Biomedical subjects

M G Sutton

Publications and source records attributed to M G Sutton.

41 records · Page 3Linked to original sources

PubMed1979

Histopathological types of cardiac fibrosis in myocardial disease.

Myocardial fibrosis is a frequently observed pathologic finding. It is a common practice to differentiate macroscopic scarring and microscopic scarring, but there has been little attempt to distinguish the various types of interstitial fibrosis, and to determine their prevalence in different cardiac disorders. In this study, we have semiquantitatively assessed microscopic scarring, interfibre and perivascular fibrosis and a distinctive type of plexiform fibrosis. We examined ten hearts with congestive cardiomyopathy, ten with hypertrophic cardiomyopathy, ten with severe valvular aortic stenosis and ten normal hearts. Perivascular and interfibre fibrosis were quantitatively closely linked and most marked in the congestive cardiomyopathy and the valvular aortic stenosis groups. Plexiform fibrosis occurred maximally in the hypertrophic obstructive cardiomyopathy group, closely associated with myocardium exhibiting muscle fibre disarray. Our study demonstrates that although different types of interstitial fibrosis have particular associations with certain disease entities, the associations are not specific. The recognition of the prevalence of one or more types of interstitial fibrosis may, however, assist in the histopathologic diagnosis of certain myocardial disorders.

Adult↗

PubMed1978

Anticoagulants and the Björk-Shiley prosthesis. Experience of 390 patients.

From September 1972 to January 1975, 390 patients underwent valve replacement using the Björk-Shiley tilting disc prosthesis. For the group as a whole hospital mortality was 13.3 per cent and was lowest in those undergoing isolated mitral or aortic valve replacement (5.3 and 9.4%, respectively). Available for follow-up were 209 patients of whom 123 were maintained on dipyridamole and 96 on warfarin. Thromboembolic complications were significantly (P less than 0.01) commoner in the dipyridamole (28 of 123, 22%) than warfarin (6 of 86, 7%) treated group. In the dipyridamole treated group the incidence of thromboembolic complications was similar whichever valve was replaced and thromboembolic complications were responsible for 14 of the 28 late deaths. In the warfarin treated group thromboembolic complications only occurred in patients with a mitral prosthesis. Anticoagulation is indicated for all patients with this prosthesis wherever inserted.

Anticoagulants↗

PubMed1978

Left ventricular relaxation and filling in hypertrophic cardiomyopathy. An echocardiographic study.

Echocardiograms showing left ventricular cavity and mitral valve cusps simultaneously were recorded in 36 patients, apex cardiograms being obtained in 26 of them. These were digitised and continuous plots made of left ventricular dimension, its rate of change, and anterior mitral leaflet velocity, and were compared with those in 20 normal subjects. Peak mitral diastolic closure rate was reduced to 120 +/- 80 mm/s, compared with normal (250 +/- 60 mm/s). Peak rate of increase of dimension was normal (13.4 cm/s), though the pattern of filling was disturbed, with the duration of rapid filling prolonged in 5, and shortened in 15, suggesting restriction. Mitral valve opening, normally synchronous with minimum dimension, was delayed by a mean of 76 ms, and during this period there was an abnormal increase in dimension. Dimension also increased by 50 +/- 25 per cent of the total diastolic excursion before the 'O' point of the apex cardiogram compared with 21 +/- 7 per cent in normals, and the timing of peak rate of increase of dimension was delayed by 50 +/- 20 ms instead of being synchronous with the 'O' point as normal. None of these findings correlated with the reduction in peak mitral diastolic closure rate. Noninvasive methods thus show that relaxation may be abnormal in hypertrophic cardiomyopathy. Delay in mitral valve opening and disturbances in the rate, duration, and co-ordination of wall movement during filling suggest the presence of segmental abnormalities of left ventricular function.

Adolescent↗

PubMed1978

Echocardiographic assessment of left ventricular filling and septal and posterior wall dynamics in idiopathic hypertrophic subaortic stenosis.

In order to study left ventricular function in idiopathic hypertrophic subaortic stenosis (IHSS), left ventricular echograms were analyzed by computer and compared with results in normal subjects. Systolic function was consistently normal or above normal even in the presence of severe diastolic abnormalities. Wide variation in diastolic function in IHSS allowed separation of patients into three groups on the basis of the left ventricular peak filling rate. Because of the severe septal hypertrophy and hypokinesia, peak left ventricular filling rate is predominantly determined by the rate of free wall thinning. Patients in group 1 had rapid left ventricular filling rates, those in group 2 had normal filling rates, and those in group 3 had slow filling rates. With reduction in left ventricular peak filling rate caused by impaired free wall thinning, there was progressive increase in 1) duration of the rapid filling phase, 2) delay of mitral valve opening, 3) asynchrony between septum and posterior wall, 4) incidence of angina, and 5) incidence of atrial fibrillation.

Adolescent↗

PubMedDate not supplied

Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction.

BACKGROUND: Expansion of an acute myocardial infarction predicts progressive left ventricular (LV) dilatation, functional deterioration, and early death. This study tests the hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting function. METHODS AND RESULTS: In 23 sheep, snares were placed around the distal left anterior descending and second diagonal coronary arteries. In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardial infarct. Snared arteries were occluded 10 to 14 days later. Serial hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained up to 8 weeks after anteroapical infarction of 0.23 of LV mass. In sheep with mesh, circulatory hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after infarction and do not change subsequently. Ventricular volumes and ejection fraction do not change after the first week postinfarction. Control animals develop large anteroapical ventricular aneurysms, increasing LV dilatation, and progressive deterioration in circulatory hemodynamics and ventricular function. At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic and end-systolic volumes, ejection fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups. CONCLUSIONS: Preventing expansion of acute myocardial infarctions preserves LV geometry and function.

Analysis of Variance↗