The role of longitudinally and circumferentially oriented fibres in left ventricular wall motion was examined by digitising echocardiograms of the mitral ring (whose motion reflects long axis change) and of the standard minor axis in 36 healthy individuals, 36 patients with coronary artery disease, 16 with left ventricular hypertrophy, 44 with mitral valve disease (24 of whom had undergone mitral valve replacement). In the controls long axis shortening significantly preceded minor axis shortening (mean (1 SD) difference 25 (40) ms) so that the minor axis increased more during isovolumic contraction (0 25 v 0 09 cm), indicating that the left ventricle became more spherical. Changes in the long and short axes were synchronous at end ejection and in early diastole in the controls. Epicardial excursion preceded endocardial excursion by 50 (20) ms at its peak. These time relations were consistently disturbed in all patient groups, irrespective of the extent of fractional shortening of the minor axis. The onset of long axis shortening was delayed, and this was often associated with premature shortening of the minor axis, the normal spherical shape change during isovolumic contraction was lost, and peak epicardial and endocardial changes became more synchronous. In patients with coronary disease these changes are the expected consequence of ischaemic injury to longitudinally orientated subendocardial fibres. In left ventricular hypertrophy their presence consistently showed systolic dysfunction when orthodox measures were still normal. They were more pronounced after mitral valve replacement when the papillary muscles had been sectioned; long axis shortening was reduced during systole and prolonged into early diastole, while normal shortening of the minor axis was maintained only by abnormal epicardial excursion.Relations between long and short axis motion in healthy individuals are characteristic, and their loss is an early index of systolic ventricular disease. These disturbances precede changes in orthodox measures such as fractional shortening or peak velocity of circumferential fibre shortening.Anatomical studies'2 have shown longitudinal as well as circumferential fibres with a continuous variation in fibre angle across the left ventricular wall. The function of these longitudinal fibres has not been extensively studied. Because effective ventricular function during ejection and filling is likely to depend upon the coordinated action of all myocardial layers, we set out to study the timing and extent of changes in the long axis, comparing them with those of the minor axis in healthy controls and those with left ventricular disease. In addition, we investigated patients after mitral valve replacement where a component of the longitudinal fibres (the papillary muscles) had been sectioned. Patients and methods CONTROLS AND PATIENTSCross sectionally guided M mode echocardiograms were recorded and analysed in 36 patients with coronary artery disease, 16 with left ventricular hypertrophy, 44 patients with mitr...

SUMMARY To define the range of cardiac involvement in the Churg-Strauss syndrome, M mode, continuous wave Doppler, and cross sectional echocardiograms were recorded in twelve patients with the disorder. The M mode recordings were digitised and the cross sectional images were recorded with standardised gain settings to determine regional myocardial echo amplitude. Left ventricular end diastolic and end systolic dimensions were increased above the normal 95% confidence interval in four patients, three of whom showed a depressed shortening fraction. Mitral regurgitation was present in six patients; this was severe enough to need valve replacement in two. Mean echo amplitude in both the septum and the posterior wall was significantly increased above normal by a mean (SD) of4-87 (2-57) dB, suggesting the presence ofmyocardial fibrosis. There was no evidence of subendocardial involvement as there is in other hypereosinophilic syndromes.Mitral regurgitation is common in the Churg-Strauss syndrome. This cannot be ascribed to involvement ofthe cusps or chordae and it occurs even when ventricular function is well preserved. It is suggested that mitral regurgitation is caused by diffuse myocardial fibrosis.The Churg-Strauss syndrome is recognised by the combination of blood eosinophilia, eosinophilic tissue infiltration, extravascular fibrinoid necrotising (allergic) epithelioid and eosinophilic granuloma formation, and disseminated necrotising vasculitis occurring in asthmatic patients.' 2 Lanham et al noted that "the histological components of the syndrome often do not coexist temporally or spatially" and suggested that the clinical pattern of a prodromal phase of allergic disease, followed by a second phase characterised by eosinophilic tissue infiltration and peripheral blood eosinophilia culminating in a third vasculitic phase, should supercede strict adherence to histopathological criteria for the purposes of diagnosis.' Myocardial fibrosis, particularly in the subendocardial region, is a characteristic feature of the idiopathic hypereosinophilic syndrome4 and it has been attributed directly to the eosinophilia itself. Possible cardiac involvement in patients with ChurgStrauss syndrome and comparable blood eosinophilia, however, is less well defined. We therefore studied a series of patients with Churg-Strauss syndrome by M mode, continuous wave Doppler, and cross sectional echocardiography to assess whether they were also at risk for heart disease.Requests for reprints to Dr J M Morgan, National Heart Hospital, London WIM 8BA.Accepted for publication 6 April 1989 Patients and methodsWe studied 12 patients in whom the diagnosis of Churg-Strauss syndrome was made on the basis of histological criteria" and clinical features.' The blood eosinophil count was raised in all (eosinophil counts ranged from 2-3 to 11 x 109 1 at presentation). The results of echocardiography were compared with those in 20 age and sex matched controls with no clinical evidence of heart disease in whom stress test had been negative at high wo...

OBJECTIVE: To assess the sensitivity and specificity of flow-volume curves in detecting central airway obstruction (CAO), and to determine whether their quantitative and qualitative criteria are associated with the location, type and degree of obstruction. METHODS: Over a four-month period, we consecutively evaluated patients with bronchoscopy indicated. Over a one-week period, all patients underwent clinical evaluation, flow-volume curve, bronchoscopy, and completed a dyspnea scale. Four reviewers, blinded to quantitative and clinical data, and bronchoscopy results, classified the morphology of the curves. A fifth reviewer determined the morphological criteria, as well as the quantitative criteria. RESULTS: We studied 82 patients, 36 (44%) of whom had CAO. The sensitivity and specificity of the flow-volume curves in detecting CAO were, respectively, 88.9% and 91.3% (quantitative criteria) and 30.6% and 93.5% (qualitative criteria). The most prevalent quantitative criteria in our sample were FEF50%/FIF50% ≥ 1, in 83% of patients, and FEV1/PEF ≥ 8 mL . L–1 . min–1, in 36%, both being associated with the type, location, and degree of obstruction (p < 0.05). There was concordance among the reviewers as to the presence of CAO. There is a relationship between the degree of obstruction and dyspnea. CONCLUSIONS: The quantitative criteria should always be calculated for flow-volume curves in order to detect CAO, because of the low sensitivity of the qualitative criteria. Both FEF50%/FIF50% ≥ 1 and FEV1/PEF ≥ 8 mL . L–1 . min–1 were associated with the location, type and degree of obstruction.

<p class="MsoNormal" style="margin-bottom: 0.0001pt; text-align: justify;"><strong><span style="font-size: 8.0pt; font-family: ";Calibri-Bold";,";sans-serif";; mso-bidi-font-family: Calibri-Bold;">Introdução</span></strong><span style="font-size: 8.0pt; mso-ascii-font-family: Calibri; mso-hansi-font-family: Calibri; mso-bidi-font-family: Calibri;">: A cannabis é a droga ilícita mais usada nas sociedades desenvolvidas. Excetuando os componentes psicoativos, a cannabis e o tabaco possuem uma mistura semelhante de tóxicos e irritantes. Muitas vezes a cannabis é misturada com o tabaco quer durante o seu consumo quer como hábito inalatório concomitante, o que torna difícil isolar os efeitos nocivos para a saúde causados por estas duas substâncias. </span><strong><span style="font-size: 8.0pt; font-family: ";Calibri-Bold";,";sans-serif";; mso-bidi-font-family: Calibri-Bold;">Objetivo</span></strong><span style="font-size: 8.0pt; mso-ascii-font-family: Calibri; mso-hansi-font-family: Calibri; mso-bidi-font-family: Calibri;">: Caracterizar os efeitos do consumo de cannabis na função respiratória. </span><strong><span style="font-size: 8.0pt; font-family: ";Calibri-Bold";,";sans-serif";; mso-bidi-font-family: Calibri-Bold;">Resultados</span></strong><span style="font-size: 8.0pt; mso-ascii-font-family: Calibri; mso-hansi-font-family: Calibri; mso-bidi-font-family: Calibri;">: O consumo de cannabis associada ou não a tabaco pode promover alterações funcionais respiratórias que se manifestam predominantemente pela diminuição da condutância específica e da relação entre o volume expiratório forçado no primeiro segundo e a capacidade vital forçada. Também outros parâmetros podem sofrer modificações, tais como o volume expiratório forçado no primeiro segundo, a resistência das vias aéreas e a capacidade de difusão do monóxido de carbono. </span><strong><span style="font-size: 8.0pt; font-family: ";Calibri-Bold";,";sans-serif";; mso-bidi-font-family: Calibri-Bold;">Conclusão</span></strong><span style="font-size: 8.0pt; mso-ascii-font-family: Calibri; mso-hansi-font-family: Calibri; mso-bidi-font-family: Calibri;">: Através da análise da literatura é possível verificar que a inalação desta substância afeta a função respiratória, majoritariamente as vias aéreas de maior calibre.</span></p>