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Background: Left ventricular hypertrophy is a heterogeneous disorder with distinct morphologies. Changes in wall thickness, left ventricular chamber diameter, and mass alter systolic wall stress of the left ventricle and may influence ischemic threshold. Thus, the goal of this study was to investigate the effect of the different patterns of left ventricular hypertrophy on the accuracy of dobutamine-atropine stress echocardiography., Methods and Results: Three-hundred eighty-six patients underwent multistage dobutamine-atropine stress echocardiography and diagnostic angiography. Echocardiograms were measured for mean and relative wall thicknesses, chamber size, left ventricular mass, and end-systolic wall stress. The patterns of ventricular hypertrophy were concentric hypertrophy (increased wall thickness and mass), eccentric hypertrophy (normal wall thickness and increased mass), and concentric remodeling (increased wall thickness and normal mass). The overall sensitivity, specificity, and accuracy of dobutamine-atropine stress echocardiography for the detection of coronary artery disease were 85%, 87%, and 86%, respectively. Increased left ventricular mass index alone did not affect accuracy. Sensitivity was markedly reduced (36%) only in those with concentric remodeling. The univariate predictors of false-negative studies were single-vessel left circumflex disease, increased wall thickness, small chamber size, hyperdynamic ejection fraction, and left ventricular concentric remodeling. Multivariate predictors were concentric remodeling (P<0.0001; odds ratio, 13.5), left ventricular ejection fraction >2 SD above normal (P<0.0001), and single-vessel left circumflex disease (P<0.0007; odds ratio, 7.6). Sensitivity was excellent in patients with small ventricles and normal wall thickness and in those with normal or large chambers regardless of wall thickness., Conclusions: Dobutamine-atropine stress echocardiography is an accurate test in most patients with left ventricular hypertrophy, but it is insensitive in the small subset with concentric remodeling.

Background: The safety of dobutamine-atropine echocardiography early after acute myocardial infarction is unknown. Its accuracy for the early detection of infarct artery stenosis and multivessel coronary artery disease is also unclear. The objective of the present study was to document its safety and accuracy during the first week after acute myocardial infarction., Methods and Results: Multistage dobutamine-atropine stress echocardiography was performed in 232 patients (age, 58 +/- 13 years; 58 women) at 5 +/- 2 days after acute myocardial infarction. The peak heart rate was 116 +/- 20 bpm. There were no episodes of sustained ventricular tachycardia, myocardial infarction, or death. Atropine with dobutamine was tolerated well. Coronary angiography was performed in 206 patients (89%). There were 171 patients (83%) with infarct artery stenosis of > or = 50% and 114 patients (55%) with multivessel disease. Ischemic or biphasic responses in the infarction zone were 82% (140 of 171) sensitive and 80% (28 of 35) specific for residual stenosis. Sensitivity was similar for occluded arteries (77%, 36 of 47) and patent but stenotic arteries (84%, 104 of 124). Wall motion abnormalities outside the infarction zone were specific (97%, 89 of 92) and moderately sensitive (68%, 77 of 114) for multivessel disease. The only determinant of sensitivity for residual infarct artery stenosis was improved wall motion at low dose (P < .01). The determinants of sensitivity for multivessel disease were peak heart rate and infarct size (P < .01)., Conclusions: Dobutamine-atropine stress echocardiography was safely used to detect residual infarct artery stenosis and multivessel disease during the first week after acute myocardial infarction. The test may be very effective for evaluating patients with acute myocardial infarction because sensitivity for residual stenosis and multivessel disease was maximal in the high-risk subsets of patients with viable, jeopardized myocardium and large infarct size.

Background: Because dobutamine stress echocardiography (DSE) provides assessment of left ventricular function and ischemia at a distance, the major determinants of adverse outcome after acute myocardial infarction (AMI), we undertook this study to determine the role of DSE in risk stratification after AMI., Methods and Results: A graded DSE in 5-minute stages was performed in 214 patients (age, 57 +/- 13 years [mean +/- SD]) at 2 to 7 days after AMI. Coronary angiography was performed in 193 patients. Follow-up data regarding major cardiac events were obtained through telephone interviews and chart reviews. All patients were followed for > or = 500 days or until a hard cardiac event occurred. The mean follow-up interval was 494 +/- 182 days after AMI. Peak heart rate and systolic blood pressure were 115 +/- 21 bpm and 135 +/- 29 mm Hg, respectively. An adverse outcome occurred in 80 of 214 patients; cardiac death occurred in 15, nonfatal AMI occurred in 15, sustained or symptomatic ventricular arrhythmia occurred in 5, congestive heart failure occurred in 14, and unstable angina occurred in 31. Significant predictors of adverse outcome by univariate analysis were prior myocardial infarction (P = .005), anterior infarction (P = .006), multivessel coronary artery disease (P < .0001), global resting left ventricular wall motion score index (P < .0001), infarction zone nonviability based on akinesis unresponsive to low-dose dobutamine (P < .0001), and ischemia/infarction at a distance (P < .0001). Furthermore, the extent of infarct zone and nonviability correlated with the severity of the cardiac event. Multivariate analysis of clinical, angiographic, and DSE variables revealed that the only independent predictors of adverse outcome were ischemia/infarction at a distance (P < .0001) and infarction zone nonviability (P < .0001). Multivessel disease identified through DSE was more predictive of adverse outcome than was angiographically determined multivessel disease., Conclusions: DSE can be used to predict adverse outcomes after AMI.

Background: Ultrasonic backscatter demonstrates a cardiac cycle-dependent modulation. The exact mechanism of the modulation is under debate. The objective of the present study was to test the hypothesis that a change in size and configuration of myofilaments from systole to diastole alters acoustic propagation properties and backscatter., Methods and Results: In vivo measurements were made of integrated backscatter at 5 MHz (IBR5), followed by in vitro measurements of ultrasonic attenuation, speed, and heterogeneity index using a scanning laser acoustic microscope at 100 MHz. Studies were performed in canine hearts (16) arrested in systole (8) with calcium chloride or arrested in diastole (8) with potassium chloride. Sarcomere length was measured with a calibrated eyepiece on a Ziess microscope. Wall thickness was measured with calipers. The attenuation coefficient of 220 +/- 34 dB/cm during systole was significantly higher than the coefficient of 189 +/- 24 dB/cm during diastole (P < .01); the IBR5 of -44.7 +/- 1.2 dB during systole was significantly greater than the IBR5 of -47.0 +/- 1.0 dB during diastole (P < .01); the ultrasonic speed of 1591 +/- 11 m/s during systole was higher than the speed of 1575 +/- 4.2 m/s during diastole (P < .01); and the heterogeneity index of 7.4 +/- 1.8 m/s during systole was significantly lower than the index of 9.0 +/- 2.0 m/s during diastole (P < .02). The sarcomere length of 1.804 +/- 0.142 microns during diastole was significantly higher than the length of 1.075 +/- 0.177 micron during systole (P < .01). Wall thickness was significantly greater during systole than during diastole (20 +/- 3 versus 9 +/- 3 mm, P < .01)., Conclusions: Ultrasonic backscatter and propagation properties are directly related to sarcomere length and myocardial thickness and may be responsible for cardiac cycle-dependent variation in backscatter.

Background: Identification of viable but stunned myocardium remains a major problem. Since stunned myocardium results in impairment of myocardial function without any structural damage and infarcted myocardium causes major structural disruption, we postulated that acoustic properties could distinguish between the two insults., Methods and Results: Anesthetized open-chest dogs underwent a total occlusion of the left anterior descending coronary artery for 15 minutes (stunned, n = 7) and 90 minutes (infarcted, n = 8), followed by reperfusion for 3 hours. Circumflex coronary artery perfusion territory (n = 15) served as normal control tissue. Regions of myocardium were quantitatively evaluated with a scanning laser acoustic microscope operating at 100 MHz and a research ultrasound system operating at 4 to 7 MHz. Four ultrasonic parameters were determined: attenuation coefficient (an index of loss per unit distance), speed of propagation, a spatial variation of propagation speed called the heterogeneity index (HI), and ultrasonic backscatter at 5 MHz (IBR5). Myocardial water, lipid, and protein contents of normal, stunned, and infarcted myocardium were also determined. The attenuation coefficient of normal myocardium (179 +/- 20 dB/cm) was significantly greater than that of stunned (136 +/- 7 dB/cm, P < .001) and infarcted (130 +/- 8 dB/cm, P < .001) myocardium. The propagation speed of normal myocardium (1597 +/- 6 m/s) was similar to that of stunned (1600 +/- 6 m/s) and significantly higher than that of infarcted (1575 +/- 7 m/s, P < .001) myocardium. The HI for specimen thicknesses of 75 to 100 microns showed an increase of 33% between normal (5.0 +/- 0.8 m/s) and stunned (7.5 +/- 2.3 m/s, P < .05) myocardium. However, for the infarcted myocardium (5.8 +/- 2.0 m/s), the HI was essentially the same as that of the normal myocardium (5.0 +/- 0.8 m/s). The IBR5 of normal (-47.1 +/- 1.0 dB) was not significantly different from that of stunned myocardium (-46.8 +/- 0.9 dB). The IBR5 of infarcted myocardium (-42.4 +/- 1.0 dB) was significantly greater than that of normal myocardium. Myocardial water and protein contents were similar in the normal and stunned myocardium. Water content in the infarcted myocardium (80.8 +/- 2%) was significantly greater (P < .05) than in the normal (72.7 +/- 1.3%), and protein content of 18.5 +/- 0.7% was significantly lower (P < .05) than the normal (21.4 +/- 0.8%). Lipid content was increased in the stunned (8.5 +/- 0.5%) and virtually absent in the infarcted myocardium (0.8 +/- 0.3%) compared with normal (5.5 +/- 0.6%)., Conclusions: We conclude that acoustic propagation properties can identify stunned and infarcted myocardium and may be related to biochemical/morphological differences.

Serial determination of left ventricular mass, right ventricular and left atrial size, fractional shortening and left ventricular systolic time intervals were made from M-mode echocardiograms in 13 long-term survivors with cardiac allografts These measurements were correlated with presence or absence of acute rejection as determined by myocardial biopsy. Left ventricular mass increased significantly, from a baseline of 129.8 +/- 11.8 (mean +/- SEM) to 310.5 +/- 13.0 g during 12 episodes of rejection. In contrast during eight episodes without rejection, the left ventricular mass did not increase significantly (baseline 175.2 +/- 11.8 to 211.9 +/- 25.6 g). There was no relationship between changes in right ventricular and left atrial size, fractional shortening or systolic time intervals and presence or absence of rejection of myocardial biopsy. An increase in left ventricular mass by M-mode echocardiography offers a reliable noninvasive method for detection of acute rejection of a cardiac allograft.

The prevalence and significance of arrhythmias after cardiac transplantation were evaluated in the absence of acute rejection in 13 long-term survivors (greater than 3 months). ECGs were obtained daily for the first 70 days 8- and 24-hour ambulatory electrocardiographic monitoring was performed 3 months after the transplantation and every 6 months thereafter. Junctional rhythm occurred during the early transplant period (less than 70 days) in nine of 13 patients. Complex premature ventricular depolarizations (Lown grade III or higher) were present in the late transplant period (greater than 70 days) in all five patients in whom severe coronary artery disease was found in the donor heart at postmortem, compared with two of the eight remaining patients (six survivors and two patients who died but did not have coronary artery disease at postmortem) (p less than 0.05). The high prevalence of junctional rhythm in the early transplant period appeared to be due to sympathetic denervation and reversible surgical damage to and ischemia of the sinus node region of the donor heart. Routine ambulatory electrocardiographic monitoring detected complex premature ventricular depolarizations, which were a sensitive marker for the subsequent mortality related to accelerated atherosclerosis of chronic rejection in the donor heart.