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Biomedical subjects

D G Gibson

Publications and source records attributed to D G Gibson.

At least 145 records · Page 8Linked to original sources

U waves in ventricular hypertrophy: possible demonstration of mechano-electrical feedback.

The relation between ventricular function and electrocardiographic evidence of hypertrophy (by voltage criteria, "strain", and U wave inversion) was examined by means of M mode echocardiography and apex cardiography in 73 patients with diseases associated with left ventricular hypertrophy and 10 normal volunteers. In patients with disease, left ventricular cavity dimension and fractional shortening were unrelated to electrocardiographic findings, but left ventricular posterior wall thickness was greater in those with strain or U wave inversion. Without U wave inversion, hypertrophy and strain were weakly related to diastolic abnormalities, but the addition of U wave inversion was strongly associated with a reduced rate of early diastolic posterior wall thinning, prolonged isovolumic relaxation time, delayed mitral valve opening after minimum cavity dimension, and a pronounced increase in transverse dimension during the isovolumic period suggesting incoordinate relaxation. It is concluded that, whereas a negative U wave frequently occurs in association with the pattern of left ventricular hypertrophy or strain, it alone is strongly related to abnormalities of isovolumic relaxation. The close relation between incoordinate relaxation and U wave inversion, events which occur virtually simultaneously during the isovolumic period, suggests a mechanical influence on U wave genesis.

Cardiomegaly↗

Regional variation in the timing and extent of left ventricular wall motion in normal subjects.

Right anterior oblique cineangiograms from 19 subjects without evidence of heart disease were analysed to assess regional non-uniformity in the time of onset of systolic inward motion, amplitude of systolic motion, time of peak inward motion, and wall motion during the isovolumic relaxation period. The left ventricular silhouette was digitised frame by frame for a full cardiac cycle. These four wall motion variables were quantitatively measured along 40 chords drawn from equally spaced points on the end diastolic silhouette to the nearest point on the end systolic silhouette. Onset of systolic inward motion was significantly non-uniform, being delayed by up to 120 ms in the anterior apical chords compared with the areas of earliest inward motion near the base of the heart. More uniformity was noted in time of peak inward motion; the differences between regions were not statistically significant. Amplitude of systolic motion was significantly less at the apical and mid-anterior segments than elsewhere in the heart. Wall motion during the isovolumic relaxation period is outward and greatest in the mid-anterior segments, but inward in the proximal inferior segments and mitral valve region. These data suggest that contraction of muscle fibres in the anterior apical segments is initially isometric due to the considerable afterload at the onset of contraction, this afterload being the result of earlier contraction elsewhere in the ventricle. This may partly explain the propensity for aneurysms to be located in the anterior apical region. When the timing and extent of wall motion in disease states are analysed, account must be taken of the non-uniformity in the normal heart.

Adult↗

Abnormal left ventricular diastolic function in chronic Chagas' disease: an echocardiographic study.

Simultaneous M-mode echocardiograms and phonocardiograms were recorded in 19 patients with chronic Chagas' disease, and were digitised and compared with normal in order to study systolic and diastolic left ventricular function. Five of the patients were in New York Heart Association class 1, 9 in class 2, and 5 in class 3. Left ventricular cavity dimensions were increased in 3 and shortening fraction reduced in 1. Peak velocity of circumferential fibre shortening was below the 95% confidence limit of normal in 9. In contrast to previous echocardiographic studies, diastolic abnormalities were common, with prolongation of isovolumic relaxation time in 9 patients and reduced rate of dimension increase in 11. However, in spite of regional disease, documented angiographically in 5 of 6 patients, there was no evidence of asynchronous wall motion during relaxation seen in patients with coronary artery disease and comparable segmental abnormalities of wall motion. The relative timing of aortic valve closure and minimum cavity dimension was normal in all but 3 patients, and a significant dimension change during isovolumic relaxation in only one. Thus diastolic disturbances are common at all stages of Chagas' disease, and may represent a fundamental aspect of the pathological process as it affects the left ventricle.

Adolescent↗

Relation between mitral valve closure and early systolic function of the left ventricle.

In order to investigate relations between mitral valve closure and mechanical events at the onset of left ventricular systole, simultaneous M mode echocardiograms and phonocardiograms were recorded with the apexcardiogram and its first differential (dA/dt) in 25 normal subjects and 88 patients with heart disease. The timing of mitral and aortic valve closure and the onset and peak rate of rise of the apexcardiogram with respect to the Q wave of the electrocardiogram were measured. There was considerable variation in the intervals from Q to mitral valve closure (Q-MVC) and from Q to peak dA/dt and in the isovolumic contraction time between normal subjects. There was no consistent abnormality of these intervals in patients with coronary artery or valvar disease, and no relation between the interval from Q to mitral valve closure and end diastolic pressure. When the timing of the first heart sound and peak dA/dt were considered together, however, clear abnormalities became apparent. In normal subjects, the intervals Q-MVC and Q to peak dA/dt were significantly correlated. In coronary artery disease, the expected relation between Q-MVC and Q to peak dA/dt was found only when end diastolic pressure was normal and was lost when end diastolic pressure was raised. Mitral stenosis was associated with delayed mitral closure in a few cases only, but in chronic aortic regurgitation closure was consistently early with respect to the apexcardiogram. In patients with atrial fibrillation and a normal mitral valve the timing of mitral valve closure with respect to the apexcardiogram was normal, which is inconsistent with an atrial contribution to the timing of mitral valve closure. Thus when considered in isolation the timing of mitral valve closure and the duration of isovolumic contraction time gave little information about cardiac function. Nevertheless, a predictable relation exists between mitral valve closure and the onset of left ventricular mechanical systole in normal subjects, which can be used to identify characteristic alterations in patients with heart disease.

Adult↗

Assessment of hypertrophic cardiomyopathy in potential aircrew.

On account of the risks of: (1) sudden death; (2) significant arrhythmias; (3) reduction in effort tolerance due to severe cardiac hypertrophy; (4) syncope; (5) systemic embolism and (6) side effects of drugs used to treat the condition, no patient with established hypertrophic cardiomyopathy should be licensed to fly. This includes those who may have undergone surgery. Those with minor degrees of hypertrophy on 2-D echo may be considered for restricted licensing subject to their having a normal exercise test and no significant arrhythmia on 24 h ambulatory electrocardiogram. If licensed, six-monthly review by a cardiologist should be required.

Adult↗

Relation between regional echo intensity and myocardial connective tissue in chronic left ventricular disease.

Cross sectional echocardiograms were recorded within one week of death in seven patients with valvular heart disease, four with coronary artery disease, and nine with congenital heart disease. Regional echo amplitude was measured from the cross sectional display by constructing histograms of pixel intensity. Parietal pericardium was used as an internal standard for setting the gain of the instrument. At necropsy myocardium was taken from the free wall of the left ventricle, the papillary muscles, and the septum. Fibrosis was assessed histologically and biochemically as hydroxyproline content. In individual samples histological and biochemical estimates were correlated. In all regions other than the septum in patients with left ventricular hypertrophy, log [collagen] correlated with median pixel intensity. The amplitude of reflected echoes from the hypertrophied septum was significantly higher than that from other samples but was similarly correlated with collagen content. Agreement between echo amplitude and histological grade was significantly less good. Thus in chronic left ventricular disease myocardial collagen content appears to be the major determinant of regional echo intensity. Reproducibility of measurements and more rigorous definition of tissue abnormalities will, however, require further study.

Adult↗

Left ventricular wall motion in patients with Chagas's disease.

The effect of early chronic Chagas's disease on the timing and extent of regional left ventricular wall motion was studied with a frame by frame analysis of left ventriculograms in nine patients and compared with those in 19 normal subjects. In all the patients there was hypokinesis or akinesis in the anteroapical region together with delay in the onset of inward movement. Hypokinesis of the proximal inferior segment was also present, but the time of onset of inward motion here was normal. These differences can be explained on the basis of regional asynchrony within the normal left ventricle, where anteroapical wall motion is delayed with respect to that elsewhere. Thus contraction of the diseased anteroapical segment starts against an appreciable pressure and so may be isometric, whereas the affected proximal inferior segment starts contracting earlier against a lower pressure and so is able to shorten. No abnormalities of wall motion were seen during isovolumic relaxation despite segmental involvement, which is a distinctly different finding from that in patients with coronary artery disease. This may be due partly to the absence of incoordinate relaxation in Chagas's disease and partly to myocardial involvement by Chagas's disease in the mid-anterior segment. This is the site of rapid early diastolic wall thinning, which has been put forward as a major mechanism of normal rapid ventricular filling and whose premature activity causes disturbances in regional wall motion before mitral valve opening when relaxation is incoordinate. Thus quantitative analysis of both the timing and amplitude of wall motion indicates fundamental differences between Chagas's disease and coronary artery disease, when a less complex analysis would have shown a similar pattern of segmental dysfunction in both. Since the effect of the same pathological process on wall motion varies with the site of ventricular involvement, the importance of the disturbances seen in Chagas's disease becomes apparent only when the non-uniformity of normal left ventricular structure and function is taken into account.

Angiocardiography↗

Assessment of mitral Björk-Shiley prosthetic dysfunction using digitised M mode echocardiography.

Digitised M mode echocardiograms were analysed in 22 patients with possible Björk-Shiley mitral prosthetic dysfunction. Patients with paraprosthetic mitral regurgitation had a significantly greater shortening fraction, an increased peak rate of dimension change during systole, and an increased peak velocity of circumferential fibre shortening than those with poor left ventricular function. Patients with a clotted prosthesis had lower values for shortening fraction and peak rate of dimension change during systole than patients with paraprosthetic regurgitation. In this latter group, the peak rate of dimension change during diastole and peak lengthening rate were greater than in either those patients with poor left ventricular function or those with a clotted prosthesis. In addition, the peak lengthening rate was greater in those with a clotted prosthesis than in those with poor left ventricular function. Thus M mode echocardiography is a useful method of assessing mitral prosthetic dysfunction and allows patients with paraprosthetic regurgitation to be distinguished from those with either poor left ventricular function or a clotted prosthesis.

Adult↗

Relation of regional echo amplitude to left ventricular function and the electrocardiogram in left ventricular hypertrophy.

In order to determine the relation between three manifestations of left ventricular hypertrophy--ST-T wave changes on the electrocardiogram, diastolic disturbances, and increased myocardial echo intensity--M mode and cross sectional echocardiograms were recorded in 12 normal subjects, 15 athletes, 16 patients with hypertrophic cardiomyopathy, and 42 patients with secondary left ventricular hypertrophy due to aortic stenosis (20), severe essential hypertension (8), coarctation (7), or subaortic stenosis (7). M mode echocardiograms were digitised and cross sectional echocardiograms were analysed for regional echo intensity. In patients with hypertrophy regional echo amplitude was significantly increased in mid and basal septum and posterior left ventricular wall. Patients with increased echo amplitude in any region showed a higher incidence of ST-T wave abnormalities than those without and of diastolic abnormalities--including prolongation of isovolumic relaxation time, delay in mitral valve opening with respect to minimum cavity dimension, and a reduction in peak rate of posterior wall thinning and dimension increase. There was a significant rank order correlation between median pixel count and these diastolic abnormalities. No significant differences were demonstrable in these relations between the diagnostic groups. By contrast, electrocardiographic findings, diastolic function, and pixel count were uniformly normal in athletes, although the increase in left ventricular mass was similar to that in the patients. Thus an increase in left ventricular mass alone is not responsible for repolarisation or wall motion abnormalities occurring in pathological left ventricular hypertrophy. These latter changes are, however, strongly associated with the change in myocardial properties detected as an increase in echo intensity and may be due to increased interstitial fibrosis.

Adult↗

Relation between electrocardiographic repolarisation changes and mechanical events in left ventricular hypertrophy.

The relation between ventricular function and the presence of electrocardiographic "strain" in patients with left ventricular hypertrophy was examined using digitised M mode echocardiography and 12 lead electrocardiograms in 64 patients with pressure overload, 21 with hypertrophic cardiomyopathy, and 14 athletes. Although all had increased left ventricular mass, those with strain had a prolonged interval from minimum cavity dimension to mitral valve opening and a reduced rate of early diastolic posterior wall thinning and dimension increase compared with those with normal ST segments and T waves. Both groups had normal systolic function (fractional shortening and peak velocity of circumferential fibre shortening), and the time between the termination of the T wave and minimum dimension was similar. In athletes, however, electromechanical systole was shorter than normal, and the end of the T wave and minimum cavity dimension were synchronous. It is concluded that abnormal electrical recovery in left ventricular hypertrophy is closely related to impaired early relaxation and may be dissociated from impaired systolic function, cavity dimension, interventricular conduction delay, and the presence of increased mass alone. The normal relation between electrical and mechanical systole is preserved even when the polarity of repolarisation is reversed.

Adolescent↗

Study of isovolumic relaxation in man.

Although isovolumic relaxation time is relatively short, occupying less than 10% of the total cardiac cycle, study of its duration and of pressure and wall movement changes occurring in it have shed considerable light on the normal synchronous pattern of left ventricular function and its loss in disease. These observations have indicated the importance of diastolic as well as systolic events in determining overall cardiac function, and have stressed the requirement for a more versatile intellectual framework for interpreting these observations than the conviction that all ventricular disease is simply the result of "depressed contractility".

Aortic Valve↗

Effect of myocardial fibre architecture on the behaviour of the human left ventricle in diastole.

Stress and deformation results from finite element analyses are presented for a series of models of the human left ventricle. The myocardium has a complex anisotropic fibre structure, are made on both fibre orientation and on the ratio are made on both fibre orientation and on the ratio of the elastic moduli along and across the fibres. The results show that, at least in diastole, when the left ventricle is considered as a passive structure under the action of the internal blood pressure, the effect of the real fibre arrangement is generally to reduce deformation and also the direct stresses. In spite of fibre angle changing across the wall, the analyses correctly predict the lack of rotation of the left ventricle about the long axis.

Biomechanical Phenomena↗

Clinical value of echocardiography in patients with 'heart failure'.

The clinical syndrome of 'heart failure' can be caused by a variety of haemodynamic disturbances, which can be analysed by echocardiography. Occasionally, occult valve disease may be present. The commonest cause is left ventricular disease. Two-dimensional echocardiography allows cavity size and shape to be studied, and when combined with colour amplitude processing, regional abnormalities of acoustic properties of the myocardium detected, and shown to have clinical significance. Digitization of combined M-mode and 2D records allows endocardial position and wall dynamics to be studied, at a repetition rate of 1000/s in known positions in the ventricle. Abnormal systolic function can be analysed in great detail, and the effects of a dilated cavity distinguished from those incoordinate wall motion. Reduced contraction velocity can also be identified, but this is rare as an isolated abnormality. A series of diastolic abnormalities can also be detected, including incoordinate relaxation in coronary artery disease, and prolonged isovolumic relaxation and reduced rate of diastolic wall motion in left ventricular hypertrophy. When simultaneous high fidelity pressure is available, myocardial power, work, and stress-strain relations can be documented. Thus 'heart failure' is not a discrete entity, and there is no single type of clinical left ventricular disease corresponding to 'depressed contractility' to be detected by echocardiography in its early or late stages. Much more valuable, however, is the use of the technique to record a series of separable abnormalities of ventricle function, to quantify them in individual patients, and to follow the effects of treatment.

Cardiomegaly↗

Effect of postextrasystolic potentiation on amplitude and timing of regional left ventricular wall motion in ischaemic heart disease.

In order to investigate the effects of postextrasystolic potentiation on left ventricular wall motion, the left ventriculograms of 30 patients were digitised frame by frame and regional movement demonstrated by contour displays. Postextrasystolic potentiation caused significant increases in end-diastolic volume, ejection fraction, and peak ejection and filling rates. The amplitude of normally moving segments increased by 5.7 +/- 2.3 mm, regardless of initial amplitude. Hypokinetic segments moved normally if the initial amplitude was greater than 5 mm, and there was a reduced or absent response if 4 mm or less. Four specific abnormalities of timing of motion were studied during isovolumic contraction, early ejection, and isovolumic relaxation. Their timing and extent were all unaffected in postextrasystolic beats. These results thus give no evidence for the entity "reversible asynergy". Rather, they suggest that the response of local wall motion to postextrasystolic potentiation depends only on basal amplitude and increased volume change in postextrasystolic beats.

Cardiac Complexes, Premature↗