Quantitative evaluation of the segmental left ventricular response to dobutamine stress by tissue Doppler echocardiography.

Tissue Doppler imaging displays color-coded myocardial velocity on-line and has potential to objectively quantify regional left ventricular function. Sixty patients, aged 56 +/- 10 years, were studied to determine the normal and abnormal segmental endocardial velocity response to dobutamine stress, and the sensitivity, specificity, and accuracy of tissue Doppler imaging for detecting abnormal wall motion at peak stress as defined by routine visual interpretation. Separate 2-dimensional routine gray scale and color tissue Doppler image sets were acquired at rest and peak dobutamine stress in a digital cineloop format. Routine wall motion interpretation from gray scale images and color-coded peak systolic endocardial velocity from tissue Doppler images were determined independently. Twenty-two patients who reached their target heart rate and had normal wall motion at peak stress served as a control group. There were 19 patients who had wall motion abnormalities at peak stress. Segmental peak endocardial velocities increased significantly in all segments in the control group. Endocardial velocity was significantly lower at peak stress in the pooled abnormal segments than in the pooled normal segments: 3.1 +/- 1.2 versus 7.2 +/- 1.9 cm/s, respectively (p < 0.05 vs normal control). However, the velocity response of abnormal apical segments could not be distinguished from normal controls by tissue Doppler imaging. Excluding apical segments, a peak velocity of < or = 5.5 cm/s with peak stress had an average sensitivity of 96%, specificity of 81%, and accuracy of 86% for identifying abnormal segments at peak stress as defined by routine 2-dimensional criteria. Tissue Doppler imaging has the potential to quantify regional left ventricular function during dobutamine stress.

Quantification of the myocardial response to low-dose dobutamine using tissue Doppler echocardiographic measures of velocity and velocity gradient.

Low-dose dobutamine echocardiography has been clinically useful in myocardial viability studies, although routine visual assessment of wall motion is subjective. The objective was to quantify the incremental myocardial response to low-dose dobutamine infusion using a new semiautomated tissue Doppler (TD) analysis system and to compare these data with routine echocardiographic measures in the same subjects. Twelve subjects had TD and routine echocardiographic studies at baseline and during 10-minute stages of dobutamine infusion at 1, 2, 3, and 5 microg/kg/min. Color TD video data were converted to a digital velocity matrix (4.5 velocity data points/mm at 500 Hz) for analysis of mitral annular velocity, endocardial velocity, and velocity gradient at each stage. Posterior wall percent thickening and ejection fraction were calculated from the routine images. Mitral annular peak systolic velocity significantly increased with only 1 microg/kg/min of dobutamine from 69 +/- 9 to 77 +/- 7 mm/s (p <0.05 vs baseline), and further incremental increases occurred with each subsequent dose. Anteroseptal and posterior wall peak endocardial velocity increased with 2 microg/kg/min of dobutamine from 33 +/- 7 to 46 +/- 15 mm/s and 50 +/- 9 to 61 +/- 10 mm/s, respectively (p <0.01 vs baseline) and further increased with 5 microg/kg/min (p <0.0001 vs 3 microg/kg/min). Posterior wall peak systolic gradient also increased with 2 microg/kg/min of dobutamine from 3.1 +/- 0.6 to 5.4 +/- 1.6 s(-1) (p <0.05 vs baseline). Routine measures of percent wall thickening or ejection fraction did not detect increases until the 3 microg/kg/min dose. TD can detect subtle alterations in contractility induced by low-dose dobutamine and has the potential to quantify regional ventricular function objectively.

Accuracy of the conductance catheter for measurement of ventricular volumes seen clinically: effects of electric field homogeneity and parallel conductance.

The conductance-volume method is an important clinical tool which allows the assessment of left ventricular function in vivo. However, the accuracy of this method is limited by the homogeneity of electric field the conductance catheter produces and the parallel conductance of surrounding structures. This paper examines these sources of error in volumes seen clinically. The characteristics of electric field within a chamber were examined using computer simulation. Nonconductive and conductive models were constructed and experimental measurements obtained using both single-field (SF) and dual-field (DF) excitation. Results from computer simulations and in vitro measurements were compared to validate the purposed theoretical model of conductance-volume method. The effects of field homogeneity and significance of parallel conductance in volume measurement were then determined. The results of this study show that DF provide a more accurate measure of intraventricular volume than SF, especially at larger volumes. However, both significantly underestimate true volume at larger volumes. In addition, the parallel conductance due to the chamber wall is significant at small volumes, but diminishes at larger volumes. Furthermore, the effect of parallel conductance beyond the chamber wall may be negligible. This study demonstrates the limitations in applying current conductance technology to patients with dilated hearts.

End-systolic pressure-dimension relationship of in situ mouse left ventricle.

The increasing popularity of genetically engineered mice in cardiovascular research has made it important to evaluate cardiac function in small animals. We have developed a system to enable simultaneous pressure-dimension analysis of the mouse left ventricle. The chest was opened under anesthesia, and a 1.4 F micromanometer catheter was inserted into the left ventricle through the apex. A pair of sonomicrometry crystals were attached to the anterior and posterior walls using tissue adhesive. Pressure and dimension were recorded simultaneously at baseline and after isoproterenol injection (1 micro g, intraperitoneally). The ascending aorta was occluded transiently to estimate the end-systolic pressure-dimension relationship (ESPDR), which was parameterized subsequently by the quadratic equation: Pes=C2 X (Des-D0)2+E0 X (Des-D0), where Pes is end-systolic pressure, Des is end-systolic dimension, D0 is the dimension axis intercept, E0 is the local slope at D0, and C2 is the curvilinearity coefficient. The maximum and minimum external dimensions at baseline were 5.82+/-0.50 (s.d.) mm and 5.49+/-0.46 mm with fractional shortening of 0.057+/-0.014 (n=12). The ESPDR was significantly curvilinear and increased convexity after isoproterenol injection (C2, -444+/-281 to -1113+/-780 mmHg/mm2, P<0. 05; E0, 536+/-175 to 889+/-276 mmHg/mm, P<0.001), while the dimension axis intercept remained relatively constant (D0, 5.39+/-0. 46 to 5.37+/-0.52 mm). In conclusion, the combination of miniature piezo-electric crystals and a micromanometer enables continuous measurement of pressure and dimension of in situ mouse left ventricle. This technology may be useful in evaluating the cardiac phenotype of genetically engineered mice.