Biomedical subjects
Publications and source records attributed to Z Vered.
Acquired left ventricular-right atrial communication due to infective endocarditis was diagnosed in a 64-year-old patient by transesophageal echocardiography and confirmed by cardiac catheterization. The patient was initially treated medically and then referred for corrective surgery.
We describe a 65-year-old patient with moderate combined mitral disease and severe tricuspid regurgitation, in whom the tricuspid regurgitant jet was oriented toward the interatrial septum. Color flow and pulsed Doppler demonstrated a late-systolic to mid-diastolic, right-to-left shunting of the tricuspid regurgitant jet through the foramen ovale. This finding was subsequently confirmed with transesophageal echocardiography.
Stress echocardiography is used increasingly in the evaluation of coronary artery disease. The echocardiographic evaluation of ischemia is based on stress-induced changes in wall motion and wall thickening of the ischemic segments. Studies have demonstrated that left ventricular volumetric changes may induce changes in wall thickness. The aim of the study was to evaluate whether significant changes in ventricular volume, wall thickness, and wall thickening occur during stress echocardiography with atrial pacing. Seven German Landrace female pigs were studied 4 weeks after the induction of a small myocardial infarction. Echocardiographic measurements were conducted in noninfarcted segments on the short-axis view at baseline and during atrial pacing at 120, 150, and 180 beats/min. End-diastolic circumferential area decreased from 12.3 +/- 2.0 cm2 at baseline to 8.9 +/- 1.9 cm2 at 180 beats/min of atrial pacing (p < 0.01). Mean wall thickness (interventricular septal plus posterior wall thickness divided by 2) increased markedly and progressively from 6.7 +/- 0.6 mm at baseline to 9.8 +/- 1.0 mm at 180 beats/min (p < 0.01). The increase in wall thickness correlated inversely with end-diastolic area (r = -0.57; p < 0.01). Percent systolic thickening decreased from 38.9 +/- 12.0 at baseline to 14.9 +/- 7.4 at 180 beats/min of atrial pacing (p < 0.01). The decrease in percent wall thickening correlated with the increase in wall thickness (r = -0.71; p < 0.01). In conclusion, this study shows that a marked increase in wall thickness (pseudohypertrophy) and decrease in percent systolic thickening are observed during rapid atrial pacing in normal myocardium and do not indicate stress-induced left ventricular dysfunction.
We report on a patient in whom significant bleeding occurred during thrombolytic therapy. The bleeding occurred after an echocardiographic study, and it resulted in blood transfusion.
We and others have shown that normal myocardium exhibits 4 to 5 dB diastolic-to-systolic cyclic variation (CV) of integrated backscatter. To investigate the effect of intramyocardial contrast on integrated backscatter, we injected 5% sonicated albumin, containing microbubbles in the range of 5 microns in diameter, into the left atrium in nine open-chest dogs. The dogs were anesthetized and placed in the right lateral decubitus position on a specially designed table with a cutout allowing ultrasound imaging from below. Ultrasonic data was obtained from the right precordium by use of a prototype M-mode integrated backscatter system implemented in a commercially available two-dimensional system. Usable data were obtained in eight of nine dogs. Integrated backscatter increased up to 13 dB after contrast injections. There was a significantly decreased CV of integrated backscatter during myocardial contrast in all eight dogs. The mean level of CV of integrated backscatter for the eight dogs decreased from 4.7 dB (530 beats analyzed) without contrast to 2.8 dB during contrast (436 beats analyzed). There was a trend to greater CV at higher levels of contrast. Septal excursion, as measured by M-mode echocardiography simultaneously with integrated backscatter by the same ultrasound beam, was similar with and without contrast (mean 8.2 vs 8.3 mm). Thus left atrium contrast injection produces quantitatively measurable integrated backscatter effects. Cyclic variation of integrated backscatter decreases with contrast. However, at higher contrast levels the decrease tends to be smaller. These effects should be considered during quantitative tissue characterization and myocardial contrast studies.
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We have previously shown that the intrinsic properties of myocardium can be characterized quantitatively by the assessment of ultrasonic integrated backscatter. In this study we utilized a novel, real-time, two-dimensional system capable of quantitative integrated backscatter imaging to determine whether zones of remote myocardial infarction in dogs could be delineated definitively by ultrasonic tissue characterization. Detection of such zones in patients is needed as a basis for management decisions related to thrombolysis, angioplasty, and coronary surgery. Integrated backscatter was measured through the closed chest from 25 myocardial sites. Zones of infarction exhibited time-averaged integrated backscatter values approximately 10 dB (9.5 +/- 0.5 dB, standard error of the mean) greater than those in normal regions (p less than 0.001). In addition, the physiologic cardiac cycle--dependent variation of integrated backscatter was blunted significantly in zones of infarction [0.8 dB +/- 0.3 vs. 3.8 +/- 0.6 (p less than 0.01) for normal regions]. Ultrasonic results matched the histopathologic features assessed directly. Thus quantitative ultrasonic tissue characterization can differentiate infarcted tissue from normal myocardium and offers promise for quantitative detection of histopathology in vivo.
A total of 145 patients with 160 mechanical prostheses of the Björk-Shiley or Starr-Edwards type (15 with double mitral plus aortic valves) underwent clinical and Doppler echocardiography analysis. In the mitral position (85 valves) 10 patients with valve-related symptoms, calculated prosthetic area less than or equal to 1 cm2, or mean transprosthetic gradient greater than 10 mm Hg by Doppler echocardiography were predefined as abnormal. Seven patients had operations, and prosthetic obstruction was confirmed in all. All patients had higher pulmonary pressures (p less than 0.001) before valve replacement. Clinical presentation was variable; however, all those with proved prosthetic thrombosis had a fulminant course and distinctive velocity curves on Doppler. In the 75 patients predefined as normal, calculated valve area (2.3 +/- 0.6 cm2, mean +/- SD, range 1.3 to 3.7 cm2) and mean gradient (4.9 +/- 1.7 mm Hg, range 1.5 to 9.5 mm Hg) were widely spread and were independent of prosthetic size greater than or equal to 27 mm. Clinically 37 of 75 patients were moderately to severely limited. Mean gradient above 5 mm Hg was associated with a higher incidence of chronic atrial fibrillation (p less than 0.05), significant tricuspid regurgitation, failure of the right side of the heart, and significant functional limitation (p less than 0.02 for all). In the aortic position (75 valves) peak gradients were 28.2 +/- 15 mm Hg (8 to 80 mm Hg). Mean gradients were 18 +/- 9.6 mm Hg (6.5 to 46.5 mm Hg). Averaged gradients derived from the average of peak and late systolic gradients were 22.4 +/- 12.7 mm Hg (6 to 62 mm Hg). In all five abnormal patients (two with endocarditis and three with hemodynamic decompensation) but also in 18 of 70 clinically normal valves, peak gradients were greater than or equal to 36 mm Hg (ranges 36 to 65 mm Hg in both). Gradients were unrelated to symptoms or to the duration of the valve in situ (3 weeks to 20 years). Gradients correlated with prosthetic size (r = 0.57) and were higher (p less than 0.001) across small (19 to 23 mm) versus large (25 to 31 mm) valves. Regurgitation was present in 40% of the mitral prostheses. It was detected in 32% of the mitral prostheses defined as normal and was estimated as mild in most. Aortic regurgitation was present in all five abnormal aortic prostheses, significant in four, and in 26 of the valves (37%) defined as normal, significant in two.(ABSTRACT TRUNCATED AT 400 WORDS)
BACKGROUND: Monitoring intravascular volume during surgery, especially in major cardiovascular procedures is necessary for appropriate fluid restoration and the maintenance of an adequate cardiac output. In estimating preload, both standard hemodynamic and echocardiographic parameters have been limited. The purpose of this study was to further define the effects of induced hypovolemia on the echocardiographic parameters. In particular, we sought to show whether a decrease in echocardiographic left ventricular area and volume was associated with a significant increase in left ventricular wall thickness (left ventricular pseudohypertrophy) and with changes in LV function. In addition, we sought to investigate the effects of rapid restoration of blood volume on cardiac dimensions and function. METHODS AND RESULTS: Seven anesthetized pigs underwent systemic and right heart pressures and cardiac output measurements. Two-dimensional echocardiographic parasternal long- and short-axis views were obtained during graded bleeding by rapid withdrawal of blood from an arterial cannula, with increments of 5% each up to 30% of calculated blood volume. After completion of the bleeding, the entire amount of the blood withdrawn was retransfused within 4 to 5 minutes. Both hemodynamic and echocardiographic measurements were performed at baseline, immediately after the completion of each stage of bleeding and after blood restoration. Mean (+/- standard deviation) left ventricular wall thickness (mean of septal and posterior wall thickness) was 6.3 +/- 0.1 mm at baseline, 8.3 +/- 1.5 mm at peak bleeding, and 6.2 +/- 0.1 after restoration (p < 0.01). Left ventricular mass did not change during the experiment. Left ventricular end-diastolic volume was 62.8 +/- 20.3 ml at baseline, 37.5 +/- 12.4 ml at peak bleeding (p < 0.0001), and 65.9 +/- 16.7 ml after blood restoration (p < 0.001 compared with 30% bleeding). H/r ratio (posterior wall thickness divided by left ventricular radius) increased from 0.29 +/- 0.07 at baseline to 0.50 +/- 0.19 at peak bleeding returning to 0.26 +/- 0.04 after restoration. Left ventricular ejection fraction was 0.53 +/- 0.10 at baseline and 0.55 +/- 0.20 at peak bleeding (not significant), decreasing to 0.38 +/- 0.11 after blood restoration (p < 0.05 compared with 30% bleeding). End-diastolic volume correlated closely with right atrial pressure (r = -0.82), capillary wedge pressure (r = -0.78), and stroke volume (r = 0.74). Left ventricular ejection fraction inversely correlated with left ventricular end-diastolic volume (r = -0.48) and with end-systolic wall stress (r = -0.62). The changes in interventricular septal and posterior wall thickness were inversely related to left ventricular end-diastolic volume (r = -0.72 and -0.35, respectively). CONCLUSIONS: This study shows that transient concentric left ventricular remodeling (pseudohypertrophy), a phenomenon previously described in cardiac tamponade and during rapid atrial pacing is commonly seen during hypovolemia. This new sign may further enhance the echocardiographic estimation of left ventricular preload.
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