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Utilizing a model effective interaction for [sup 3]He atoms in a [sup 4]He film that consists of two-body potentials, phonon exchange, and ripplon exchange, we calculate the [sup 3]He equation of state. The energy and pressure are determined in the Hartree-Fock approximation allowing for [sup 3]He population of multiple discrete transverse states. In this work we use a two-state approximation and self-consistently solve the matrix Dyson equation for the 2[times]2 self-energy matrix. We find that the many-body self-energy decreases the gap between the lowest and first excited transverse state from the noninteracting model but that no clear evidence exists for a self-bound state.

Increasing experience with the arterial switch procedure has revealed that, in some instances, obstruction of the newly created sub-pulmonary outflow tract is a major problem. In this study, we examined the right ventricular outflow tract in 51 specimens of complete transposition, 18 of which were associated with a ventricular septal defect. We focussed our attention on the musculature which made up the outflow region and considered variations from that found in the normal right ventricle. Our gross observations showed differences in morphology which produced a sharper angulation between inflow and outflow when compared to the normal. Discrete outflow obstruction was found in 11 hearts (8 with ventricular septal defect and 3 with an intact ventricular septum). The obstruction was due to deviation of the outlet septum in 5, and anomalous muscle bundle in 1, hypertrophy of septomarginal and septoparietal trabeculations in 3 and circumferential infundibular hypertrophy in 2 hearts. Coexisting obstruction of the left ventricular outflow was present in 3 hearts. The anatomical substrates of discrete obstruction should be identified by preoperative cross-sectional echocardiography and/or angiography. Modifications in surgical techniques or radical resection of the obstructing musculature could then be performed to avoid the problem of subpulmonary obstruction after the arterial switch procedure.

Background: Air pollution is associated with total mortality. This association may be confounded by uncontrolled time-varying risk factors such as influenza epidemics. Methods: We analyzed independent data on influenza epidemics from 7 European cities that also had data on mortality associated with particulates (PM10). We used 10 methods to control for epidemics (5 derived from influenza data and 5 from respiratory mortality series) and compared those results with analyses that did not control for these epidemics. Results: Adjustment for influenza epidemics increased the PM10 effect estimate in most cases (% change in the pooled regression coefficient: -1.9 to 38.9 for total mortality and 1.3 to 25.5 for cardiovascular mortality). A 10-mug/m(3) increase in PM10 concentrations (lag 0-1) was associated with a 0.48% (95% confidence interval = 0.27-0.70%) increase in daily mortality unadjusted for influenza epidemics, whereas under the various methods to control for epidemics the increase ranged from 0.45% (0.26-0.69%) to 0.67% (0.46-0.89%). The corresponding figures for cardiovascular mortality were 0.85% (0.53-1.18%) with no adjustment and from 0.86% (0.53-1.19%) to 1.06% (0.74-1.39%) with the methods of control. Conclusions: The association between air pollution and mortality is not weakened by control for influenza epidemic irrespective of the method used. To adjust for influenza epidemics, one can use methods based on respiratory mortality counts instead of counts of influenza cases if the latter are not available. However, adjustment for influenza by any method tested did not markedly alter the air pollution effect estimate.

Short-term changes in ambient particulate matter with aerodynamic diameters < 10 mum (PM10) have been associated with short-term fluctuations in mortality or morbidity in many studies. In this study, we tested whether those deaths are just advanced by a few days or weeks using a multicity hierarchical modeling approach for all-cause, respiratory, and cardiovascular deaths, for all ages and stratifying by age groups, within the APHEA-2 (Air Pollution and Health: A European Approach) project. We fit a Poisson regression and used an unconstrained distributed lag to model the effect of PM10 exposure on deaths up to 40 days after the exposure. In baseline models using PM10 the day of and day before the death, we found that the overall PM10 effect (per 10 mug/m(3)) was 0.74% [95% confidence interval (95% CI), -0.17 to 1.66] for respiratory deaths and 0.69% (95% CL 0.31-1.08) for cardiovascular deaths. In unrestricted distributed lag models, the effect estimates increased to 4.2% (95% Cl, 1.08-7.42) for respiratory deaths and to 1.97% (95% Cl, 1.38-2.55) for cardiovascular deaths. Our study confirms that most of the effect of air pollution is not simply advanced by a few weeks and that effects persist for more than a month after exposure. The effect size estimate for PM10 doubles when we considered longer-term effects for all deaths and for cardiovascular deaths and becomes five times higher for respiratory deaths. We found similar effects when stratifying by age groups. These larger effects are important for risk assessment.

Current nomenclature for the AV junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with anteroposterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, whereas the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and AV nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and from the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions and establish the principles of this new nomenclature.

Current nomenclature for atrioventricular junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, while the mouth of the coronary sinus is shown as being posterior. While this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal re-entry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology, and the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value as regards the description of the atrioventricular junctions, establishing the principles of this new nomenclature.

This review is the first of a two-part series of articles on "atrioventricular [AV] nodal reentry." The early clinical literature as well as the experimental studies are reviewed, and more recent morphologic data are presented, with the aim of clarifying whether the reentrant circuit is confined to the AV node, or consists in part of extranodal components. Most of the evidence supports the concept that atrial tissue is an essential link in the reentrant pathway. Arguments will be presented to indicate that within the AV node, the separation between antegrade and retrograde pathways is functional, not anatomical, and that both pathways are in electrotonic contact.

It has been suggested that the fetal heart rate response to fetal stimulation in labour is an indication of fetal condition. This study was designed to evaluate scalp stimulation at the time of fetal blood sampling. All labours requiring fetal scalp pH measurement during one year at the John Radcliffe Maternity Hospital were reviewed to determine the association between pH result and the fetal heart rate response to the first scalp blood sample. Sixty-nine (50%) cases showed an acceleration and none had a scalp blood pH less than 7.20. Six (8.7%) of the cases which did not show an acceleration of the fetal heart rate had a pH less than 7.20 and this group had a greater incidence of analgesia usage and twice as many caesarean sections (39%). The detection rate for non-acidaemia using a fetal heart rate acceleration at the time of fetal blood sampling was 52 percent but the specificity and positive predictive value were both 100 percent. The false negative rate was 91 percent. Thus, whilst an acceleration was reassuring, the absence of an acceleration at the time of fetal blood sampling was not a good predictor of fetal acidaemia. These results are compared with the data from four other published reports.

OBJECTIVES: We aimed to test the diagnostic accuracy of cardiovascular magnetic resonance (CMR) imaging in distinguishing pathological left ventricular non-compaction (LVNC) from lesser degrees of trabecular layering seen in healthy volunteers and, in those with cardiomyopathies and concentric left ventricular hypertrophy, potential differential diagnoses. We hypothesized that pathological trabeculation could be distinguished by determining the ratio of non-compacted to compacted myocardium (NC/C ratio). BACKGROUND: Left ventricular non-compaction is characterized by a non-compacted myocardial layer in the left ventricle. Cardiovascular magnetic resonance images this layer with unprecedented quality, particularly in the ventricular apex, where echocardiography has inherent difficulties. METHODS: We analyzed magnetic resonance cine images, using the 17-segment model in 45 healthy volunteers, 25 athletes, 39 patients with hypertrophic cardiomyopathy and 14 with dilated cardiomyopathy, 17 with hypertensive heart disease, and 30 with aortic stenosis, as well as images from 7 patients previously diagnosed with LVNC whose diagnoses were supported by additional features. RESULTS: Areas of non-compaction were common and occurred more frequently in all groups studied in apical and lateral, rather than in basal or septal, segments. A NC/C ratio of >2.3 in diastole distinguished pathological non-compaction, with values for sensitivity, specificity, and positive and negative predictions of 86%, 99%, 75%, and 99%, respectively. CONCLUSIONS: Left ventricular non-compaction is diagnosed accurately with CMR using the NC/C ratio in diastole.

As this translation of Fallot's conclusions makes clear, he emphasized the clinical diagnostic usefulness of his findings because of the high frequency of this malformation in cyanotic congenital heart disease. Terming this anomaly "tetralogy," he clearly and simply delineated its four cardinal features. He stated that cyanosis was not due to a patent foramen ovale. He attributed the morphogenesis of the tetralogy to an intrauterine pathologic process at the level of the pulmonary valve leaflets and the subpulmonary infundibulum. The tetralogy and Fallot's contribution are reassessed in the light of present understanding.

Anatomical studies have shown that the pathognomonic feature of primitive ventricle is absence of that portion of the interventricular septum which interposes between the atrioventricular valves. The relation of this posterior septum to the atrioventricular valves is such that echocardiography should be a particularly suitable technique for showing its presence or absence. When a posterior septum is present, it is seen on an echocardiogram as a double echo between the two atrioventricular valves. It presence limits posterior movement of the septal cusp of the anterior atrioventricular valve. Absence of the posterior septum should, therefore, be seen echocardiographically as more than mere absence of the double septal echo. It should be possible to show unusual posterior excursion of the "septal" cusp of the anterior atrioventricular valve and apposition of the "septal" cusps of the atrioventricular valves during diastole. In most instances it should also be possible to demonstrate that the posterior great artery is in continuity with both atrioventricular valves. We have shown these echocardiographic features in 26 patients. The diagnosis of primitive ventricle has been confirmed at necropsy or at operation in 4 patients. In the other 22 patients in angiographic data are compatible with a diagnosis of primitive ventricle. Demonstration of these positive features at echocardiography is, therefore, of considerable value in the initial diagnosis of primitive ventricle and in particular its differentiation from other congenital malformations.