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Embolization of atheroma from the ascending aorta is a principal cause of stroke after cardiac operations. We have previously shown that intraoperative ultrasonographic scanning of the aorta rapidly, safely, and accurately identifies atheromatous disease in the ascending aorta. Intraoperative ultrasonography of the ascending aorta was performed in 500 of a consecutive series of 540 patients 50 years of age or older (mean 68 years) who underwent a variety of cardiac operations. Eighty-nine percent required bypass grafting. Sixty-eight patients (13.6% of the total) with a mean age of 72 years (range 55 to 85 years) had significant atheromatous disease in the ascending aorta and were considered to be at increased risk for embolization. Palpation identified the atheromatous disease in only 26 (38%) of these patients and underestimated its severity. A total of 168 modifications in the standard techniques for cannulation and clamping of the aorta were implemented in the 68 patients (mean 2.5 per patient) and included alterations in the sites of aortic cannulation (50 patients), aortic clamping (54 patients), attachment of the vein grafts (35 patients), and cannulation for infusion of cardioplegic solution (29 patients). Ten patients with severe diffuse atheromatous disease underwent graft replacement of the ascending aorta with hypothermic circulatory arrest without aortic clamping. Fourteen patients with symptoms or with high-grade carotid artery occlusive disease were treated by concomitant carotid endarterectomy. Thirty-day mortality for the entire group was 3.4% (17 patients). Permanent neurologic deficits occurred in five (1.0%) of the patients in the entire group but in none of the 68 patients with significant atheromatous disease in whom modifications in technique were used. One patient in the latter group had a reversible ischemic neurologic deficit. Modification of standard cannulation and clamping techniques based on ultrasonography may reduce the frequency of stroke related to atheromatous embolization.

We report a case acute lower extremity ischemia caused by emboli in which the initial diagnostic evaluation, including standard aortoiliofemoral arteriography and routine transthoracic two-dimensional echocardiography, failed to reveal the offending source. Because of the strong clinical suspicion that the origin of the arterial occlusion was embolic, transesophageal echocardiography was performed. Transesophageal echocardiography demonstrated an aortic valvular lesion and cardiac surgery was performed on an emergency basis. The use of transesophageal echocardiography in evaluating the heart and thoracic aorta as a source of distal emboli is also discussed.

To provide an approach suitable for on-line analysis of ventricular function, a conventional two-dimensional ultrasound imaging system was modified to detect and track blood-tissue interfaces in real time based on their quantitative acoustic properties. This modification permitted on-line display of the left ventricular cavity area, fractional area change, volumes and ejection fraction on a beat by beat basis. Images were obtained from 54 patients and 12 normal subjects with broad ranges of ventricular dimensions and systolic function. On-line measurements of cavity areas were compared with off-line measurements of cavity areas (analysis of videotaped conventional images). Left ventricular cavity areas measured on-line from short-axis views correlated closely with off-line views as did areas from apical views. On-line fractional area change correlated well with ejection fraction calculated off-line. More than 70% of patients could be studied adequately with the approach developed. Thus, automatic boundary detection based on quantitative assessment of tissue acoustic properties permits on-line quantitation of ventricular cavity areas and indexes of function.

Pulmonary arteriovenous (A-V) malformation is frequently a manifestation of Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia). We identified 14 patients (9 men and 5 women) with A-V malformation by contrast echocardiography; 10 patients with atrial right-to-left shunt served as control subjects. Agitated saline solution (10 ml) was injected through a peripheral vein during echocardiographic imaging. The delay in the appearance of microcavitations in the left atrium was measured (in number of frames) after right atrial appearance. The degree of left ventricular opacification was graded 1 to 4+ (where 4+ = intense left ventricular endocardial outline, and 1+ = minimal opacification). Results indicated patients with A-V malformation had a significant delay (p less than 0.001) in left atrial appearance of microcavitations compared with those with atrial right-to-left shunt (66 +/- 27 vs 21 +/- 7 frames, mean +/- 1 standard deviation). In the group with A-V malformation, abnormal blood gases were present in only 6 of 14 patients and chest x-ray was positive in 7. Pulmonary angiography was performed in 11 of 14 patients with positive contrast echocardiography, and all 11 had A-V malformation identified. In patients with 3 to 4+ left ventricular opacification (n = 8), large (greater than 5 mm feeding vessel) or multiple malformations were present, whereas patients with small or isolated malformation had 1 to 2+ left ventricular opacification. Balloon occlusion of malformations was performed in all 11 of these patients; repeat contrast echocardiography revealed significant diminution of right-to-left shunt in 9, and 2 required repeat embolotherapy for an additional previously undetected A-V malformation.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrasonic tissue characterization provides quantitative assessment of myocardial function and viability. We have previously reported that normal myocardium is characterized by a diastolic-to-systolic cyclic variation of integrated backscatter (IB), whereas ischemic myocardium exhibits blunting of this pattern. To define the applicability of this measurement to characterize the left ventricular myocardium in the operating room, we studied 26 consecutive patients undergoing open heart surgery (12 coronary artery bypass graft, 13 valvular, 1 other) with 5 MHz transesophageal echocardiography. Images of the left ventricle were obtained in the short-axis plane (papillary muscle level) before cardiopulmonary bypass. M-mode acquisition of myocardial IB was attempted from the anterior and inferior segments in each patient. The cyclic variation of IB was measured in at least two consecutive cycles in addition to a qualitative assessment of wall motion. Quantitative measurement of IB was possible in 39/52 (75%) myocardial segments. Cyclic variation of IB averaged 5.7 +/- 1.4 dB (SD) in segments with normal wall motion (n = 25); no difference was noted in the cyclic variation of IB among anterior or inferior walls. Hypokinetic segments demonstrated significant reduction of the cyclic variation (3.8 +/- 1.8 dB; p less than 0.001). Difficulty with obtaining myocardial IB was related to near-field artifact or lateral displacement of the left ventricular wall during systole. Transesophageal echocardiography holds promise for the evaluation of myocardial function and its preservation during cardiac surgery.

Dislodgement of atheromatous plaque from the ascending aorta following manipulation is one of the principal causes of stroke following cardiac surgery. To define clinical correlates that predict the presence of severe atherosclerosis, we performed ultrasonographic evaluation of the ascending aorta at the time of cardiac surgery in 100 consecutive patients. The ascending aorta was divided into three equal segments for analysis, and the severity of atherosclerosis was determined as mild when intimal thickening (less than 3 mm) was localized to one segment, moderate when intimal thickening (greater than 3 mm) was present in one or two segments, and severe when intimal thickening (greater than 3 mm) was present throughout the entire circumference in all three segments. Thirty-eight percent of the studies were normal, mild atherosclerosis was present in 33%, moderate atherosclerosis in 19%, and severe atherosclerosis in 10% of the patients. Palpation of the ascending aorta to detect atherosclerosis significantly underestimated the presence (p less than 0.001) and severity (p less than 0.001) of atherosclerosis when compared with ultrasonography. Age, carotid artery disease, diabetes, gender, smoking, and hypertension were evaluated for their ability to discriminate between normal and severely atherosclerotic aortas. Stepwise logistic regression analysis showed age (p less than 0.02) and diabetes (p less than 0.04) to be significant independent predictors of the presence of severe atherosclerosis in the ascending aorta. Based on the ultrasonographic findings, the operative procedure was altered to reduce the risk of embolization in 17% of the patients. We conclude that high-resolution images of the ascending aorta for identification of atherosclerosis can be obtained by ultrasonography.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of isoflurane in patients with coronary artery disease remains controversial because of the possibility of "coronary steal". In this study, the effects of isoflurane and halothane on global and regional myocardial blood flow and metabolism were compared, and the relationship between steal-induced myocardial ischemia and the administered volatile anesthetic was investigated in 40 patients with steal-prone coronary anatomy undergoing elective coronary artery bypass operations. The patients were randomly assigned to receive either isoflurane or halothane (0.5 MAC inspired concentration) immediately after induction with fentanyl (50 micrograms/kg). Hemodynamic measurements and blood samples were obtained at preinduction, postintubation, preincision, poststernotomy, at 60 min after beginning isoflurane or halothane, and precannulation (a total of 238 study events). Throughout the study, heart rate was kept constant by atrial pacing at approximately postintubation values while arterial pressure was maintained within 10% of postintubation values with fluid administration or phenylephrine infusion. Overall, systemic hemodynamic changes observed during the study were similar in the two groups. Myocardial ischemic episodes were defined as a new electrocardiographic ST-segment shift of greater than or equal to 0.1 mV, new echocardiographic regional wall motion abnormalities (RWMA) and/or myocardial lactate production (MLP). A total of 18 new ischemic episodes were detected in 15 patients (7 episodes during isoflurane in 7 patients and 11 during halothane in 8 patients). Ten (56%) episodes were related to acute hemodynamic abnormalities, whereas 8 (44%) were random and unrelated to changes. Seven episodes were detected by echocardiography (38%), 6 by MLP (33%) and 1 by ECG (6%) only, whereas concomitant echocardiographic abnormalities and MLP were observed during 2 episodes (11%), echocardiographic and ECG during 1 (6%), and ECG and MLP during 1 other (6%). Ratios of regional to global coronary venous flow, coronary vascular resistance, myocardial oxygen content, and lactate extraction, along with hemodynamic data obtained during these episodes, do not support coronary steal for the development of myocardial ischemia. We conclude that in patients with steal-prone coronary anatomy anesthetized with fentanyl, neither isoflurane nor halothane administered at concentrations used in the current study is likely to cause myocardial ischemia by the coronary steal mechanism.

Left ventricular (LV) outflow obstruction may result from retaining the anterior mitral leaflet when a mitral prosthesis is inserted in the mitral anulus. We retrospectively reviewed the echocardiograms (two-dimensional Doppler and Doppler color flow imaging, or transesophageal with color flow imaging) obtained in seven patients with preoperative mitral regurgitation who had a prosthesis implanted with the native mitral leaflets left intact. Systolic anterior motion of the native anterior mitral leaflet, as seen in dynamic LV outflow tract obstruction, was observed in six of seven patients. LV fractional shortening preoperatively was less than or equal to 0.25 in all (mean 0.20 +/- 0.04) and did not significantly (p = ns) increase postoperatively (mean 0.27 +/- 0.12). Color flow imaging revealed disturbed systolic flow in the LV outflow tract in five patients, and all had systolic anterior motion of the native anterior mitral leaflet. Continuous wave Doppler detected significant systolic LV outflow tract jets in five patients averaging 4.1 +/- 0.9 m/sec. Mitral prosthetic function was normal (pressure half-time of 81 +/- 25 msec and mean gradient of 7 +/- 3 mm Hg +/- SD) in five patients. Clinical follow-up revealed that all had died, six of them within 2 months of their operation. Thus systolic anterior motion of the native anterior mitral leaflet occurs commonly after prosthetic mitral valve insertion with the native leaflets left intact. Continuous wave Doppler often demonstrates increased systolic LV outflow tract velocities consistent with dynamic LV outflow obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Postcardiotomy right ventricular (RV) failure after institution of mechanical left ventricular (LV) support is poorly understood. Using a canine model supported by cardiopulmonary bypass (CPB), the animals underwent 30 min of aortic clamping or no ischemia and were weaned to an LV assist device (LVAD). Echocardiographic measurements of LV and RV cavity size off support allowed calculation of percentage change in cavity area (fractional shortening). There were no differences at baseline. After 2 hrs on LVAD, there were significant differences between ischemic and control groups in both LV (38 +/- 12 vs. 61 +/- 6) and RV (15 +/- 3 vs. 55 +/- 12). The ischemic RV also had significantly decreased function compared with the LV (38 +/- 12 vs. 15 +/- 3). The control group demonstrated no differences in ventricular function. The authors concluded that global ischemia diminishes LV and RV function, and this effect is accentuated in the RV after LVAD support. In controls, RV function is not affected by LVAD support, but after ischemia, LVAD support alone often will be inadequate.

Although worksite health promotion programs have proliferated, little is known about the population they reach. This study of employees of a large utility company compared whether the same characteristics which predict recruitment also predict extended participation. The study also prospectively assessed how risk factors are related to employees' on-going extended participation. The findings demonstrate that sociodemographic predictors of recruitment are almost mirror images of the predictors of extended participation. Over time employees who are at higher risk for cardiovascular disease participated in on-going sessions less frequently. Data suggest that referral to targeted sessions does not result in higher rates of attendance by employees with a particular risk factor, although there is no evidence of selective avoidance. Organizational influences on participation evident from the beginning are sustained through four sessions. Programs targeting higher risk employees nested within worksite-wide programs may be useful to increase the extended participation of individuals at elevated risk for heart disease.

To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)

Contrast techniques have been used to improve detection of peak velocities by Doppler spectral analysis. To define the effect of contrast enhancement on the tricuspid regurgitation (TR) jet area and length, 29 patients were studied (25 transthoracic, 4 transesophageal) with 2-dimensional color flow imaging. Three- to 5-ml of agitated saline was injected and images were obtained from 4-chamber views at 12- or 16-cm depth setting. Color gain was optimized to display TR jet at baseline and then reduced to minimal settings before injection. Measurements of TR jet area and length were made in 3 to 5 consecutive cycles. A ratio of TR jet area to 2-dimensional area was derived. TR jet area at baseline was 4.7 +/- 3.6 cm2 and increased significantly (p less than 0.0001) in 26 patients to 8.1 +/- 6.3 cm2 after contrast enhancement. Jet length at baseline was 3.4 +/- 1.7 cm and increased significantly (p less than 0.0001) in 20 patients to 4.1 +/- 1.8 cm after contrast enhancement. The ratio of TR jet area to right atrial area also increased significantly (p less than 0.0001) to greater than 0.20 in 18 of 28 patients after enhancement. Increases in jet area and length were not associated with changes in TR jet or diastolic inflow velocities measured by continuous wave Doppler at baseline and after contrast. Thus, contrast enhancement increases the amplitude of Doppler signals responsible for transvalvular and regurgitant flow. By reducing the effect of attenuation and improving signal-to-noise ratio, it improves delineation of the TR jet using color flow imaging.

To define the frequency, natural history and clinical correlates of the murmur of mitral regurgitation (MR) detected after myocardial infarction, clinical data from 849 patients with documented acute myocardial infarction were analyzed. A murmur suggestive of MR was present on admission in 76 patients (9%). Patients with MR on admission were older and more apt to be female and nonwhite. They also had a significantly greater frequency of prior infarction and signs and symptoms of congestive heart failure. There was no difference in the location (anterior or inferior) of infarction. Patients with MR on admission had a 36% mortality compared to 16% for those who developed MR later in the hospitalization and 15% for those without MR by auscultation (p less than 0.001). Correction for differences in baseline variables indicated that the presence of MR on admission did not contribute independently to mortality. Thus, the murmur of MR derives its prognostic significance from integration of multiple clinical, radiographic and electrocardiographic characteristics.

We have previously shown that cardiac cycle-dependent variation of integrated backscatter occurs in normal myocardium. To determine whether myocardial ischemia and reperfusion can be distinguished by real-time integrated backscatter imaging we performed 10 min balloon occlusion of the Left Anterior Descending (LAD) coronary artery followed by reperfusion in 10 closed-chest anesthetized dogs. Images were obtained at baseline, during occlusion, and up to 120 min after reperfusion. We measured the magnitude and delay of cyclic variation of integrated backscatter in segments with and without asynergy. Radiolabeled microspheres were used to verify both ischemia and reperfusion. Ischemic segments exhibited decreased magnitude and increased normalized delay of cyclic variation of integrated backscatter (from 3.3 +/- 0.3 dB to 1.4 +/- 0.2 dB, mean +/- SE; and from 0.95 +/- 0.03 to 1.67 +/- 0.15, respectively, all p less than or equal to 0.001). Reperfusion promptly restored the magnitude of cyclic variation toward normal. However, the delay of the cyclic variation was restored only partially. Wall motion analysis of the ischemic sites revealed persistent abnormalities throughout the reperfusion interval despite return to normal of the magnitude and delay of cyclic variation. Thus, real-time integrated backscatter imaging permits detection and differentiation of changes in myocardial acoustic properties indicative of ischemia and of subsequent reperfusion.

To define the incidence of mitral regurgitation (MR) and elucidate its potential contribution to the development of severe congestive heart failure after acute myocardial infarction (AMI), Doppler echocardiograms were obtained within 48 hours of onset of AMI in 59 patients. The presence of MR was determined from the apical 4-chamber and parasternal long-axis views with pulsed Doppler. MR was detected in 23 of the 59 patients (39%) and was similarly frequent in patients with anterior (11 of 24 or 46%) and inferior AMI (12 of 34 or 35%). Patients with MR were older (71 +/- 3 vs 62 +/- 2 years, p less than 0.005), had a higher incidence of prior AMI (8 of 23 vs 4 of 36, p less than 0.05) and larger end-diastolic volume indexes by radionuclide ventriculography (112 +/- 9 vs 72 +/- 4, p less than 0.005). A systolic murmur was heard in only 10 of 23 patients with MR detected by Doppler. Mortality determined 8 to 14 months after the index AMI was 48% (11 of 23) in patients with MR but only 11% (4 of 30) in those without it (p less than 0.01). Thus, this study determined that clinically silent MR frequently complicates AMI and its presence is associated with and is a potential determinant of severe congestive heart failure and mortality.

The diagnosis of combined ventricular septal rupture and mitral regurgitation complicating acute myocardial infarction is difficult and in previously reported cases has required right and left heart catheterization. This study utilized simultaneous Doppler and two-dimensional echocardiography to diagnose these combined lesions in two cases. Doppler echocardiography should have its greatest impact in the early noninvasive diagnosis of these complications.

An algorithm for quantitative description of cardiac cycle dependent variation of integrated backscatter (cyclic variation) has been developed and is shown to be suitable for analysis of nonsinusoidal data typical of ultrasonic tissue characterization measurements from myocardium in vivo. The algorithm produces estimates of the magnitude of variation and of the time delay relative to the electrocardiographically recorded QRS-complex. To validate the algorithm, 246 integrated backscatter measurements were analyzed both manually and by the automated method. The magnitude and time delay estimates from the two methods correlated closely. With a separate set of data, the algorithm produced reasonable descriptions of the cyclic variation for 89 of 101 integrated backscatter measurements. Only modest computational power is required for effective implementation of this algorithm, facilitating inclusion of online automated analysis capabilities in quantitative ultrasonic tissue characterization systems.

Progress in tissue characterization of myocardium with ultrasound suggests that quantitative recognition of ischemic or scarred tissue will be achieved. Despite the increasing recognition and importance of cardiomyopathy, its diagnosis generally requires invasive procedures such as cardiac catheterization and biopsy. To investigate methods that permit the characterization of longitudinal cardiomyopathic changes that might ultimately be extended for noninvasive studies in patients, quantitative ultrasonic methods were utilized for in vitro tissue characterization of hearts from Syrian hamsters of selected age of either 2 to 3 or 5 to 7 months. Normal hamsters were used as controls. Myocardial sites (n = 600) from the young Syrian hamsters exhibited values (+/- standard error) of integrated ultrasonic backscatter averaging -53.87 +/- 0.26 dB, which were significantly different from values (n = 500) in age-matched control hamsters (-58.07 +/- 0.08 dB; p less than 0.001). Cardiomyopathic hearts from older animals exhibited backscatter values (n = 500 sites) averaging -50.87 +/- 0.22 dB, again significantly different from values (n = 300 sites) in age-matched control hamsters (-55.91 +/- 0.11 dB; p less than 0.001). In addition, ultrasonic attenuation was significantly different for hearts from the control and cardiomyopathic hamsters of both age ranges. The results correlated with sequential calcification and fibrosis characteristics assessed histopathologically. This study indicates that quantitative characterization of myocardium with ultrasound may permit longitudinal assessment of cardiomyopathic changes in diverse disease entities and their response to therapy.

A method for estimating infarct size from 12-lead ECGs has been developed but not extensively validated. To assess its accuracy, ECG scores from 62 patients admitted to the coronary care unit at Barnes Hospital were compared to infarct size calculated from plasma MB creatine kinase (MB-CK) activity. A second cohort of 29 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS) was evaluated as a test set and to provide pathologic correlates. Patients with conduction system disease, ventricular hypertrophy, or multiple infarctions were excluded, as were those in the Barnes group who had undergone thrombolytic therapy. ECGs obtained early (days 3 to 7 in the Barnes group and day 3 in the MILIS group) or late (days 8 to 14 in the Barnes group) were scored manually and by computer. QRS scores from early ECGs of patients with anterior infarctions correlated closely with MB-CK estimates of infarct size (r = 0.71 [Barnes] and 0.85 [MILIS] and with anatomic data (r = 0.78). Enzymatic and pathologic infarct size also correlated well (r = 0.85). Correcting for body surface area by means of total CK-derived infarct size or use of QRS scores from late ECGs did not alter the correlation coefficients. Among patients with inferior infarctions QRS scores corresponded poorly with MB-CK infarct size (r = 0.28 [Barnes] and r = -0.42 [MILIS]) and pathologic infarct size (r = -0.20), despite a significant relationship between pathologic and MB-CK estimates (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical manipulation of the atherosclerotic ascending aorta in elderly patients is often accompanied by serious complications. To reduce the risk of disrupting highly degenerated but nonpalpable plaques, we used quantitative ultrasonic techniques to intraoperatively image the ascending aorta in 33 patients (mean age, 71 years) as a guide to selection of cross-clamping or cannulation sites. Two-dimensional, integrated backscatter images (integration time, 1.6 mu sec) were obtained with a 5-MHz transducer wrapped in a sterile sheath and placed directly on the aorta. Significant atherosclerotic disease was detected in 18 patients. Calcified lesions were found in 13 patients, and fibrofatty lesions were found in five. In four patients undergoing repair of degenerative aneurysms, the extent and distribution of ultrasonically delineated regions of calcification and fibrosis were confirmed histologically. In eight (24%) patients, the composition, severity, and location of plaques delineated ultrasonically led to selection of alternate cannulation sites without resultant atheroembolism. Thus, ultrasonic tissue characterization sensitively delineates the extent of aortic atherosclerosis, and its use may decrease the risk of atheroembolism.

Embolization of atherosclerotic material from the ascending aorta resulting from placement of cannulas or vascular clamps is a major cause of stroke during cardiac surgical procedures. In an effort to identify atherosclerotic disease of the ascending aorta which might predispose to embolization, intraoperative B-mode ultrasonography was performed in 50 patients. The aorta was imaged from the aortic annulus to the origin of the innominate artery in transverse and longitudinal views. The results were compared with visual and tactile examination of the aorta for the presence of atherosclerosis. Ultrasonic imaging demonstrated atherosclerotic disease in 29 patients (58%). Visual examination and palpation identified atherosclerosis in 12 patients (24%). The amount and location of plaque was sufficient to require a change in the site of arterial cannulation or the proximal vein graft anastomoses or the technique of cardiopulmonary perfusion in 12 of the 50 patients (24%). All 12 patients were 65 years of age or older. Palpation underestimates the presence of atherosclerotic disease in the ascending aorta. Intraoperative ultrasonography accurately identifies patients with atherosclerotic disease of the ascending aorta. This allows the surgeon to modify cannulation, perfusion, and operative techniques to reduce the risk of perioperative stroke due to the embolization of atherosclerotic debris from the ascending aorta.

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.

To determine whether quantitative ultrasound tissue characterization differentiates normal myocardial regions from segments of remote infarction, 32 consecutive patients with a diagnosis of previous myocardial infarction were evaluated. Images were obtained in real time with a modified two-dimensional ultrasound system capable of providing continuous signals in proportion to the logarithm of integrated backscatter along each A line. In 15 patients, adequate parasternal long-axis images that delineated both normal and infarct segments were obtained with standard time-gain compensation. Image data were analyzed to yield both magnitude and delay (electrocardiographic R wave to nadir normalized for the QT interval) of the cyclic variation of backscatter. Cyclic variation was present in 55 of 56 normal myocardial sites, averaging (mean +/- SEM) 3.2 +/- 0.2 dB in magnitude and exhibiting a mean normalized delay of 0.87 +/- 0.03. The magnitude of cyclic variation in infarct segments was significantly reduced to 1.1 +/- 0.2 dB (42 sites), and the delay was markedly increased to 1.47 +/- 0.12 (21 sites) (p less than 0.0001 for both). In 20 of 42 infarct sites, no cyclic variation was detectable. Thus, ultrasound tissue characterization quantitatively differentiated infarct segments from normal myocardium in patients with remote myocardial infarction.