Myocarditis--a case of mistaken identity?
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Biomedical subjects
Publications and source records attributed to E G Olsen.
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A retrospective study has been carried out on the necropsy material from 30 patients who have died after a clinically diagnosed myocardial infarction. This study has been undertaken to compare the reliability of the fluorescence of infarcted myocardium when stained by haematoxylin and eosin and an adjacent section stained by the haematoxylin basic fuchsin picric acid (HBFP) method to detect early ischaemia. The results showed that the fluorescence technique is reliable, reproducible and coincides with the findings obtained by HBFP stain.
The studies leading up to the unitarian concept suggesting that endomyocardial fibrosis, described in the tropics, and Löffler's endocarditis parietalis fibroplastica (Löffler's endomyocardial disease), described in the temperate zone, belong to the same disease spectrum are detailed. Evidence that the eosinophil is involved in the pathogenesis of endomyocardial diseases, irrespective of the geographical origin, is presented. The findings of a similar abnormality in these cells obtained from patients in the tropical and temperate zones are briefly mentioned. In view of the evidence it is proposed that endomyocardial disease, associated with abnormal eosinophils, hitherto classified under the restrictive type of cardiomyopathy, be removed from this classification and reclassified under 'specific heart muscle disease'.
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.
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.
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The rabbit cornea endothelium has been studied with specular and scanning electron microscopy after exposure with a commercially available ultraviolet lamp. The animals were plased 50 cm from the source, and most experiments were run with a 20 min exposure time. In the specular microscope, the endothelium revealed numerous circumscript reflex-free areas, which were observed from 4 days up to 8 months after the irradiation. A wide variety of changes were found in the scanning electron microscope. One day after the exposure the cells showed indistinct outlines, and they were bulging into the anterior chamber. In some regions the pattern was dominated by marked grooves preferentially along the cell demarcations, whereas other regions showed rough surfaced cells because of cytoplasmic projections and grainy deposits. At the 3 days stage there was a marked pleomorphy, and some cells were on their way to being rejected. After one week the cobblestone appearance of the endothelium was about to decline. Partly rejected cells were still common. In addition, distinct, ringshaped local impressions occurred imitating the previous described grooves. This phenomenon along with some single endothelial cells studied with microvilli were the abnormal findings 8 months after the damage. It is concluded that although ultraviolet radiation is largely absorbed in the cornea, the threshold dose for damage of the endothelium is not beyond those used for practical purpose. The endothelium was surprisingly resistant towards repeated radiation damage.
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Pathological studies in seven hearts from patients with dilated cardiomyopathy have shown that the number of neurons is significantly reduced in these compared with five hearts from normal subjects. The number of ganglion cells was counted in a strip of right atrial wall between the venae cavae and sectioned serially. The mechanism responsible for the neuronal depopulation in this type of cardiomyopathy could not be determined. Previous viral infection may be causally related. Three hearts of patients suffering from chronic Chagas's heart disease were also studied. Depopulation of neurons was most severe in the hearts with Chagas's disease and less severe in those with dilated cardiomyopathy, though neurons were still significantly reduced in number in the latter compared with normal controls. Despite the lack of a specific, definite cause for the depopulation of neurons, physiological evidence of parasympathetic impairment in patients with dilated cardiomyopathy is in agreement with the pathological findings. It is suggested that on the basis of our findings neuronal depopulation in some patients with dilated cardiomyopathy may be of aetiological significance.
Porcine aortic valves stored in various concentrations of sucrose (50-80%) for up to 52 weeks were examined both histologically and by electron microscopy. The valves were compared with porcine aortic valves stored in a nutrient and antibiotic medium for 12 weeks. Overall preservation was better in those porcine valves stored in sucrose solution than in nutrient and antibiotic medium, the best preservation being in 50% sucrose. Despite wide separation of collagen at that concentration seen on electron microscopy (not noted histologically), tissue preservation was good after storage in sucrose solutions at concentrations up to 80%, at which clumping of collagen and distortion of fibroblasts occurred. It is suggested that sucrose solution is acceptable for the long-term preservation of biological valves.
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Autonomic function was investigated in patients with congestive (dilated) cardiomyopathy and compared with that in controls. Heart-rate and blood-pressure were recorded during physiological and pharmacological interventions and plasma noradrenaline concentration was measured at rest and when the physiological interventions produced a peak response. The results indicate that even at an early (pre-failure) stage of the disease parasympathetic function is impaired but no significant increase in sympathetic activity occurs at this stage.
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