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Why does C-reactive protein increase in non-ST elevation acute coronary syndromes? Role of myocardial damage.

INTRODUCTION: C-reactive protein is an important prognostic indicator for early risk stratification in patients with an acute coronary syndrome. The mechanisms underlying the elevation of C-reactive protein in these patients have not been fully understood. We studied the factors related to the increase of this acute-phase reactant. METHODS AND RESULTS: Within a single-centre registry, 419 consecutive patients admitted for a non-ST elevation acute coronary syndrome were studied. Serum high sensitivity C-reactive protein was measured late (median 3 days) after admission. Clinical, electrocardiographic, biochemical and angiographic variables were recorded. In the multivariate analysis, an increased C-reactive protein (n=162) was related to high levels of troponin I (OR 2.5 (1.6-4) P<0.001) and to a Killip class>1 at presentation (OR 2.9 (1.6-5.4) P<0.001). The coronary angiographic characteristics were not related to C-reactive protein. Finally, in 52 patients with no previous heart disease in whom regional dysfunction was quantified by left ventriculography the presence of a significant (>6 chords) regional dysfunction was significantly related to C-reactive protein (OR 5.1 (1.7-15.3) P=0.006) CONCLUSION: Our results indicate that in acute coronary syndromes elevated levels of C-reactive protein late after admission are mainly related to clinical, biochemical and angiographic evidences of myocardial damage. The prognostic utility of this parameter could be in part explained by its relationship with a major regional dysfunction.

Acute Disease↗

H-2-incompatible bone marrow chimeras produce donor-H-2-restricted Ly-2 suppressor T-cell factor(s).

To study adaptive-differentiation phenomena of T lymphocytes, suppressor T-cell factors (TsF) produced by Ly-2+ splenic T cells from fully allogeneic mouse bone marrow chimeras were analyzed. AKR mice irradiated and reconstituted with B10 marrow cells (B10----AKR chimeras) produced an Ly-2+ TsF after hyperimmunization with sheep erythrocytes. The TsF suppressed primary antibody responses (to sheep erythrocytes) generated with spleen cells of mice of H-2b haplotype but not those of H-2k haplotype. Thus, this suppressor factor was donor-H-2-restricted. The immunoglobulin heavy chain variable region gene (Igh-V)-restricting element was not involved in this form of suppression. Similar results were obtained when TsF from B6----BALB/c and BALB/c----B6 chimeras were analyzed. The TsF from B10----AKR chimeras suppressed responses of B10.A(3R) and B10.A(5R) mice but not those of B10.A(4R). This finding showed that identity between the factor-producing cells and target spleen cells is required on the left-hand side of the E beta locus of the H-2 region and that the putative I-Jb locus is not involved in this form of suppression. The present results support the postulate that post-thymic differentiation in the presence of continued or repeated stimulation with antigen and donor-derived antigen-presenting cells generates donor-H-2-restricted T-cell clones that may predominate within the repertoire of the specific antigen being presented.

Alleles↗

Modification of regional myocardial performance caused by blood withdrawal and infusion in acute ischaemic canine heart.

The effect of changes in preload on regional myocardial motion in acute ischaemia was examined by miniature ultrasonic gauges after left anterior descending coronary artery occlusion in eight open chest dogs with the pericardium preserved. Left ventricular end-diastolic pressure was varied by blood withdrawal and infusion. When preload changed, isovolumetric shortening in the non-ischaemic region was inversely related to that in the ischaemic region. When preload decreased, stroke volume decreased and was accompanied by a decrease in end-diastolic length and ejection shortening in the non-ischaemic region together with an increase in isovolumetric bulging in the ischaemic region. When preload increased, these variables changed in opposite directions. These results indicate that in acute ischaemia: (1) changes in isovolumetric shortening in the non-ischaemic and ischaemic regions were related with each other when the level of volume expansion varied, and suggest that; (2) stroke volume is affected by end-diastolic length, ejection shortening in the non-ischaemic region and isovolumetric bulging in the ischemic region.

Animals↗

Effects of permanent dual chamber pacing on myocardial perfusion in symptomatic hypertrophic cardiomyopathy.

OBJECTIVE: Angina and the presence of myocardial ischaemia are common in hypertrophic cardiomyopathy. Dual chamber pacing results in clinical improvement in these patients. This study evaluates the effects of permanent dual chamber pacing on absolute regional myocardial perfusion and perfusion reserve. SETTING: University hospital. PATIENTS AND DESIGN: Six patients with hypertrophic cardiomyopathy and severe symptoms of angina received a dual chamber pacemaker. Absolute myocardial regional perfusion and perfusion reserve (dipyridamole 0.56 mg/kg) were measured by dynamic positron emission tomography with 13N-ammonia both during sinus rhythm and 3 months after pacemaker insertion. Results were compared with those from 28 healthy volunteers. RESULTS: Pacing resulted in a reduction of anginal complaints and a reduction in intraventricular pressure gradient from 65 (SD 30) mm Hg to 19 (10) mm Hg. During sinus rhythm, baseline perfusion was higher in patients with hypertrophic cardiomyopathy than controls (184 (31) v 106 (26) ml/min/100 g, P < 0.01), and perfusion reserve was lower (1.6 (0.4) v 2.8 (1.0), P < 0.05). During pacing myocardial perfusion decreased to 130 (27) ml/min/100 g (P < 0.05), with variable responses in terms of perfusion reserve. Pacing caused a redistribution of myocardial stress perfusion and perfusion reserve. The coefficient of regional variation of myocardial stress perfusion decreased from 19.7 (7.0)% to 14.6 (3.9)% during pacing (12.9 (3.8)% in controls, P < 0.01). The coefficient of regional variation of perfusion reserve decreased from 16.7 (6.6)% to 11.4 (2.6)% during pacing (9.8 (4.1)% in controls, P < 0.01). CONCLUSIONS: Pacing caused a decrease of resting left ventricular myocardial blood flow and blood flow during pharmacologically induced coronary vasodilatation. Although global perfusion reserve remained unchanged, myocardial perfusion reserve became more homogeneously distributed.

Adult↗

The effects of unilateral forced nostril breathing on the heart.

Three experiments are described that employ impedance cardiography to monitor the effects of unilateral forced nostril breathing (UFNB) on the heart. Experiment 1 includes 7 subjects (4 males, 3 females) with a respiratory rate of 6 breaths/min (BPM). Experiment 2 includes 16 trials using one subject to examine the intraindividual variability, at 6 BPM. Experiment 3 includes 10 trials with the same subject in experiment 2, but with a respiratory rate of 2-3 breaths/s. This rapid rate of respiration is a yogic breathing technique called "breath of fire" or "kapalabhatti" and employs a very shallow but rapid breath in which the abdominal region acts like a bellows. All 3 experiments demonstrated that right UFNB increases heart rate (HR) compared to left. Experiment 1 gave 7 negative slopes, or lowering in HR with left nostril breathing and 7 positive slopes, or increases in HR with right nostril breathing, p = .001. The second and third experiments showed differences in HR means in which right UFNB increases HR more than left, p = .013, p = .001, respectively. In experiment 2 stroke volume was higher with left UFNB, p = .045, compensating for lower HR. Left UFNB increased end diastolic volume as measured in both experiments 1 and 2, p = .006, p = .001, respectively. These results demonstrate a unique unilateral effect on sympathetic stimulation of the heart that may have therapeutic value.

Activity Cycles↗

[Left ventricular myocardial geometry in arterial hypertension in patients with stenosing cerebral atherosclerosis].

The aim of the study was to define more exactly correlations between circulatory disturbances in the common carotid artery (CCA) basin, and hemodynamic disturbances and structural myocardial remodeling in patients suffering from arterial hypertension (AH) and cerebral atherosclerosis. The subjects were 83 patients evaluated by means of carotid arterial Doppler ultrasonography and echoCG; the variables of central homodynamic were measured as well. The study revealed that patients with AH and moderate CCA stenosis displayed hyperkinetic hemodynamic type more often than patients with severe CCA stenosis, of whom hypodynamic hemodynamic type was more typical. Left ventricular (LV) myocardial remodeling was more frequent in the latter group of patients; asymmetric LV hypertrophy prevailed. The study shows that the process of remodeling, caused by dissociation between central and regional hemodynamics, develops together with the progress of atherosclerotic arterial lesion.

Cardiomyopathy, Hypertrophic, Familial↗

Factors related to end-systolic volume are important determinants of peak early diastolic transmitral flow velocity.

BACKGROUND: Three important determinants of left ventricular (LV) peak early diastolic filling rate, which is related directly to the magnitude of the transmitral pressure difference, are the rate of LV isovolumic pressure fall (T1/2), left atrial (LA) pressure at mitral valve opening (X1), and end-systolic volume (ESV). METHODS AND RESULTS: To delineate the relative degrees to which these factors contribute to the magnitude of peak early diastolic filling rate, we measured LA and regional intra-LV pressures with micromanometers, LV volume with contrast angiography, and peak transmitral flow velocity (E) with transesophageal Doppler echocardiography in 16 anesthetized closed-chest dogs. E did not correlate significantly with either X1 (r = -0.255) or T1/2 (r = -0.281). Multivariate analysis, with E entered as the dependent variable and X1 and T1/2 as independent variables, also failed to reach significance (R = 0.310). E correlated significantly with ESV (r = -0.633, p less than 0.009). Using multivariate analysis, the major determinants of ESV were found to be LV contractility (+dP/dt), afterload (aortic diastolic pressure, AOdias), and preload (end-diastolic volume, EDV) (R = 0.848, p less than 0.001). E correlated significantly with two of the determinants of ESV (+dP/dt and AOdias) (R = 0.906, p less than 0.001); however, the addition of EDV did not significantly improve the multivariate relation (R = 0.911). To determine whether X1 or T1/2 would add significantly to the above multivariate relation, these factors were entered individually along with +dP/dt and AOdias as third independent variables. Neither the addition of X1 (R = 0.906) or T1/2 (R = 0.926) resulted in a significant improvement in the prediction of E. CONCLUSIONS: Our observations confirm the importance of factors related to ESV as important determinants of early diastolic filling. These relations suggest that the process of early diastolic function is intimately related to systolic function.

Animals↗

The effect of dexmedetomidine on nutrient organ blood flow.

The alpha 2-adrenergic agonist dexmedetomidine decreases not only heart rate, myocardial contractility, and oxygen demand, but also cardiac output (Q). To investigate whether this reduction in Q could critically impair perfusion of individual organs, we studied the effect of dexmedetomidine on nutrient blood flow to the heart, brain, kidney, spleen, skin, intestine, liver, and arteriovenous anastomoses using the radioactive microsphere technique. Studies were conducted in 14 dogs with an open chest and anesthetized with either chloralose/urethane (CU) or fentanyl/halothane (FH), to create different baseline conditions. Hemodynamic variables, organ blood flow, arterial and mixed venous oxygen, and lactate content were measured before and after administration of 0.1, 1, and 10 micrograms/kg dexmedetomidine intravenously (IV). After 10 micrograms/kg dexmedetomidine Q decreased in both groups by 50%. The decrease in blood flow varied greatly between the organs. While flow through arteriovenous anastomoses and skin decreased by 70% to 90%, renal blood flow decreased by 30%, cerebral blood flow only when baseline blood flow was high (FH dogs), and left ventricular blood flow only in the CU group, where the largest decrease in hemodynamic variables occurred. Oxygen consumption decreased only in CU dogs, but so did arterial lactate levels. These data indicate that dexmedetomidine causes considerable redistribution of Q, predominantly reducing blood flow to less vital organs and shunt flow.

Adrenergic alpha-Agonists↗

Quality of medical care and excess mortality in older patients with mental disorders.

BACKGROUND: This study investigated whether differences in quality of medical care might explain a portion of the excess mortality associated with mental disorders in the year after myocardial infarction. METHODS: This study examined a national cohort of 88 241 Medicare patients 65 years and older who were hospitalized for clinically confirmed acute myocardial infarction. Proportional hazard models compared the association between mental disorders and mortality before and after adjusting 5 established quality indicators: reperfusion, aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, and smoking cessation counseling. All models adjusted for eligibility for each procedure, demographic characteristics, cardiac risk factors and history, admission characteristics, left ventricular function, hospital characteristics, and regional factors. RESULTS: After adjusting for the potential confounding factors, presence of any mental disorder was associated with a 19% increase in 1-year risk of mortality (hazard ratios [HR], 1.19; 95% confidence interval [CI], 1.04-1.36). After adding the 5 quality measures to the model, the association was no longer significant (HR, 1.10; 95% CI, 0.96-1.26). Similarly, while schizophrenia (HR, 1.34; 95% CI, 1.01-1.67) and major affective disorders (HR, 1.11; 95% CI, 1.02-1.20) were each initially associated with increased mortality, after adding the quality variables, neither schizophrenia (HR, 1.23; 95% CI, 0.86-1.60) nor major affective disorder (HR, 1.05; 95% CI, 0.87-1.23) remained a significant predictor. CONCLUSIONS: Deficits in quality of medical care seemed to explain a substantial portion of the excess mortality experienced by patients with mental disorders after myocardial infarction. The study suggests the potential importance of improving these patients' medical care as a step toward reducing their excess mortality.

Adrenergic beta-Antagonists↗

Quantification of the contractile response to injury: assessment of the work-length relationship in the intact heart.

We used a sonomicrometric determination of ventricular dimension to examine the effect of ischemia and reperfusion on the work-length relationship in the intact heart to develop a useful and precise variable of ventricular contractile response to injury. Twenty anesthetized dogs were instrumented with epicardial ultrasonic dimension transducers to record right ventricular free wall chord length and left ventricular minor-axis length, micromanometers to record ventricular pressures, and an electromagnetic probe to record pulmonary arterial (n = 8) or aortic (n = 7) flow. Dogs were subjected to either 20 min (n = 7) or 30 min (n = 13) of global cardiac ischemia supported by cardiopulmonary bypass. Data were acquired over a range of end-diastolic volumes produced by transient (5 to 10 sec) vena caval occlusion before and after ischemia. In both ventricles, systolic epicardial dimensional shortening correlated with flow probe-measured stroke volume (mean r = .969) and regional stroke work calculated as the integral of instantaneous ventricular pressure and epicardial dimension correlated with measured global stroke work (mean r = .960), confirming the validity of dimensional measurements. Regression analysis demonstrated a highly linear relationship between calculated regional stroke work and end-diastolic length in the right ventricle (mean r = .973) and left ventricle (mean r = .967), quantifiable by a slope (Mw) and x intercept (Lw). Change in afterload produced by pulmonary arterial or aortic constriction resulted in no significant changes in Mw or Lw in either ventricle. Ischemia and reperfusion decreased Mw and shifted Lw to the right in both ventricles. The decrease in Mw with 30 min ischemia exceeded the decrease with 20 min ischemia by 29% in the right ventricle and by 32% in the left (p less than .04) with up to 1 hr of reperfusion. Changes in Lw were not related to severity of injury. After ischemia, infusion of calcium increased Mw by 177% in the right ventricle and by 67% in the left (p less than .03) without significant changes in Lw. Independent of load conditions, the slope Mw, of the linear stroke work vs end-diastolic length relationship is a valid and precise index of right and left ventricular contractile response to global ischemia in the intact circulation. This variable may be useful in evaluating therapies designed to limit myocardial injury and enhance ventricular functional performance.

Animals↗

Regional fibre stress-fibre strain area as an estimate of regional blood flow and oxygen demand in the canine heart.

1. In the present study the relation between regional left ventricular contractile work, regional myocardial blood flow and oxygen uptake was assessed during asynchronous electrical activation. 2. In analogy to the use of the pressure-volume area for the estimation of global oxygen demand, the fibre stress-fibre strain area, as assessed regionally, was used to estimate regional oxygen demand. The more often used relation between the pressure-sarcomere length area and regional oxygen demand was also assessed. 3. Experiments were performed in six anaesthetized dogs with open chests. Regional differences in mechanical work were generated by asynchronous electrical activation of the myocardial wall. The ventricles were paced from the right atrium, the left ventricular free wall, the left ventricular apex or the right ventricular outflow tract. Regional fibre strain was measured at the epicardial anterior left ventricular free wall with a two-dimensional video technique. 4. Regional fibre stress was estimated from left ventricular pressure, the ratio of left ventricular cavity volume to wall volume, and regional deformation. Total mechanical power (TMP) was calculated from the fibre stress-fibre strain area (SSA) and the duration of the cardiac cycle (tcycle) using the equation: TMP = SSA/tcycle. Regional myocardial blood flow was measured with radioactive microspheres. Regional oxygen uptake was estimated from regional myocardial blood flow values and arteriovenous differences in oxygen content. 5. During asynchronous electrical activation, total mechanical power, pressure-sarcomere length area, myocardial blood flow and oxygen uptake were significantly lower in early than in late activated regions (P < 0.05). 6. Within the experiments, the correlation between the pressure-sarcomere length area and regional oxygen uptake was not significantly lower than the one between total mechanical power (TMP) and regional oxygen uptake (VO2,reg). However, variability of this relation between the experiments was less for total mechanical power. Pooling all experimental data revealed: VO2,reg = k1 TMP+k2, with k1 = 4.94 +/- 0.31 mol J-1 k2 = 24.2 +/- 1.9 mmol m-3 s-1 (means +/- standard error of the estimate). 7. This relation is in quantitative agreement with previously reported relations between the pressure-volume area and global oxygen demand. The results indicate that asynchronous electrical activation causes a redistribution of mechanical work and oxygen demand and that regional total mechanical power is a better and more general estimate of regional oxygen demand than the regional pressure-sarcomere length area.

Animals↗

Brain activations in schizophrenia during a graded memory task studied with functional neuroimaging.

BACKGROUND: Functional neuroimaging experiments have implicated prefrontal cortex (PFC) in memory processes. Several studies of schizophrenic patients have shown failure of activation in the dorsolateral region of PFC (DLPFC). We used a graded memory challenge to characterize functional neuroanatomical differences between schizophrenic and control subjects. The graded manipulation of task demands enabled us to assess group differences in the context of normal and abnormal psychological task performance. METHODS: Memory-related activity was assessed using positron emission tomography in schizophrenic patients and age-matched controls during performance of a graded memory task. Subjects underwent scanning while learning and recalling word lists of variable length. RESULTS: We used a model that assessed linear and nonlinear effects of memory load. Nonlinear group differences in DLPFC activation were observed. Controls showed a steepening slope of DLPFC increase as task demands increased. By contrast, schizophrenic subjects showed initial DLPFC increases that fell away with increasing memory load. The DLPFC response in schizophrenic subjects was closely related to measured task performance. In addition, schizophrenic subjects failed to show task-related decreases in activity in the left superior temporal and inferior parietal gyrus. CONCLUSIONS: Patients with schizophrenia showed a failure in DLPFC activation only in the face of diminished performance measures, suggesting that a full characterization of task-related changes in DLPFC activation must consider performance levels. However, striking failures of deactivation in superior temporal and inferior parietal regions were independent of task performance, possibly reflecting a core abnormality of the condition.

Adult↗

Determination of lumbar muscular activity in helicopter pilots: a new approach.

BACKGROUND: Discomfort in the lumbar region is a frequent complaint of helicopter pilots. Two factors that helicopter crewmembers relate to back pain are exposure to vibration and poor posture during flight, because during flight the seat and controls force the pilot to adopt an asymmetric posture. Repeated exposure to these adverse flight conditions could cause pathological changes in the spine. The purpose of this study was to compare right and left sided lumbar muscular activity in helicopter pilots under real flight conditions, using surface electromyography (SEMG) to demonstrate the effects of asymmetrical posture on the musculoskeletal system. An attempt was also made to correlate lumbar muscular activity with environmental factors and such variables as type of flight, type of helicopter, duration of flight, age, physical fitness, and height. METHODS: Right- and left-sided lumbar electrical activity were measured using two-channel SEMG during 35 flights in 2 types of helicopter and a cockpit mock-up. RESULTS: There was a statistically significant increase in right-sided lumbar activity when related to the duration of flight. CONCLUSIONS: The data showed that when the pilot used the manual controls during flight, he did not maintain a symmetrical posture and contracted one side more than the other. We think the relationship between the greatest right-sided contraction and flight duration is due to maintaining an asymmetric posture over a long period. We also noted a tendency towards greater right lumbar musculature activity in older pilots.

Adult↗

Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size.

OBJECTIVES: We sought to identify advantages of contrast-enhanced magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling. BACKGROUND: Although sequential measurements of ventricular volumes, internal dimensions, and total ventricular mass have provided important insights into postinfarction left ventricular remodeling, it has not been possible to define serial, directionally opposite changes in resorption of infarcted tissue and hypertrophy of viable myocardium and effects of these changes on commonly used indices of remodeling. METHODS: Using gadolinium-enhanced MRI, the time course and geometry of changes in infarcted and noninfarcted regions were assessed serially in dogs subjected to coronary occlusion for 45 min, 90 min, or permanently. RESULTS: Infarct mass decreased progressively between three days and four to eight weeks following coronary occlusion; terminal values averaged 24 +/- 3% of those at three days. Radial infarct thickness also decreased progressively, whereas changes in circumferential and longitudinal extent of infarction were variable. The ability to define the circumferential endocardial and epicardial extents of infarction allowed radial thinning without epicardial expansion to be distinguished from true infarct expansion. The mass of noninfarcted myocardium increased by 15 +/- 2% following 90-min or permanent occlusion. However, the time course of growth of noninfarcted myocardium differed systematically from that of infarct resorption. Measurements of total ventricular mass frequently failed to reflect concurrent changes in infarcted and noninfarcted regions. Reperfusion accelerated infarct resorption. Histologic reductions in nucleus-to-cytoplasm ratios corresponded with increases in noninfarcted ventricular mass. CONCLUSIONS: Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.

Animals↗

Differential ventricular ischemic injury: an experimental model of right ventricular failure with a variable degree of left ventricular dysfunction.

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.

Adenine Nucleotides↗

Effects and interactions of nitrous oxide, myocardial ischemia, and reperfusion on left ventricular diastolic function.

The effects of nitrous oxide on left ventricular diastolic function and its potential interactions with ischemia-induced diastolic dysfunction have not been described. Accordingly, we investigated the effects of nitrous oxide in ischemic and remote nonischemic myocardium during baseline, 90 min severe low-flow myocardial ischemia (systolic bulge), and reperfusion in 11 open-chest dogs. Anesthesia was maintained with fentanyl infusion (2 micrograms.kg-1.min-1), animals were ventilated with 60% nitrogen in oxygen, and hemodynamic variables were recorded prior to and after the replacement of nitrogen by 60% nitrous oxide. During baseline, nitrous oxide moderately increased chamber stiffness (+ 10%), myocardial stiffness (+33%), and unstressed length (+4%) and decreased the peak lengthening rate (-10%). Moreover, nitrous oxide decreased regional contractility during baseline (-12% at apex, -8% at base) as well as in nonischemic myocardium during myocardial ischemia (-9%) and reperfusion (-8%). However, nitrous oxide did not modify ischemia-induced systolic or diastolic dysfunction in ischemic myocardium during ischemia and reperfusion. Myocardial ischemia (+45%) and reperfusion (+57%) were associated with an increase in myocardial stiffness of nonischemic myocardium regardless of the anesthetic technique used. This study is the first to demonstrate that in addition to its well established negative inotropic effect, nitrous oxide affects regional diastolic function.

Anesthetics, Inhalation↗

Computed tomography measurements of brain density in Schizophrenia.

Although previous studies have reported differences in computed tomography (CT) scan attenuation values between patients with schizophrenia and controls, interpretation of these findings has been hindered by methodological shortcomings such as the failure to control for head size, scanner calibration differences, and other confounding variables. In the present study of CT attenuation values in multiple brain regions in 20 patients with chronic schizophrenia and an equal number of age- and sex-matched normal subjects we controlled for head size and normalized the attenuation values for each scan to an internal standard. No significant differences emerged between the patients with schizophrenia and the controls. However, in the controls only, the mean density of white matter in the left frontal area was significantly higher (t = -2.83, p = 0.01) than that in the right. The results, although possibly suggestive of deviant lateralization in schizophrenia, raise questions about the sensitivity and validity of regional CT attenuation values in detecting subtle anatomic abnormalities in patients with this illness.

Adult↗

Developmental dyslexia.

Developmental dyslexia, or specific reading disability, is a disorder in which children with normal intelligence and sensory abilities show learning deficits for reading. Substantial evidence has established its biological origin and the preponderance of phonological disorders even though important phenotypic variability and comorbidity have been recorded. Diverse theories have been proposed to account for the cognitive and neurological aspects of dyslexia. Findings of genetic studies show that different loci affect specific reading disability although a direct relation has not been established between symptoms and a given genomic locus. In both children and adults with dyslexia, results of neuroimaging studies suggest defective activity and abnormal connectivity between regions crucial for language functions--eg, the left fusiform gyrus for reading--and changes in brain activity associated with performance improvement after various remedial interventions.

Adult↗