volume traveled into the left ventricle, indicating lower severity scores. AR severity scores reflected mean left atrial pressure poorly when variations in tissue properties were present., Conclusions: Simulating altered AR hemodynamics caused by variations in cardiovascular tissue properties led to inconsistent severity scores when evaluating the severity using RF, regurgitant volume, and PHT. In this situation, pulmonary congestion is poorly reflected by AR severity as quantified by ROA, RF, and PHT. Cardiac and aortic tissue properties should therefore be taken into account to improve clinical assessment of AR severity., (Copyright © 2016 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

Background: Tissue Doppler cross-correlation analysis has been shown to be associated with long-term survival after cardiac resynchronization defibrillator therapy (CRT-D). Its association with ventricular arrhythmia (VA) is unknown., Methods: From two centers 151 CRT-D patients (New York Heart Association functional classes II-IV, ejection fraction ≤ 35%, and QRS duration ≥ 120 msec) were prospectively included. Tissue Doppler cross-correlation analysis of myocardial acceleration curves from the basal segments in the apical views both at baseline and 6 months after CRT-D implantation was performed. Patients were divided into four subgroups on the basis of dyssynchrony at baseline and follow-up after CRT-D. Outcome events were predefined as appropriate antitachycardia pacing, shock, or death over 2 years., Results: Mechanical dyssynchrony was present in 97 patients (64%) at baseline. At follow-up, 42 of these 97 patients (43%) had persistent dyssynchrony. Furthermore, among 54 patients with no dyssynchrony at baseline, 15 (28%) had onset of new dyssynchrony after CRT-D. In comparison with the group with reduced dyssynchrony, patients with persistent dyssynchrony after CRT-D were associated with a substantially increased risk for VA (hazard ratio [HR], 4.4; 95% CI, 1.2-16.3; P = .03) and VA or death (HR, 4.0; 95% CI, 1.7-9.6; P = .002) after adjusting for other covariates. Similarly, patients with new dyssynchrony had increased risk for VA (HR, 10.6; 95% CI, 2.8-40.4; P = .001) and VA or death (HR, 5.0; 95% CI, 1.8-13.5; P = .002)., Conclusions: Persistent and new mechanical dyssynchrony after CRT-D was associated with subsequent complex VA. Dyssynchrony after CRT-D is a marker of poor prognosis., (Copyright © 2015 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

Background: Response to cardiac resynchronization therapy is variable. The aim of this study was to test the hypothesis that left ventricular (LV) lead position in proximity to myocardial scar is associated with less favorable outcomes., Methods: A total of 149 patients were included in this substudy of the Speckle Tracking Assisted Resynchronization Therapy for Electrode Region trial using echocardiographic radial strain for basal and middle LV segments and transverse strain for apical segments to estimate scar. Sixty-four patients with high-dose rest (99m)Tc sestamibi single-photon emission computed tomographic imaging were used for validation in 508 LV free-wall segments. The relationship of LV lead position to segments estimated as scar was defined as concordant, adjacent, or remote. The prespecified primary end point was heart failure hospitalization or death over 2 years., Results: Wall thickening < 10% by radial strain in LV free wall segments was associated with absent (99m)Tc sestamibi uptake indicative of scar with 77% sensitivity and 89% specificity and strain < 10% was accordingly used as the surrogate for scar. Event-free survival was most favorable in patients with nonischemic disease (79%), similarly favorable in patients with ischemic disease and LV leads remote from scar (74%), but significantly worse in patients with ischemic disease and LV leads adjacent to (61%) or within scar (41%) (P = .004). Preserved wall thickening at the LV lead site was independently associated with favorable outcome and additive to pacing at the site of latest mechanical activation (P = .001) and remained significant after adjusting for scar burden., Conclusions: Echocardiographic speckle-tracking strain has the potential to estimate free wall scar in patients with ischemic cardiomyopathy and influence LV lead positioning away from scar to improve clinical outcomes after cardiac resynchronization therapy., (Copyright © 2014 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.)

Echocardiographic strain imaging, also known as deformation imaging, has been developed as a means to objectively quantify regional myocardial function. First introduced as post-processing of tissue Doppler imaging velocity converted to strain and strain rate, strain imaging has more recently also been derived from digital speckle tracking analysis. Strain imaging has been used to gain greater understanding into the pathophysiology of cardiac ischemia and infarction, primary diseases of the myocardium, and the effects of valvular disease on myocardial function, and to advance our understanding of diastolic function. Strain imaging has also been used to quantify abnormalities in the timing of mechanical activation for heart failure patients undergoing cardiac resynchronization pacing therapy. Further advances, such as 3-dimensional speckle tracking strain imaging, have emerged to provide even greater insight. Strain imaging has become established as a robust research tool and has great potential to play many roles in routine clinical practice to advance the care of the cardiovascular patient. This perspective reviews the physiology of myocardial strain, the technical features of strain imaging using tissue Doppler imaging and speckle tracking, their strengths and weaknesses, and the state-of-the-art present and potential future clinical applications., (Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

The strain delay index is reportedly a marker of dyssynchrony and residual myocardial contractility. The aim of this study was to test the hypothesis that a relatively simple version of the strain dyssynchrony index (SDI) can predict response to cardiac resynchronization therapy (CRT) and that combining assessment of radial, circumferential, and longitudinal SDI can further improve the prediction of responders. A total of 52 patients who underwent CRT were studied. The SDI was calculated as the average difference between peak and end-systolic strain from 6 segments for radial and circumferential SDI and 18 segments for longitudinal SDI. Conventional dyssynchrony measures were assessed by interventricular mechanical delay, the Yu index, and radial dyssynchrony by speckle tracking strain. Response was defined as a ≥15% decrease in end-systolic volume after 3 months. Of the individual parameters, radial SDI ≥6.5% was the best predictor of response to CRT, with sensitivity of 81%, specificity of 81%, and an area under the curve of 0.87 (p <0.001). Circumferential SDI ≥3.2% and longitudinal SDI ≥3.6% were also found to be predictive of response to CRT, with areas under the curve of 0.81 and 0.80, respectively (p <0.001). Moreover, radial, circumferential, and longitudinal SDI at baseline were correlated with reduction of end-systolic volume with CRT. In addition, the response rate in patients with 3 positive SDIs was 100%. In contrast, rates in patients with either 1 or no positive SDIs were 42% and 22%, respectively (p <0.005 and p <0.001 vs 3 positive SDIs). In conclusion, the SDI can successfully predict response to CRT, and the combined approach leads to more accurate prediction than using individual parameters., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objectives: The goals of this study were to compare patterns of mechanical activation in patients with chronic right ventricular (RV) pacing with those with left bundle branch block (LBBB) using 2-dimensional and novel 3-dimensional speckle tracking, and to compare ejection fraction (EF) response and long-term survival after cardiac resynchronization therapy (CRT)., Background: Several randomized CRT trials have excluded patients with chronic RV pacing, and current guidelines for CRT include patients with intrinsically widened QRS, typically LBBB., Methods: We studied 308 patients who were referred for CRT: 227 had LBBB, 81 were RV paced. Dyssynchrony was assessed by tissue Doppler, routine pulsed Doppler, and 2-dimensional speckle-tracking radial strain. 3D strain was assessed using speckle tracking from a pyramidal dataset in a subset of 57 patients for mechanical activation mapping. Survival after CRT was compared with survival in a group of 46 patients with attempted, but failed, CRT., Results: Patients with chronic RV pacing and LBBB had similar intraventricular dyssynchrony, with opposing wall delays by tissue Doppler of 82 +/- 45 ms versus 87 +/- 63 ms and anteroseptum-to-posterior delays by speckle tracking of 225 +/- 142 ms, versus 211 +/- 107 ms, respectively. RV-paced patients, however, had greater interventricular dyssynchrony: 44 +/- 24 ms versus 35 +/- 21 ms (p < 0.01), which correlated with their greater QRS duration (p < 0.001). Sites of latest mechanical activation were most often posterior or lateral in both groups, but RV-paced patients had sites of earliest activation more often from the inferior-septum and apex (p < 0.05). EF response was similar in RV-paced and LBBB groups, and survival free from transplantation or mechanical support after CRT was similarly favorable as compared with failed CRT patients over 5 years (p < 0.01)., Conclusions: RV-paced patients, when compared with LBBB patients, had similar dyssynchronous patterns of mechanical activation and greater interventricular dyssynchrony. Importantly, RV-paced patients had similar EF response and long-term outcome as those with LBBB, which supports their candidacy for CRT., (Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objective: To determine the subclinical effects of isolated obesity and its duration on cardiac function by using routine echocardiography and tissue Doppler myocardial strain rate., Methods: Forty-nine subjects were enrolled in this study; 29 with isolated obesity defined as a body mass index > or = 30 kg/m(2) with no other cardiovascular comorbidities, and 20 nonobese controls. All subjects underwent two-dimensional and Doppler echocardiography including tissue Doppler imaging and myocardial strain rate., Results: The average duration of obesity was 12.1 years (4-18 years). Abnormalities of left ventricular (LV) wall thickness, mass, diastolic function, and left atrial size were detected in obese individuals, despite having preserved ejection fractions. The LV global longitudinal peak strain rate was significantly lower in obese subjects compared to nonobese control subjects (1.07 +/- 0.14 vs. 1.38 +/- 0.12, P < 0.001). Using multivariate analysis, the duration of obesity (ss=-0.76, P < 0.001), body mass index (ss=-0.35, P = 0.023), and age (ss=-0.29, P = 0.009) were independent predictors of the decreased LV global longitudinal peak strain rate, while the duration of obesity (ss=-0.66, P < 0.001) and body mass index (ss=-0.28, P = 0.037) were independent predictors of the decreased right ventricular (RV) peak strain rate., Conclusion: The presence and the duration of obesity were associated with impairment of subclinical biventricular systolic and diastolic function. These findings have the potential to increase awareness of subclinical cardiac manifestations in patients with isolated obesity and influence their early management.

Background: Although several echocardiographic approaches exist to quantify mechanical dyssynchrony, the comparative ability of different manufacturers' speckle-tracking software programs to predict response to cardiac resynchronization therapy (CRT) is unknown., Methods: Eighty-four patients with heart failure referred for CRT were studied (mean age, 64 +/- 12 years; mean ejection fraction [EF], 26 +/- 7%; mean QRS duration, 157 +/- 26 ms). Dyssynchrony was assessed using the same midventricular short-axis digital cine loop for each patient with 3 different offline speckle-tracking strain analysis programs: software A, speckle-tracking two-dimensional strain; software B, velocity vector imaging strain; and software C, speckle-tracking strain. Significant dyssynchrony was defined as an anterior septum-to-posterior wall delay > or =130 ms. Follow-up was available for 57 patients (mean, 7 +/- 4 months). Response to CRT was defined as an EF increase > or =15%., Results: Variability between software results was observed when patients had large degrees of dyssynchrony (> or =200 ms), with limits of agreement from 123 to 214 ms. However, close agreement for identifying patients with significant dyssynchrony was observed: 91% for software A versus B, 96% for software A versus C, and 93% for software B versus C. Importantly, the 3 software approaches' ability to predict EF outcome had similar sensitivities, specificities, and areas under receiver operating characteristic curves: 0.87, 0.86, and 0.86, respectively., Conclusions: Radial strain dyssynchrony analyses by 3 different speckle-tracking software programs were similarly able to predict EF response to CRT. Although variability in absolute values of dyssynchrony was observed, there was close agreement for determining the presence or absence of significant dyssynchrony. Speckle-tracking echocardiography has potential as a means to quantify dyssynchrony in a multicenter clinical trial or clinical practice.

Objectives: The purpose of this study was to test the hypothesis that a combined echocardiographic assessment of longitudinal dyssynchrony by tissue Doppler imaging (TDI) and radial dyssynchrony by speckle-tracking strain may predict left ventricular (LV) functional response to cardiac resynchronization therapy (CRT)., Background: Mechanical LV dyssynchrony is associated with response to CRT; however, complex patterns may exist., Methods: We studied 190 heart failure patients (ejection fraction [EF] 23 +/- 6%, QRS duration 168 +/- 27 ms) before and after CRT. Longitudinal dyssynchrony was assessed by color TDI for time to peak velocity (2 sites in all and 12 sites in a subgroup of 67). Radial dyssynchrony was assessed by speckle-tracking radial strain. The LV response was defined as > or =15% increase in EF., Results: One hundred seventy-six patients (93%) had technically sufficient baseline and follow-up data available. Overall, 34% were EF nonresponders at 6 +/- 3 months after CRT. When both longitudinal dyssynchrony by 2-site TDI (> or =60 ms) and radial dyssynchrony (> or =130 ms) were positive, 95% of patients had an EF response; when both were negative, 21% had an EF response (p < 0.001 vs. both positive). The EF response rate was lowest (10%) when dyssynchrony was negative using 12-site TDI and radial strain (p < 0.001 vs. both positive). When either longitudinal or radial dyssynchrony was positive (but not both), 59% had an EF response. Combined longitudinal and radial dyssynchrony predicted EF response with 88% sensitivity and 80% specificity, which was significantly better than either technique alone (p < 0.0001)., Conclusions: Combined patterns of longitudinal and radial dyssynchrony can be predictive of LV functional response after CRT.

Velocity vector imaging is a novel quantitative echocardiographic technique that was applied to routine grayscale echocardiographic images of 23 patients with heart failure who underwent cardiac resynchronization therapy. The hypothesis was tested that velocity vector imaging can quantify left ventricular mechanical dyssynchrony and predict response to resynchronization therapy. Tissue velocities were determined by the automated tracking of periodic B-mode image patterns on digital cine loops from standard apical 4-chamber, 2-chamber, and long-axis views, with the user tracing the mid left ventricular wall from a single frame. Dyssynchrony was determined as the greatest opposing wall peak longitudinal systolic velocity delay from the 3 views. Responders, defined as those with >or=15% increases in the ejection fraction, had greater baseline dyssynchrony than nonresponders (opposing wall velocity delays of 131 +/- 83 vs 52 +/- 60 ms, p <0.05), and >or=75 ms predicted response with 85% sensitivity and 80% specificity when followed 8 +/- 5 months after resynchronization therapy. Baseline electrocardiographic QRS duration was not predictive in the same patients. In conclusion, echocardiographic velocity vector imaging has potential for clinical utility.

Our objective was to test the hypothesis that novel angle-corrected radial strain imaging can quantify left ventricular dyssynchrony associated with contractile impairment and improved with biventricular pacing. Eight open-chest dogs were studied by novel angle-corrected color-coded radial strain imaging and high-fidelity pressure-conductance catheters recording pressure-volume loops. Heart rate was controlled by right atrial pacing and all timing intervals were corrected by R-R interval (corrected interval = measured interval/(R-R interval)(1/2)). Left bundle branch block, simulated by right ventricular free wall pacing, resulted in marked radial dyssynchrony, which we defined as maximal time difference between peak segmental strain, from 39 +/- 17 to 354 +/- 49 milliseconds and stroke work decreased from 157 +/- 40 to 60 +/- 37 mJ, (P < .005 vs baseline). Depression of contractility by high-dose esmolol (end-systolic pressure-volume relationship from 5.7 +/- 2.4 to 3.6 +/- 1.0 mm Hg/mL) was associated with augmented dyssynchrony to 388 +/- 53 milliseconds (P < .05 vs baseline right ventricular pacing). Biventricular pacing improved dyssynchrony to 55 +/- 19 milliseconds and stroke work to 143 +/- 33 mJ (P < .05 vs right ventricular pacing). Changes in radial dyssynchrony correlated significantly with 6-site average regional strain (r = -0.93 +/- 0.05 individually, r = 0.80 overall) and stroke work (r = -0.88 +/- 0.12 individually, r = -0.82 overall). Angle-corrected radial strain imaging has clinical potential to quantify mechanical dyssynchrony and effects of biventricular pacing.

The Tei index is clinically useful to quantify left ventricular (LV) function, but it requires sequential Doppler recordings from two different views. A related myocardial performance index (MPI) using tissue Doppler (TD) can be rapidly calculated from a single beat; however, its ability to quantify contractility and the effects of acute changes in loading have not been determined. Our aim was to test the hypothesis that TD MPI can quantify contractile state but is affected by acute alterations in loading, using LV pressure-volume relations in an animal model. Eight dogs were studied by using mitral annular TD, high-fidelity pressure, and conductance catheters. TD MPI was calculated as (a' - b')/b', where a' was the duration of mitral annular velocity during diastole and b' was the duration of the systolic wave. End-systolic elastance (Ees), the time constant of isovolumic relaxation (tau), and peak positive and negative first derivative of pressure (dP/dtmax and dP/dtmin, respectively) were used as measures of LV function. Data were obtained at baseline, at dobutamine and esmolol infusion to alter contractile state, and at inferior vena cava and aortic occlusion to alter preload and afterload. TD MPI decreased from 0.83 (SD 0.19) to 0.62 (SD 0.20) with dobutamine and increased to 1.19 (SD 0.26) with esmolol. TD MPI significantly correlated with dP/dtmax (r = -0.76), Ees (r = -0.68), dP/dtmin (r = 0.82), and tau (r = 0.78); however, it was affected by acute decreases in preload [from 0.83 (SD 0.19) to 1.09 (SD 0.36)] and acute increases in afterload [to 1.23 (SD 0.17)]. All the above increases and decreases and r values were significant (P < 0.05 vs. baseline). In conclusion, TD MPI can rapidly quantify alterations in LV contractile state but is affected by acute alterations in preload and afterload.

An 80-year-old woman with severe symptomatic heart failure (ejection fraction of 13%), and left bundle branch block (QRS duration of 160 ms) underwent cardiac resynchronization therapy (CRT). She had significant baseline dyssynchrony with a septal to posterior wall delay of 160 ms by echocardiographic tissue synchronization imaging (TSI). Despite exhaustive efforts, a stable posterior-lateral coronary vein lead position could not be achieved with the standard percutaneous approach, resulting in anterior coronary vein lead placement. This resulted in no improvement in the patient's symptoms or ventricular function. Follow-up TSI revealed earlier activation of the anteroseptal site and worsened dyssynchrony with septal to posterior wall delay of now 290 ms. This information prompted surgical revision of the left ventricular (LV) lead position via limited thoracotomy and posterior-lateral epicardial lead implantation. Pacing at the new lead site resulted in a 30% increase in stroke volume and symptomatic improvement. TSI in this case redirected lead position in a clinical nonresponder, resulting in a favorable response to CRT.

Study Objectives: Early diastolic mitral annular velocity (E') by tissue Doppler echocardiography (TD) has been reported to be a load-independent index of left ventricular (LV) diastolic function, allowing the early diastolic mitral inflow velocity (E)/E' ratio to be used clinically to predict LV filling pressures. However, preload independence of E' has remained controversial, and E/E' may not consistently be predictive of LV filling pressures. Our objectives were to test the hypotheses that E' is affected by preload, and that alterations of preload, afterload, and contractility also affect E/E'. DESIGN, INTERVENTIONS, AND MEASUREMENTS: An open-chest dog model was used (n = 8). High-fidelity pressure and conductance catheters were used for pressure-volume relations, and E' was obtained by pulsed TD from the apical four-chamber view. Changes in preload and afterload were induced by vena caval and partial aortic occlusions, respectively. Data were collected during control phase and during infusions of dobutamine and esmolol to alter contractility., Results: E' was consistently and significantly associated with acute decreases in LV end-diastolic pressure in each dog (n = 200 beats; r = 0.93 +/- 0.06 [mean +/- SD]). Similar results occurred with dobutamine and esmolol infusions. This preload sensitivity was reflected in E/E', which was inversely (rather than directly) correlated with LV diastolic pressure (r = - 0.67). E/E' was less affected by preload when diastolic dysfunction was induced by sustained partial aortic occlusion (time constant of relaxation increased from 46 +/- 19 to 53 +/- 21 ms, p < 0.001)., Conclusions: E' was significantly influenced by preload with preserved LV function and low filling pressures (< 12 mm Hg); accordingly, E/E' was less predictive of LV filling pressures in this scenario. E/E' was more predictive of LV filling pressures in the presence of diastolic dysfunction.

Tissue Doppler echocardiography (TDE) is a relatively recent addition to the diagnostic ultrasonographic examination. This is similar to routine Doppler ultrasonography to assess blood flow, but technologic features focus on lower velocity frequency shifts. Two techniques are used to assess myocardial function: pulsed TDE and color-coded TDE. A great deal of data has been generated on TDE over the last 5 years, and this review allows for only a small portion of these emerging data to be discussed. One clinical application is to assess peak systolic mitral annular velocity from the apical windows as an index of global ventricular function. The six-site average for peak systolic mitral annular velocity by the color-coded TDE method of greater than 5.4 cm/sec is predictive of an ejection fraction greater than 50% with an 88% sensitivity and a 97% specificity. An emerging application is to use pulsed-TDE to assess ventricular filling pressures. The mitral annular to inflow ratio (E/Ea) greater than 10 is predictive of a mean pulmonary capillary wedge pressure greater than 15 mm Hg with a 92% sensitivity and 80% specificity. Another application is to use peak early diastolic velocity to help differentiate constrictive pericarditis from restrictive cardiomyopathy. Peak early diastolic velocity is blunted with restrictive cardiomyopathy and preserved with constrictive pericarditis. These are just a few of the many evolving clinical applications of this new quantitative diagnostic ultrasonographic method.

TDI is a new echocardiographic technique that calculates and displays color-coded myocardial velocity on-line. To determine the feasibility of endocardial velocity throughout the cardiac cycle as a means to quantify regional function, 20 normal subjects aged 30 +/- 5 years and 12 patients with heart disease aged 62 +/- 17 years were studied with a prototype TDI system. TDI M-mode images were acquired by using a multicolored velocity map (display range, -30 to 30 mm/sec; temporal resolution, 90 Hz). Color-coded velocity data were then converted to numeric values off-line at 50 msec intervals. Posterior wall velocities throughout the cardiac cycle by TDI were closely correlated with velocity calculations from the first derivative of routine digitized M-mode tracings (group mean r = 0.88 +/- 0.03, SEE = 7.0 +/- 1.1 mm/sec). Anteroseptal TDI color-coded systolic velocity occurred 164 +/- 84 msec from the onset of the electrocardiographic QRS compared with 203 +/- 33 msec in the posterior wall (P < 0.05) in normal subjects, consistent with normal electrical activation. Significant differences in systolic and diastolic posterior wall TDI velocity data were observed in patients with hypokinetic or akinetic segments assessed by independent routine study when compared with normal controls. Calculated systolic and early diastolic posterior wall TDI indexes correlated significantly with percentage of wall thickening. Of abnormal anteroseptal segments, TDI systolic time velocity integrals were significantly different than normal and correlated with percentage of wall thickening. TDI has potential to quantitatively assess regional left ventricular function.

Mitral annular descent has been described as an index of left ventricular (LV) systolic function, which is independent of endocardial definition. Echocardiographic tissue Doppler imaging is a new technique that calculates and displays color-coded cardiac tissue velocities on-line. To evaluate mitral annular descent velocity as a rapid index of global LV function, we performed tissue Doppler imaging studies in 55 patients, aged 56 +/-15 years, within 3 hours of radionuclide ventriculographic ejection fraction. Tissue Doppler M-mode studies were obtained from each of 6 mitral annular sites, as follows: inferoseptal and lateral from apical 4-chamber views, anterior and inferior from apical 2-chamber views, and anteroseptal and posterior from apical long-axis views. Only 1 patient with severe mitral annular calcification was excluded. The group mean 6-site average peak mitral annular descent velocity was 5.5 +/- 1.9 cm/s (range 2.4 to 10.5), and the group mean ejection fraction was 49 +/- 18% (range 17 to 80%). The 6-site average peak annular descent velocity correlated linearly with LV ejection fraction (r = 0.86, SEE = 1.02 cm/s): LV ejection fraction = 8.2 (average peak mitral annular descent velocity) + 3%. The 6-site peak mitral annular descent velocity average >5.4 cm/s was 88% sensitive and 97% specific for ejection fraction >50%. The peak mitral annular descent velocity from the apical 4-chamber view (average from inferoseptal and lateral sites) correlated most closely with the LV ejection fraction (r = 0.85) as an individual view. Peak mitral annular descent velocity by tissue Doppler imaging has the potential to estimate rapidly the global LV function.

A new method to measure cardiac output using transgastric continuous-wave Doppler was evaluated in 31 consecutive patients undergoing cardiac surgery with simultaneous measurement of cardiac output by the thermodilution technique. A 5 MHz single-plane imaging/5 MHz continuous-wave Doppler transesophageal transducer was used to image the left ventricular outflow tract, aortic valve and ascending aorta from a modified transgastric short-axis plane. The continuous-wave Doppler cursor was aligned parallel with blood flow across the aortic valve to obtain the maximal Doppler velocity spectra. Stroke volume was obtained by multiplying the mean Doppler flow velocity integral by the aortic annulus area, which was calculated from its diameter measured from the esophageal 5-chamber view. The stroke volume was multiplied by heart rate to yield cardiac output. A total of 57 simultaneous thermodilution and Doppler studies were attempted. Doppler data were technically limited for 2 patients both before and after cardiopulmonary bypass and for 3 patients before cardiopulmonary bypass with a result of 50 adequate studies of 57 (88%) attempted. The Doppler-derived cardiac outputs were correlated with the simultaneous measurements of cardiac output by the thermodilution technique. Linear regression analysis revealed a close correlation with R = 0.91, SEE = 0.8 liter/min, and y = 1.01x + 0.2 (p < 0.001). In conclusion, transgastric continuous-wave Doppler across the aortic valve is a promising new technique that may be used in selected patients for accurate measurement of cardiac output.

A completely noninvasive method for estimating left atrial pressure in patients with congestive heart failure and mitral regurgitation has been devised with the use of continuous-wave Doppler echocardiography and brachial sphygmomanometry. Of 46 patients studied with mitral regurgitation, 35 (76%) had jets with distinct Doppler spectral envelopes recorded. The peak ventriculoatrial gradient was obtained by measuring peak mitral regurgitant velocity in systole and using the modified Bernoulli equation. This gradient was then subtracted from peak brachial systolic blood pressure, an estimate of left ventricular systolic pressure, to yield left atrial pressure (left atrial pressure = systolic blood pressure - mitral regurgitant pressure gradient). Noninvasive estimates of left atrial pressure from 35 patients were plotted against simultaneous recordings of mean pulmonary capillary wedge pressure resulting in the correlation y = 0.88x + 3.3, r = 0.88, standard error of estimate = +/- 4 mm Hg (p less than 0.001). Therefore, continuous-wave Doppler echocardiography and sphygmomanometry may be used in selected patients with congestive heart failure and mitral regurgitation for noninvasive estimation of left atrial pressure.

The effect of percutaneous transluminal coronary angioplasty (PTCA) on left ventricular (LV) diastolic function has not been systematically investigated in patients treated for unstable angina or ischemia after acute myocardial infarction (AMI). To assess the relation between reduction of stenosis severity and improvement in diastolic function in this setting, 42 patients with either unstable angina (n = 22) or post-AMI ischemia (n = 20) were serially monitored by Doppler echocardiography 8 +/- 5 hours before and 2 +/- 1 days after PTCA. Doppler LV filling indexes included isovolumic relaxation time, mitral deceleration time, E/A peak velocity ratio and atrial filling fraction. Eighteen aged-matched control subjects served to establish normal values for comparison. Before PTCA, both groups exhibited abnormal diastolic function demonstrated by prolonged isovolumic relaxation time and mitral deceleration time, decreased E/A ratio and increased atrial filling fraction. After PTCA isovolumic relaxation time and deceleration time decreased 18 +/- 28 (p less than 0.005) and 33 +/- 43 ms (p less than 0.002) in the unstable angina group and 18 +/- 23 (p less than 0.003) and 14 +/- 34 ms (difference not significant), respectively, in the post-AMI ischemia group. An increase in E/A ratio and a decrease in atrial filling fraction occurred in both groups; however, these changes were significant only in patients with post-AMI ischemia (+21%, p less than 0.03 and -11.4%, p less than 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)