Prediction of cardiac mortality after myocardial infarction: the role of maximal treadmill stress echocardiography.

Patients frequently undergo low-level exercise treadmill testing after acute myocardial infarction (MI) and, in the absence of inducible ischemia, a maximal test several weeks later. This study examines 203 patients who had 2-dimensional echocardiography before and after a maximal Bruce protocol exercise treadmill test performed 4 to 6 weeks after MI. The subjects were followed for a mean of 43 months (range 1 to 77 months). Predictors of cardiac mortality by multivariate or univariate analysis included an ejection fraction < or =40%, diabetes, age > or=70 years, and ischemia by exercise echocardiography but not by electrocardiography. Therefore, standard electrocardiographic monitoring during exercise treadmill testing 6 weeks after MI fails to predict cardiac mortality. The addition of pre-exercise and post-exercise treadmill stress echocardiography to readily available clinical parameters identifies those patients at greatest risk for cardiac death (resting ejection fraction < or=40%) and detects residual exercise-induced ischemia that may be of additional prognostic value.

Prognostic value of exercise echocardiography in women in the community setting.

Treadmill stress echocardiography was performed in 1,136 women with known or suspected coronary artery disease whose clinical course was then evaluated a mean of 33 months later (range 12 to 60). The strongest predictor of an adverse outcome was the presence of a resting or an exercise-induced wall motion abnormality.

Exercise echocardiography: detection of coronary artery disease in patients with normal left ventricular wall motion at rest.

Most studies investigating the ability of exercise two-dimensional echocardiography to identify patients with coronary artery disease have included patients with left ventricular wall motion abnormalities at rest. This has the effect of increasing sensitivity because patients with only abnormalities at rest are detected. To determine the diagnostic utility of exercise echocardiography in patients with normal wall motion at rest, 64 patients were studied with exercise echocardiography in conjunction with routine treadmill exercise testing before coronary cineangiography. All 24 patients who had no angiographic evidence of coronary artery disease had a negative exercise echocardiogram (100% specificity). Nine of 40 patients with coronary artery disease (defined as greater than or equal to 50% narrowing of at least one major vessel) also had a negative exercise echocardiogram (78% sensitivity). Of the nine patients with a false negative exercise echocardiographic study, six had single vessel disease. Among 25 patients with single vessel disease, exercise echocardiography was significantly more sensitive (p = 0.01) than treadmill exercise testing alone (76 versus 36%, respectively). Among 15 patients with multivessel disease, the two tests demonstrated similar sensitivity (80%). In conclusion, exercise echocardiography is highly specific and moderately sensitive for the detection of coronary artery disease in patients with normal wall motion at rest. Although exercise echocardiography is significantly more sensitive than treadmill exercise electrocardiographic testing alone in patients with single vessel disease, the two tests are similar in their ability to detect coronary artery disease in patients with multivessel disease and normal wall motion at rest.

Failure of fluosol DA to enhance the ultrasonic image of infarcted myocardium.

The perfluorocarbon Fluosol DA has been reported to increase the subjective echogenicity of infarcted myocardium. To investigate this phenomenon, two-dimensional echocardiograms were recorded in 20 closed-chest dogs before and 24,48,72, and 96 h following permanent coronary artery occlusion. Low-dose Fluosol, 10 ml/kg (LDF) (four dogs), high-dose Fluosol, 25 ml/kg (HDF) (eight dogs), or lactated Ringers 25 ml/kg (LR) (eight dogs) was administered 48 h after occlusion. Left ventricular sections corresponding to the short-axis echocardiographic examination plane were stained with nitroblue tetrazolium 48 h after Fluosol administration. Short-axis echocardiographic studies were evaluated by two blinded observers who found no consistent increase in the echogenicity of the infarcted area in any group. Videodensitometry of the infarcted area, normalized to the average value of two remote areas, confirmed mean post-Fluosol increases of 66% in LR dogs, 65% in LDF dogs, and 107% in HDF animals (p less than 0.001 for all dogs; all intergroup comparisons NS). The increase in videodensity observed in all groups may have occurred as a consequence of volume administration, although changes in infarct intensity occurring over time cannot be excluded.