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Biomedical subjects

M H Picard

Publications and source records attributed to M H Picard.

At least 73 records · Page 4Linked to original sources
PubMed1994

Natural history of vegetations during successful medical treatment of endocarditis.

Although initial morphologic features of vegetations have been related to the risk of early complications, there is little information about the natural history of the vegetations during medical treatment or the relation of morphologic changes in vegetation to late complications. To assess the evolution of valvular vegetations by echocardiography during treatment of infective endocarditis and to relate the morphologic changes in vegetation to late prognosis, serial echocardiograms of patients with successful medical treatment for native valve infective endocarditis were reviewed to assess the presence and morphologic features of valvular vegetations at the onset and at the end of therapy. The evolution of vegetation size, mobility, consistency, the extent of the disease, and the severity of valvular regurgitation were related to late complications such as embolism, valve replacement, or death occurring after the end of therapy. Forty-one vegetations were identified in 32 patients on initial echocardiograms. At the end of treatment, 29 vegetations were still present; 59% had no significant change in size and 52% appeared to be denser in consistency. Morphologic changes did not relate to late complications, but the presence of severe valvular regurgitations was associated with late valve replacement. The echocardiographic persistence of vegetations is common after successful medical treatment of infective endocarditis. In the absence of severe valvular dysfunction, however, persistent vegetations are not independently associated with late complications.

Adult↗
PubMed1994

Quantification of pericardial effusions by three-dimensional echocardiography.

OBJECTIVES: The purpose of this study was to examine the accuracy of three-dimensional echocardiography for the quantification of asymmetric pericardial effusion volume and to compare this new technique with two-dimensional echocardiography. BACKGROUND: Quantification of pericardial effusion by two-dimensional echocardiography relies on a symmetric distribution of the fluid. Three-dimensional echocardiography can quantitate volume without these limitations, but its accuracy for pericardial effusion volume has not yet been assessed. METHODS: In six open chest dogs, 41 different asymmetrically distributed pericardial effusions of known volume were created by serial infusions of fluid through a pericardial catheter. The hearts were imaged using an automated echocardiographic method that integrates three-dimensional spatial and imaging data. The surfaces of the pericardial sac and heart were then reconstructed, and the volumes of pericardial effusions were calculated. Two-dimensional echocardiography was performed simultaneously, and volumes were calculated using the prolate ellipsoid method. Asymmetric distribution of the fluid was obtained by applying localized hydrostatic pressure to the pericardium. RESULTS: The volumes of pericardial effusion quantified using three-dimensional echocardiography correlated well with actual volumes (y = 1.0x - 1.4, SEE = 7.7 ml, r = 0.98). Two-dimensional echocardiography had an acceptable correlation (y = 1.0x + 2.3, SEE = 23 ml, r = 0.84), but a marked degree of variation from the true value was observed for any individual measurement. CONCLUSIONS: Three-dimensional echocardiography accurately quantifies pericardial effusion volume in vivo, even when the fluid is distributed asymmetrically, whereas two-dimensional echocardiography is less reliable. This new technique may be of clinical value in quantitating pericardial effusion, especially in the serial evaluation of asymmetric or loculated effusions.

Algorithms↗
PubMed1994

Three-dimensional echocardiography. In vivo validation for right ventricular volume and function.

BACKGROUND: Current two-dimensional echocardiographic measures of right ventricular volume are limited by the asymmetrical and crescentic shape of the ventricle and by difficulty in obtaining standardized views. Three-dimensional echocardiographic reconstruction, which does not require geometric assumptions or standardized views, may therefore have potential advantages for determining right ventricular volume. Three-dimensional techniques, however, have not been applied to the right ventricle in vivo, where cardiac motion and contraction could affect accuracy. The purpose of this study was to determine the feasibility and accuracy of three-dimensional echocardiographic reconstruction for quantifying right ventricular volume and function in vivo. In particular, it was designed to test the accuracy of a newly developed system that provides rapid, efficient, and automated three-dimensional data collection (minimizing motion effects) and takes advantage of the full three-dimensional data set to obtain volume. METHODS AND RESULTS: The three-dimensional system was applied to reconstruct the right ventricle and measure its volume and function during 20 hemodynamic stages created in five dogs. Actual instantaneous volumes were measured continuously by an intracavitary balloon connected to an external column. Hemodynamics were varied by volume loading and induction of ischemia. Three-dimensional reconstruction successfully reproduced right ventricular volume compared with actual values at end diastole (y = 1.0 chi-3.4, r = .99, SEE = 1.8 mL) and end systole (y = 1.0 chi+ 2.0, 4 = .98, SEE = 2.5 mL). The mean difference between calculated and actual volumes throughout the cycle was 2.1 mL, or 4.9% of the mean. Ejection fraction also correlated well with actual values (y = 0.96 chi-0.3, r = .98, SEE = 3.3%). CONCLUSIONS: Despite the irregular crescentic shape of the right ventricle, this newly developed three-dimensional system and surfacing algorithm can accurately reconstruct its shape and quantitate its volume and function in vivo without geometric assumptions. The increased efficiency of the system should increase applicability to issues of clinical and research interest.

Algorithms↗
PubMed1993

Benefit of late coronary reperfusion on ventricular morphology and function after myocardial infarction.

OBJECTIVES: This study was designed to examine the relation between the timing and adequacy of perfusion of the infarct bed and changes in ventricular size and the extent of abnormal wall motion after acute myocardial infarction. METHODS: A validated echocardiographic mapping technique was used to measure the left ventricular endocardial surface area index and the extent of abnormal wall motion over a 3-month period in 91 patients who had either 1) no anterograde or collateral flow to the infarct bed (n = 14), 2) only collateral flow to the infarct bed (n = 18), 3) restoration of anterograde flow to the infarct bed within hours of chest pain (early [n = 43]), or 4) restoration of anterograde flow to the infarct bed within a mean of 5 days after acute myocardial infarction (late [n = 16]). RESULTS: Over the follow-up period, a progressive and significant increase in endocardial surface area index was observed only in the group of patients without anterograde or collateral flow to the infarct bed (entry 64 +/- 3.4 cm2/m2 vs. 3 months 75.9 +/- 6.4 cm2/m2, p < 0.005). In contrast, a progressive reduction in the extent of abnormal wall motion was evident in the group of patients in whom anterograde flow to the infarct bed was restored within hours (entry 26.7 +/- 2.5 cm2 vs. 3 months 11.8 +/- 2.9 cm2, p < 0.001) or days (entry 22.1 +/- 3.6 cm2 vs. 3 months 11.8 +/- 3.3 cm2, p < 0.001) of coronary occlusion. Multiple stepwise linear regression analysis confirmed that by 3 months, 1) ventricular size was independently related to endocardial surface area index and abnormal wall motion at entry (p < 0.0001) and to the change in abnormal wall motion over the follow-up period (p < 0.0001), and 2) the change in abnormal wall motion was related to the presence of anterograde flow to the infarct bed (p < 0.0001) independent of the timing of reperfusion, infarct site or the extent of abnormal wall motion on admission. CONCLUSIONS: After myocardial infarction, the process of ventricular remodeling is influenced by changes in the extent of abnormal wall motion, which in turn are related to the adequacy rather than the timing of perfusion of the infarct bed.

Collateral Circulation↗
PubMed1993

A new integrated system for three-dimensional echocardiographic reconstruction: development and validation for ventricular volume with application in human subjects.

OBJECTIVES: The purpose of this study was to improve three-dimensional echocardiographic reconstruction by developing an automated mechanism for integrating spark gap locating data with corresponding images in real time and to validate use of this mechanism for the measurement of left ventricular volume. BACKGROUND: Initial approaches to three-dimensional echocardiographic reconstruction were often limited by inefficient reconstructive processes requiring manual coordination of two-dimensional images and corresponding spatial locating data. METHODS: In this system, a single computer overlays the binary-encoded positional data on the two-dimensional echocardiographic image, which is then recorded on videotape. The same system allows images to be digitized, traced, analyzed and displayed in three dimensions. This system was validated by using it to reconstruct 11 ventricular phantoms (19 to 271 ml) and 11 gel-filled excised ventricles (21 to 236 ml) imaged in intersecting long- and short-axis views and by apical rotation. To measure cavity volume, a surface was generated by an algorithm that takes advantage of the full three-dimensional data set. RESULTS: Reconstructed cavity volumes agreed well with actual values: y = 0.96x + 2.2 for the ventricular phantoms in long- and short-axis views (r = 0.99, SEE = 2.7 ml); y = 0.95x + 2.9 for the phantoms, reconstructed by apical rotation (r = 0.99, SEE = 2.7 ml); and y = 0.99x + 0.11 ml for the excised ventricles (reconstructed in long- and short-axis views; r = 0.99, SEE = 5.9 ml). The mean difference between three-dimensional and actual volumes was 3% of the mean (3.0 ml) for the phantoms and 6% (4.6 ml) for the excised ventricles. Observer variability was 2.3% for the phantoms and 5.6% for the excised ventricles. Application to 14 normal subjects demonstrated feasibility of left ventricular reconstruction, which provided values for stroke volume that agreed well with an independent Doppler measure (y = 0.97x + 0.94; r = 0.95, SEE = 3.2 ml), with an observer variability of 4.9% (2.4 ml). CONCLUSIONS: A system has therefore been developed that automatically integrates locating and imaging data in no more time than the component two-dimensional echocardiographic scans. This system can accurately reconstruct ventricular volumes in vitro over a wide range and is feasible in vivo, thus laying the foundation for further applications. It has increased the efficiency of three-dimensional reconstruction and enhanced our ability to address clinical and research questions with this technique.

Adult↗
PubMed1993

Long-term effects of acute thrombolytic therapy on ventricular size and function.

To investigate the influence of thrombolytic therapy on the natural history of left ventricular size and regional function after myocardial infarction, 32 patients treated with acute thrombolytic therapy (treatment group) were studied by echocardiography on admission to the hospital and at 1 week, 3 months, and 1 year after myocardial infarction; they were compared with 40 patients who did not receive acute intervention (control group). The endocardial surface area index (cm2/m2) and the area of abnormal wall motion (cm2) were calculated from left ventricular dimensions and measurements of abnormal wall motion. Although no differences in the endocardial surface area index were noted over the year for the groups as a whole, a significant difference was noted in treated anterior infarctions with early functional infarct expansion compared with untreated infarct expansion (treatment group: 85.8 +/- 2.0 cm2/m2 [entry] to 77.4 +/- 2.7 cm2/m2 [1 week] to 69.9 +/- 4.2 cm2/m2 [3 months] to 67.2 +/- 6.4 cm2/m2 [1 year] versus control group: 84.0 +/- 6.4 cm2/m2 [entry] to 83.7 +/- 8.5 cm2/m2 [1 week] to 96.3 +/- 8.6 cm2/m2 [3 months] to 81.5 +/- 4.2 cm2/m2 [1 year]; p < 0.01). When early expansion was present, those receiving thrombolysis exhibited a consistent decrease in the initially enlarged endocardial surface area in contrast to control subjects, who demonstrated continued increases in endocardial surface area during the first 3 months. In all groups a decrease in the area of abnormal wall motion was observed during the year of follow-up. However, the magnitude and timing of the improvement was accelerated in the treatment group. Thus acute thrombolytic therapy alters the natural history of left ventricular size and function with a more rapid recovery of abnormal endocardial segments and reversal of functional infarct expansion.

Case-Control Studies↗
PubMed1993

Three-dimensional echocardiography. In vivo validation for left ventricular volume and function.

BACKGROUND: Current two-dimensional quantitative echocardiographic methods of volume assessment require image acquisition from standardized scanning planes. Left ventricular volume and ejection fraction are then calculated by assuming ventricular symmetry and geometry. These assumptions may not be valid in distorted ventricles. Three-dimensional echocardiography can quantify left ventricular volume without the limitations imposed by the assumptions of two-dimensional methods. We have developed a three-dimensional system that automatically integrates two-dimensional echocardiographic images and their positions in real time and calculates left ventricular volume directly from traced endocardial contours without geometric assumptions. METHODS AND RESULTS: To study the accuracy of this method in quantifying left ventricular volume and performance in vivo, a canine model was developed in which instantaneous left ventricular volume can be measured directly with an intracavitary balloon connected to an external column. Ten dogs were studied at 84 different cavity volumes (4 to 85 cm3) and in conditions of altered left ventricular shape produced by either coronary occlusion or right ventricular volume overload. To demonstrate clinical feasibility, 19 adult human subjects were then studied by this method for quantification of stroke volume. Left ventricular volume, stroke volume, and ejection fraction calculated by three-dimensional echocardiography correlated well with directly measured values (r = .98, .96, .96 for volume, stroke volume, and ejection fraction, respectively) and agreed closely with them (mean difference, -0.78 cm3, -0.60 cm3, -0.32%). In humans, there was a good correlation (r = .94, SEE = 4.29 cm3) and agreement (mean difference, -0.98 +/- 4.2 cm3) between three-dimensional echocardiography and Doppler-derived stroke volumes. CONCLUSIONS: Three-dimensional echocardiography allows accurate assessment of left ventricular volume and systolic function.

Adult↗
PubMed1992

Isovolumic relaxation time varies predictably with its time constant and aortic and left atrial pressures: implications for the noninvasive evaluation of ventricular relaxation.

The isovolumic relaxation time (IVRT) is an important noninvasive index of left ventricular diastolic function. Despite its widespread use, however, the IVRT has not been related analytically to invasive parameters of ventricular function. Establishing such a relationship would make the IVRT more useful by itself and perhaps allow it to be combined more precisely with other noninvasive parameters of ventricular filling. The purpose of this study was to validate such a quantitative relationship. Assuming isovolumic relaxation to be a monoexponential decay of ventricular pressure (pv) to a zero-pressure asymptote, it was postulated that the time interval from aortic valve closure (when pv = p(o)) until mitral valve opening (when pv = left atrial pressure, pA) would be given analytically by IVRT = tau[log(p(o))-log(pA)], where tau is the time constant of isovolumic relaxation and log is to the base e. To test this hypothesis we analyzed data from six canine experiments in which ventricular preload and afterload were controlled nonpharmacologically. In addition, tau was adjusted with the use of beta-adrenergic blockade and calcium infusion, as well as with hypothermia. In each experiment data were collected before and after the surgical formation of mitral stenosis, performed to permit the study of a wide range of left atrial pressures. High-fidelity left atrial, left ventricular, and aortic root pressures were digitized, the IVRT was measured from the aortic dicrotic notch until the left atrioventricular pressure crossover point, and tau was calculated by nonlinear least-squares regression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The effect of late patency of the infarct-related coronary artery on left ventricular morphology and regional function after thrombolysis.

The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESAj; cm2/m2) and extent of abnormal wall motion were quantitated in those with a patent (n = 20) and those with an occluded (n = 10) infarct-related artery on coronary angiography performed 8 +/- 6 days after thrombolysis. Mean ESAi increased from (53 +/- 7 to 61 +/- 10 cm2/m2; p less than 0.02) in the occluded group during the follow-up period but remained unchanged (60 +/- 11 to 62 +/- 11 cm2/m2; p = NS) in the patient group. Mean percentage of abnormal wall motion decreased in the patent group (27 +/- 16% to 18 +/- 16%; p less than 0.01), whereas no significant change was noted in the occluded group (20 +/- 13% to 23 +/- 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attenuated left ventricular dilatation.

Cardiomegaly↗
PubMed1992

Progressive changes in ventricular structure and function during the year after acute myocardial infarction.

To investigate the long-term changes in left ventricular structure and function after myocardial infarction, 51 patients with a first myocardial infarction (17 anterior, 23 inferior, and 11 non-Q wave) were studied by two-dimensional echocardiography at the time of entry into the hospital, at 3 months, and 1 year after infarction. The left ventricular endocardial surface was reconstructed from these echocardiograms, and the endocardial surface area (ESA) index (in cm2/m2) and area of abnormal wall motion (AWM in cm2) were quantitated. Despite different trends in the ESA index between entry and 3-month values in those with and without early infarct expansion, a decrease in the ESA index from 3 months to 1 year was noted in anterior and non-Q wave infarctions (anterior with early expansion: 96.3 +/- 8.6 to 81.5 +/- 4.2 cm2/m2, p less than 0.05; anterior without early expansion: 59.7 +/- 2.0 to 54.7 +/- 2.0 cm2/m2, p less than 0.01; non-Q wave: 64.1 +/- 3.5 to 57.9 +/- 4.4 cm2/m2, p less than 0.01). The mean decline in ESA from 3 months to 1 year of 8.9 +/- 2.5 cm2 was independent of initial infarct size. Regional function, as represented by the area of AWM, was also improved but the timing of the improvement was related to the location and size of the infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1992

New perspectives in the assessment of cardiac chamber dimensions during development and adulthood.

The use of body surface area to assess the normalcy of cardiac dimensions has several limitations. To determine whether cardiac dimensions can be assessed by other indexes of body size and growth, this study evaluated the relations between cardiac dimensions assessed by two-dimensional echocardiography and age, height, weight and body surface area. The study group included 268 normal persons aged 6 days to 76 years of age. The dimensions examined included the aortic anulus, left atrium and left ventricular end-diastolic diameter, each measured in the parasternal long-axis plane, and left ventricular length measured from the apical two-chamber view. The analysis confirmed that the heart and great vessels grow in unison and at a predictable rate after birth, reaching 50% of their adult dimensions at birth, 75% by 5 years and 90% by 12 years. Although each cardiac dimension related linearly with height (aortic anulus, r = 0.96; left atrium, r = 0.91; left ventricular diameter, r = 0.94; left ventricular length, r = 0.93), the relations among age, weight and body surface area were best expressed by quadratic equations. Multiple regression confirmed that after adjustment for height, other indexes including age, gender, weight and body surface area had no independent effect on the prediction of each dimension. Therefore, because height is a nonderived variable that relates linearly with cardiac dimensions independent of age, it offers a simple yet accurate means of assessing the normalcy of cardiac dimensions in children and adults.

Adolescent↗
PubMed1991

Echocardiographic assessment of patients with infectious endocarditis: prediction of risk for complications.

To enhance the echocardiographic identification of high risk lesions in patients with infectious endocarditis, the medical records and two-dimensional echocardiograms of 204 patients with this condition were analyzed. The occurrence of specific clinical complications was recorded and vegetations were assessed with respect to predetermined morphologic characteristics. The overall complication rates were roughly equivalent for patients with mitral (53%), aortic (62%), tricuspid (77%) and prosthetic valve (61%) vegetations, as well as for those with nonspecific valvular changes but no discrete vegetations (57%), although the distribution of specific complications varied considerably among these groups. There were significantly fewer complications in patients without discernible valvular abnormalities (27%). In native left-sided valve endocarditis, vegetation size, extent, mobility and consistency were all found to be significant univariate predictors of complications. In multivariate analysis, vegetation size, extent and mobility emerged as optimal predictors and an echocardiographic score based on these factors predicted the occurrence of complications with 70% sensitivity and 92% specificity in mitral valve endocarditis and with 76% sensitivity and 62% specificity in aortic valve endocarditis.

Adult↗
PubMed1991

Immediate regional endocardial surface expansion following coronary occlusion in the canine left ventricle: disproportionate effects of anterior versus inferior ischemia.

The exact time of onset of functional expansion after acute myocardial infarction/ischemia remains unclear in spite of its potential link to chronic pathologic infarct expansion and its potential implications for therapy. To examine this early change in ventricular morphology, 14 open-chest dogs were studied with two-dimensional echocardiography before and after occlusion (10 minutes) of the left anterior descending coronary artery (LAD, n = 7) or circumflex artery (CIRC, n = 7). The endocardial surface area (ESA) and the area of abnormal wall motion (AWM) were reconstructed from the echocardiographic data using a previously reported technique for quantitatively mapping the ESA and extent of AWM. For the total group (N = 14), the mean ESA before occlusion was 48.9 +/- 9.8 cm2, increasing to 65.7 +/- 18.9 cm2 at 10 minutes occlusion (p less than 0.001). For the LAD subgroup, the mean ESA before occlusion was 50.7 +/- 9.3 cm2, increasing to 79.1 +/- 14.1 cm2 at 10 minutes following occlusion (p less than 0.001). For the CIRC subgroup, the mean ESA before occlusion was 47.1 +/- 10.8 cm2, increasing to 52.3 +/- 12.6 cm2 at 10 minutes after occlusion (p less than 0.001). The ESA increase for the LAD subgroup was significantly larger than that of the CIRC subgroup (LAD range 14.5 to 49.9 cm2 versus CIRC range 1.5 to 9 cm2, p less than 0.0001). Coronary occlusion resulted in similarly sized regions of AWM for both subgroups (LAD, 31.3 +/- 12.2 cm2 versus CIRC, 25.9 +/- 10.3 cm2, p = n.s.). For the LAD group, the largest increase in endocardial circumference occurred within the zone of AWM at the apex (39.9 +/- 12%). The endocardial surface area therefore expands immediately after coronary occlusion and the magnitude of this process is primarily related to the site (anteroapical) rather than to the extent of AWM.

Animals↗
PubMed1991

Quantitative relation between increased intrapericardial pressure and Doppler flow velocities during experimental cardiac tamponade.

To establish whether a quantitative relation exists between pericardial pressure and respiratory variation in intracardiac blood flow velocities, a spontaneously breathing closed chest canine model of pericardial tamponade was created. In seven dogs, pericardial pressure was sequentially increased in stages from a mean of -4 +/- 1 to 10 +/- 2 mm Hg while aortic and pulmonary Doppler flow velocities, pleural pressure changes (respiratory effort), blood pressure and cardiac output were measured. The variation in the Doppler-detected peak transaortic velocity (AV) during inspiration (IV) increased linearly from -5 +/- 3% at baseline (pericardial pressure -4 mm Hg) to -32 +/- 9% at a pericardial pressure of 10 mm Hg [IVAV = -2 (pericardial pressure)--13.1; r = 0.78, p less than 10(-6)]. The inspiratory variation in the peak transpulmonary velocity increased from 13 +/- 3% at baseline to 71 +/- 19% at a pericardial pressure of 10 mm Hg. The inspiratory variation in the pulmonary Doppler peak velocity (IVPV) was dependent on both pericardial pressure and degree of respiratory effort [IVPV = 3.8 (pericardial pressure) + 2.6 (respiratory effort) + 10.9; r = 0.88, p less than 10(-8)]. Thus, quantitative relations exist between increases in intrapericardial pressure and increases in inspiratory variation of peak aortic and pulmonary flow velocities. Additionally, pulmonary artery flow velocity is influenced more than aortic velocity by intrathoracic pressure.

Animals↗
PubMed1991

Impact of impinging wall jet on color Doppler quantification of mitral regurgitation.

BACKGROUND: In clinical color Doppler examinations, mitral regurgitant jets are often observed to impinge on the left atrial wall immediately beyond the mitral valve. In accordance with fluid dynamics theory, we hypothesized that a jet impinging on a wall would lose momentum more rapidly, undergo spatial distortion, and thus have a different observed jet area from that of a free jet with an identical flow rate. METHODS AND RESULTS: To test this hypothesis in vivo, we studied 44 patients with mitral regurgitation--30 with centrally directed free jets and 14 with eccentrically directed impinging wall jets. Maximal color jet areas (cm2) (with and without correction for left atrial size) were correlated with mitral regurgitant volumes, flow rates, and fractions derived from pulsed Doppler mitral and aortic forward flows. The groups were compared by analysis of covariance. Mean +/- SD mitral regurgitant fraction, regurgitant volume, and mean flow rate averaged 37 +/- 17%, 3.06 +/- 2.65 l/min, and 147 +/- 118 ml/sec, respectively. The maximal jet area from color Doppler imaging correlated relatively well with the mitral regurgitant fraction in the patients with free mitral regurgitant jets (r = 0.74, p less than 0.0001) but poorly in the patients with impinging wall jets (r = 0.42, p = NS). Although the mitral regurgitant fraction was larger (p less than 0.05) in patients with wall jets (44 +/- 20%) than in those with free jets (33 +/- 15%), the maximal jet area was significantly smaller (4.78 +/- 2.87 cm2 for wall jets versus 9.17 +/- 6.45 cm2 for free jets, p less than 0.01). For the same regurgitant fraction, wall jets were only approximately 40% of the size of a corresponding free jet, a difference confirmed by analysis of covariance (p less than 0.0001). CONCLUSIONS: Patients with mitral regurgitation frequently have jets that impinge on the left atrial wall close to the mitral valve. Such impinging wall jets are less predictable and usually have much smaller color Doppler areas in conventional echocardiographic views than do free jets of similar regurgitant severity. Jet morphology should be considered in the semiquantitative interpretation of mitral regurgitation by Doppler color flow mapping. Future studies of the three-dimensional morphology of wall jets may aid in their assessment.

Adult↗
PubMed1990

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

To investigate the natural history of regional dyssynergy and left ventricular size after myocardial infarction, 57 patients with a first Q wave myocardial infarction (18 anterior, 35 inferior, and four apical by echocardiography) were studied by two-dimensional echocardiography and compared with 30 control patients. Measurements from the echocardiograms were used to construct maps of the left ventricular endocardial surface from which the endocardial surface area index (ESAi) and the percent of the endocardial surface area involved by abnormal wall motion (%AWM) were calculated. The maps from entry and 3-month echocardiograms were used to classify patients based on changes in ESAi and abnormal wall motion. Two subgroups of patients were identified at entry--those with a normal ESAi (group 1, n = 50) and those with an increased ESAi (group 2, n = 7). Group 1 patients was subdivided at 3 months by changes occurring in ESAi (1A, 5% increase [n = 19]; 1B, no change [n = 23]; 1C, 5% decrease [n = 8]). The increase in ESAi (64.9 +/- 5.2 to 75.4 +/- 7.5 cm2/m2, p less than 0.0001) in group 1A was associated with global ventricular dilatation (n = 11) and clinically silent infarct extension (n = 8). Groups 1B and 1C were composed predominantly of patients with inferior infarctions, and all exhibited either no change or a significant decrease in infarct size (infarct regression). Group 2 patients demonstrated a continued increase in ESAi by 3 months (88.2 +/- 10.0 to 101.4 +/- 15.5 cm2/m2, p less than 0.007). This group comprised only patients with anterior infarctions, and all exhibited infarct expansion at the left ventricular apex. The changes in left ventricular size and functional infarct size are heterogeneous after acute myocardial infarction and relate to the initial endocardial surface area, infarct location, and functional infarct size.

Acute Disease↗