Clinical correlates and reference intervals for pulmonary artery systolic pressure among echocardiographically normal subjects.

BACKGROUND: Data in normal human subjects on the factors affecting pulmonary artery systolic pressure (PASP) are limited. We determined the correlates of and established a reference range for PASP as determined by Doppler transthoracic echocardiography (TTE) from a clinical echocardiographic database of 102 818 patients, of whom 15 596 (15%) had a normal Doppler TTE study. METHODS AND RESULTS: A normal TTE was based on normal cardiac structure and function during complete Doppler TTE studies. The PASP was calculated by use of the modified Bernoulli equation, with right atrial pressure assumed to be 10 mm Hg. Among TTE normal subjects, 3790 subjects (2432 women, 1358 men) from 1 to 89 years old had a measured PASP. The mean PASP was 28.3+/-4.9 mm Hg (range 15 to 57 mm Hg). PASP was independently associated with age, body mass index (BMI), male sex, left ventricular posterior wall thickness, and left ventricular ejection fraction (P<0.001). The estimated upper 95% limit for PASP among lower-risk subjects was 37.2 mm Hg. A PASP >40 mm Hg was found in 6% of those >50 years old and 5% of those with a BMI >30 kg/m(2). CONCLUSIONS: Among 3790 echocardiographically normal subjects, PASP was associated with age, BMI, sex, wall thickness, and ejection fraction. Of these subjects, 28% had a PASP >30 mm Hg, and the expected upper limit of PASP may include 40 mm Hg in older or obese subjects. These findings support the use of age- and BMI-corrected values in establishing the expected normal range for PASP.

Doppler mitral pressure half-time: a clinical tool in search of theoretical justification.

The Doppler determination of the mitral pressure half-time has gained widespread acceptance as a reliable estimate for mitral valve area, despite little theoretical basis for its "independence" of other hemodynamic variables. A simple model of the left atrium and mitral valve has been developed and a governing equation derived from fluid dynamics fundamentals. Solution of this equation indicates that the pressure half-time should vary inversely with mitral valve area, but also proportionally to net left atrial and ventricular compliance and to the square root of the peak transmitral gradient. This complex relation is apparently masked in the typical clinical situation because pressure and compliance tend to change in opposite directions, thereby partly offsetting each other. In several clinical settings, such as balloon mitral valvotomy, left ventricular hypertrophy and aortic regurgitation, changes in initial pressure and compliance may be large enough to alter the relation between mitral area and pressure half-time. This study reviews the development of the pressure half-time concept, presents an overall method for studying mitral valve flow using mathematical modeling and describes the effects of factors other than mitral valve area on pressure half-time.

Fluid dynamics model of mitral valve flow: description with in vitro validation.

A lumped variable fluid dynamics model of mitral valve blood flow is described that is applicable to both Doppler echocardiography and invasive hemodynamic measurement. Given left atrial and ventricular compliance, initial pressures and mitral valve impedance, the model predicts the time course of mitral flow and atrial and ventricular pressure. The predictions of this mathematic formulation have been tested in an in vitro analog of the left heart in which mitral valve area and atrial and ventricular compliance can be accurately controlled. For the situation of constant chamber compliance, transmitral gradient is predicted to decay as a parabolic curve, and this has been confirmed in the in vitro model with r greater than 0.99 in all cases for a range of orifice area from 0.3 to 3.0 cm2, initial pressure gradient from 2.4 to 14.2 mm Hg and net chamber compliance from 16 to 29 cc/mm Hg. This mathematic formulation of transmitral flow should help to unify the Doppler echocardiographic and catheterization assessment of mitral stenosis and left ventricular diastolic dysfunction.

Contrast echocardiography in acute myocardial ischemia. II. The effect of site of injection of contrast agent on the estimation of area at risk for necrosis after coronary occlusion.

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.

Adjacent solid boundaries alter the size of regurgitant jets on Doppler color flow maps.

Recent studies have attempted to predict the severity of regurgitant lesions from jet size on Doppler flow maps. Jet size is a function of both regurgitant volume and fluid entrained from the receiving chamber and, for a free jet, is a function of its momentum at the orifice. However, regurgitant jets often approach or attach to cardiac walls, potentially altering their momentum and ability to expand by entrainment. Therefore, this study addressed the hypothesis that adjacent walls influence regurgitant jet size as seen on Doppler flow maps. Steady flow was driven through circular orifices (0.02 to 0.05 cm2) at physiologic velocities of 2 to 5 m/s. At a constant flow rate and orifice velocity, orifice position was varied to produce three jet geometries: free jets, jets adjacent to a horizontal chamber wall lying 1 cm below the orifice and wall jets with the orifice at the level of the wall. Doppler color flow imaging was performed at identical instrument settings for all jets. Two long-axis views of the jet were obtained: a vertical view perpendicular to the wall, resembling that most commonly used in patients to image the length of the jet, and a horizontal view parallel to the chamber wall. Velocities along the jet were also measured by Doppler mapping.(ABSTRACT TRUNCATED AT 250 WORDS)

Calculation of atrioventricular compliance from the mitral flow profile: analytic and in vitro study.

The quantitative assessment of ventricular diastolic function is an important goal of Doppler echocardiography. Hydrodynamic analysis predicts that the net compliance (Cn) of the left atrium and ventricle can be quantitatively predicted from the deceleration rate (dv/dt) of the mitral velocity profile by the simple expression: Cn = - A/rho dv/dt, where A is effective mitral valve area and rho is blood density. This formula was validated using an in vitro model of transmitral filling where mitral valve area ranged from 0.5 to 2.5 cm2 and net compliance from 0.012 to 0.023 cm3/(dynes/cm2) (15 to 30 cm3/mm Hg). In 34 experiments in which compliance was held constant throughout the filling period, net atrioventricular compliance was accurately calculated from the E wave downslope and mitral valve area (r = 0.95, p less than 0.0001). In a second group of experiments, chamber compliance was allowed to vary as a function of chamber pressure. When net compliance decreased during diastole (as when the ventricle moved to a steeper portion of its pressure-volume curve), the transorifice velocity profile was concave downward, whereas when net compliance increased, the velocity profile was concave upward. Application of the preceding formula to these curved profiles allowed instantaneous compliance to be calculated throughout the filling period (r = 0.93, p less than 0.001). Numeric application of a mathematic model of mitral filling demonstrated the accuracy of this approach in both restrictive and nonrestrictive orifices.(ABSTRACT TRUNCATED AT 250 WORDS)

Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans.

To determine the effect of filling pressure on the pattern of left ventricular filling in humans, the mitral flow velocity profile was measured by pulsed wave Doppler echocardiography during right and left heart catheterization in 11 patients before and during nitroglycerin infusion. Nitroglycerin reduced mean arterial pressure from 90 +/- 9 to 80 +/- 11 mm Hg (p less than 0.001) and mean pulmonary capillary wedge pressure from 9 +/- 4 to 4 +/- 2 mm Hg (p less than 0.001). Cardiac output fell from 6.6 +/- 1.5 to 5.5 +/- 1.4 liters/min (p less than 0.001) and heart rate increased from 60 +/- 13 to 65 +/- 14 beats/min (p less than 0.002). The time constant of isovolumic relaxation (TI.) decreased from 51 +/- 9 to 46 +/- 8 ms (p less than 0.01), indicating faster left ventricular relaxation. Nitroglycerin altered the Doppler characteristics of the early filling (E) wave but not those of the atrial contraction (A) wave. Peak velocity of the E wave decreased from 56 +/- 14 to 44 +/- 9 cm/s (p less than 0.001), peak velocity of the A wave did not change and the ratio of peak velocities of the E and A waves decreased from 0.97 +/- 0.33 to 0.77 +/- 0.20 (p less than 0.02). The deceleration of the E wave decreased from 289 +/- 138 to 186 +/- 71 cm/s2 (p less than 0.02). The ratio of velocity-time integral of the A wave to total velocity-time integral (that is, contribution of atrial contraction to total filling) increased from 0.31 +/- 0.09 to 0.36 +/- 0.08 (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical significance of incomplete tricuspid valve closure seen on two-dimensional echocardiography.

Incomplete closure of the tricuspid valve without apparent cusp disease was noted on two-dimensional echocardiography in 31 patients. This abnormality was defined as a failure of the tricuspid valve leaflet tips to reach the plane of the tricuspid valve anulus by at least 1 cm in the standard apical four chamber view at the point of maximal systolic closure. This resulted in a final systolic leaflet position deeper within the right ventricular cavity than is normally seen. The finding was present in the following diagnostic subgroups: Group A, pulmonary hypertension (11 patients); Group B, rheumatic heart disease (4 patients); Group C, dilated cardiomyopathy (9 patients) and Group D, previous myocardial infarction (7 patients). Right atrial, right ventricular and tricuspid anulus measurements were made and compared with those from a group of 67 normal subjects. The results were as follows: right atrial endsystolic area = 27.2 +/- 8.6 cm2 (normal = 13.4 +/- 2.0); right ventricular end-systolic area = 25.6 +/- 8.7 cm2 (normal = 10.9 +/- 2.9); right ventricular end-diastolic area = 31.5 +/- 9.1 cm2 (normal = 20.1 +/- 4.9) and tricuspid valve anular end-systolic dimension = 4.0 +/- 0.6 cm (normal = 2.2 +/- 0.3). The differences from the normal data were all statistically significant (p less than 0.001). Incomplete closure of the tricuspid valve, although a nonspecific diagnostic finding, is primarily associated with right-sided chamber enlargement. Tricuspid regurgitation may be present. The mechanism could be related to geometric changes in valve apparatus dynamics secondary to right-sided cardiac enlargement and tricuspid valve anular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the early transmitral Doppler velocity curve: effect of primary physiologic changes and compensatory preload adjustment.

Left ventricular filling (as assessed by Doppler echocardiography) has previously been shown to depend in a complex fashion on ventricular diastolic function (compliance and relaxation) as well as other variables, such as atrial pressure and compliance, ventricular systolic function and mitral valve impedance. To study the effect of isolated physiologic alterations on individual Doppler indexes, a mathematic model of mitral flow was analyzed. By varying one physiologic variable at a time, it was shown that mitral velocity acceleration is affected directly by atrial pressure and inversely by the ventricular relaxation time constant, with relatively little impact of chamber compliance. Deceleration rate was directly influenced by mitral valve area, atrial pressure and ventricular systolic dysfunction and inversely affected by atrial and ventricular compliance relations, with little impact of relaxation unless it was so delayed as to be incomplete during deceleration. Peak velocity was directly affected most strongly by initial left atrial pressure, and lowered somewhat by prolonged relaxation, low atrial and ventricular compliance and systolic dysfunction. Strikingly different filling patterns emerged when the primary physiologic alterations were accompanied by simultaneous compensatory changes in atrial pressure designed to maintain stroke volume constant. Low ventricular compliance with preload compensation produced characteristic E waves with very short acceleration and deceleration times and high peak velocity. Thus, mathematic analysis of ventricular filling helps to explain the physical and physiologic basis for the transmitral velocity curve.

Influence of orifice geometry and flow rate on effective valve area: an in vitro study.

Fluid dynamics suggests that orifice geometry is a determinant of discharge properties and, therefore, should influence empiric constants in formulas (such as the Gorlin formula) to calculate stenotic valve area. An in vitro study utilizing a model of transmitral flow was conducted to investigate how the discharge coefficient changes with 1) orifice eccentricity (ratio of long to short diameter), 2) absolute area, 3) the presence of a nozzle-like inlet, and 4) varying flow. Twenty-three orifices with areas varying between 0.3 and 2.5 cm2 and eccentricities from 1:1, or circular, to 5:1, or elliptic, were tested. The calculated discharge coefficients ranged between 0.675 and 0.93. For a given area, the discharge coefficient decreased by a mean value (+/- SD) of 5.5 +/- 1.3% between circular orifices and 5:1 ellipses. Discharge coefficients increased by a mean of 8.9 +/- 3.5% from 0.3 to 2.5 cm2 area within each eccentricity class. A gradually tapering inlet (nozzle) raised the discharge coefficient by 8.8 +/- 3.9%, leading to a discharge coefficient between 0.81 and 0.93 for round orifices. The discharge coefficient did not change appreciably with flow. The concept of the discharge coefficient and its role in assessing restrictive orifices in general by hydraulic formulas (for example, the Gorlin and pressure half-time calculations) are discussed.

Osteogenic sarcomas mimicking left atrial myxomas: clinical and two-dimensional echocardiographic features.

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.

Optimal stage duration in dobutamine stress echocardiography.

OBJECTIVES: This study attempted to determine the benefit of a 5-min dobutamine stress echocardiographic stage versus a 3-min stage in a canine model. BACKGROUND: Dobutamine stress echocardiography, as currently performed, uses a variety of different protocols. Among the many aspects of dobutamine stress echocardiographic protocols that vary is stage duration. Because dobutamine has specific pharmacodynamics, it is possible that stages of different durations may have different cardiovascular effects. METHODS: Paired dobutamine stress echocardiograms were obtained in 10 open chest instrumented dogs. The stage duration for the initial dobutamine stress echocardiogram was randomly allocated to either 3 or 5 min, and all hemodynamic and echocardiographic variables were allowed to return to baseline before the second dobutamine stress echocardiogram was obtained using the alternative stage duration. At each stage, heart rate, systolic blood pressure, coronary flow, myocardial wall thickness and left ventricular cavity area were recorded. Cavity obliteration, hypotension, ventricular tachycardia or a maximal dose of 40 micrograms/kg body weight per min served as the dobutamine stress echocardiographic end point. RESULTS: At baseline, no difference was detected between the 3- or 5-min protocols for heart rate, systolic blood pressure, rate-pressure product, coronary blood flow, wall thickness or percent area change. Heart rate, systolic blood pressure and coronary flow increased more by the 10-micrograms/kg per min dose with the 5-min protocol than with the 3-min protocol. The dobutamine stress echocardiographic end points were achieved at a lower dobutamine dose (15.0 +/- 4.1 vs. 11.0 +/- 2.1 micrograms/kg per min [mean +/- SD], p = 0.01) with the longer stage duration. CONCLUSIONS: In this canine model, a longer stage produced a greater hemodynamic effect at a lower peak dose. Thus, extending stage duration in clinical dobutamine stress echocardiography may achieve equivalent physiologic stress at lower doses and contribute to the optimization of dobutamine stress echocardiographic protocols.

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.

Impact of orifice geometry on the shape of jets: an in vitro Doppler color flow study.

To investigate the influence of orifice geometry on the three-dimensional shape of jets, an in vitro Doppler color flow study was performed. Jets were formed by discharging blood through round orifices and through orifices with major/minor axis ratios of 2:1, 3:1 and 5:1. These were repeated with orifice areas of 0.1, 0.3 and 0.5 cm2. For turbulent and laminar jets formed by these orifices, Doppler color flow images were obtained from two orthogonal scanning planes aligned with the major and minor orifice axes. Jet width was measured at 1 cm intervals from 0 to 5 cm from the orifice and used to calculate jet eccentricity (ratio of major to minor axis widths) and the rate of divergence of the jet walls. Jets were observed to diverge more rapidly along walls aligned with the orifice minor axis rather than along the major axis. This differential spreading led to the development of circular symmetry at a short distance from the orifice. Jet divergence (theta) occurred more rapidly for turbulent jets and for jets formed by larger orifices: theta (zero) = 0.80 + 6.3.A + 7.0.T + 0.47.E-OR (r = 95, p less than 0.0001, n = 48), where A is orifice area (cm2); T is 0 for laminar jets, 1 for turbulent jets and E-OR combines orifice eccentricity and scanning orientation, ranging from -5 for 5:1 orifices imaged along the major axis, 0 for circular orifices to 5 for 5:1 orifices imaged along the minor axis. Within the jet, eccentricity decayed approximately exponentially with distance from the orifice, more rapidly for turbulent jets, more slowly for the larger and more eccentric orifices.(ABSTRACT TRUNCATED AT 250 WORDS)

Reconsideration of echocardiographic standards for mitral valve prolapse: lack of association between leaflet displacement isolated to the apical four chamber view and independent echocardiographic evidence of abnormality.

Mitral valve prolapse by current echocardiographic criteria can be diagnosed with surprising frequency in the general population, even when preselected normal subjects are examined. In most of these individuals, however, prolapse is present in the apical four chamber view and absent in roughly perpendicular long-axis views. Previous studies have shown that systolic annular nonplanarity can cause apparent prolapse in the four chamber view without actual leaflet displacement above the most superior points of the anulus, and there is evidence for such nonplanarity in vivo. It is then reasonable to ask whether superior leaflet displacement limited to the four chamber view has any pathologic significance or complications. The purpose of this study, therefore, was to address the following hypothesis: that patients with superior leaflet displacement confined to the four chamber view have no higher frequency of associated echocardiographic abnormalities than do patients without displacement in any view. Such abnormalities, which would provide independent evidence of mitral valve pathology or dysfunction, include leaflet thickening, left atrial enlargement and mitral regurgitation. Leaflet displacement was measured in the parasternal long-axis and apical four chamber views in 312 patients who were studied retrospectively and selected for the absence of forms of heart disease other than mitral valve prolapse. Leaflet thickness and left atrial size were measured and mitral regurgitation was graded. Patients with leaflet displacement limited to the four chamber view were no more likely to have associated abnormalities than were patients without displacement in any view (0 to 2% prevalence, p greater than 0.5). In contrast, patients with leaflet displacement in the long-axis view were significantly more likely to have associated abnormalities (12 to 24%, p less than 0.005), the frequency of which increased with the extent of leaflet displacement in that view (p less than 0.0001). These results suggest that displacement limited to the apical four chamber view is, in general, a normal geometric finding unassociated with echocardiographic evidence of pathologic significance.

Limits of normal left ventricular dimensions in growth and development: analysis of dimensions and variance in the two-dimensional echocardiograms of 268 normal healthy subjects.

The majority of studies generating normal echocardiographic reference values for left ventricular dimensions have been based on blindly performed M-mode measurements, and there are no previous reports based on two-dimensional echocardiography that provide a comprehensive analysis of the two-dimensional measurements from infancy to old age. This report presents the results of analyzing the left ventricular internal dimensions from cross-sectional echocardiographic studies on 268 normal healthy subjects (none were hospitalized for any reason) whose ages ranged from 6 days to 76 years. The mean data are reported as functions of body surface area and, in addition, the variance is modeled as a function of body surface area to provide an accurate and clinically useful determination of normal limits and to model changes in the cardiac dimensions and in their variance representing normal growth and development. The data fit well to the exponential growth model (r values 0.85 to 0.95). Variance about the central values also depended significantly on body size; that relation is represented effectively by a quadratic function of body surface area (r values 0.82 to 0.98). The model parameters allow calculation of normal limits at any desired level of confidence. Areas determined by hand planimetry have significantly greater variance compared with variance of linear dimensions, and also compared with variance of cross-sectional area using ellipses generated from the anteroposterior and mediolateral dimensions. This implies that either biologic variations in the amount of infolding or errors in freehand planimetry constitute a significant source of variance; this may be remedied by filtering out high frequency oscillations of contour. There is no significant difference in midnormal values and confidence limits for corresponding dimensions measured from orthogonal views. Furthermore, the anteroposterior and mediolateral dimensions of the left ventricle superimpose at each body size, consistent with circular cross section for normal subjects throughout growth and development. The data presented should comprise a useful set of reference standards for interpretation of cross-sectional echocardiograms.

Doppler and two-dimensional echocardiographic diagnosis of Björk-Shiley prosthetic valve malfunction: importance of interventricular septal motion and the timing of onset of valve flow.

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.

Contrast echocardiography in acute myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis.

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.

Papillary muscle traction in mitral valve prolapse: quantitation by two-dimensional echocardiography.

Previous angiographic observations in patients with mitral valve prolapse have suggested that superior leaflet displacement results in abnormal superior tension on the papillary muscle tips that causes their superior traction or displacement. It has further been postulated that such tension can potentially affect the mechanical and electrophysiologic function of the left ventricle. The purpose of this study was to confirm and quantitate this phenomenon noninvasively by using two-dimensional echocardiography to determine whether superior displacement of the papillary muscle tips occurs and its relation to the degree of mitral leaflet displacement. Directed echocardiographic examination of the papillary muscles and mitral anulus was carried out in a series of patients with classic mitral valve prolapse and results were compared with those in a group of normal control subjects. Distance from the anulus to the papillary muscle tip was measured both in early and at peak ventricular systole. In normal subjects, this distance did not change significantly through systole, whereas in the patient group it decreased, corresponding to a superior displacement of the papillary muscle tips toward the anulus in systole (8.5 +/- 2.6 vs. 0.8 +/- 0.7 mm; p less than 0.0001). This superior papillary muscle motion paralleled the superior displacement of the leaflets in individual patients (y = 1.0x + 0.8; r = 0.93) and followed a similar time course.(ABSTRACT TRUNCATED AT 250 WORDS)

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.