超声组织定征在心血管疾病诊断中的应用

超声组织定征(Ultrasonic Tissue Characterization,UTC)技术是通过检测组织的声学参数来定量描述正常和病理组织的物理(声学)特性。研究表明,背向散射积分作为组织定征的参数,可以识别缺血心肌、顿抑心肌、梗死心肌、左心室心肌肥厚及心脏移植排斥反应,评价和分析系统性疾病如糖尿病等引起的弥漫性心肌受累的状态、心腔内血栓和动脉斑块的成份等。因而UTC技术具有很大的临床价值和发展潜力,将成为常规超声心动图诊断的辅助手段。本文就超声组织定征技术在心血管疾病诊断中的应用及进展作一综述。     

Estimation of myocardial infarct size with ultrasonic tissue characterization

BACKGROUND. Ultrasonic tissue characterization (UTC) can distinguish normal from infarcted myocardium. Infarcted myocardium shows an increase in integrated backscatter and loss of cardiac cycle-dependent variation in backscatter. The cyclic variation of backscatter is closely related to regional myocardial contractile function; the latter is a marker of myocardial ischemia. The present study was designed to test the hypothesis that intramural cyclic variation of backscatter can map and estimate infarct size. METHODS AND RESULTS. Transmural myocardial infarction was produced in 12 anesthetized, open-chest dogs by total occlusion of the left anterior descending coronary artery for 4 hours. A real-time ultrasonic tissue characterization instrument, which graphically displays integrated backscatter Rayleigh 5, cardiac cycle-dependent variation, and patterns of cyclic variation in backscatter, was used to map infarct size and area at risk of infarction. Staining with 2,3,4-triphenyltetrazolium chloride (TTC) and Patent Blue Dye was used to estimate infarct size and the area at risk, respectively. The ratio of infarct size to area at risk of infarction determined with UTC correlated well with that determined with TCC (r = 0.862, y = 23.7 +/- 0.792x). Correlation coefficients for infarct size and area at risk were also good (r = 0.736, y = 12.3 +/- 737x for infarct size and r = 0.714, y = 5.80 +/- 1.012x for area at risk). However, UTC underestimated both infarct size and area at risk. CONCLUSIONS. Ultrasonic tissue characterization may provide a reliable, noninvasive method to estimate myocardial infarct size.     

Structural remodeling of human myocardial tissue after infarction. Quantification with ultrasonic backscatter.

BACKGROUND. Remodeling of myocardial tissue after infarction may culminate in the development of either a well-healed scar or a thin, expanded heart wall segment that predisposes to ventricular aneurysm formation, congestive heart failure, or ventricular tachycardia. The three-dimensional architecture of mature human infarct tissue and the mechanisms that determine it have not been elucidated. We have previously shown that quantitative ultrasonic backscatter can be used to define the transmural organization of human myofibers in the normal ventricular wall by measuring the dependence of backscatter on the angle of insonification, or ultrasonic anisotropy. We propose that measurement of ultrasonic anisotropy of backscatter may permit quantitative characterization of the transmural architecture of tissue from areas of myocardial infarction and facilitate identification of fundamental mechanisms of remodeling of the ventricular wall. METHODS AND RESULTS. We measured integrated backscatter in 33 transmural sections from 12 cylindrical biopsy specimens (1.4-cm diameter) sampled from central regions of mature infarction in six explanted fixed human hearts. Tissue samples were insonified in two-degree steps around their entire circumference at successive transmural levels with a 5-MHz broad-band piezoelectric transducer. Backscatter radio frequency data were gated from the center of each specimen, and spectral analysis was performed on the gated radio frequency for the computation of integrated backscatter. Histological morphometric analysis was performed on each specimen for determination of the predominant fiber orientation and the percentage of tissue infarcted at consecutive transmural levels. The average percentage of tissue infarcted for all transmural levels was 49 +/- 3% (range, 13-80%). Histological attributes varied from patchy fibrosis to extensive confluent zones of scar tissue. The angle-averaged integrated backscatter for all transmural levels in infarct tissue was approximately 5 dB greater than that previously measured in normal tissue in our laboratory (-48.3 +/- 0.5 versus -53.4 +/- 0.4 dB, infarct versus normal). Marked anisotropy of backscatter was observed in tissue from areas of infarction and was characterized by a sinusoid-like dependence on the angle of insonification at each transmural level. Insonification perpendicular to infarct fibers yielded values for integrated backscatter 14.8 +/- 0.5 dB greater than those for insonification parallel to these fibers. Juxtaposition of the sinusoid-like anisotropy functions from all consecutive transmural levels demonstrated a progressive shift in the orientation of scar tissue elements from epicardial to endocardial levels of 14.6 +/- 1.5 degrees/mm of tissue. The transmural shift in fiber orientation per millimeter of tissue from the area of infarction exceeded that previously measured for normal tissue (9.2 +/- 0.7 degrees/mm) by 59%. This marked augmentation in angular shift per millimeter of tissue results from a generalized structural rearrangement (or reorientation) of fibers across the entire ventricular wall in the infarct zone that we hypothesize is determined in part by dynamic mechanical forces, imposed by the surrounding functional normal tissue, that tether the "infarcted" tissue. CONCLUSIONS. Myocardial tissue from areas of myocardial infarction manifests substantial anisotropy of ultrasonic scattering that may be useful for quantitative characterization of the alignment and overall three-dimensional anatomic organization of mature infarct scars.     

Detection of ischemic myocardium in vivo through the chest wall by quantitative ultrasonic tissue characterization

Quantitative analysis of ultrasound offers a potentially valuable method for noninvasive differentiation of specific types of cardiac disease and for assessment of their severity. Clinical application necessitates quantitative measurement of the ultrasonic properties of myocardium through the chest wall. This study was designed to determine whether such measurements could be made noninvasively with the aid of conventional M mode echocardiographic guidance and to characterize the quantitative effects of intervening tissue (chest wall) on the ultrasonic signals backscattered by ischemic and normal myocardium. Frequency-dependent ultrasonic backscatter (2 to 7 MHz) from normal myocardium was measured in dogs in vivo through the closed chest with the use of M mode guidance and with the chest open, directly from the myocardium. Closed-chest and open-chest measurements were repeated after ligation of the left anterior descending coronary artery in the same animals. Closed-chest data were compensated by correcting for the average value for the slope of the attenuation-frequency function of chest wall, which was determined from measurements obtained by analysis on excised tissue. Compensated closed-chest measurements correlated with measurements obtained from the epicardial surface of the heart. The differentiation of normal from ischemic myocardium with both the closed- and open-chest measurements was consistent (p < 0.005). The successful differentiation of normal from ischemic myocardium by determination of quantitative backscatter through the intervening chest wall supports the concept that tissue characterization by quantitative analysis of backscattered ultrasound is a potentially useful, clinically applicable approach to noninvasive detection and differentiation of intrinsic properties of normal and diseased myocardium.     

Quantitative ultrasonic tissue characterization with real-time integrated backscatter imaging in normal human subjects and in patients with dilated cardiomyopathy

We have shown previously that the physical properties of myocardium in dogs can be characterized with quantitative ultrasonic integrated backscatter and that interrogation of the tissue with ultrasound can delineate cardiac cycle-dependent changes in ultrasonic backscatter in normal tissue that disappear with ischemia and reappear with reperfusion if functional integrity is restorable. To determine whether this approach can be applied to man, we implemented an automatic gain compensation and continuous data acquisition system to characterize myocardium with quantitative ultrasonic backscatter and to detect cardiac cycle-dependent changes in real time. We developed a two-dimensional echocardiographic system with quantitative integrated backscatter imaging capabilities for use in human subjects that can automatically differentiate ultrasonic signals from blood as opposed to those obtained from tissue and adjust the slope of the gain compensation appropriately. Real-time images were formed from a continuous signal proportional to the logarithm of the integrated backscatter along each A-line. In our initial investigation, 15 normal volunteers (ages 17 to 40 years, heart rates 44 to 88 beats/min) and five patients with dilated cardiomyopathy (ages 22 to 52, heart rates 82 to 120 beats/min) were studied with conventional parasternal long-axis echocardiographic views. Diastolic-to-systolic variation of integrated backscatter in the interventricular septum and left ventricular posterior wall was seen in each of the normal subjects averaging 4.6 +/- 1.4 dB (SD) and 5.3 +/- 1.5 dB (n = 127 sites), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of unique transmural architecture of human idiopathic cardiomyopathy by ultrasonic tissue characterization.

BACKGROUND. Noninvasive approaches to the evaluation of idiopathic cardiomyopathy are limited. Recent work from our laboratory has used quantitative ultrasound to define the three-dimensional structure of normal human myocardium and the myocardial remodeling associated with infarction. Our goal was to define the role of ultrasonic tissue characterization for detection of specific alterations in the three-dimensional transmural architecture of idiopathic dilated cardiomyopathy. METHODS AND RESULTS. We measured frequency-dependent backscatter from 22 cylindrical biopsy specimens from nine explanted fixed hearts of patients who underwent heart transplantation for idiopathic cardiomyopathy, seven specimens from normal portions, and 12 specimens of infarcted tissue from six explanted fixed human hearts. Consecutive transmural levels from each specimen were insonified with a 5-MHz broadband transducer. The dependence of apparent (uncompensated for attenuation) backscatter, B(f), on frequency (f) was computed from radiofrequency (rf) data as: magnitude of B(f)2 = afn, where n is an index that reflects in part the size of the dominant scatterers in myocardial tissue. Myofiber diameter and percentage fibrosis were determined at each transmural level for each specimen. For cardiomyopathic tissue, the frequency dependence of backscatter (n) increased progressively from epicardial to endocardial (0.02 +/- 0.37 to 1.01 +/- 0.12, p less than 0.05) levels in conjunction with a progressive decrease in myofiber diameter (29.5 +/- 0.9 to 21.4 +/- 0.6 microns, p less than 0.0001). In contrast, in tissue from areas of infarction, the frequency dependence decreased progressively from epicardium to endocardium (0.91 +/- 0.20 to 0.23 +/- 0.21, p less than 0.05) in conjunction with a progressive increase in the percentage of fibrosis (23.5 +/- 9.4% to 54.5 +/- 4.9%, p less than 0.005). Normal tissue exhibited no significant transmural trend for frequency dependence, myofiber diameter, or percentage fibrosis. CONCLUSIONS. These data indicate the presence of a heterogenous transmural distribution of scattering structures associated with human idiopathic cardiomyopathy and myocardial infarction that may be detected by ultrasonic tissue characterization. The divergence of these transmural trends for frequency dependence of backscatter reflects distinct mechanisms of structural heterogeneity for different pathological processes that comprise a transmural gradation of cell size and fibrosis for idiopathic cardiomyopathy and infarction, respectively.     

Transmural heterogeneity of myocardial integrated backscatter in diabetic patients without overt cardiac disease

It is important to detect early changes in diabetic myocardium, because some diabetic patients suffer from diabetic cardiomyopathy, especially those with poorer glycemic control or hypertension (HT). To clarify whether ultrasonic tissue characterization can noninvasively detect ultrastructural changes in diabetic myocardium, we analyzed the transmural heterogeneity in myocardial integrated backscatter (THIB) in 20 diabetic patients and 16 normal subjects. THIB was defined as the absolute value of difference of integrated backscatter between the endocardial and epicardial half of the myocardium. THIB in diabetic patients was significantly greater than that in normal subjects. In diabetic patients, there was a significant correlation between glycosylated hemoglobin and THIB, and the greater THIB was shown in patients with HT compared with those without HT. Early changes in the myocardium, related to increased interstitial collagen deposition or other occult cardiomyopathic changes, may be detected on the basis of quantitative analysis of THIB in diabetic patients.     

Ultrasound integrated backscatter tissue characterization of remote myocardial infarction in human subjects

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.     

Quantitative ultrasonic imaging: Tissue characterization and instantaneous quantification of cardiac function

Quantitative myocardial tissue characterization is being developed to complement and expand conventional echocardiography by delineating the physical state of myocardium under diverse pathophysiologic conditions. Real-time quantitative integrated backscatter imaging has already been applied to patients with ischemic heart disease, hypertrophic cardiomyopathy, and cardiac allograft rejection in clinical investigations performed in the United States, Europe, and Japan. A recently introduced modification of imaging processing algorithms employed for characterization of tissue facilitates automatic detection of endocardial-blood interfaces and on-line quantification of ventricular size and function. Further progress and anticipated developments in quantitative ultrasonic imaging will undoubtedly augment the clinical applications of tissue characterizations based on myocardial integrated backscatter for improved diagnosis, elucidation of pathophysiology, and assessment of cardiac function.     

Myocardial ultrasonic tissue characterization for estimating histological abnormalities in hypertrophic cardiomyopathy: comparison with endomyocardial biopsy findings.

AIMS: In this study, we investigated the clinical usefulness of ultrasonic tissue characterization with integrated backscatter for the evaluation of myocardial histological abnormalities in comparison with endomyocardial biopsy findings in patients with hypertrophic cardiomyopathy. METHODS: Twenty patients with hypertrophic cardiomyopathy and 20 normal subjects were enrolled in this study. We measured two parameters for the ultrasonic tissue characterization with integrated backscatter: the magnitude of the cardiac-cycle-dependent variation in integrated backscatter signals (cdv-IB) and the mean value of integrated backscatter signals calibrated by the pericardium (cal-IB). These parameters were measured at both the interventricular septum and the left ventricular posterior wall. Histological findings of right ventricular endomyocardial biopsy specimens were analyzed by computer image analyzer. RESULTS: cdv-IB was significantly lower and cal-IB significantly higher in both the interventricular septum and the left ventricular posterior wall in patients with hypertrophic cardiomyopathy compared with normal subjects. In patients with hypertrophic cardiomyopathy, the degree of myocardial disarray, interstitial fibrosis, and nonhomogeneity of myocyte size showed positive correlations with cal-IB and negative correlations with cdv-IB. CONCLUSIONS: Ultrasonic tissue characterization with IB enables the noninvasive evaluation of myocardial histological abnormalities in patients with hypertrophic cardiomyopathy.     

Detection of oxygen-derived free radical generation in the canine postischemic heart during late phase of reperfusion

To define the relation between oxygen-derived free radical (oxy-radical) generation in the reperfused ischemic myocardium and the progression of myocardial damage, we measured oxy-radical generation in the ischemic myocardium and the propagating infarct size in a model of canine coronary occlusion (90 minutes) and reperfusion. We used electron paramagnetic resonance spin-trapping techniques (5,5-dimethyl-1-pyrroline N-oxide [DMPO]) to detect oxy-radicals in the rapidly frozen myocardial samples taken by needle biopsy. There was no detectable generation of DMPO adducts in the normal myocardium before or after reperfusion. In the reperfused ischemic myocardium, electron paramagnetic resonance signals of DMPO-OOH (superoxide anion) and DMPO-OH (hydroxyl radical) were detected, with peak concentrations at 1 hour after reperfusion for DMPO-OOH and at 3 hours after reperfusion for DMPO-OH, respectively. These DMPO adducts were also detected during the early phase (15 seconds) of reperfusion, but the concentrations of these signals were much less than those during the late phase of reperfusion. Treatment with human recombinant superoxide dismutase (2.5 mg/kg/hr) and catalase (2.5 mg/kg/hr) during the course of experiments abolished DMPO-OOH formation but had little effect on DMPO-OH formation. Infarct size (percent of risk area infarcted), quantified by a dual staining method with Evans blue dye and triphenyltetrazolium chloride, was 18.3 +/- 4.8% (mean +/- SEM) at 90 minutes of occlusion. After 5 hours of reperfusion, infarct size increased to 43.6 +/- 7.2%. These results indicate that a greater magnitude of oxy-radical generation was sustained in the ischemic myocardial tissue during the late phase (1-3 hours) of reperfusion, associated with the progression of myocardial infarction. The concurrent appearance of oxy-radicals and progressive infarction may support the view that a chain reaction of oxy-radicals contributes to the propagation of myocardial cell damage in the postischemic heart.     

Correlation of acute myocardial infarct scintigraphy with postmortem studies.

Acute myocardial infarct scintigraphy with technetium-99m-pyrophosphate was performed in a patient with an acute massive transmural infarct. The patient died 12 hours later, and postmortem tracer studies demonstrated a tracer concentration ratio of 13:1 between acutely infarcted myocardium and normal myocardium remote from the infarct. The concentration of tracer in tissue bordering on the infarct but without histologic evidence of acute infarction was 1.5 times that in normal tissue remote from the infarct. In vitro scintigraphy of the excised heart revealed a pattern of tracer distribution similar to that of scintiscans obtained before death. The biologic distribution of 99mTc-pyrophosphate, with large tracer concentrations only within the acutely infarcted tissue, suggests that acute myocardial infarct scintigraphy can be used to estimate the extent of an acute myocardial infarct.     

Measurement of infarct size and percentage myocardium infarcted in a dog preparation with single photon-emission computed tomography, thallium-201, and indium 111-monoclonal antimyosin Fab

Single photon-emission tomography (SPECT) and indium 111-labeled monoclonal antimyosin Fab fragments were used to measure myocardial infarct size in 12 dogs, six subjected to balloon catheter-induced coronary artery occlusion for 6 hr (late reperfusion) and six subjected to occlusion with reperfusion at 2 hr (early reperfusion). Tomographic imaging was performed 24 hr after the intravenous injection of labeled Fab fragments with the use of a dual-head SPECT camera with medium-energy collimators. Immediately after the first tomographic scan, thallium-201 was injected into nine of 12 dogs and imaging was repeated. Estimated infarct size in grams was calculated from transaxially reconstructed, normalized, and background-corrected indium SPECT images with the use of a threshold technique for edge detection. Estimated noninfarcted myocardium in grams was calculated from obliquely reconstructed thallium SPECT images by a similar method. The animals were killed and infarct size in grams and true infarct size as a percentage of total left ventricular myocardial volume were measured by triphenyl tetrazolium chloride staining. Estimated infarct size from indium SPECT images showed an excellent correlation with true infarct size (r = .95, SEE = 4.1 g). Estimated percentage myocardium infarcted was calculated by dividing estimated infarct size from indium images by the sum of estimated infarct size plus estimated noninfarcted myocardium obtained from thallium images. Correlation between the estimated percentage of myocardium infarcted and true percentage of myocardium infarcted was excellent (r = .93, SEE = 4.4%). We conclude that dual-isotope SPECT with indium 111-monoclonal antimyosin antibodies and thallium-201 can accurately estimate infarct size and percentage myocardium infarcted.     

Ultrasonic tissue characterization with integrated backscatter. Acute myocardial ischemia, reperfusion, and stunned myocardium in patients

We have previously shown in studies of experimental animals that myocardium exhibits a cardiac cycle-dependent variation of integrated backscatter that reflects regional myocardial contractile performance and that is blunted promptly after arterial occlusion and recovers after reperfusion. To define the clinical utility of ultrasonic tissue characterization with integrated backscatter for detection of acute myocardial infarction and reperfusion, 21 patients (14 men and seven women) were studied in the cardiac care unit within the first 24 hours (mean time, 11.3 hours; range, 3.5-23.8 hours) after the onset of symptoms indicative of acute myocardial infarction with conventional two-dimensional and M-mode echocardiography and with analysis of integrated backscatter. The magnitude of cyclic variation of integrated backscatter was measured from several sites within acute infarct regions and normal regions remote from the infarct zone for each patient. The average magnitude of cyclic variation among all patients (n = 21) was 4.8 +/- 0.5 dB in normal regions compared with 0.8 +/- 0.3 dB in infarct regions (p less than 0.05) within the first 24 hours after the onset of symptoms. Among the patients who had two studies, 15 (mean, 7.1 days; range, 2-31 days for second study) underwent coronary arteriography to define vessel patency. In patients with vessels with documented patency (n = 10), the magnitude of cyclic variation in infarct regions increased over time from 1.3 +/- 0.6 to 2.5 +/- 0.5 dB from the initial to final study (p less than 0.05). Patients with occluded infarct-related arteries (n = 5) exhibited no significant recovery of cyclic variation (0.3 +/- 0.3-0.6 +/- 0.3 dB). A blinded analysis of standard two-dimensional echocardiographic images revealed no significant recovery of wall thickening in either group over the same time intervals. Ultrasonic tissue characterization promptly detects acute myocardial infarction and may delineate potential beneficial effects of coronary artery reperfusion manifest by restoration of cyclic variation of integrated backscatter in the presence of severe wall motion abnormalities.     

Temporal and spatial development of myocardial infarcts in porcine hearts without significant collateral blood flow

To evaluate the time-dependent beneficial effect of reperfusion on infarct size, we investigated the temporal and spatial development of infarcts in porcine hearts. The left anterior descending coronary artery was occluded in 17 pigs for different periods of time. Ischemia was always followed by 4 hours of reperfusion. After 60 minutes of ischemia, transmural needle biopsies subdivided into subendocardial and subepicardial halves were removed from the ischemic apex to determine the tissue concentrations of adenosine triphosphate and nicotinamide adenine dinucleotide. The myocardium at risk was determined with a fluorescent dye, and the infarcted tissue with nitroblue tetrazolium stain. Infarct size was expressed as the ratio of the infarcted myocardium over the risk region. Ischemic cell death began in the jeopardized left ventricular subendocardial septum after about 30 minutes of ischemia. Further progress involved the right subendocardial septum and the subendocardium of the left anterior free wall. After 75 minutes of ischemia, most of the myocytes were already irreversibly injured. Tissue damage from the infarctions was complete after 90 to 120 minutes of ischemia. These results indicate that in hearts without a significant collateral blood flow, reperfusion can only reduce infarct size if initiated within 60 to 75 minutes of ischemia. As in canine hearts, infarctions in porcine hearts progress from the ischemic subendocardium toward the outer layers.     

Tritiated digoxin. XX. Tissue distribution in experimental myocardial infarction

The role and potential hazards of digitalis glycoside administration in acute myocardial infarction remain controversial. We investigated the concentration of tritiated digoxin in normal, ischemic, and infarcted left ventricular myocardium of the dog after ligation of the anterior interventricular coronary artery. The normal homogeneous distribution of tritiated digoxin in the normal canine left ventricle was altered following acute myocardial infarction. The ischemic and infarcted zones exhibited a marked diminution in digoxin concentration. Oxidative phosphorylation determinations confirmed tissue hypoxia in the infarcted zone. The gradient of digoxin concentration between normal, ischemic, and infarcted zones of myocardium may potentiate the development of an arrhythmia in the electrically unstable infarcted myocardium.     

Enhanced detection of ischemic but viable myocardium by QT interval dispersion on treadmill exercise electrocardiograms of patients with healed anterior wall myocardial infarcts

BACKGROUND: The presence of ischemic but viable myocardium in infarcted areas is an important indication for coronary revascularization, but is often difficult to detect with the use of treadmill exercise electrocardiography (ECG). HYPOTHESIS: QT interval dispersion (QTd) is a sensitive method for detecting myocardial ischemia and may improve the accuracy of treadmill exercise ECG testing for detecting ischemic but viable myocardium in infarcted areas. METHODS: Forty-five patients with Q-wave anterior wall myocardial infarctions who underwent treadmill exercise ECG, exercise reinjection thallium-201 (201Tl) scintigraphy, radionuclide angiocardiography, and coronary angiography 1 month after infarction were enrolled in this study. The presence of viable myocardium in the infarct area was determined by exercise reinjection 201Tl scintigraphy. Patients who had no redistribution in the infarct area after reinjection were included in Group 1, and those with redistribution were included in Group 2. RESULTS: QTd immediately after exercise, and the difference between QTd before and immediately after exercise, were significantly greater in Group 2 than in Group 1. The sensitivity, specificity, and accuracy of conventional ST-segment depression criteria for detecting viable myocardium in the infarct area were 48, 64, and 56%, respectively. The measurement of QTd immediately after exercise (abnormal: > or = 70 ms; normal: < 70 ms) improved the sensitivity, specificity, and accuracy to 78, 82, and 80%, respectively. CONCLUSIONS: This novel diagnostic method using QTd-based criteria significantly improves the clinical usefulness of treadmill exercise ECG testing for detecting ischemic but viable myocardium in infarct areas in patients with healed Q-wave anterior wall myocardial infarctions.     

Ultrasonic characterization of porcine liver tissue at frequency between 25 to 55 MHz

AIM: To study the relation between acoustic parameters and histological structure of biological tissue and to provide the basis for high-resolution image of biological tissues and quantitative ultrasonic diagnosis of liver disease. METHODS: Ultrasonic imaging and tissue characterization of four normal porcine liver and five cirrhotic liver tissue samples were performed using a high frequency imaging system. RESULTS: The acoustic parameters of cirrhotic liver tissue were larger than those of normal liver tissue. The sound velocity was 1577 m/s in normal liver tissue and 1631 m/s in cirrhotic liver tissue. At 35 MHz, the attenuation coefficient was 3.0 dB/mm in normal liver tissue and 4.1 dB/mm in cirrhotic liver tissue. The backscatter coefficient was 0.00431 dB/Srmm in cirrhotic liver tissue and 0.00303 dB/Srmm in normal liver tissue. The backscatter coefficient increased with the frequency. The high frequency images coincided with their histological features. CONCLUSION: The acoustic parameters, especially the sound backscatter coefficient, are sensitive to the changes of liver tissues and can be used to differentiate between the normal and pathological liver tissues. High frequency image system is a useful device for high-resolution image and tissue characterization.     

Cell therapy enhances function of remote non-infarcted myocardium

Cell transplantation improves cardiac function after myocardial infarction; however, the underlying mechanisms are not well-understood. Therefore, the goals of this study were to determine if neonatal rat cardiomyocytes transplanted into adult rat hearts 1 week after infarction would, after 8–10 weeks: 1) improve global myocardial function, 2) contract in a Ca²⁺ dependent manner, 3) influence mechanical properties of remote uninjured myocardium and 4) alter passive mechanical properties of infarct regions. The cardiomyocytes formed small grafts of ultrastructurally maturing myocardium that enhanced fractional shortening compared to non-treated infarcted hearts. Chemically demembranated tissue strips of cardiomyocyte grafts produced force when activated by Ca²⁺, whereas scar tissue did not. Furthermore, the Ca²⁺ sensitivity of force was greater in cardiomyocyte grafts compared to control myocardium. Surprisingly, cardiomyocytes grafts isolated in the infarct zone increased Ca²⁺ sensitivity of remote uninjured myocardium to levels greater than either remote myocardium from non-treated infarcted hearts or sham-operated controls. Enhanced calcium sensitivity was associated with decreased phosphorylation of cTnT, tropomyosin and MLC2, but not changes in myosin or troponin isoforms. Passive compliance of grafts resembled normal myocardium, while infarct tissue distant from grafts had compliance typical of scar. Thus, cardiomyocyte grafts are contractile, improve local tissue compliance and enhance calcium sensitivity of remote myocardium. Because the volume of remote myocardium greatly exceeds that of the grafts, this enhanced calcium sensitivity may be a major contributor to global improvements in ventricular function after cell transplantation.     

In vivo ultrasonic tissue characterization of human intracardiac masses

Interactions between an ultrasonic signal and cardiac tissue have been used to characterize the histologic state of myocardium in vitro. To assess the utility of in vivo ultrasonic tissue characterization, stochastic analysis was applied to the digitized echocardiographic signals from 15 patients with 2-dimensional echocardiograms suggesting intracardiac masses. Ten subjects with echocardiograms suggesting mural thrombi underwent subsequent surgery or necropsy, which confirmed thrombi in 6 and revealed no thrombi (designated artifact) in 4. Five other patients had intracardiac tumors. The amplitudes within the digitized ultrasonic signals were displayed as histograms, which were described by a parameter k that represented the degree to which each histogram departed from a totally random probability density function. In 5 of 6 thrombi, k = 0, but in all 4 artifacts, k greater than 0. The sixth thrombus had k = 0.5 due to the specular effect of the interface between the thrombus' 2 lobes. All 5 tumors had k greater than 0. Ultrasonic tissue characterization using a stochastic analysis of backscatter can be performed in vivo and helps differentiate thrombus from artifact and tumor in the heart.