A specific search for intramyocardial platelet aggregates was made in 90 patients who died suddenly of ischemic heart disease. Platelet aggregates in small intramyocardial vessels were found in 27 (30%). There was a significant difference (p < .05) in the incidence of platelet aggregates in patients with chest pain of recent onset (unstable angina) before death (16/36, 44.4%) and that in those without it (1 1/54, 20.4%). Multifocal microscopic necrosis with involvement of the full thickness of the ventricular wall, including the subpericardial zone, was significantly more common (p = < .005) in the patients with platelet emboli (55.6% vs 12.7%). With one exception, aggregates were confined to the segment of myocardium immediately downstream of a major epicardial coronary artery containing an atheromatous plaque that had undergone fissuring and on which mural thrombus had developed. The results support the view that platelet aggregates in the myocardium represent an embolic phenomenon and are a potential cause of unstable angina. The association of myocardial necrosis with such emboli could precipitate sudden death from ventricular fibrillation. Circulation 73, No. 3, 418-427, 1986. WHEN PATIENTS with stable and unstable angina are compared the degree and distribution of stenosis is similar, but unstable angina is associated with stenotic lesions that have a characteristic angiographic morphology.' These type II lesions have morphologic features, including an irregular outline and the presence of intraluminal filling defects outlined by contrast medium,2 that are observed on postmortem angiograms.3'4 Under these circumstances histologic examination reveals atheromatous plaques that have undergone fissuring, rupture, or ulceration and over which nonocclusive (mural) thrombus has formed.When thrombus projects into, but does not totally occlude, the lumen of an artery, there is the potential for emboli to pass distally into the segment of myocardium supplied by that artery. Such embolization has been postulated to be responsible for the crescendo
Sudden ischaemic death results either from an episode of acute myocardial ischaemia consequent upon coronary thrombosis or from an arrhythmia arising within a scarred left ventricle. Very different proportions of these two groups have been reported in both clinical studies in resuscitated subjects with out-of-hospital ventricular fibrillation, and in necropsy series. In 168 cases of sudden death due to ischaemic heart disease coming to necropsy 73 (43.5%) had mural intraluminal coronary thrombi, 50 (29.8%) had occlusive intraluminal thrombi, and 45 (26.7%) had no intraluminal thrombi, giving a ratio of 2.7:1 for those with and without coronary thrombosis. Single vessel disease, the presence of acute infarction at autopsy and prodromal symptoms were positively associated with the presence of coronary thrombosis. Conversely, the presence of old myocardial infarction at necropsy, a known clinical history of ischaemic heart disease and triple vessel disease were associated with the absence of acute thrombosis. The reported variation in the incidence of coronary thrombi in sudden ischaemic death can be largely explained by selection of subjects with those clinical characteristics which are positively or negatively associated with coronary thrombosis.
Three patients (6%) each had five separate segments of stenosis with a vasospastic potential.The results indicate that even in a population of men with stable angina in whom diabetes is excluded the distribution of types of atheromatous lesions is very heterogenous.In vivo coronary angiograms demonstrate that pharmacological intervention can lead to significant changes in the diameter of the residual lumen in some stenotic coronary arteries.' The variation of lumen diameter showed by such coronary angiograms and referred to as "dynamic stenosis" has been reviewed2 and is thought to occur in the presence of plaques that are eccentric and thus retain an arc of arterial wall containing medial muscle capable of contraction. While stenotic segments with such a Requests for reprints to Dr J R W Hangartner,
The total weight of the normal adult human heart as well as that of each ventricle is proportional to body size. Body weight is superior to height as a predictor of total heart and isolated ventricular weights. Ventricular wall thickness is an insensitive means of assessing ventricular hypertrophy. Heart weight is a poor predictor of isolated right ventricular mass but a slightly better predictor of isolated left ventricular mass. The only method of determining the presence or absence of hypertrophy with confidence is to use the Fulton technique for isolated ventricular weights. The use of an arbitrary upper and lower limit, as currently used, for isolated ventricular weights obtained by Fulton's method may, however lead to errors in determining the presence or absence of ventricular hypertrophy.
The histological, immunocytochemical, and electron microscopic findings in a case of malignant primary pulmonary paraganglioma are reported. The existence of this rare tumour is evidence for the presence of pulmonary chemoreceptors. Case report A 49 year old nursing auxiliary, a non-smoker, presented with a three month history of pleuritic pain in the right shoulder and a cough with white sputum; she had noticed increased breathlessness during this period. On examination there were diminished breath sounds over the right upper lobe. A chest radiograph showed a shadow in the right upper lobe, which extended anteriorly to the pleura.Right anterior mediastinotomy through the second intercostal space disclosed a group of enlarged lymph nodes overlying the main pulmonary artery and a separate large mass within the right upper lobe of the lung. At bronchoscopy the anterior segment of the right upper lobe bronchus was found to be obstructed. Endobronchial biopsy specimens showed no mucosal abnormality. As no other primary lesion was found the patient underwent a right pneumonectomy through the fifth intercostal space. A tumour occupied the greater part of the right upper lobe: a mass of enlarged subcarinal and paratracheal nodes surrounded the main bronchus and extended round the right pulmonary artery. The right lung and the enlarged nodes were excised and she made an uneventful recovery. Repeat computed tomography at three months showed no recurrence. She remains well with
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