DiscussionThese results show that AH 7725 when given by mouth can inhibit the immediate bronchial response to inhaled antigen in asthmatic patients. It has no bronchodilator effect (Gayrard, 1974) and its activi.ty is most likely to be explained by the inhibition of release of mediators of immediate-type allergic responses, which has already been shown in laboratory work.AH 7725 has similar inhibitory properties to those of disodium cromoglycate and also to those of its own predecessors AH 6556 and AH 7079 (Assem, 1973; Assem and McAllen, 1973 b). It is, however, exceptional in being active when given by mouth. So far as we know this is the first report on a d1rug for the prophylaxis of asthma which is active when given by mouth.Our Journal, 1974, 2, 95-96 Patienits with left atrial myxoma characteristically present with a history of progressive shortness of breath, often punctuated by syncopal attacks, and physical signs of miitral valve obstruction (Goodwin, 1963;Greenwood, 1968; Harvey, 1968). Predominant or "pure" mitral regurgitation due to left atrial myxoma has been reported but is uncommon (Cohen et al., 1963;Penny et al., 1967;Wittenstein et al., 1959). This report describes a patient with a calcified left atrial myxoma who presented with sudden severe mitral regurgitation due to ruptured chordae tendineae.Case Report A 44-year-old machinist, previously well and active, abruptly developed dyspnoea and orthopnoea during the first week of December 1972. He was admitted to his local hospital where he was found to have cardiac enlargement, pulmonary oedema, and bilateral pleural effusion. The electrocardiogram showed sinus rhythm with evidence of left atrial enlargement. A heart murmur had been heard one year earlier, but he was told "not to worry" about his heart. There was no history of rheumatic fever, chest pain, calf tendemess or swelling, or fever or chills. Digitalis (digoxin 0-25 mg/day) and a diuretic (Lasix Cardiology Section, Medical Service, Eastern Maine Medical Center, Bangor, Maine, 0441, U.S.A. JOE R. WISE, juN., M.D., Attending Physician 40 mg/day) were given but dyspnoea, orthopnoea, and fatigue persisted, atrial fibrillation developed, and he was referred for consultation.On examination he was very thin and dyspnoeic at rest. Atrial fibrillation was present, the blood pressure was 110/60 mm Hg, there were no signs of peripheral embolism, and the optic fundi were normal. The carotid pulse was small and rapid, the venous pressure was raised, and there was prominent systolic pulsation of the neck veins. The apex beat was in the mid-clavicular line and there was a prominent, diffuse systolic pulsation in the third to fifth interspaces midway between the sternum and the apex. The pulmonary valve closure sound was increased and the aortic component normal. A loud first heart sound was followed by a grade III/VI regurgitant murmur heard best at the apex. There was a prominent early third heart sound and a faint mid-diastolic apical murmur. The lungs were clear. The liver was palpable 2 cm b...

The slope of the posterior left ventricular wall motion in diastole (LVDS) was determined by echocardiography in 25 normal subjects and 21 patients with mitral stenosis. Patients with mitral stenosis had reduced LVDS that was related to the degree of mitral stenosis determined by calculated mitral valve area (r = 0.92). The mitral valve area correlated more closely with the LVDS than with the left atrial emptying index derived from the posterior aortic wall motion. Three patients with mitral stenosis had an increased LVDS after mitral valvotomy or mitral valve replacement. One patient with a stenotic mitral valve prosthesis had reduced LVDS. The results of this study suggest that analysis of the LVDS would be useful in predicting the severity of mitral stenosis and may be beneficial in evaluating patients with suspected prosthetic mitral valve malfunction.

Eleven cases of catheter proven ventricular septal defect with left-to-right shunting in the absence of pulmonary hypertension were studied by phonocardiography. All showed wide and relatively fixed splitting of the second heart sound. Reasons for the relative fixation of the split are suggested, and the point is made that such fixed splitting is not necessarily a sign of atrial septal defect.The wide and fixed splitting of the two components of the second heart sound in patients with atrial septal defect is well established and is regarded as an important clue to the diagnosis of this condition (Aygen and Braunwald, I962; Dexter, I956). In one study of II5 patients with atrial septal defect, 87 showed no respiratory variation of these two components while in 28 there was an average increase of only o0oi sec an inspiration (Johnston, I957). The second heart sound in patients with ventricular septal defects, on the other hand, though recognized as being widely split, is generally thought to show normal movement with respiration. Leatham investigated 23 patients with ventricular septal defects of varying size, and found that in 17 of these subjects the second heart sound was widely split. On inspiration the width of the splitting increased 'normally' -that is, the split was wide but not fixed. However, the average amount of increase in splitting on inspiration in these patients was only 0eo2 sec (from an average of 0X045 sec in expiration to an average of o-o65 in inspiration) (Leatham and Gray, I956 Because it was our clinical impression that the respiratory variation of the A2-P2 interval in patients with ventricular septal defect was less than normal, we undertook the following study. Subjects and methodsPatients with ventricular septal defect were studied by phonocardiography. The criteria used for patient selection were:i Presence of a ventricular septal defect with left-to-right shunt confirmed by cardiac catheterization. 2 Absence of additional cardiac defects (for example, atrial septal defect, pulmonary stenosis, etc). 3 Absence of complete right or left bundlebranch block. 4 Absence of pulmonary hypertension due to raised pulmonary vascular resistance. Two patients with modestly raised pulmonary artery pressures associated with large left-to-right shunts were included. 5 Patient age sufficient to allow co-operation during sound recordings.Phonocardiograms were recorded at the pulmonary valve area and at the left sternal edge during and after held expiration and inspiration and during a prolonged period of exaggerated respiration. Valsalva manoeuvre was avoided. All recordings were made on a Cambridge Multichannel Recorder (Type 72II2) using mid-frequency filters and paper speeds of 75 and I00 mm/sec. All tracings were then measured to determine the minimum and maximum splitting