Study of left ventricular function by echocardiography.
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Biomedical subjects
Publications and source records attributed to D G Gibson.
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The effects of trinitrin and propranolol on left ventricular function were compared with those of saphenous bypass grafting in patients with ischaemic heart disease. Simultaneous echocardiograms, apexcardiograms and phonocardiograms were recorded and digitized before and after drug administration or operation. As expected, trinitrin caused a reduction in left ventricular cavity size, an increase in peak VCF and an increase in heart rate, while propranolol consistently reduced heart rate and peak VCF. Asynchronous onset of wall movement was unaffected by propranolol or trinitrin, but when present preoperatively, consistently improved after saphenous bypass grafting. Abnormalities of relaxation, usually due to asynchronous termination of contraction, were aggravated by trinitrin or propranolol in those patients in whom contraction was initially incoordinate, but after operation, they tended to improve along with systolic abnormalities. The time interval, Q to minimum LV cavity dimension is frequently reduced in patients with ischaemic heart disease, and treatment with propranolol increases the frequency of this abnormality. Saphenous bypass grafting, however, was associated with a consistent return towards normal, regardless of changes in heart rate. Thus although trinitrin, propranolol and saphenous bypass grafting all relieve angina, their effects on left ventricular function are significantly different.
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To assess the acute and chronic effects of propranolol on left ventricular wall motion, simultaneous, echo-, apex-, and phonocardiograms were recorded in 10 normal subjects and in 16 patients with ischaemic heart disease, nine with co-ordinate (group A) and seven with incoordinate (group B) contraction in the control site. Records were made after 0.1 mg/kg intravenous or oral therapeutic dose for one week. In all, propranolol caused small reductions in heart rate and peak VCF. In normal subjects, intravenous and oral propranolol caused rate-related increases in the intervals Q to A2, Q to minimum dimension, and Q to mitral valve opening. The effects were different in patients with ischaemic heart disease. In group A, inward wall movement ceased 80 ms early, and this was not attributable to a change in heart rate. Diastolic events were unaltered. In group B, minimum dimension already occurred early. Propranolol did not alter systolic events further, but increased delay in mitral valve opening, 'O' point, prolonged isovolumic relaxation, reduced peak rate of dimension increase, and aggravated incoordinate relaxation. It is concluded that the effects of propranolol in patients with ischaemic heart disease are modified in a manner that cannot be predicted from observations made in normal subjects. It also appears that complex drug effects can be assessed in man from the measurement of time intervals derived from multiple non-invasive techniques.
Six patients with early systolic closure of the aortic valve are described with mitral regurgitation, double outlet right ventricle, left ventricular diverticulum, congestive cardiomyopathy, Eisenmenger ventricular septal defect, and aortic regurgitation with an aneurysmal ascending aorta, respectively. None had evidence of subaortic stenosis. Early sytolic closure of the aortic valve is thus not diagnostic of subvalvular aortic stenosis but is a non-specific finding.
Regional abnormalities of left ventricular function are frequently determined from superimposed cavity outlines at end-diastole and end-systole. The timing of end-diastole is standardised with respect to the electrocardiogram, but that of end-systole is undefined, and frequently determined by simple inspection. To examine the effect of variation in the timing of the end-systolic frame on apparent regional wall motion, 35 left ventricular angiograms from patients wit ischaemic heart disease were digitised frame by frame, and the timing of aortic valve closure and mitral valve opening superimposed on contour displays. In 15 patients, the pattern in the two frame display with end-systole taken as aortic valve closure was similar to that when it was taken as mitral valve opening. In the remaining 20, however, there were major discrepancies between the two, because of changes in cavity shape during isovolumic relaxation. These shape changes were the result of asynchronous termination of systole in different regions of the ventricle. In addition, there was a significant increase in left ventricular cavity area of 3.9 +/- 1.7 per cent during isovolumic relaxation, corresponding to an increase in calculated volume of 8.1 +/- 4.5 per cent. Estimates of ejection fraction derived from end-systole taken at end-ejection were thus consistently greater than those at mitral valve opening. These differences in the apparent pattern of regional wall motion resulting from lack of definition of end-systole are large compared with those reported after intervention angiography, or surgery. Thus, if two frame methods are to be used, the timing of end-systole must be standardised. We suggest that end-ejection be used. Changes of shape during isovolumic relaxation should be considered separately.
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The human left ventricle in diastole can be modelled as a passive structure with incremental internal pressure change being considered as the load. Recent developments in engineering stress analysis provide techniques for predicting the behaviour of structures with complex geometry and material properties, as is the case with the left ventricle. That which is most appropriate is the finite element method which requires the use of a large digital computer. The ventricles of 2 patients have been studied during diastole, the geometries having been derived from cineangiographic data (biplane), and the pressure by means of catheter-tip manometers. Various descriptions of myocardial stress/strain relations have been assumed and applied to the left ventricular wall in order to obtain the best match between the calculated and observed deformation patterns. The manner in which the value and distribution of stiffness in the left ventricle influences the shape change can therefore be determined, and possible clinical implications deduced.
Left ventriculograms of 45 patients with angina and normal coronary arteriograms were digitised frame by frame in order to detect regional abnormalities of wall movement. Though left ventricular pressures, end-diastolic volume, and ejection fraction were normal in all, regional outward movement during early systole was present in 10 patients, and abnormal inward wall movement during isovolumic relaxation also in 10, involving the apex or inferior surface. Both were present together in 8 patients, and affected segments showed normal amplitude and peak velocity of movement during ejection. These disturbances of wall movement were associated with inferior T wave changes on the electrocardiogram, and mitral prolapse, particularly when the latter resulted from delayed movement of the valve during ejection. It is suggested that the onset of contraction is delayed in affected areas, but that it proceeds normally thereafter. The resulting persistence of tension into the period of relaxation of the remainder of the ventricle may interfere locally with coronary flow, particularly during tachycardia, thus causing manifestations of regional ischaemia.
Three patients with mitral stenosis are described, in whom the haemodynamic findings at cardiac catheterisation were more suggestive of left ventricular myocardial disease, in that the left ventricular diastolic pressure was high and the mitral valve gradient small. However, their echocardiograms showed abnormal wall movement during diastole characteristic of severe inflow obstruction, with slow and protracted filling, and at operation mitral stenosis was confirmed. Left ventricular wall stress was estimated throughout the cardiac cycle in one patient, and the diastolic stress-strain relation shown to be abnormal. The effects of mitral stenosis on left ventricular function are complex, and are not explicable simply by reduction in size of the mitral orifice.
M-Mode echocardiography in patients with univentricular heart allows the number and relations of the AV valves to be established. The absence of a posterior septum can be documented with some certainty and in many cases a stradding AV valve suspected. In addition, reduced amplitude of diastolic closure velocity is very suggestive of valve atresia or dysplasia. This information is of practical significance if corrective surgery is planned.
In order to investigate the basis of ventricular dysfunction in patients with univentricular heart, cineangiograms of 20 patients aged between 3 weeks and 22 years were digitized frame by frame and compared with left ventriculograms of patients with other cardiac malformations. Ejection fraction was at least normal (58% to 95%) and peak rate of systolic minor axis shortening was normal in all. However in only 3 patients was the change in volume achieved by virtue of the normal change in cavity shape; in 17 the end-systolic outline was abnormally circular and shape index, 4 pi (area)/(perimeter)2, changed by less than normal (p less than 0.01). In addition, abnormalities of regional wall movement were found in 12 patients. 11 showed a consistent pattern, unlike that found in ischaemic heart disease or other congenital lesions, of delayed systolic inward movement of the antero-apical wall, associated in 9 with hypokinesis. Four of these showed secondary delay of relaxation in the same region. One patient had an isolated abnormality of isovolumic relaxation. These findings were independent of age, volume overload or degree of cyanosis, but were more common in patients with absent atrioventricular connexion. We conclude that the architectural abnormalities in univentricular hearts lead to disturbances of myocardial function which particularly affect the apex. These are detectable from an early age.