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Biomedical subjects

J F Goodwin

Publications and source records attributed to J F Goodwin.

At least 55 records · Page 3Linked to original sources
PubMed1983

Myocarditis in siblings leading to chronic heart failure.

Two brothers, aged 7 and 9, presented 4 years apart with progressive heart failure following a probable viral infection. Electrocardiograms of both showed widespread precordial Q waves. Cardiac catheterization in each case revealed almost equal right atrial, right ventricular and pulmonary artery pressures and poorer contraction of the right than left ventricle. High neutralizing antibody titres to Coxsackie B4 virus were found in the siblings and their mother. Widespread post-myocarditic scarring of both ventricles was found at autopsy on the elder brother. These findings provide further evidence that Coxsackie myocarditis accounts for some cases of dilated cardiomyopathy and suggest that familial factors may be important.

Adolescent↗
PubMed1983

'Pseudo' systolic anterior motion in patients with hypertensive heart disease.

The systolic motion of the mitral apparatus in patients with hypertensive heart disease and hypertrophic cardiomyopathy was studied in order to quantify the difference. Twelve out of 37 patients with severe systemic hypertension were found to have abnormal systolic anterior motion and had significantly small left ventricular end-systolic dimension (P less than 0.05) and greater ejection fraction and mean velocity of circumferential fibre shortening (P less than 0.01 for each) than the other hypertensive patients without abnormal systolic anterior motion. A comparison between systolic anterior motion in 12 hypertensive patients and mild or moderate systolic anterior motion in 28 patients with hypertrophic cardiomyopathy showed a clear cut difference. 'Pseudo' systole anterior motion reached its peak at end-systole when the posterior wall had contracted fully. 'True' systolic anterior motion, however, reached its peak much earlier than maximum movement of the posterior wall--approximately after two-thirds of systole had been completed. At the time of mitral valve opening, 'pseudo' systolic anterior motion had not yet returned to this initial level, whereas 'true' systolic anterior motion returned prior to the opening of the mitral valve. Anterior chordal motion in hyperdynamic ventricle appears to play a role in the production of 'pseudo' systolic anterior motion.

Adolescent↗
PubMed1983

Echocardiographic features of tropical endomyocardial disease in South India.

Fifteen patients with tropical endomyocardial disease which had been proved angiographically were studied using M-mode and cross-sectional echocardiography to determine the extent to which specific features of this disease could be recognised by these non-invasive methods. Tethering of the posterior mitral valve leaflet to the ventricular wall in combination with areas of echo-dense material in the posterior left ventricular wall and associated papillary muscle appeared to be a constant diagnostic feature of this disease. Colour coding of regional echo amplitude showed high intensity echoes in a distribution corresponding closely to that of the fibrosis known to occur in this condition. Though M-mode echocardiography did not contribute diagnostic information, it was useful in defining the functional consequences of myocardial or mitral valve disease. Digitisation of records allowed a restrictive pattern of left ventricular filling to be observed. It was concluded that cross-sectional echocardiography, particularly when supplemented by colour coded amplitude processing, can make a confident non-invasive diagnosis of tropical endomyocardial disease and so could be useful in assessing its progression or response to treatment.

Adolescent↗
PubMed1983

Endomyocardial disease--clinical features.

The clinical features of tropical and temperate zone endomyocardial fibrosis (EMF) are the same, allowing for certain regional, environmental and possibly genetic variations. For example, the seasonal incidence in rainy humid areas probably reflects the large and repeated parasitic infestations in tropical EMF, while the absence of tissue eosinophilia in organs other than the heart in tropical EMF may reflect racial and environmental differences between tropical and western geographical areas that have still to be elucidated. That EMF occurs in Europeans who have lived in the tropics is undoubted, but the absence of right ventricular involvement in Europeans in the tropics, but not in temperate climes, is unexplained; perhaps it is a chance finding. It is also apparent that the extreme degrees of right ventricular EMF that are commonly seen in the tropics, with almost complete obliteration of the ventricular cavity are not usually seen in eosinophilic EMF in temperate areas. Involvement of both ventricles and of both atrioventricular valves is, however, common both in the tropics and in temperate climate EMF.

Endomyocardial Fibrosis↗
PubMed1983

Clinical features of fifteen patients with the hypereosinophilic syndrome.

Fifteen patients with the hypereosinophilic syndrome were studied during a period of 6.5 years. The mean age at onset was 36 years. Two were female. The commonest presenting symptoms were nocturnal sweating with or without severe coughing attacks, symptoms of cardiovascular disease, anorexia and weight loss, neurological and gastrointestinal symptoms and itching with or without skin lesions. The mean blood eosinophil counts at presentation were 20.1 X 10(9)/l. Eight patients had previous allergic or parasitic disease which could have predisposed them to the development of hypereosinophilia. Eight patients had raised serum immunoglobulin levels: IgM in five, IgE in four and IgG in one. Five of nine patients had raised serum eosinophil cationic protein levels. Episodes of clinical relapse occurred with increased white blood counts and were treated with prednisolone and cytotoxic drugs. Thrombotic and embolic complications developed in 10 patients, despite treatment with anticoagulants and inhibitors of platelet function, and were the cause of death in three. Two patients with severe endomyocardial fibrosis responded well to cardiac surgery, and a third required emergency mitral valve replacement. The 12 surviving patients have lived 0.8-11.5 years (mean 4.4), since the onset of their illness. It is concluded that the hypereosinophilic syndrome has distinctive features with an episodic course. The principal complications affect the cardiovascular system, especially endomyocardial fibrosis and thromboembolic occlusion of large and small blood vessels in many organs. Although treatment is usually effective in overcoming relapses, the underlying disease process appears to be unaffected. Despite this, patients can have prolonged periods of remission and may survive for many years.

Adolescent↗
PubMed1983

Cardiovascular features of 11 patients with eosinophilic endomyocardial disease.

This report describes the clinical features, cardiac investigations and treatment of eleven patients with biventricular eosinophilic endomyocardial disease, who were followed up for a mean of 3.2 years. Three patients died. Five patients presented with heart disease and hypereosinophilia. Six other patients presented with hypereosinophilia and developed cardiac disease later. Histological studies showed early acute necrotic lesions in five patients, later thrombotic lesions in one and late fibrotic lesions in three patients. Endomyocardial biopsy was the method of choice for diagnosing early acute necrotic and thrombotic lesions. Late fibrotic lesions were best shown by amplitude processed 2D echocardiography and angiocardiography. Episodes of heart failure responded well to treatment with prednisolone which appeared to inhibit progression of heart disease in two patients. Three patients with severe ventricular disease and valvular regurgitation responded well to surgical treatment. This longitudinal study has shown that eosinophilic endomyocardial disease can now be investigated and treated effectively at each stage from early sub-clinical lesions to late incapacitating endomyocardial fibrosis.

Adult↗
PubMed1982

Platelet kinetics in congenital heart disease.

The survival of 111indium labelled platelets has been determined in a series of 47 subjects comprising nine with cyanotic congenital disease (Eisenmenger's syndrome), seven with congenital heart disease associated with left to right shunts, six with primary pulmonary hypertension, six with peripheral vascular disease, 11 with cardiac disorder associated with low cardiac output and eight normal volunteers. Compared with the value in the normals of 9.5 days, mean survival was significantly shortened in those with Eisenmenger's syndrome (8.4 days) and with peripheral vascular disease (8.5 days). It was normal in patients with left to right shunts (9.5 days). Gamma camera imaging in selected patients failed to reveal any abnormal sites of deposition of labelled platelets except in one patient with peripheral vascular disease who had bilateral abnormal activity in his lower limbs and a shortened platelet survival (8.0 days). From theoretical considerations, it was concluded that the reduction in platelet survival in Eisenmenger's syndrome was such that, had it been the result of pulmonary intravascular platelet deposition, abnormal activity should have been visible on chest scanning with the gamma camera. The absence of scintigraphic evidence of abnormal platelet deposition in the lungs of these patients, combined with the linear configuration of their platelet survival curves, suggests that the accelerated platelet destruction is in the reticuloendothelial (RE) system rather than intravascular. Indirect evidence in favour of increased RE destruction of platelets in Eisenmenger's syndrome was the finding of an approximate doubling of intrasplenic platelet transit time, indicating abnormal platelet pooling within the spleen.

Blood Platelets↗
PubMed1982

Non-invasive assessment of diastolic function in hypertrophic cardiomyopathy on and off beta adrenergic blocking drugs.

Beta adrenergic blocking drugs in hypertrophic cardiomyopathy provide symptomatic relief but their effect on long-term prognosis is uncertain. Thirty patients were studied non-invasively by simultaneous recordings of echocardiogram, apex-cardiogram, phonocardiogram, and electrocardiogram in order to assess diastolic abnormalities on and off oral beta adrenergic blocking drugs. While on treatment these patients had a mean dose of propranolol 200 mg/day. The treatment was stopped for one week and then non-invasive assessment was repeated. The following diastolic time intervals were studied: isovolumic relaxation period (A2-mitral valve opening); rapid relaxation period (A2-O point of the apexcardiogram), and the period from mitral valve opening to the O point of the apexcardiogram (Mo-O) when most of the filling of the left ventricle occurs. The prolongation of the rapid relaxation period reflects a reduced rate of fall of the left ventricular pressure when the pressure differential does not change between A2 and the O point of the apexcardiogram, and in this study this period was prolonged in 19, shortened in eight, and remained the same in three patients after beta blockade. The Mo-O point was prolonged in 22, shortened in seven, and was unchanged in one patient after beta adrenergic blocking drugs. All these results were independent of heart rate. In conclusion the response of diastolic time intervals to beta blocking drugs in hypertrophic cardiomyopathy was variable but there was a significant number of patients in whom the time available for filling of the left ventricle was prolonged, suggesting better filling possibly because of improved distensibility of the left ventricle after beta adrenergic blocking drugs.

Adolescent↗
PubMed1982

Echocardiographic features of eosinophilic endomyocardial disease.

Nine patients with eosinophilic endomyocardial disease who had undergone angiocardiography with histological staging of their disease, were studied by M-mode and two dimensional echocardiography to determine the extent to which specific features of the disease could be evaluated by these non-invasive methods. In seven patients, amplitude processed two dimensional echocardiography showed regions where the relative intensity of endomyocardial echoes was greater than normal, and their distribution corresponded to known areas of fibrosis. Standard two dimensional echocardiography was normal in all but three patients. In eight patients M-mode echocardiography showed only non-specific abnormalities, but appeared to be useful in assessing the functional consequences of myocardial or mitral valve disease. After digitisation a reduction in the duration and an increase in the peak rate of dimension increase during filling was prolonged. It was concluded that amplitude processed two dimensional echocardiography might be useful in diagnosing the extent and severity of endomyocardial disease in patients with hyperosinophilia. These noninvasive techniques may thus provide a means for the early diagnosis of endomyocardial fibrosis and could be useful in assessing in progression or response to treatment.

Adult↗
PubMed1982

The natural history of left ventricular hypertrophy in hypertrophic cardiomyopathy: an electrocardiographic study.

The natural history of electrocardiographic left ventricular hypertrophy was assessed in relation to clinical features, treatment with propranolol and prognosis in 100 patients with hypertrophic cardiomyopathy who were followed 5--20 years (mean 8 years). Seventy-one patients received propranolol, 120--800 mg/day (mean 240 mg). At diagnosis, the voltage measurement from SV1 + RV5 was 37 +/- 20 mm, the R wave in aVL was 12 +/- 6 mm and the mean frontal plane voltage was 15 +/- 10 mm. After 5 years, these values were increased to 43 +/- 22 mm (p less than 0.0002), 14 +/- 6 mm (p less than 0.003) and 17 +/- 10 mm (p less than 0.01), respectively. Neither a left ventricular outflow tract gradient nor propranolol treatment influenced these voltage changes. Twenty patients had an increase of more than 10 mm in SV1 + RV5, which was associated with exertional chest pain (p less than 0.006) and death (p less than 0.02). Four patients had a decrease of more than 10 mm in SV1 + RV5. Two of these received high-dose propranolol, one 720 mg/day for 12 years and another 800 mg/day for 12 years. No other patient received more than 480 mg of propranolol daily. In hypertrophic cardiomyopathy there is electrocardiographic evidence of progressive hypertrophy, which is associated with poor prognosis and is not influenced by treatment with propranolol in moderate dosage. Regression of hypertrophy is rare and may be related to long-term treatment with high-dose propranolol.

Adolescent↗