Biomedical subjects

J L Weiss

Publications and source records attributed to J L Weiss.

At least 37 records · Page 2Linked to original sources

PubMed1996

Prolonged impairment of regional contractile function after resolution of exercise-induced angina. Evidence of myocardial stunning in patients with coronary artery disease.

BACKGROUND: Delayed recovery of contractile function in spite of normal perfusion (ie, "stunning") has been described in animal models of exercise-induced myocardial ischemia. Therefore, we investigated whether stunning may result from effort angina in patients. METHODS AND RESULTS: Patients with coronary artery disease underwent exercise testing combined with quantitative measurements of contractile function for up to 240 minutes after exercise determined by either measurement of regional ejection fraction (99mTc radionuclide angiography; n = 17, group A) or computer-assisted measurement of systolic wall thickening (n = 14, group B). In the latter group, myocardial perfusion was also evaluated by 99mTc-sestamibi tomographic imaging. Angina induced marked contractile dysfunction. Hemodynamic and ECG changes brought about by ischemia were promptly normalized. Furthermore, no perfusion defects could be detected in group B patients 30 minutes after exercise, yet contractile function remained impaired well after cessation of exercise. Thirty minutes into recovery, regional ejection fraction of previously ischemic areas was still 82.6 +/- 4.6% of baseline in group A (P < .05). Similarly, in group B patients, systolic thickening of previously ischemic segments was still significantly impaired 60 minutes after exercise, averaging 33.8 +/- 2.8% versus 40.5 +/- 2.7% at baseline (P < .05). Contractile impairment was fully reversible, as the functioning of previously ischemic segments normalized between 60 and 120 minutes of recovery. CONCLUSIONS: Prolonged yet ultimately reversible impairment of regional myocardial function may occur in patients after exercise-induced angina in the absence of perfusion abnormalities. These findings indicate that myocardial stunning may ensue after effort angina in patients with severe coronary artery disease.

Adult↗

PubMed1996

A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis.

BACKGROUND: Platelet glycoprotein IIb/IIIa is a membrane receptor for fibrinogen and von Willebrand factor, and it has an important role in platelet aggregation. It is known to be involved in the pathogenesis of acute coronary syndromes. Previously, we found a high frequency of a particular polymorphism, PlA2, of the gene encoding glycoprotein IIIa in kindreds with a high prevalence of premature myocardial infarction. METHODS: To investigate the relation between the PlA2 polymorphism and acute coronary syndromes, we conducted a case-control study of 71 case patients with myocardial infarction or unstable angina and 68 inpatient controls without known heart disease. The groups were matched for age, race, and sex. We used two methods to determine the PlA genotype: reverse dot blot hybridization and allele-specific restriction digestion. RESULTS: The prevalence of PlA2 was 2.1 times higher among the case patients than among the controls (39.4 percent vs. 19.1 percent, P=0.01). In a subgroup of patients whose disease began before the age of 60 years, the prevalence of PlA2 was 50 percent, a value that was 3.6 times that among control subjects under 60 years of age (13.9 percent, P=0.002). Among subjects with the PlA2 polymorphism, the odds ratio for having a coronary event was 2.8 (95 percent confidence interval, 1.2 to 6.4). In the patients less than 60 years of age at the onset of disease, the odds ratio was 6.2 (95 percent confidence interval, 1.8 to 22.4). CONCLUSIONS: We observed a strong association between the PlA2 polymorphism of the glycoprotein IIIa gene and acute coronary thrombosis, and this association was strongest in patients who had had coronary events before the age of 60 years.

Acute Disease↗

PubMed1996

Three-dimensional mapping of acute ischemic regions using artificial neural networks and tagged MRI.

Many methods for mapping ischemic myocardial regions by functional analysis have been suggested. However, the complicated relationship between myocardial function and perfusion, and the inherent limitations of the imaging techniques used, have led to a generally low mapping accuracy. We show herein, that highly accurate mapping can be obtained by combining tagged magnetic resonance imaging (MRI), three-dimensional (3-D) analysis, and artificial neural networks. Nine canine hearts with acute ischemia were studied using multiplanar tagged MRI. Twenty-four myocardial cuboids were tagged in each heart and reconstructed in 3-D at end diastole (ED) and end systole (ES). The cuboids were arranged in three slices approximately 1 cm thick and covered most of the left ventricle (LV). Transmural thickening and endocardial area strain were calculated for each cuboid. Applying a post-mortem (PM) analysis, the percent ischemia in each cuboid was estimated using monastral blue dye; the PM analysis served as a "gold standard." An artificial neural network (ANN), designed to estimate the percent ischemia in each cuboid from the functional indexes, was then created. The ANN "learned" the function-ischemia relationship in 192 cuboids taken from eight of the hearts and was asked to estimate the percent ischemia in the 24 cuboids of the ninth heart. The process was repeated nine times, each time using a different heart as test case. The average accuracy of mapping, i.e., the accuracy with which the ANN has mapped the normal and ischemic cuboids using the functional parameters, was 87.5% +/- 7.8 (s.d.). This accuracy was superior to the accuracy obtained by optimal thresholding of the same thickening (80.1%) and endocardial strain (76.9%) data.

Animals↗

PubMed1996

Effects of afterload on regional left ventricular torsion.

OBJECTIVE: To determine if left ventricular torsion, as measured by magnetic resonance tissue tagging, is afterload dependent in a canine isolated heart model in which neurohumoral responses are absent, and preload is constant. METHODS: In ten isolated, blood perfused, ejecting, canine hearts, three afterloads were studied, while keeping preload constant: low afterload, high afterload (stroke volume reduced by approx. 50% of low afterload), and isovolumic loading (infinite afterload). RESULTS: There were significant effects of afterload on both torsion (P < 0.05) and circumferential shortening (P < 0.0005). Between low and high afterloads, at the anterior region of the endocardium only, where torsion was maximal, there was a significant reduction in torsion (15.1 +/- 2.2 degrees to 7.8 +/- 1.8 degrees, P < 0.05). Between high afterload and isovolumic loading there was no significant change in torsion (7.8 +/- 1.8 degrees to 6.2 +/- 1.5 degrees, P = NS). Circumferential shortening at the anterior endocardium was significantly reduced both between low and high afterload (-0.19 +/- 0.02 to -0.11 +/- 0.02, P < 0.0005), and also between high afterload and isovolumic loading (-0.11 +/- 0.02 to 0.00 +/- 0.02, P < 0.05). Plots of strains with respect to end-systolic volume demonstrated a reduction in both torsion and shortening with afterload-induced increases in end-systolic volume. Torsion, but not circumferential shortening, persisted at isovolumic loading. CONCLUSIONS: Maximal regional torsion of the left ventricle is afterload dependent. The afterload response of torsion appears related to the effects of afterload on end-systolic volume.

Animals↗

PubMed1995

Effect of early enalapril therapy on left ventricular function and structure in acute myocardial infarction.

Infarct expansion starts within hours to days after transmural myocardial injury. Previous echocardiographic and left ventriculographic studies demonstrated that angiotensin-converting enzyme (ACE) inhibitor therapy limits left ventricular dilatation, particularly in patients with anterior wall acute myocardial infarction (AMI) or impaired left ventricular function. Forty-three patients with an acute Q-wave AMI were randomized within 24 hours of symptom onset to intravenous enalaprilat (1 mg) or placebo. Patients were then given corresponding oral therapy and followed for 1 month. Predrug and 1-month gated blood pool scans were obtained in 32 patients to evaluate changes in cardiac volumes and ejection fraction. Twenty-three patients underwent magnetic resonance imaging at 1 month to evaluate left ventricular infarct expansion. Blood pressure decreased at 6 hours but returned to baseline in both groups after 1 month of therapy. The change in cardiac volumes from baseline to 1 month differed between the placebo (end-diastolic volume +16 +/- 5 ml, end-systolic volume +8 +/- 6 ml), and enalapril (end-diastolic volume -8 +/- 9 ml and end-systolic volume -14 +/- 7 ml) groups (p < 0.05 vs placebo). Global and infarct zone ejection fractions improved significantly at 1 month in the enalapril group (+6 +/- 3% and 19 +/- 5%, respectively) but did not change over 1 month in the placebo group. Infarct segment length and infarct expansion index by magnetic resonance imaging were significantly less in those treated with enalapril, suggesting less infarct expansion in this group. Thus, early administration of enalaprilat to patients presenting with a first Q-wave AMI prevents cardiac dilatation and infarct expansion.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Distribution of myocardial strains: an MRI study.

Quantification of myocardial strains is essential for understanding cardiac mechanics. Previous techniques for assessing regional myocardial strains have been mainly limited to invasive procedures. A technique by which tagging can be added to magnetic resonance images (MRI) has recently been introduced and allows for noninvasive measurement of myocardial deformations. We have applied MRI tagging to two sets of orthogonal planes and have obtained three dimensional (3D) reconstructions of 24 myocardial cuboids at end-diastole (ED) and at end-systole (ES). Applying finite strain analysis to these cuboids we were able to study the longitudinal distribution of the endocardial and epicardial principal strains (PS) in the normal canine heart. In addition we have calculated the longitudinal distribution of the left ventricular (LV) transmural thickening using a 3D approach. Our results show similarity in the longitudinal distribution of endocardial PS and transmural thickening. These results imply that endocardial strains are determined not only by endocardial fiber deformations but mainly by geometrical coupling through transmural thickening.

Animals↗

PubMed1995

A noninvasive comparative study of myocardial strains in ischemic canine hearts using tagged MRI in 3-D.

Regional reduction in myocardial function has long been utilized for noninvasive detection and localization of ischemic regions in the left ventricle. In this study, we compared the ability of 13 different myocardial strain indexes to discriminate between ischemic and nonischemic tissue. Using magnetic resonance imaging with tagging and three-dimensional reconstruction, we noninvasively tracked the deformation of 24 myocardial cuboids in each of nine canine hearts with acute ischemia induced by coronary artery ligation. Monastral blue staining was used for postmortem assessment of ischemia. The ability of each index to discriminate between normal and ischemic zones was evaluated using the "t" statistic. The best discrimination was obtained by the endocardial area strain [t = 7.5 +/- 3.0 (SD)], a local measure of systolic shrinkage on the endocardial surface, and by the magnitude of the endocardial principal strain (t = 7.0 +/- 1.9). Transmural wall thickening (t = 6.1 +/- 2.3) was the third best functional index. The same three indexes correlated most closely with perfusion, as assessed by monastral blue staining. These findings imply that these are the preferable functional indexes for mapping of ischemic myocardial regions.

Animals↗

PubMed1994

Rotational deformation of the canine left ventricle measured by magnetic resonance tagging: effects of catecholamines, ischaemia, and pacing.

OBJECTIVE: The aim was to investigate the generation of rotation of the left ventricular apex with respect to the base by magnetic resonance tagging, a non-invasive method of labelling the myocardium, in a canine model. METHODS: 18 dogs were imaged at baseline and during: (1) inotropic stimulation with dobutamine; (2) chronotropic stimulation with atrial pacing; (3) anterior wall ischaemia; (4) posterior wall ischaemia; and (5) varying left ventricular activation site; six dogs underwent each intervention. Apical rotation of the apex (torsion) was quantified. The epicardium and the endocardium were considered separately, as were the anterior and posterior walls. RESULTS: Mean torsion of the epicardium [anterior 3.1(SEM 1.2) degrees, posterior 9.9(1.0) degrees] was less than that of the endocardium [anterior 8.1(2.6) degrees, posterior 14.9(2.0) degrees, p < 0.05 for both]. Anterior torsion was less than posterior torsion for both the epicardium, p < 0.05, and the endocardium, p < 0.05. Dobutamine increased torsion of both the epicardium [anterior 13.3(2.2) degrees, posterior 12.6(1.7) degrees, p < 0.05 for both] and the endocardium [anterior 24.6(2.3) degrees, posterior 16.5(2.1) degrees, p < 0.05 for both]. Atrial pacing at 160% baseline rate increased torsion of both the anterior wall [epicardium 6.6(1.0) degrees, endocardium 11.3(1.2) degrees, p < 0.05] and the posterior wall [epicardium 13.0(1.3) degrees, endocardium 19.4(1.9) degrees, p < 0.05]. Anterior wall ischaemia reduced torsion of the anterior wall only [epicardium -2.0(1.0) degrees, endocardium 6.7(2.3) degrees, both p < 0.05]. Posterior wall ischaemia reduced torsion of the posterior wall of the epicardium only [7.1(1.2) degrees, p < 0.05] but also reduced torsion of the anterior wall [epicardium 0.7(1.0) degrees, endocardium 2.4(1.6) degrees, p < 0.05 for both]. Altering the pattern of left ventricular activation by atrioventricular pacing reduced torsion of the posterior wall of the epicardium [6.6(1.2) degrees, p < 0.05] and of the anterior [3.6(1.9) degrees, p < 0.05] and posterior [7.1(1.6) degrees, p < 0.05] walls of the endocardium. CONCLUSIONS: Rotational deformation of the left ventricle is dependent on the pattern of left ventricular activation and the contractile state. That a decrease in the contractile state in one area (by ischaemia) can cause a decrease in rotation in another suggests that this rotation depends on the complex fiber arrangement of the whole ventricle.

Animals↗

PubMed1994

Relation of regional cross-fiber shortening to wall thickening in the intact heart. Three-dimensional strain analysis by NMR tagging.

BACKGROUND: The mechanism by which small amounts of myofiber shortening lead to extensive wall thickening is unknown. When isolated fibers shorten, they thicken in the two orthogonal directions. In situ fibers, however, vary in their orientation through the wall, and each is tethered to near or distant neighbors, which allows shortening to occur both in the direction of the fibers and also perpendicular to them. This "cross-fiber" shortening may enable the wall to shorten in two directions and thereby thicken extensively in the third. METHODS AND RESULTS: Nuclear magnetic resonance tagging is a noninvasive method of labeling and tracking myocardium of the entire heart in three dimensions that does not interfere with myocardial motion. To investigate the presence and importance of cross-fiber shortening in the intact left ventricle, 10 closed-chest dogs were studied by nuclear magnetic resonance tagging. Five short-axis and four long-axis images were acquired to reconstruct 32 cubes of myocardium in each dog at end diastole and end systole. Pathological dissection was performed to determine the fiber direction at the epicardium, midwall, and endocardium of each cube. Strain was computed from the three-dimensional cube coordinates in the fiber and cross-fiber directions for epicardial and endocardial surfaces, and thickening of the full wall and its epicardial and endocardial halves was determined. Shear deformations were also calculated. Fiber strain at the epicardium and endocardium was -6.4 +/- 0.7% and -8.5 +/- 0.6% (mean +/- SEM), respectively (difference, P > .05). Cross-fiber strain at epicardium and endocardium was -0.6 +/- 0.5% and -25 +/- 0.6%, respectively (difference, P < .05). Thickening of the full wall reached 32.5 +/- 1.0%, composed of epicardial thickening of 25.5 +/- 0.6% and endocardial thickening of 43.3 +/- 1.0% (difference, P < .05). Fiber/cross-fiber shear strain was small (< 3%). Significant regional differences were present in all strains. A significant correlation was found between the extents of regional thickening and cross-fiber shortening. CONCLUSIONS: Cross-fiber shortening at the endocardium, therefore, far exceeds cross-fiber shortening at the epicardium and fiber shortening at both epicardium and endocardium. Since no active shortening can occur locally in the cross-fiber direction, the extensive endocardial cross-fiber shortening must result from interaction with differently aligned fibers at a distance. The correlation between regional thickening and cross-fiber shortening supports the hypothesis that this interaction is the mechanism for amplifying small amounts of fiber shortening to cause extensive endocardial thickening.

Animals↗

PubMed1993

Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction.

Previous investigators have hypothesized that myocardial "stunning" may result either from a primary impairment in excitation or from electromechanical dissociation. Thrombolytic therapy and angioplasty have increased the importance of understanding the electrophysiologic effects of brief ischemia followed by reperfusion. We investigated the electrophysiologic properties of mechanically dysfunctional stunned myocardium in 18 dogs anesthetized with pentobarbital (30 mg/kg, intravenously administered). After thoracotomy, the proximal anterior descending coronary artery was occluded for 15 minutes, which was followed by 20 minutes of reperfusion. At baseline, peak ischemia, and 20 minutes of reperfusion, local electrogram durations, activation times, and refractory periods were measured from 12 standardized sites within the ischemic and border zones. Echocardiographic percentage of systolic wall thickening confirmed normal preischemic and markedly reduced postischemic function in the investigated region. Despite the marked electrophysiologic abnormalities observed in the ischemic zone during ischemia, mean electrogram duration, calculated conduction velocity, and mean effective refractory period after 20 minutes of reperfusion had returned almost to baseline values 39.2 +/- 11.5 msec versus 37.2 +/- 12.1 msec, 0.65 +/- 0.15 m/sec versus 0.68 +/- 0.15 m/sec, and 134 +/- 14 msec versus 131 +/- 8 msec, respectively. Corresponding mean values within the ischemic border zone were similarly close to baseline values after reperfusion. There was no significant difference in local heterogeneity (coefficient of variation) within the ischemic or border zone after reperfusion versus baseline values. Although the postischemic electrophysiologic status returned to normal, systolic thinning and dyskinesis persisted in the region of measurement. The contractile dysfunction that results from reperfusion-induced injury can thus occur in the setting of apparent excitation-contraction uncoupling.

Analysis of Variance↗

PubMed1993

Accurate systolic wall thickening by nuclear magnetic resonance imaging with tissue tagging: correlation with sonomicrometers in normal and ischemic myocardium.

OBJECTIVES: This study examined whether the correlation of systolic wall thickening (%WT) by nuclear magnetic resonance (NMR) imaging with wall thickening by sonomicrometry (SM) is improved by using a three-dimensional volume element model of the left ventricular wall. BACKGROUND: Left ventricular wall obliquity with respect to the imaging plane causes overestimation of wall thickness by planar imaging techniques. Wall thickness perpendicular to the endocardial surface can be accurately calculated by three-dimensional reconstruction of left ventricular wall segments. METHODS: Sonomicrometers were placed transmurally in 11 dogs (left anterior descending artery territory) with an imaging marker, visible on NMR imaging, sewn to the epicardial crystal. Two adjacent NMR short-axis image planes were radially segmented by four perpendicular spin-saturated planes (tags), dividing the myocardium into eight volume elements, one of which contained the sonomicrometer crystal pair. Left ventricular thickness and thickening were calculated by four methods: 1) linear = distance between epicardium and endocardium at midpoint in the segment with the sonomicrometer; 2) planar = area of that segment divided by the mean of the endocardial and epicardial arc lengths; 3) biplanar = average of wall thicknesses calculated by the planar method from the segment with sonomicrometers and the corresponding segment located in the adjacent short-axis imaging plane; and 4) three-dimensional = volume of the element with the sonomicrometers divided by the mean of the endocardial and epicardial surface areas. RESULTS: Regressions for all methods using pooled data from control periods and during ischemia: Linear %WT = 0.59 + 1.31 SM%WT (r = 0.71, SEE = 0.28, p < 0.0002) Planar %WT = 1.43 + 1.62 SM%WT (r = 0.87, SEE = 0.19, p < 0.0001) Biplanar %WT = 2.09 + 1.46 SM%WT (r = 0.90, SEE = 0.15, p < 0.0001) Three-dimensional %WT = 0.19 + 1.49 SM%WT (r = 0.95, SEE = 0.10, p < 0.0001) CONCLUSIONS: Nuclear magnetic resonance imaging with tissue tagging allows accurate noninvasive assessment of systolic wall thickening. The three-dimensional volume element approach, by accounting for obliquity between the image plane and the left ventricular wall, provides the strongest correlation between NMR imaging and percent systolic wall thickening by sonomicrometer crystals.

Animals↗

PubMed1993

Small apex-to-base heterogeneity in radius-to-thickness ratio by three-dimensional magnetic resonance imaging.

Reported large base-to-apex differences in endocardial area ejection fraction may suggest large variability in myocardial function and load. To test ventricular load heterogeneities, we measured the ratio of radius of curvature to wall thickness (R/T), as a stress index reflecting myocardial load. End-diastolic (ED) and end-systolic (ES) magnetic resonance cross-sectional images were obtained in 15 open-chest dogs at 5 levels from base to apex, from which 4 three-dimensional thick disks were generated from adjacent image planes. The average R/T for each disk was calculated by planar and three-dimensional methods, using both midwall and endocardial radii of curvature. R/T was normalized to the apical value to quantify the relative changes in myocardial load. Normalized R/T using the midwall three-dimensional approach was 1.08, 1.11, 1.06, and 1.0 for ED (P = NS) and 1.25, 1.013, 1.08, and 1.0 for ES (P < 0.02), base to apex, respectively, while the other methods yielded higher values. Therefore, R/T calculated by the three-dimensional midwall approach shows only small apex-to base variations at ED (< 11%) and ES (< 25%), which is substantially less than the variability in area ejection fraction (102%). This suggests only small base-to-apex load heterogeneities, in spite of large changes in the area ejection fraction, an index reflecting specific ventricular geometry rather than local myocardial function.

Animals↗

PubMed1993

Noninvasive quantification of principal strains in normal canine hearts using tagged MRI images in 3-D.

Previous studies of myocardial strains have been largely limited to invasive procedures in isolated regions. Utilizing images from tagged magnetic resonance imaging (MRI) in three dimensions (3-D), we noninvasively quantified in vivo endocardial (endo) and epicardial (epi) principal strains (PS) throughout the left ventricle (LV) and tested their uniformity. Seven normal hearts in paced reclosed-chest dogs were studied. Combining long- and short-axis images, 24 myocardial cuboids were tagged at end diastole (ED), imaged at end systole and ED, and reconstructed in 3-D. The cuboids were circumferentially arranged in three parallel approximately 1-cm-thick short-axis slices (8 cuboids/slice). By application of finite strain analysis to each cuboid, the major PS (i.e., magnitude and angle with respect to the circumferential direction of maximal shortening) was calculated for each face. when strains are averaged globally (i.e., using all regions), the average magnitude of endo PS exceeded epi PS approximately twofold: -0.24 +/- 0.07 (SD) vs. -0.11 +/- 0.05 (P < 0.05). On the other hand, the PS angle with respect to the circumferential direction at epi exceeded the angle at endo (P < 0.05) by 33 +/- 36 degrees. Average PS direction at epi, 59 +/- 32 degrees, aligned with the expected fiber direction but was perpendicular to it at endo, 26 +/- 30 degrees. However, significant regional variations were observed from wall to wall and from apex to base. When variations in location were accounted for, the pooled SD for the PS magnitudes dropped to 0.032 and for the direction to only 15 degrees. Furthermore, it was found that the anterior-posterior pair of walls contracted differently (P < 0.05) from the septal-lateral pair of walls. These observations indicate that regional myocardial function is heterogeneous and is location dependent.

Animals↗

PubMed1992

Dissociation between left ventricular untwisting and filling. Accentuation by catecholamines.

BACKGROUND: Efficient early diastolic filling is essential for normal cardiac function. Diastolic suction, as evidenced by a decreasing left ventricular pressure during early filling, could result from restoring forces (the release of potential energy stored during systolic deformation) dependent on myofilament relaxation. Although these restoring forces have been envisioned within individual myofibers, recent studies suggest that gross fiber rearrangement involving the connective tissue network occurs easy in diastole. This may lead to the release of potential energy stored during systole and suction-aided filling. METHODS AND RESULTS: To establish precisely the timing and extent of restoration of the systolic torsional deformation of the left ventricle with respect to early filling at baseline and with enhanced relaxation, we studied untwisting during control conditions and with catecholamine stimulation. Using noninvasive and nondestructive magnetic resonance tagging, torsional deformation of the left ventricle was measured at 20-msec intervals in 10 open-chest, atrially paced dogs, starting at aortic valve closure. Eight equiangular tags intersected the epicardium and endocardium in three short-axis imaging planes (base, mid, and apex). From the intersection points, epicardial and endocardial circumferential chord and arc lengths were measured and angular twist of mid and apical levels with respect to the base (maximal torsion and its reversal, untwisting) was calculated. Echo-Doppler provided timing of aortic valve closure and of mitral valve opening. Zero torsion was defined at end diastole. Torsion at the apical level reversed rapidly between its maximum and the time immediately after mitral valve opening: from 7.0 +/- 5.8 degrees to 3.2 +/- 5.4 degrees and 12.0 +/- 8.5 degrees to 6.9 +/- 7.8 degrees (mean +/- SD, both p less than 0.01) at the epicardium and endocardium, respectively. During the same period, no significant circumferential segment length changes occurred. As expected, after mitral valve opening, filling resulted in significant circumferential segment lengthening, whereas further reversal of torsion was small and nonsignificant. During dobutamine infusion, torsion at end systole was greater and reversal during isovolumic relaxation was much more rapid and greater in extent (p less than 0.01). Torsion reversed from 11.5 +/- 4.3 degrees to 5.7 +/- 4.8 degrees and 17.4 +/- 6.4 degrees to 6.9 +/- 7.7 degrees at epicardium and endocardium. CONCLUSIONS: Untwisting occurs principally during isovolumic relaxation before filling and is markedly enhanced in speed and magnitude by catecholamines. This partial return of the left ventricle to its preejection configuration before mitral valve opening could represent an important mechanism for the release of potential energy stored in elastic elements during the systolic deformation. These myocardial restoring forces would be markedly enhanced by physiological changes consequent to catecholamines such as during exercise, offsetting the concomitant shortening of the filling period.

Animals↗

PubMed1991

Myocardial infarct expansion: recognition, significance and pathology.

Infarct expansion can be defined pathologically as a distortion of ventricular topography produced by thinning and disproportionate dilation of the infarct segment. Large transmural infarcts tend to be associated with greater propensity for infarct expansion. Two-dimensional echocardiography has made it feasible to detect these acute alterations in cardiac topography by serial examination of patients with acute myocardial infarction. A practical approach to the echocardiographic quantification of expansion involves analysis of end-diastolic cross-sectional echo views at the papillary muscle level, which can be used as fixed internal landmarks to divide the left ventricle into 2 segments, anterior and posterior. An off-line computer system can be used to track relative lengths of these segments as well as their thicknesses over time. In the initial clinical study, one third of patients with acute anterior transmural infarcts showed an average 50% increase in the infarct segment length beginning within the first 3 days of infarction, characterized by disproportionate progressive dilation and transmural thinning of this zone. These patients demonstrated a significantly higher mortality than those without expansion. Later studies demonstrated not only continuing dilation of the infarcted anterior wall, but also progressive dilation of the noninfarcted posterior wall, underscoring the importance of continuing long-term noninvasive follow-up. Not only is expansion associated with a poor clinical outcome; it has also been shown experimentally and clinically to be modifiable or even preventable by various therapeutic maneuvers, which may well improve survival. Because of the limitations of the echocardiographic window, it is often possible to obtain only a single cross-sectional view of high quality, and even then technical quality may not be sufficiently high to enable detailed quantitative analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Reduced left ventricular cavitary activity ("black hole sign") in thallium-201 SPECT perfusion images of anteroapical transmural myocardial infarction.

Apparently reduced left ventricular (LV) cavitary thallium activity in both planar and tomographic perfusion images has been previously observed by these and other investigators. With single-photon emission computerized tomography, we have clinically noted that this "black hole sign" was associated with an aneurysm in the setting of a transmural anterior or anteroapical perfusion defect. We have now prospectively studied the etiology and predictive value of this sign in 84 consecutive patients with an anterior, anteroapical transmural perfusion defect. Of the 84 patients, 49 had both LV aneurysm (confirmed by contrast ventriculography, echocardiography or gated blood pool studies) and a black hole sign. Only 1 patient with an aneurysm did not have the black hole sign, and 2 without aneurysm did. Thus, it is concluded that this sign is highly accurate in diagnosing LV aneurysm. Because thallium-201 single-photon emission computerized tomography imaging is often performed as one of the first diagnostic tests soon after myocardial infarction, this has important clinical management implications.

Adult↗

PubMed1991

Usefulness of OPC-8212, a quinolinone derivative, for chronic congestive heart failure in patients with ischemic heart disease or idiopathic dilated cardiomyopathy.

To evaluate the safety and efficacy of the inotropic agent OPC-8212 in patients with chronic congestive heart failure, 76 patients with impaired cardiac function and diminished exercise tolerance were studied. They were randomized to 12 weeks of double-blind therapy with either 60 mg/day of OPC-8212 or placebo. The study drug was added to their baseline medical regimen. The primary study outcome was the combined outcome of the time to either mortality (of all cause) or substantial worsening of heart failure (major morbidity), whichever occurred first. Treatment with OPC-8212 significantly (p less than 0.01) decreased the combination of major morbidity/mortality over 12 weeks of therapy. Quality of life, assessed by the Sickness Impact Profile questionnaire, was significantly improved in patients receiving OPC-8212 (p less than 0.01). Furthermore, ventricular premature contractions as assessed by 24-hour Holter monitoring were not increased with OPC-8212 treatment. Although patients treated with OPC-8212 were able to reach a significantly higher peak oxygen uptake and exercise longer during symptom-limited exercise, when data were analyzed as percent change from baseline, the absolute increases were small. These results suggest that OPC-8212 is beneficial in treating patients with congestive heart failure and that further evaluation of this new inotropic agent is warranted.

Adolescent↗

PubMed1991

Estimating WAIS-R IQ from the Shipley Institute of Living Scale: a replication.

Zachary, Crumpton, and Spiegel (1985) introduced a linear regression and continuous norming procedure for estimating Full Scale WAIS-R IQ from the Shipley Institute of Living Scale. The present study replicated their method with 55 adult psychiatric inpatients and day hospital patients. A high correlation (r = .85), an extremely small mean difference in IQ (.8 points), and an acceptable average absolute difference (7.6 points) were found between estimated and obtained WAIS-R. Sines and Simmons tables (1959) for Shipley estimates of WAIS IQ produced a high correlation (r = .86), but large mean and average absolute differences (13.1 and 13.6 points, respectively). The study supports use of the Zachary et al. procedure for estimating WAIS-R IQ from Shipley scores in a psychiatric population.

Adolescent↗