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Bioprosthetic valve dysfunction (BVD) and bioprosthetic valve failure (BVF) may be caused by structural or nonstructural valve dysfunction. Both surgical and transcatheter bioprosthetic valves have limited durability because of structural valve deterioration. The main objective of this summary of experts participating in a virtual workshop was to propose standardized definitions for nonstructural and structural BVD and BVF following aortic or mitral biological valve replacement with the goal of facilitating research reporting and implementation of these terms in clinical practice. Definitions of structural BVF, based on valve reintervention or death, underestimate the true incidence of BVF. However, definitions solely based on the presence of high transprosthetic gradient at a given echocardiogram during follow-up overestimate the incidence of structural BVD and BVF. Definitions of aortic or mitral structural BVD must therefore include the confirmation by imaging of permanent structural changes to the leaflets alongside evidence of deterioration in valve hemodynamic function at echocardiography follow-up., Competing Interests: Funding Support and Author Disclosures Dr Pibarot has received funding from Edwards Lifesciences, Medtronic, Pi-Cardia, and Cardiac Phoenix for echocardiography core laboratory analyses and research studies in the field of transcatheter valve therapies, for which he received no personal compensation; and has received lecture fees from Edwards Lifesciences and Medtronic. Dr Herrmann has received institutional research funding from Abbott, Boston Scientific, Edwards Lifesciences, Highlife, Medtronic, and WL Gore; has received consulting fees from Edwards Lifesciences, Medtronic, Wells Fargo, and WL Gore; and has equity in Holistick Medical and Microinterventional Devices. Dr Hahn has received speaker fees from Abbott Structural, Edwards Lifesciences, and Philips Healthcare; has institutional consulting contracts for which she receives no direct compensation with Abbott Structural, Boston Scientific, Edwards Lifesciences, Medtronic and Novartis; and has equity in Navigate. Dr Abbas has received research grants and consulting fees from Edwards Lifesciences. Dr Dweck has served as a consultant to Edwards Lifesciences and Medtronic; has received research funding from Edwards Lifesciences and Medtronic; and has received speaking fees from NVT. Dr Leipsic has served as a consultant for Circle CVI and MVRX; and has received institutional funding for CT core laboratory analyses from Edwards Lifesciences, Neovasc, Abbott, Medtronic, Boston Scientific, PI Cardia, and Conformal. Dr Rogers has served as a consultant and physician proctor for Edwards Lifesciences and Medtronic; has served as an advisory board member for Medtronic; and holds equity interest in Transmural Systems. Dr Sathananthan has served as a consultant to Edwards Lifesciences and Medtronic; has received research funding from Edwards Lifesciences and Medtronic; and has received speaking fees from NVT. Dr Guerrero has received institutional research grant support from Edwards Lifesciences. Dr Ternacle has served as a consultant for Philips Healthcare and Abbott Medical. Dr Barbanti has served as a consultant for Edwards Lifesciences and Boston Scientific. Dr Généreux has served as a consultant and advisor for and received speaker fees from Abbott Vascular, Abiomed, BioTrace Medical, and Medtronic; has served as a consultant for Boston Scientific, GE Healthcare, iRhythm Technologies, Opsens, Siemens, and Teleflex; has served as a consultant, PI Eclipse Trial, for Cardiovascular System Inc; has served as a consultant, advisor, and proctor for and received speaker fees and research grant from Edwards LifeSciences for the PI EARLY-TAVR and PI PROGRESS trials; has served as a consultant for and has equity in Pi-Cardia, Puzzle Medical, Saranas, and Soundbite Medical Inc; has served as a consultant for and received speaker fees from Shockwave; and has served as a consultant for the PI Feasibility study for 4C Medical. Dr Kaneko has served as a consultant for Edwards Lifesciences, Medtronic, and Abbott Structural. Dr Wood has served as a consultant to and his institution (CCI-CIC) receives grant support from Edwards Lifesciences, Abbott Vascular, and Medtronic. Dr Gillam has served as a consultant to Philips and Bracco; is an advisory board member for Edwards Lifesciences; and has core lab contracts with Edwards Lifesciences, Medtronic, and Abbott for which she receives no direct compensation. Dr Reardon has served as a consultant for Medtronic, Boston Scientific, Abbott Medical, and Gore Medical; all fees for such are to his department. Dr Rodes-Cabau has received institutional research grants from Edwards Lifesciences, Medtronic, and Boston Scientific. Dr Thourani has performed consulting/research for Abbott Vascular, Boston Scientific, Cryolife, Edwards Lifesciences, Medtronic, and Shockwave. Dr Bax’s institution (Department of Cardiology, LUMC, the Netherlands) has received research grants from Medtronic, Biotronik, Edwards Lifesciences, and Boston Scientific. Dr Mack has served as a co-principal investigator for clinical trials for Abbott and Edwards Lifesciences; and has served as study chair for a trial for Medtronic; all roles were uncompensated. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: The decision to undergo mitral valve surgery is often made on the basis of echocardiographic criteria and clinical assessment. Recent changes in treatment guidelines recommending surgery in asymptomatic patients make the accurate assessment of mitral regurgitation (MR) severity even more important., Objectives: The purpose of this study was to compare echocardiography and magnetic resonance imaging (MRI) in the assessment of MR severity using the degree of left ventricular (LV) remodeling after surgery as the reference standard., Methods: In this prospective multicenter trial, MR severity was assessed in 103 patients using both echocardiography and MRI. Thirty-eight patients subsequently had isolated mitral valve surgery, and 26 of these had an additional MRI performed 5 to 7 months after surgery. The pre-surgical estimate of regurgitant severity was correlated with the postoperative decrease in LV end-diastolic volume., Results: Agreement between MRI and echocardiographic estimates of MR severity was modest in the overall cohort (r = 0.6; p < 0.0001), and there was a poorer correlation in the subset of patients sent for surgery (r = 0.4; p = 0.01). There was a strong correlation between post-surgical LV remodeling and MR severity as assessed by MRI (r = 0.85; p < 0.0001), and no correlation between post-surgical LV remodeling and MR severity as assessed by echocardiography (r = 0.32; p = 0.1)., Conclusions: The data suggest that MRI is more accurate than echocardiography in assessing the severity of MR. MRI should be considered in those patients when MR severity as assessed by echocardiography is influencing important clinical decisions, such as the decision to undergo MR surgery., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Cardiovascular imaging has enjoyed both rapid technological advances and sustained growth, yet less attention has been focused on quality than in other areas of cardiovascular medicine. To address this deficit, representatives from cardiovascular imaging societies, private payers, government agencies, the medical imaging industry, and experts in quality measurement met, and this report provides an overview of the discussions. A consensus definition of quality in imaging and a convergence of opinion on quality measures across imaging modalities was achieved and are intended to be the start of a process culminating in the development, dissemination, and adoption of quality measures for all cardiovascular imaging modalities.

Objectives: The echocardiographic contrast-enhancing effects and safety profile of ALBUNEX (a suspension of air-filled albumin microspheres) were compared with the new contrast agent OPTISON (formerly FS069: a suspension of albumin microspheres containing the gas perfluoropropane) in 203 patients with inadequate noncontrast echocardiograms., Background: The efficacy of ALBUNEX has been limited by its short duration of action. By using perfluoropropane instead of air within the microsphere, its duration of action is increased., Methods: Each patient received ALBUNEX (0.8 and 0.22 mL/kg) and OPTISON (0.2, 0.5, 3.0, and 5.0 mL) on separate days a minimum of 48 hours apart. Echocardiograms were evaluated for increase in left ventricular (LV) endocardial border length, degree of LV opacification, number of LV endocardial border segments visualized, conversion from a nondiagnostic to a diagnostic echocardiogram, and duration of contrast enhancement. A thorough safety evaluation was conducted., Results: Compared with ALBUNEX, OPTISON more significantly improved every measure of contrast enhancement. OPTISON increased well-visualized LV endocardial border length by 6.0+/-5.1, 6.9+/-5.4, 7.5+/-4.7, and 7.6+/-4.8 cm, respectively, for each of the four doses, compared with only 2.2+/-4.5 and 3.4+/-4.6 cm, respectively, for the two ALBUNEX doses (p < 0.001). 100% LV opacification was achieved in 61%, 73%, 87%, and 87% of the patients with the four doses of OPTISON, but in only 16% and 36% of the patients with the two ALBUNEX doses (p < 0.001). Conversion of nondiagnostic to diagnostic echocardiograms with contrast occurred in 74% of patients with the optimal dose of OPTISON (3.0 mL) compared with only 26% with the optimal dose of ALBUNEX (0.22 mL/kg) (p < 0.001). The duration of contrast effect was also significantly greater with OPTISON than with ALBUNEX. In a subset of patients with potentially poor transpulmonary transit of contrast (patients with chronic lung disease or dilated cardiomyopathy), OPTISON more significantly improved the same measures of contrast enhancement compared with ALBUNEX and did so to the same extent as in the overall population. Side effects were similar and transient with the two agents., Conclusion: OPTISON appears to be a safe, well-tolerated echocardiographic contrast agent that is superior to ALBUNEX.

Objectives: This study was designed to study apoptosis in hypoperfused hibernating myocardium subtending severe coronary stenosis., Background: Apoptosis contributes to myocyte death in acute myocardial infarction., Methods: A left anterior descending coronary artery stenosis was created in 13 pigs and maintained for 24 h (n = 4), 7 days (n = 5) and 4 weeks (n = 4) to reduce coronary blood flow by a mean of 34% with severe regional myocardial systolic dysfunction, as documented by echocardiography. Apoptosis was detected with an in situ end-labeling method and confirmed by "deoxyribonucleic acid laddering" on agarose-gel electrophoresis. The severity of apoptosis was expressed as the percentage of apoptotic myocyte nuclei and nonapoptotic myocardial nuclei., Results: Myocardial blood flow of the anterior left ventricular wall was reduced from 1.00 +/- 0.18 to 0.66 +/- 0.21 ml/min per g (p < 0.01), with a severe reduction of anterior regional wall thickening from a mean (+/-SD) of 39 +/- 4% to 9 +/- 8% (p < 0.01). There was no myocardial infarction in five pigs and minimal patchy infarction of < or = 6% of the area at risk in eight pigs. Apoptotic myocytes were observed in the hibernating myocardial region in all pigs (4.8 +/- 2.3%). Myocyte apoptosis was patchy in distribution and was found predominantly in the subendocardial myocardium (9.8 +/- 4.6%) and rarely in the subepicardial myocardium (0.32 +/- 0.45%). Apoptosis was found not only around focal fibrosis areas, but also in areas without fibrosis or patchy infarction. Apoptosis was found not only in 24-h hypoperfused myocardium, but also in 4-week hypoperfused myocardium. The severity of myocyte apoptosis correlated significantly with regional coronary blood flow reduction (r = 0.75, p < 0.01). No apoptosis was found in the normal control region., Conclusions: This study demonstrates that there is ongoing myocyte death through myocyte apoptosis in hypoperfused hibernating myocardium.

Objectives: This study was designed to examine the effects of a beta-adrenergic blocking agent on the ischemic response to dobutamine stress and to determine the degree to which these effects can be abolished by the addition of atropine., Background: Whether beta-blockade affects the sensitivity of dobutamine stress echocardiography for the diagnosis of coronary artery disease has been controversial., Methods: In nine pigs, a left anterior descending coronary artery stenosis was created to reduce flow reserve (maximal/rest flow) to 1.1 to 1.9 without baseline regional wall motion abnormalities. This corresponded to a 50% to 90% diameter stenosis. Wall thickening was measured using epicardial echocardiography. Regional lactate production and coronary venous pH were monitored from an adjacent cardiac vein. A standard protocol of dobutamine stress echocardiography was first performed. After normalization of the ischemic abnormalities elicited with this infusion, esmolol was infused at 50 micrograms/kg body weight per min and the dobutamine test was repeated, with 1.0 mg of atropine added at the maximal dobutamine dose., Results: Without esmolol, dobutamine stress induced myocardial ischemia with a reduction in regional wall thickening and lactate production in all nine pigs. Multiple regression analysis revealed that coronary flow per heartbeat (p < 0.01) and lactate production (p < 0.05) independently correlated with regional wall thickening during dobutamine stress. The beta-blocker significantly reduced heart rate and regional oxygen consumption and altered the relation between coronary flow per heartbeat and regional wall thickening (p < 0.05) during dobutamine stress. Esmolol prevented dobutamine-induced ischemia (lactate production and wall motion abnormalities) in seven of nine pigs. The addition of atropine induced lactate production and a reduction in wall thickening in five of seven pigs in which ischemia had been prevented by beta-blockade. However, lactate production was higher and regional venous pH was lower with the baseline dobutamine infusion than with that performed after esmolol with atropine added at the maximal dobutamine dose (p < 0.05)., Conclusions: A correlation between regional wall thickening and coronary flow per heartbeat was demonstrated during baseline dobutamine stress. Beta-blockade shifted this relation so that dobutamine stress-induced myocardial ischemia was attenuated. The mechanisms by which beta-blockade prevents dobutamine-induced ischemia appeared to be mainly through decreases in heart rate and rate of rise in left ventricular pressure, improvement of regional coronary flow per heartbeat and attenuation of regional ischemic lactate production. Adding atropine in conventional doses enhanced the ability of dobutamine stress to induce myocardial ischemia but did not completely abolish the effects of beta-blockade on either the severity of dobutamine-induced wall thickening abnormalities or regional metabolic disturbances.

Objectives: This study was designed to assess the feasibility of calculating left ventricular volumes using intracardiac ultrasound., Background: Previous studies have validated transthoracic echocardiographic determinations of left ventricular volumes and have indicated the superiority of Simpson rule reconstruction algorithms. The feasibility of imaging the left ventricle with intracardiac ultrasound has also been demonstrated., Methods: The determination of left ventricular volumes with Simpson rule reconstruction of intracardiac ultrasound images was evaluated in two phases. In vitro validation was performed in 29 animal hearts preserved in either a nondistended or distended state. Latex cast volumes were the reference standard. In vivo studies used 14 pigs, and compared intracardiac ultrasound volumes and ejection fraction with single-plane contrast angiographic values. A 12.5-MHz device was used to record short-axis images at 0.5-cm intervals. These were used to reconstruct the ventricle as a stack of cylindric elements using all imaged levels as well as sections recorded every 1 and 2 cm and at a single midventricular level., Results: In the in vitro hearts, when all recorded sections were used, there was excellent agreement between intracardiac ultrasound and latex cast volumes (intracardiac ultrasound volume = 0.89 latex cast volume + 2.22, r = 0.95; intracardiac ultrasound volume = 0.97 latex cast volume + 0.91, r = 0.99) for nondistended and distended hearts, respectively. In vivo, there was again close correspondence between ultrasound and angiographic volumes (intracardiac ultrasound volume = 1.04 angiographic volume - 3.6, r = 0.91). The relation between intracardiac ultrasound and angiographic ejection fraction was fair (intracardiac ultrasound ejection fraction = 1.00 angiographic ejection fraction + 6.85, r = 0.69). Excellent correlations for the volumes were maintained as the number of cross sections was reduced to those recorded every 1 and 2 cm (r = 0.87 to 0.99). With a single midventricular site more variable but generally good correlations were obtained (r = 0.77 to 0.99)., Conclusions: The application of Simpson rule reconstruction to short-axis images of the left ventricle obtained with intracardiac ultrasound provides accurate determination of left ventricular volumes in animal hearts. This technique may prove useful in the analysis of left ventricular structure and function.

Objectives: This study was designed to assess the feasibility of using hydrogel-coated balloons to deliver biologically active agents to the blood vessel wall., Background: The local intramural delivery of therapeutic agents during balloon angioplasty has been proposed as an adjunctive technique for preventing early intracoronary thrombosis and late restenosis., Methods: To assess the efficacy of delivery and depth of penetration in vitro, local delivery of horseradish peroxidase was performed in 40 porcine peripheral arteries, and delivery of fluoresceinated heparin was performed in 20 porcine peripheral arteries and 7 human atheromatous arteries. To determine the persistence of these agents in the vessel wall in vivo, horseradish peroxidase was delivered to 18 porcine peripheral arteries that were harvested at intervals of 45 min to 48 h. Fluoresceinated heparin was delivered to 22 porcine peripheral arteries, 14 with the use of a protective sleeve, harvested at intervals of 30 s to 24 h., Results: In vitro agent delivery was successful in all specimens. The depth of penetration of horseradish peroxidase was directly related to both balloon pressure (p < 0.04) and duration of inflation (p < 0.01). In vivo peroxidase staining was evident at 45 and 90 min but not thereafter. With the use of a protective sleeve, heparin was present in all arteries harvested at 30 s, with marked dissipation at 1 and 24 h. Without a sleeve, no fluorescein staining was detected in any artery. With both agents, delivery occurred consistently over broad regions of the vessel wall that were free of architectural disruption., Conclusions: Hydrogel-coated balloons can deliver biologically active agents to the vessel wall without gross tissue disruption and may provide an atraumatic method for the local delivery of therapeutic agents during balloon angioplasty.

Objectives: The purpose of this study was to evaluate the efficacy of radiofrequency-powered thermal balloon angioplasty in an in vivo porcine model., Background: Various modes of thermal energy used adjunctively during balloon angioplasty have demonstrated the potential to enhance the results of acute lumen dilation., Methods: In normal pigs, 75 peripheral arteries were dilated with a newly designed, radiofrequency-powered, thermal angioplasty balloon. All inflations were performed at 2-atm pressure for 85 s. Dilations were performed either with (hot) or without (cold) the application of heat. Lumen dimensions and vessel morphology were assessed with intravascular ultrasonography. At the end of each study, dilated arterial segments were harvested for histologic examination., Results: Single cold balloon inflations resulted in a 12.7% increase in arterial cross-sectional area whereas single hot inflations resulted in a 22.9% increase (p < 0.03). Similarly, when multiple cold inflations were compared with multiple hot inflations, two, three and four sequential hot inflations resulted in a significantly greater increase in cross-sectional area than an equivalent number of cold inflations (p < 0.03). Histologic examination demonstrated a temperature-dependent effect on the depth of medial necrosis and extent of arterial wall thinning (p < 0.001) as well as evidence for uniform alteration of elastic tissue fibers at temperatures of > or = 60 degrees C (p < 0.03)., Conclusions: Low pressure radiofrequency thermal balloon angioplasty results in a greater increase in cross-sectional area in porcine peripheral arteries than does nonheated conventional balloon angioplasty. The pathologic basis for this enhanced dilation may be a temperature-dependent effect on medial necrosis, thinning of the arterial wall or alteration of vascular elastic fibers, alone or in combination.

Objectives: This study was designed to determine the clinical utility and feasibility of using 12.5-MHz ultrasound catheters for intracardiac echocardiography., Background: Intracardiac echocardiography is a potentially useful technique of cardiac imaging and monitoring in certain settings. The feasibility of intracardiac echocardiography using 20-MHz ultrasound catheters in patients has been demonstrated. High resolution images of normal cardiac structures as well as cardiac abnormalities have been obtained. However, imaging has been limited by the shallow depth of field inherent in high frequency ultrasound imaging., Methods: Intracardiac echocardiography with 12.5-MHz catheters was performed in eight mongrel dogs and 92 patients. Catheters were introduced percutaneously in 80 patients studied in the catheterization laboratory and directly into the heart in 12 patients in the operating room. Right heart imaging was performed in 68 patients and arterial and left heart imaging in 35 patients., Results: When these catheters were introduced into the venous system, the right atrium, tricuspid valve, right ventricle, pulmonary valve and pulmonary artery were visualized. Pericardial effusion, intracardiac masses and atrial septal defects were correctly identified. The left ventricle, left atrium, mitral valve, aortic valve, aorta and coronary arteries could be imaged from the arterial circulation. Diseases identified included valvular aortic stenosis, subvalvular aortic stenosis and Kawasaki disease. Average imaging time was 10 min. No complications occurred as a result of intracardiac echocardiography., Conclusions: Intracardiac echocardiography with 12.5-MHz ultrasound catheters is safe and feasible; it also provides anatomic and physiologic information. This feasibility study provides a foundation for wider clinical use of intracardic echocardiography.

Mitral valve areas determined by Doppler pressure half-time were compared with areas obtained by planimetry in two groups of patients with mitral stenosis: 24 patients without aortic regurgitation and 32 patients with more than grade 1 aortic regurgitation. The severity of aortic regurgitation was assessed by color flow mapping; 17 patients had grade 2, 10 had grade 3 and 5 had grade 4 aortic regurgitation. Regression equations for pressure half-time area versus planimetry mitral valve area were calculated separately for the aortic regurgitation (r = 0.88) and the nonaortic regurgitation group (r = 0.86); analysis of covariance revealed a significant (p less than 0.001) difference between the two groups leading to overestimation of planimetry area by the pressure half-time method in the aortic regurgitation group. The mitral valve areas in the group without regurgitation were best calculated with the expression 239/T1/2 (r = 0.77) as compared with a best fit of 195/T1/2 (r = 0.85) for the aortic regurgitation group. To elucidate the mechanisms affecting pressure half-time in aortic regurgitation, an in vitro model of mitral inflow in the presence of varying regurgitant volumes and different ventricular chamber compliances was used. Aortic regurgitation shortened directly measured pressure half-time proportional to the regurgitant fraction but an increase in left ventricular compliance could offset this effect. Finally, in a mathematic model of mitral inflow the competing effects of aortic regurgitation and chamber compliance could be confirmed. In conclusion, aortic regurgitation results clinically in a significant net shortening of pressure half-time leading to mitral valve area overestimation. However, the effect is moderate and individually unpredictable because of changes in chamber compliance.

Previous studies have shown that Doppler echocardiographic methods based on the continuity equation can accurately determine aortic valve area in patients with clinically significant aortic stenosis; nonetheless, methods based on the continuity equation are time-consuming and may not be technically possible in all subsets of patients. The purpose of this study was to develop and prospectively evaluate a simpler new noninvasive method for determining aortic valve area. With this new method, aortic valve area is obtained by dividing the percent fractional anteroposterior shortening at the midventricular level by 4V2, where V is the peak instantaneous Doppler-derived flow velocity across the aortic valve. In the first part of the study, the fractional shortening-velocity ratio was used to examine a group of 25 patients evaluated retrospectively. There was a highly significant linear relation between the fractional shortening-velocity ratio (FSVR) and the aortic valve area (AVA) determined by the Gorlin formula at cardiac catheterization: FSVR = 1.1(AVA) - 0.1 (r = 0.88; significance of slope p less than 0.001). Furthermore, a fractional shortening-velocity ratio less than 1.1 reliably identified all patients with clinically significant aortic stenosis (aortic valve area less than 1 cm2), whereas a fractional shortening-velocity ratio less than 0.8 reliably identified all patients with critical aortic stenosis (aortic valve area less than 0.7 cm2). This new method was then validated by prospectively applying the fractional shortening-velocity ratio to a group of 44 patients from two separate institutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific information regarding the relation between infarct thickness and regional systolic function is important to the overall understanding of both the pathophysiology of acute and subacute myocardial infarction and the functional benefits of myocardial salvage interventions designed to limit the transmural extent of infarction and thereby preserve left ventricular function. In the present study, quantitative computer-assisted two-dimensional echocardiography was used to define the relation between infarct thickness and systolic function in the acutely and subacutely infarcted canine left ventricle. Echocardiograms were obtained at the mid-papillary muscle level at baseline and 6 h after occlusion (acute infarction) in eight animals and at baseline and 72 h after occlusion (subacute infarction) in nine animals. Systolic function was assessed by measuring the extent of fractional radial shortening along each of 36 evenly spaced endocardial targets from end-diastole to end-systole; the transmural extent of infarction was determined from the triphenyltetrazolium chloride-staining deficit at 6 and 72 h. The relation between systolic function and transmural extent of infarction was analyzed in two ways. First, the extent of fractional radial shortening in each group was examined as a function of quartile (25%) increments in transmural infarct thickness. This analysis revealed 1) a significant overall loss of fractional radial shortening with increasing transmural extent of infarction in both groups; and 2) significant differences in the extent of systolic dysfunction between successive quartile increments of infarction. Second, the relation between infarct thickness and systolic dysfunction was modeled mathematically by fitting the data from each infarct series to linear, logarithmic and exponential functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-dimensional echocardiography has proved to be reliable in the diagnosis of mitral, aortic and pulmonary stenosis. Its role in the diagnosis of rheumatic tricuspid stenosis is still being defined; therefore, the tricuspid valve echograms of 147 patients with rheumatic heart disease were examined. Thirty-eight of these patients also underwent hemodynamic evaluation. Tricuspid stenosis was defined echocardiographically as diastolic anterior leaflet doming, thickening and restricted excursion of the other two tricuspid leaflets and decreased separation of the leaflet tips. Using these criteria, the sensitivity and specificity of the echocardiogram in detecting tricuspid stenosis were 69 and 96%, respectively, in the group of 38 patients who had both echocardiographic and hemodynamic evaluations. However, when the smaller group of 17 patients who had simultaneous right atrial and right ventricular pressure recordings were considered separately, there was complete agreement between the echocardiographic and hemodynamic data. Thus, the two-dimensional echocardiogram is a sensitive and specific test for diagnosing rheumatic tricuspid stenosis. In addition, these data provided an opportunity to determine the prevalence of tricuspid stenosis in this group of patients with chronic rheumatic valvular disease. Tricuspid stenosis was present in 14 (9.5%) of the total group of 147 patients who had two-dimensional echocardiograms, and in 10 (26.3%) of the 38 who had both echocardiographic and hemodynamic studies. In patients with rheumatic heart disease about to undergo cardiac catheterization, an echocardiographic study should prove useful in making the diagnosis of tricuspid stenosis.

To define the in vivo relation between abnormal wall motion and the area at risk for necrosis after acute coronary occlusion, 11 open chest dogs were studied. Five dogs underwent left anterior descending coronary artery occlusion and six underwent left circumflex artery occlusion. Area at risk was defined at five short-axis levels (mitral valve, chordal, high and low papillary muscle and apex) using myocardial contrast echocardiography. Wall motion was measured in the cycles preceding injection of contrast medium. Two observers used two different methods to measure wall motion. In method A, end-diastolic to end-systolic fractional radial change for each of 32 endocardial targets was determined. The extent of abnormal wall motion was then calculated using three definitions of wall motion abnormality: akinesia/dyskinesia, fractional inward endocardial excursion of less than 10%, and fractional inward endocardial excursion of less than 20%. In method B, the information from the entire systolic contraction sequence was analyzed and correlated with a normal contraction pattern. The best linear correlation between area at risk (AR) and abnormal wall motion (AWM) was achieved using method B and expressed by the following linear regression: AWM = 0.92 AR + 3.0 (r = 0.92, p less than 0.0001, SEE = 1.7%). Of the three definitions of abnormality used in method A, the best correlation was achieved between area at risk and less than 10% inward endocardial excursion and was expressed by the following polynomial regression: AWM = -0.01 AR2 + 1.5 AR -0.14 (r = 0.92, p less than 0.001, SEE = 1.7%). These data demonstrate that there is a definite relation between area at risk and abnormal wall motion but that this relation varies depending on the method used to analyze wall motion. However, wall motion during acute ischemia is also influenced by the loading conditions of the heart. Because these may vary in a manner that is independent of the ischemic process, measurement of both risk area and abnormal motion may provide a more comprehensive assessment of cardiac function in myocardial ischemia than is provided by the measurement of either alone.

Myocardial contrast echocardiography can define in vivo the area at risk for necrosis after coronary occlusion. However, if this technique is to be used, it cannot be intrinsically toxic to the heart or other critical organs. To determine the functional and pathologic effects of contrast echocardiography, six intracoronary, six intrarenal and six intracarotid artery injections of 2 to 6 cc of a commonly employed contrast agent (agitated Renografin-saline solution) were performed in five dogs. A sixth dog served as a sham to assess any deleterious effects of the model preparation. Two-dimensional echocardiographic images and electrocardiograms were recorded during intracoronary injections, and heart rate, blood pressure, left ventricular end-diastolic pressure and rate of rise of left ventricular pressure (dP/dt) were continuously monitored. At 24 hours, echocardiographic and hemodynamic measurements were repeated, the dogs were killed and the heart, brain and kidneys were removed and prepared for light microscopic examination. Quantitative analysis of left ventricular wall motion was performed on control, peak contrast, post-contrast and 24 hour studies. With each intracoronary injection, there were transient decreases in blood pressure (p = 0.05 versus control) and increases in left ventricular end-diastolic pressure (p = 0.04 versus control). These were associated with depression of wall motion in contrast-enhanced regions (p = 0.01 versus control) and ST-T segment changes on the electrocardiogram. No significant change in heart rate or left ventricular dP/dt was noted. All variables normalized with the clearance of the contrast effect and remained normal to 24 hours. Light microscopic examination revealed no myocardial or cerebral changes attributable to the contrast agent injections.(ABSTRACT TRUNCATED AT 250 WORDS)

A new technique for quantitatively mapping the three-dimensional left ventricular endocardial surface was developed, using measurements from standard cross-sectional echocardiographic images. To validate the accuracy of this echocardiographic mapping technique in an animal model, the endocardial areas of 15 excised canine ventricles were calculated using measurements made from echocardiographic studies of the hearts and compared with areas determined with latex casts of the same ventricles. Close correlation (r = 0.87, p less than 0.001) between these two measures of endocardial area provided preliminary confirmation of the accuracy of the maps. To further characterize the mapping algorithm, it was translated into computer format and used to map the surfaces of idealized hemiellipsoids. Areas measured with this mapping technique closely approximated the actual areas of idealized surfaces with a wide spectrum of shapes; maps were particularly accurate for ellipsoids with shapes similar to those of undistorted human ventricles. Also, the accuracies of area calculations were relatively insensitive to deviation from the assumed positions of the echocardiographic short-axis planes. Finally, although the accuracy of the mapping technique improved as data from more transverse planes were added, the procedure proved reliable for estimating surface areas when data from only three planes were used. These studies confirm the accuracy of the echocardiographic mapping technique, and they suggest that the resulting planar plots might be useful as templates for localizing and quantifying the overall extent of abnormal wall motion.

Two-dimensional echocardiography was employed to define the natural history of regional wall motion abnormalities in a canine model of acute experimental myocardial infarction. Serial short-axis two-dimensional echocardiograms were recorded in 11 closed chest dogs before coronary occlusion and 10, 30, 60, 180 and 360 minutes after permanent coronary ligation. Radiolabeled microsphere-derived blood flows were obtained in each study period and the histochemical (triphenyltetrazolium chloride) extent of infarction was determined at 6 hours. Previously published methods were used to quantitate field by field (every 16.7 ms) excursion of 36 evenly spaced endocardial targets. The circumferential extent of abnormal wall motion was followed sequentially using previously published definitions of abnormality: 1) systolic fractional radial change of less than 20%; 2) dyskinesia (systolic bulging) at the point in time (echocardiographic field) in which there is maximal dyskinesia; and 3) correlation with composite normal ray motion falling outside the 95% confidence limits defined in the control period. On the basis of the triphenyltetrazolium chloride staining pattern, the ventricle was divided into five zones: central infarct zone, zone with greater than 25% transmural infarction, total infarct zone, border zones and normal zone. Mean systolic fractional radial change was calculated for each zone and used as an index of the magnitude of abnormal wall motion. Regardless of the definition of abnormality employed, the circumferential extent of abnormal wall motion manifested at 10 minutes after occlusion did not significantly change, even up to 6 hours later. Similarly, 10 minutes after coronary occlusion the three infarct zones and border zones demonstrated significantly reduced systolic fractional radial change. This remained stable over the remainder of the 6 hour study period. It is concluded that once established at 10 minutes after coronary occlusion, the circumferential extent and magnitude of abnormal wall motion do not significantly change in the immediate postinfarct (6 hour) period.

A convenient noninvasive method of mapping the left ventricular endocardial surface has been developed that can be used to display regional dysfunction and calculate the total area of abnormal endocardial excursion from data obtained in two orthogonal apical and three or more short-axis cross-sectional echocardiographic images. Visually identified regions of abnormal systolic function are plotted on end-diastolic, planar endocardial surface maps, and the extent of dysfunction can be expressed either as an absolute area or as a fraction of the total endocardial surface area involved. The extent of the left ventricular surface moving abnormally, calculated with this echocardiographic mapping technique, was compared with two histochemical measures of infarct size in a series of 11 closed chest dogs with acute circumflex coronary artery occlusions. Overall extent of abnormally moving left ventricular wall correlated closely with both the fraction of the endocardial area overlying infarct (r = 0.92, p less than or equal to 0.001) and the fraction of the myocardial volume infarcted (r = 0.86, p less than or equal to 0.001). This suggests that the echocardiographic mapping technique can be used to accurately quantify the global extent of abnormal systolic function in the presence of regional wall motion abnormalities.

The effect of infarct maturation on the temporal sequence of contraction within infarct zones has not previously been described. Accordingly, the time-varying pattern of contraction within ischemic/infarct zones was studied with use of cross-sectional echocardiography in 17 dogs at 10 min to 6 weeks after acute experimental myocardial infarction. Left ventricular short-axis images were digitized from end-diastole to end-systole and endocardial fractional radial change along 36 evenly spaced rays was calculated. The circumferential extent of dyskinesia and the number of rays that exhibited maximal dyskinesia were determined for each decile of the normalized contraction sequence. Between 10 min and 1 week after infarction, the greatest circumferential extent of dyskinesia occurred between the 3rd and 4th deciles of the normalized contraction sequence. However, as the infarct matured, the greatest spatial expanse of dyskinesia was noted to occur progressively earlier in the contraction sequence (second decile at 6 weeks), and the extent of mid- to late-systolic dyskinesia decreased markedly. Whereas end-systolic dyskinesia was present in 30% to 50% of ischemic/infarct zone rays from 10 min to 48 h, end-systolic dyskinesia was no longer observed at 6 weeks. Similarly, the maximal amplitude of dyskinesia was most commonly observed during midsystole from 10 min to 48 h, but occurred progressively earlier as the infarct matured, falling during the first decile at 6 weeks after infarction. These data suggest that maximal circumferential extent and amplitude of dyskinesia occur progressively earlier in the systolic contraction sequence as the infarct matures.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial contrast echocardiography has been shown to accurately assess the area at risk for necrosis after acute coronary occlusion in the experimental model. The area at risk as determined by this method, however, has been defined in different ways depending on the model used. Some investigators have injected the contrast agent proximal to the site of coronary occlusion (left main coronary artery or aorta) and defined the area at risk as the segment of myocardium not showing a contrast effect (negative risk area). Others have injected the contrast agent directly into the occluded vessel and have defined the area at risk as that showing contrast enhancement (positive risk area). To evaluate whether the areas at risk determined by these two techniques are identical, six open chest dogs were studied using both methods. The area at risk was slightly but significantly larger when the contrast agent was injected into the occluded vessel than when it was injected proximally into the left main coronary artery (4.98 +/- 1.69 versus 3.97 +/- 1.27 cm2, p less than 0.01). It is concluded that the site of injection of the contrast agent significantly influences the determination of area at risk. Therefore, data obtained by the two techniques should not be used interchangeably, and in a given study the area at risk should be measured consistently using one technique.

Continuous wave Doppler echocardiography has proved useful in detecting and quantitating the high velocity flow disturbances that characterize many stenotic and regurgitant valvular lesions. Pulsed Doppler echocardiography, in contrast, is limited in its ability to quantitate the high velocities that are detected. Recently, new pulsed Doppler systems have been developed that employ high pulse repetition frequencies and can theoretically measure higher flow velocities than those measured by the standard pulsed Doppler systems. To determine the ability of high pulse repetition frequency Doppler echocardiography to accurately measure high velocity flow signals in comparison with the continuous wave method, 80 patients undergoing routine echocardiographic examination for the assessment of valvular heart disease were studied using both techniques. A total of 113 high velocity flow disturbances were detected in 68 patients. In 41 instances, the maximal velocities by the two methods were within 0.5 m/s of each other. In 68 of the 113 high velocity lesions, however, the high pulse repetition frequency technique underestimated the peak velocity found with continuous wave Doppler echocardiography by more than 0.5 m/s. Comparison of the peak velocities recorded by the two methods for the total group showed no significant correlation (r = 0.04, p = NS). Comparison of the difference in peak velocities obtained by the two techniques with the maximal continuous wave velocity (n = 94, r = 0.70, slope = 0.71) suggested that the underestimation becomes greater as the peak velocity increases. Fifteen of the study patients with aortic stenosis subsequently underwent catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

In a 69 year old woman with a "sticking" Björk-Shiley mitral prosthesis, the diagnosis was suggested by both the two-dimensional and the Doppler ultrasound examinations. In particular, the findings of early diastolic paradoxic septal motion, intermittent delayed opening of the prosthetic disc and variable timing of the onset of mitral valve inflow were believed to be diagnostic of a sticking tilting disc prosthesis.

Two patients presenting with acute pulmonary edema were found to have a left atrial cardiac osteogenic sarcoma (primary and secondary). The two-dimensional echocardiographic appearance in both cases mimicked that of atrial myxoma. However, two echocardiographic features (that is, tumor extension into pulmonary veins and origin from nonseptal atrial walls) suggested the presence of a nonmyxomatous cardiac tumor.