Digital storage and retrieval: the future in echocardiography.
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Echocardiography↗
Biomedical subjects
J D Thomas
Publications and source records attributed to J D Thomas.
Physical and physiological determinants of pulmonary venous flow: numerical analysis.
To study the physical and physiological determinants of transmitral and pulmonary venous flow, a lumped-parameter model of the cardiovascular system has been created, modeling the instantaneous pressure, volume, and influx/efflux of the pulmonary veins, left atrium and ventricle, systemic arteries and veins. right atrium and ventricle, and pulmonary arteries. Initial validation has been obtained by direct comparison with transesophageal echocardiographic recordings of mitral and pulmonary venous velocity for the following clinical situations: normal diastolic function, delayed ventricular relaxation, restrictive filling due to severe systolic dysfunction, severe mitral regurgitation before and after valve repair surgery, and premature atrial contraction occurring during ventricular systole. Sensitivity analysis has been performed with a Jacobian matrix, representing the proportional change in a group of output indexes (yi) in response to isolated changes in input parameters (xj), [(delta yi/yi)/ ([delta xj/xj)], demonstrating the complementary nature of mitral and pulmonary venous A-wave velocity for predicting ventricular stiffness and atrial systolic function. This unified numerical-experimental programming environment should facilitate model refinement and physiological data exploration, in particular guiding more accurate interpretations of Doppler echocardiographic data.
Animals↗
Novel mutations and a mutational hotspot in the MODY3 gene.
Maturity-onset diabetes of the young 3 (MODY3) is a type of NIDDM caused by mutations in the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha) located on chromosome 12q. We have identified four novel HNF-1alpha missense mutations in MODY3 families. In four additional and unrelated families, we observed an identical insertion mutation that had occurred in a polycytidine tract in exon 4. Among those families, one exhibited a de novo mutation at this location. We propose that instability of this sequence represents a general mutational mechanism in MODY3. We observed no HNF-1alpha mutations among 86 unrelated late-onset diabetic patients with relative insulin deficiency. Hence mutations in this gene appear to be most strongly associated with early-onset diabetes.
Chromosomes, Human, Pair 12↗
Detecting and preventing ventricular remodeling after MI.
Infarct expansion carries a poor prognosis. Echocardiography can identify this condition by identifying distortion of the ventricular topography. In this review we discuss the acute and long-term effects of thrombolysis on infarct expansion and subsequent left ventricular remodeling after acute myocardial infarction.
Echocardiography↗
MK-801 administration during ethanol withdrawal in neonatal rat pups attenuates ethanol-induced behavioral deficits.
Alcohol exposure during development can produce central nervous system dysfunction, resulting in a wide range of behavioral alterations. The various mechanisms by which alcohol causes these behavioral changes, however, remain unknown. One mechanism that has been suggested is NMDA receptor-mediated excitotoxic cell death produced by ethanol withdrawal. The present study examined whether MK-801, an antagonist of the NMDA receptor that has been shown to protect against NMDA receptor-mediated excitotoxicity, could block alcohol's adverse effects on behavior. Sprague-Dawley rat pups were exposed to alcohol (6.0 g/kg) in a binge-like manner on postnatal day 6 using an artificial rearing procedure. Subjects then received an injection of MK-801 (0.1 mg/kg) or vehicle during withdrawal, 21 hr after ethanol exposure. At postnatal day 40, all subjects were tested on a serial spatial discrimination reversal task. Ethanol-exposed subjects were impaired in both discrimination and reversal learning, and committed a significantly greater number of perseverative-type errors, compared with controls. MK-801 administration during ethanol withdrawal significantly attenuated ethanol-induced deficits in reversal learning and increases in perseverative-type errors, whereas MK-801 exposure by itself had no significant effect on performance. Thus, exposure to MK-801 during ethanol withdrawal partially protected against alcohol-related disruptions in spatial reversal learning. These results support the suggestion that NMDA receptor-mediated excitotoxicity may be one mechanism by which alcohol induces behavioral teratogenicity.
Alcohol Withdrawal Delirium↗
Application of color Doppler M-mode echocardiography in the assessment of ventricular diastolic function: potential for quantitative analysis.
Color Doppler M-mode echocardiography provides a spatiotemporal map of blood distribution (v(s,t)) within the heart, with a typical temporal resolution of 5 ms, a spatial resolution of 300 microns, and a velocity resolution of 3 cm/s. M-mode echocardiographic data can be obtained along a streamline from the mid-left atrium to the mid-left ventricle from either the apical transthoracic window or the basal transesophageal window. A key parameter of the color Doppler M-mode is the transmitral propagation velocity, the slope of the leading edge of the M-mode derived E-wave. This propagation velocity is significantly less than the velocities measured within the E-wave by pulsed Doppler echocardiography and appears to provide important independent information about left ventricular filling pressures and diastolic function. Furthermore, color M-mode velocities can be processed quantitatively by the Euler equation to yield estimates of the small (< 2 mmHg) pressure gradients between the base and apex during filling, the first time such gradients have been measured noninvasively.
Diastole↗
Mechanical response of an artery using a standard nonlinear solid.
INTRODUCTION: The stress and deformation in an artery are determined from an axisymmetric analysis of thick-walled cylinder with a time-dependent internal pressure. The purpose is to understand how different constitutive, loading, and geometric conditions affect the stress and deformation state within the artery. MATERIALS AND METHODS: The equilibrium, compatibility, and constitutive equations are applied at N discretized points in the arterial wall, in an efficient scheme using Mathcad software on a desktop computer. The constitutive equations are a modification to a standard linear solid, so that one of the linear elements is nonlinear, and so that the 3-D response is anisotropic and dissipates energy only under deviatoric (shearing) stress states. Solution at each successive time increment requires inversion of a 6N by 6N matrix. RESULTS: The model reproduces experimental stress relaxation data with a correlation coefficient of 0.985 and can reproduce quasi-static stress strain data with equal accuracy. Features such as conditioning of the tissue are understood in terms of the time-dependent properties of the tissue. CONCLUSION: The program can produce transient and steady-state responses that closely mimic tissue response. The analysis allows for quick and stable determination of the stress and strain states for a variety of loading conditions.
Arteries↗
Left ventricular function after valve repair for chronic mitral regurgitation: predictive value of preoperative assessment of contractile reserve by exercise echocardiography.
OBJECTIVES: We evaluated the value of preoperative assessment of left ventricular contractile reserve in predicting ventricular function after valve repair for minimally symptomatic mitral regurgitation. BACKGROUND: The optimal timing for operation in minimally symptomatic patients with significant mitral regurgitation is controversial. Accurate preoperative assessment of left ventricular function is difficult, and the ability to predict postoperative function is limited. Previous studies in patients undergoing mitral valve replacement may not be applicable in the present era of valve repair. METHODS: We performed exercise echocardiography in 139 patients with isolated mitral regurgitation and no coronary disease, 74 of whom subsequently underwent uncomplicated valve repair. We measured rest left ventricular end-systolic dimension, end-systolic wall stress and positive first derivative of left ventricular pressure (dP/dt). End-diastolic and end-systolic volumes and ejection fraction were measured preoperatively at rest, immediately after exercise and postoperatively. RESULTS: Ejection fraction decreased postoperatively to 55 +/- 10% from a rest preoperative value of 64 +/- 9% (p < 0.001). Compared with patients with a postoperative ejection fraction > or = (n = 56), patients with postoperative ejection fraction < 50% (n = 18) had a significantly lower preoperative exercise ejection fraction (57 +/- 11% vs. 73 +/- 9%, p < 0.0005), a larger exercise end-systolic volume index (32 +/- 8 vs. 18 +/- 7 cm3/m2, p < 0.0005) and a lower change in ejection fraction with exercise (-4 +/- 8% vs. 9 +/- 10%, p < 0.005). Preoperative rest indexes, including dP/dt, end-systolic wall stress and end-systolic volume index were less predictive, whereas exercise capacity, rest ejection fraction and end-systolic dimension were not predictive of post-repair ejection fraction. An exercise end-systolic volume index > 25 cm3/m2 was the best predictor of postoperative dysfunction, with a sensitivity and specificity of 83%. CONCLUSIONS: In minimally symptomatic patients with mitral regurgitation, latent ventricular dysfunction may be indicated by a limited contractile reserve, manifest at exercise as an inadequate increase in ejection fraction and a larger end-systolic volume. These variables may also be used to predict left ventricular function after repair.
Aged↗
Prediction of right ventricular dysfunction after left ventricular assist device implantation.
BACKGROUND: Right ventricular dysfunction (RVD) significantly affects mortality and morbidity after left ventricular assist device (LVAD) implantation, and its occurrence often is unpredictable. The aim of the present study was to identify predictors of RVD after LVAD implantation. METHODS AND RESULTS: We studied right ventricular (RV) hemodynamics in 28 patients before and after LVAD implantation with a rapid-response thermistor pulmonary artery catheter. Measurements included mean right atrial pressure (RAP), mean pulmonary arterial pressure (PAP), cardiac index, transpulmonary gradient (TPG), pulmonary vascular resistance (PVR), RV end-diastolic and end-systolic volume indexes (EDVI and ESVI, respectively), and RV ejection fraction (RVEF). We regarded patients who had RAP > or = 15 mm Hg at LVAD explantation (n = 8) or who required an RV assist device (n = 3) as the RVD group (n = 11). The other patients were categorized as the RV nondysfunctional group (RVN, n = 17). Before LVAD implantation, the RVD group had larger RV volumes (200 +/- 107 versus 125 +/- 46 mL/m2 for EDVI; 177 +/- 109 versus 104 +/- 48 mL/m2 for ESVI) and higher preload (23 +/- 6 versus 17 +/- 6 mm Hg for RAP) and afterload (20 +/- 9 versus 13 +/- 6 mm Hg for TPG; 5.9 +/- 3.0 versus 3.8 +/- 2.0 Wood units for PVR) than the RVN group (P < .05 for all). RVEF and PAP did not differ significantly. LVAD implantation remarkably improved RV hemodynamics in both groups, decreasing RV volumes, preload, and afterload and increasing RVEF in all patients, but post-LVAD PAP tended to be higher in the RVD group. Multivariate logistic regression analysis revealed that RAP and TPG before LVAD implantation and an acute decrease (delta) in PAP by LVAD were significant predictors of RVD (P < .05). The sensitivity for predicting RVD by a combination of at least two of these three predictors (RAP > or = 20 mm Hg, TPG > or = 16 mm Hg, and delta PAP < or = 10 mm Hg) was 82%, and the specificity was 88%. CONCLUSIONS: Dilated right ventricle with increased RV preload and afterload predisposes to RVD after LVAD implantation. Not only baseline parameters but also the immediate hemodynamic response to the LVAD are predictive, and a combination of these parameters may be useful in predictions of the occurrence of RVD after LVAD implantation.
Adult↗
Resting echocardiographic features of latent left ventricular outflow obstruction in hypertrophic cardiomyopathy.
We determined resting echocardiographic features predictive of latent left ventricular (LV) outflow obstruction in 50 consecutive patients with nonobstructive hypertrophic cardiomyopathy (26 provocable, 24 nonprovocable with amyl nitrite inhalation) to have a better understanding of the pathophysiology of this condition and to identify such patients without pharmacologic provocation. Measurements included wall thickness, type of hypertrophy, LV outflow tract diameter, degree of mitral systolic anterior motion, outflow pressure gradient, and ventricular volume. The direction of the ejection streamline was measured to assess the magnitude of the drag force acting on the mitral valve. Thirteen of 16 patients (81%) with proximal septal bulge were provocable, whereas only 3 of 8 patients (38%) with asymmetric septal hypertrophy and 10 of 26 (38%) with concentric hypertrophy were provocable (p < 0.05). LV outflow tract was significantly narrower and the angle between the ejection flow and the mitral valve was larger in provocable patients. The sensitivity for predicting provocable patients by a combination of a narrow outflow tract (< or = 2 cm) and a large angle (> or = 35 degrees) was 65%, with a specificity of 80% and a positive predictive value of 79%. When these criteria were combined with the presence of septal bulge, the sensitivity was 35%, but the specificity and the positive predictive value were both 100%. Patients with nonobstructive hypertrophic cardiomyopathy with proximal septal bulge, a narrow LV outflow tract, and an oblique angle between the ejection flow and the mitral valve appeared to be predisposed for latent outflow obstruction. These features are consistent with the presence of the large Venturi and drag forces. Thus, the left ventricle, which is capable of increasing both the Venturi and the drog forces on the basis of the morphologic change, contributes to the development of outflow obstruction with amyl nitrite inhalation.
Cardiomyopathy, Hypertrophic↗
Gender and referral for coronary angiography after treadmill thallium testing.
Considerable controversy exists regarding whether women are less likely than men to be referred to coronary angiography after an abnormal noninvasive test. This prospective cohort study analyzed consecutive subjects (2,351 men and 1,318 women) with no prior history of invasive cardiac procedures who were referred for treadmill thallium testing at the Cleveland Clinic Foundation. The primary end point was performance of coronary angiography within 90 days of treadmill thallium testing. A secondary end point was all-cause mortality during 1.8 years of follow-up. Women were less likely than men to undergo coronary angiography (6% vs 14%, odds ratio [OR] 0.42, 95% confidence interval [Cl] 0.33 to 0.54, p < 0.001), but were also less likely to have an abnormal thallium scan (8% vs 29%, p < 0.001). In logistic regression analyses with adjustment for thallium result and age, women were as likely as men to be referred for coronary angiography (adjusted OR 1.00, 95% Cl 0.75 to 1.34, p > 0.9). Women were less likely to have severe coronary disease on angiography (15% vs 30%, p = 0.006). During 1.8 years of follow-up there were 26 deaths (2%) among women and 84 deaths (4%) among men. After adjusting for age, thallium abnormalities, and clinical characteristics in Cox regression analyses, women had a lower mortality rate than men (relative risk 0.58, 95% Cl 0.36 to 0.94, p = 0.03). Thus, gender-related differences in referral for coronary angiography after treadmill thallium testing can be explained by a higher rate of abnormal tests in men. No evidence of a post-test gender bias was detected, but a pretest bias affecting referral to nuclear testing cannot be excluded. Furthermore, women have a lower prevalence of severe coronary disease and a lower adjusted mortality rate.
Aged↗
Plasma volume and its regulatory factors in congestive heart failure after implantation of long-term left ventricular assist devices.
BACKGROUND: Congestive heart failure is associated with blood volume expansion caused by stimulation of the renin-aldosterone system and arginine vasopressin. The use of left ventricular assist devices as bridges to heart transplantation has improved the survival of patients during this critical period. In studying heart failure physiology on support devices, we hypothesized that improvement of cardiac function by a left ventricular assist device is associated with normalization of volume load secondary to normalization of its regulatory substances. METHODS AND RESULTS: We studied 15 patients (13 men, 2 women: age 51 +/- 8 years) with end-stage heart failure who were cardiac transplant candidates eligible for HeartMate implantation. We measured plasma volume and plasma levels of atrial natriuretic peptide, aldosterone, renin, and arginine vasopressin sequentially before HeartMate implantation (baseline), after HeartMate implantation (weeks 4 and 8), and after transplantation. Baseline plasma volume was 123 +/- 20% of normal; it was 122 +/- 22% at week 4 and decreased to 115 +/- 14% at week 8. Atrial natriuretic peptide was 359 +/- 380 pg/mL at baseline, 245 +/- 175 pg/mL at week 4, and 151 +/- 66 pg/mL at week 8. Plasma aldosterone fell from 68 +/- 59 ng/dL at baseline to 17 +/- 16 ng/dL at week 4 (P < .05 versus baseline) and was 32 +/- 50 ng/dL at week 8. Plasma renin activity decreased from 80 +/- 88 ng/dL at baseline to 11 +/- 12 ng/dL at week 4 and was 16 +/- 38 ng/dL at week 8 (both P < .05 versus baseline). Arginine vasopressin fell from 5.0 +/- 4.8 fmol/mL at baseline to 1.1 +/- 0.7 fmol/mL at week 4 and 1.2+/-0.8 fmol/mL at week 8 (both P < .05 versus baseline). CONCLUSIONS: The reduction of plasma renin activity, plasma aldosterone, and arginine vasopressin occurred earlier than the reduction of plasma volume and atrial natriuretic peptide after HeartMate implantation, possibly because of decreased pulmonary congestion and improved renal perfusion. The reduction of atrial natriuretic peptide cannot be responsible for the lack of adequate decrease of plasma volume; its reduction can be taken as a marker of improved cardiac pump function and decreased atrial stretch.
Blood Volume↗
Left ventricular echocardiographic and histologic changes: impact of chronic unloading by an implantable ventricular assist device.
OBJECTIVES: We studied the effects of chronic left ventricular unloading by a ventricular assist device and assessed left ventricular morphologic and histologic changes. BACKGROUND: The implantable left ventricular assist device has been effective as a "bridge" to cardiac transplantation. Although there are reports documenting its circulatory support, little is known about the effects of chronic left ventricular unloading on the heart itself. METHODS: We performed intraoperative transesophageal echocardiography at the insertion and explanation of a HeartMate left ventricular assist device in 19 patients with end-stage heart failure. They were supported by the assist device for 3 to 153 days (mean [+/-SD] 68 +/- 33). Measurements were taken retrospectively to obtain left atrial and ventricular diameters and interventricular septal and posterior wall thicknesses. Histologic examinations were made from the left ventricular myocardial specimens of 15 patients at the times of insertion and explanation for heart transplantation. Insertion and explanation specimens were compared qualitatively (0 to 3 scale) for wavy fibers, contraction band necrosis and fibrosis, with quantitative measurement of minimal myocyte diameter across the nucleus. RESULTS: Left atrial and left ventricular diastolic and systolic diameters decreased immediately after insertion of the left ventricular assist device (from 46 to 35, 63 to 41 and 59 to 36 mm, respectively, all p < 0.001). Left ventricular wall thickness increased from 10 to 14 mm (p < 0.001) for the interventricular septum and from 10 to 13 mm for the posterior wall (p<0.001). No echocardiographic measurements showed significant subsequent changes at the chronic stage. Myocardial histologic findings demonstrated a reduction in myocyte damage (from 1.9 to 0.5, p<0.001, for wavy fiber and from 1.3 to 0.2, p<0.01, for contraction band necrosis) and an increase in fibrosis (from 1.3 to 1.9, p<0.05), but without significant change in myocyte diameter (from 15.6 to 16.8 micrometer, p=0.065). CONCLUSIONS: Left ventricular unloading with the implantable assist device induces an immediate increase in wall thickness, consistent with the reduction in chamber size, thereby decreasing wall stress. Chronic unloading allows myocardial healing and fibrosis without evidence for ongoing myocyte damage or atrophy. Left ventricular assist device insertion may have a role in "resting" the ventricle for selected patients with heart failure.
Adult↗
Dynamic magnetic resonance imaging assessment of the effect of ventricular wall curvature on regional function in hypertrophic cardiomyopathy.
We hypothesized that contraction within the ventricular septum in hypertrophic cardiomyopathy (HC) may be related to its abnormal morphology because ventricular wall stress is related to wall curvature by the Laplace equation. To test this, we studied 17 HC patients with various septal morphologies using dynamic magnetic resonance imaging techniques. Short- and long-axis curvatures of the basal septal and basal lateral walls were determined on cine images as the reciprocal of the radius of the arc best fit to the endocardial contour, which was negative if the wall was convex to the cavity of the left ventricle. Endocardial and epicardial intramyocardial circumferential shortening (% circumferential shortening) was measured in the septal and lateral walls on basal short-axis myocardial tagging images. Septal walls were flatter in the short-axis plane and more convex toward the left ventricular cavity in the long-axis plane than lateral walls, as indicated by smaller short- and long-axis curvatures. Septal percent circumferential shortening was significantly lower than the lateral percent circumferential shortening, suggesting reduced septal contraction. Endocardial and epicardial percent circumferential shortening showed significant positive correlations with wall curvatures. Multiple stepwise linear regression analysis revealed that both short- and long-axis curvatures significantly contributed to percent circumferential shortening (r=0.87 for endocardial and r=0.70 for epicardial, both p<0.0001). In conclusion, wall curvature is related to wall function in HC; the more convex toward the left ventricular cavity the wall is, the less it contracts. Reduced contraction of the septum in HC may be partly due to its abnormal curvature.
Cardiomyopathy, Hypertrophic↗
Impact of wall constraint on velocity distribution in proximal flow convergence zone. Implications for color Doppler quantification of mitral regurgitation.
OBJECTIVES: This study sought to elevate the effect of proximal flow constraint induced by the left ventricular wall on the accuracy of calculated flow rates and to assess a possible correction factor to adjust the proximal convergence angle. We further defined under which hydrodynamic and geometric conditions it is necessary to apply the corrected convergence angle. BACKGROUND: The proximal flow convergence method has been proposed as a new approach to quantify valvular regurgitation. However, significant overestimation of the calculated regurgitant flow rate has been reported, particularly in patients with mitral valve prolapse and severe mitral regurgitation. METHODS: We used an in vitro flow model and induced various degrees of proximal flow constraint. The accuracy of the proposed convergence angle formula, alpha = tau + 2 tan-1 d/r (d = wall distance; r = isovelocity radius) was tested in vitro and in a three-dimensional numerical simulation. RESULTS: With a constraining wall near the orifice, overstimulation of regurgitant flow rates was noted and was most significant with the constraining wall positioned closest to the orifice (calculated flow rate [Qc]/true flow rate [Qo] = 1.85 +/- 0.55 [mean +/- SD]). These findings were similar to the results of the numerical simulation. Applying the correction factor nearly completely eliminated the overestimation of the calculated flow rates (cQc), with cQc/Qo = 1.13 +/- 0.25. CONCLUSIONS: In the presence of a constraining wall, significant overestimation of calculated flow rates is observed when hemispheric symmetry of the flow field is assumed. In this situation, it is necessary to apply the corrected convergence angle formula to improve the accuracy of the proximal flow convergence method.
Bias↗
Acute and long-term effects of thrombolysis after anterior wall acute myocardial infarction with serial assessment of infarct expansion and late ventricular remodeling.
This study investigates the impact of thrombolysis on infarct expansion and subsequent left ventricular (LV) remodeling in patients with anterior wall acute myocardial infarction (AMI). We evaluated 51 consecutive patients (24 treated with thrombolysis) with anterior wall AMI by 2-dimensional echocardiography in the following sequence: days 1, 2, 3, and 7, after 3 and 6 weeks, and after 3, 6, and 12 months. LV end-diastolic and end-systolic volume indexes were determined from apical 2- and 4-chamber views using Simpson's biplane formula. Infarct and total LV perimeters were determined in the same views and their ratio expressed as infarct percentage. Infarct expansion was defined as: (1) an increase in infarct percentage and total perimeter >5% on days 2 to 3 in either of the views, or (2) initial infarct percentage >50% with an increase in total perimeter >5% on days 2 to 3. Coronary angiography was performed in 43 patients before discharge, and patency of the infarct-related artery was assessed using Thrombolysis in Myocardial Infarction trial criteria. Infarct expansion was detected in 23 patients. Infarct perimeter steadily decreased in patients with versus without thrombolysis and in patients with patent versus occluded infarct-related arteries. Furthermore, by logistic regression, thrombolysis (p = 0.007) and potency of the infarct-related artery (p = 0.02) were strong negative predictors of expansion, whereas initial infarct perimeter (p = 0.009) was directly associated with subsequent expansion. End-systolic volume index was higher in patients with expansion from day 1 (p = 0.003) through the end of the study (p = 0.021), and end-diastolic volume index was higher in these patients from day 2 (p = 0.012) through 12 months (p = 0.015). Thus thrombolysis, initial infarct size, and infarct-related artery patency are major predictors of infarct expansion after anterior wall AMI.
Confounding Factors, Epidemiologic↗
Serial assessment of left ventricular chamber stiffness after acute myocardial infarction.
Left ventricular (LV) systolic function after acute myocardial infarction (AMI) has been the subject of detailed studies during the last decade, but diastolic phenomena during and after AMI are less well understood. Recently, it has been shown that early filling deceleration time accurately predicted LV chamber stiffness in an experimental model. To assess changes of LV stiffness after AMI, we studied 116 consecutive patients with 2-dimensional and Doppler echocardiographic examinations 1, 2, 3, 7, 21, and 42 days after AMI. Coronary angiography was performed in 101 patients. For the entire study group, deceleration time decreased nonsignificantly on day 2 and subsequently increased on days 3 (p = 0.001) and 7 (p = 0.036), returning toward initial values afterward. Deceleration time was shorter in large (peak creatine kinase level >1,000 U/L) versus small infarcts (p = 0.0008) and in patients with anterior versus inferior AMI (p = 0.02); there was no difference between patients with good and poor (< or = 45%) ejection fraction. These data indicate that increased LV stiffness can be detected 24 to 48 hours after AMI, but returns to normal within several days. Chamber stiffness is higher in large and anterior infarcts, but appears to be independent of LV systolic function.
Aged↗
Behavioral deficits induced by bingelike exposure to alcohol in neonatal rats: importance of developmental timing and number of episodes.
The importance of the timing and number of episodes of bingelike alcohol exposure in neonatal rats on subsequent behavioral outcomes was evaluated with a parallel bar task and a spatial conditional alternation task. Different groups of Sprague-Dawley rat pups were exposed to alcohol delivered via artificial rearing procedures either on postnatal Days (PD) 4 and 5, on PD 8 and 9, or on both PD 4/5 and 8/9 (Combined), producing daily peak blood alcohol concentrations around 400 mg/dl. Controls included an artificially reared group and a normally reared group. Exposure during PD 4/5 produced significantly more severe motor deficits and significantly more severe reductions in cerebellar and brainstem weights than did exposure on PD 8/9. Combined exposure produced greater deficits on these measures than either of the limited exposures. Significant deficits in the acquisition rates for conditional alternation were found only with the Combined exposure, although both the PD 8/9 and Combined groups committed significantly more within-trial errors. All three alcohol treatments produced significant and comparable reductions in forebrain weight. The type and severity of behavioral and neural deficits induced by neonatal bingelike alcohol exposure depend on the timing and number of exposures.
Alcoholic Intoxication↗