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To examine the effects of acute myocardial infarction on mitral valve diastolic velocity, echocardiograms were performed in 18 patients on admission, daily in the Coronary Care Unit, and at 3-day intervals during the remainder of hospitalization. These patients were divided into three groups based on the time interval between onset of symptoms and initial echocardiogram. Five of six patients admitted within 5 hours of onset of myocardial infarction had a triphasic response of mitral valve diastolic velocity with a transient rise above initial values, followed by a fall to below initial values, and then a slow rise during recovery. Seven of eight patients admitted 1-2 days after onset of myocardial infarction had a biphasic response, i.e., a fall from initial values and then a slow rise. Four patients admitted later in the course of myocardial infarction had a monophasic response, i.e. low initial velocity followed by a slow recovery. We conclude that in patients with myocardial infarction the mitral valve diastolic velocity following myocardial infarction shows a triphasic response which may appear biphasic or monophasic depending on the interval between myocardial infarction and admission. The temporal pattern of mitral valve diastolic velocity changes may reflect the dynamic alterations of myocardial function and compliance that are occurring after acute myocardial infarction and during the recovery period.

Studies were made with standard time motion and B-scan echocardiography on 48 patients including 5 with idiopathic hypertrophic subaortic stenosis (hypertrophic obstructive cardiomyopathy), undergoing diagnostic cardiac catheterization. The dimensions of the left ventricular outflow (O) and inflow (I) tracts were measured on the B-scan images. The outflow tract was significantly narrowed in idiopathic hypertrophic subaortic stenosis at both end-systole (1-1+/-0-1 cm) and end-diastole (1-3+/-0-1 cm) when compared with the average width in other patients (2-6+/-0-1 and 3-0+/-0-1 cm, at end-systole and end-diastole, respectively) (P less than 0-001) or normal subjects (2-4+/-0-3 and 2-9+/-0-2 cm) (P less than 0-01). Furthermore, the O/I ratio differed significantly in idiopathic hypertrophic subaortic stenosis (0-5+/-0-1 at end-systole and 0-6+/-0-1 at end-diastole) from that in all other groups (1-4+/-0-1 at both end-systole and end-diastole) (P less than 0-005). There was no appreciable change in the width of the outflow tract from mid- to end-systole in the two patients in whom this was examined. The data support the contention that the anterior leaflet of the mitral valve assumes an abnormally anterior position in idiopathic hypertrophic subaortic stenosis. Though the systolic anterior movement of the tip of the anterior leaflet of the mitral valve shown by M-mode echocardiography could not readily be confirmed with B-scans, we believe that the narrowed outflow tract found in the present investigation contributes to the obstruction that occurs in this disease. We suggest that this outflow tract narrowing is probably caused by hypertrophy of the ventricular septum which in itself contributes to the narrowing, but which also displaces the papillary muscles and thus produces abnormal traction on the mitral valve and striking anterior displacement of the valve apparatus.

The syndrome of mitral valve prolapse with associated auscultatory-electrocardiographic findings is now well documented. Two representative cases of repetitive tachyarrhythmias in patients with mitral valve prolapse are discussed as well as an analysis of the 589 cases in the English literature of arrhythmias in patients with mitral valve prolapse. The average age of the patients was 38 years; 70 per cent of them were women. Symptoms were variable, but palpitations occurred in 44 per cent, lightheadedness in 12 per cent and syncope in 4 per cent. Premature atrial and/or ventricular contractions were found in 55 per cent, premature ventricular contractions in 45 per cent, supraventricular tachycardia in 6.1 per cent and ventricular tachycardia in 6.3 per cent. Sudden death was noted in 1.4 per cent. A discussion of the pathogenesis of arrhythmias and therapy concludes this review.

A history, heart murmur, electrocardiogram and chest X-ray film suggesting an atrial septal defect associated with an echocardiogram revealing paradoxical motion of the interventricular septum with a dilated right ventricle may be considered indicative of a secundum or primum defect in a young adult or child. Two patients who fulfill all these criteria and had the presumptive diagnosis of an atrial septal defect were found at cardiac catheterization to have no demonstrable left to right shunt or other significant abnormality. The results of standard T-M mode echocardiograms were verified with B scan ultrasonograms. These cases may represent an early stage in the development of a cardiomyopathy. There is no echocardiogram pathognomonic of an atrial septal defect, and patients whose history and echocardiogram suggest this defect should have further diagnostic evaluation including technetium scan or cardiac catheterization.

Left ventricular function and motion in 12 adults with an ostium secundum atrial septal defect were analyzed utilizing biplane cineangiography. Values for left ventricular end-diastolic volume index, stroke volume index, ejection fraction, left ventricular end-diastolic pressure and mean rate of circumferential fiber shortening were compared with values in an age-matched group of 11 normal subjects. Comparisons of ventriculographic and echocardiographic data were also made in 5 patients and 10 control subjects. Cardiac index was smaller in patients than in the normal subjects (3.6 vs. 4.5 liters/min per m2, P less than 0.01). Although left ventricular end-diastolic pressure was similar (8 mm Hg in both groups), the end-diastolic volume index was significantly smaller in patients than in normal subjects (56 vs. 76 ml/m2, P less than 0.05). Stroke volume index was also significantly smaller in patients (40 vs. 52 ml/m2, P less than 0.01). The two groups had similar values for ejection fraction (65 +/- 2 percent [standard error of the mean] in patients vs. 68 +/- 2 percent in normal subjects), circumferential fiber shortening velocity (1.67 +/- 0.13 vs. 1.81 +/- 0.15 circumferences/sec.), heart rate (91 +/- 7 vs. 90 +/- 5 beats/min) and mean systemic arterial pressure (92 +/- 5 vs. 87 +/- 3 mm Hg). Early systolic bulging of the upper ventricular septum toward the right ventricle was seen in 10 of 12 patients with an atrial septal defect but in no normal subject. Echocardiographic data supported these findings. No other abnormalities of motion were consistently noted. It is concluded that the left ventricle of patients with an atrial septal defect is subnormal in volume and abnormal in sequence of contraction of the septum and is characterized by apparent decreased distensibility.

The pioneering work of Edler in Sweden [1] and Eifert in Germany [2] has made echocardiography a widely used tool to detect structural and functional abnormalities of the human heart. The reflection of pulsed ultrasound waves is unique in its ability to record the motion of intracardiac structures noninvasively. High quality recordings of the contractile pattern of the left ventricular posterior wall, the motion of the interventricular septum and the mitral valve leaflets are examples for the great diagnostic value of echocardiography [3]. Because in patients with Preexcitation Syndrome (PES) disturbed patterns of contraction of the heart have been reported in the literature [4, 5], we examined an unselected group of those patients with conventional echocardiographic methods.

1. Segments of skinned frog muscle fibres were immersed in solutions in which the calcium ion concentration, and therefore the steady isometric force, was controlled with an EGTA buffer system. The contraction kinetics were measured when the load was quickly reduced to values less than the isometric force. 2. The velocity of shortening following release from steady force was a hyperbolic function of relative load. The minimum quick displacement required to reduce the force from the steady isometric value to half this value was about 1% of the fibre segment length. 3. The relative force—velocity relation was independent of pCa in the range 5·0-6·75. Thus calcium ions appear to control the number of sites at which cross-bridges can be formed but have no significant effect on the kinetic properties of an individual bridge. 4. Cross-bridges along the length of a myofilament appear to act independently of each other. 5. The force—velocity relations reported for intact muscle fibres during relaxation, when compared with those of skinned fibres at different calcium levels, indicate that the time course of the fall in force after a stimulus is essentially that of calcium removal from the myofilaments.