PubMed Health⌕ Search

Biomedical subjects

J R Hangartner

Publications and source records attributed to J R Hangartner.

7 recordsLinked to original sources
PubMed1989

Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death.

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.

Acute Disease↗
PubMed1989

Malignant primary pulmonary paraganglioma.

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.

Female↗
PubMed1986

Morphological characteristics of clinically significant coronary artery stenosis in stable angina.

All segments of clinically significant stenosis in the coronary arteries of 54 men with stable angina were categorised according to the position of the plaques (eccentric or concentric) and the presence or absence of a pool of extracellular lipid. In the group as a whole, stenosis of greater than 50% by diameter was caused by concentric fibrous plaques in 48% of lesions, by concentric lipid plaques in 28%, by eccentric fibrous plaques in 12%, and by eccentric lipid plaques in 12%. In addition, 43 of the 54 patients had one or more stenoses with multiple channels (recanalisation). Eccentric plaques with an arc of normal vessel wall occupying more than 16% of the circumference of the residual lumen were considered to have a vasospastic potential and made up 15% of all lesions with stenosis of greater than 50% by diameter. Forty four per cent of plaques causing stenosis between 30% and 50% by diameter were eccentric and retained a considerable arc of normal media. These lesions were often in series with segments of higher grade stenosis that did not have an arc of normal media. The overall frequency of plaque types gave no indication of the proportions of different plaque types within an individual. In 15% of patients all the plaques causing greater than 50% diameter stenosis were fibrous and in 13% of patients all the plaques were of the lipid type. Most patients had mixtures of all plaque types in varying proportions. Plaques with a large pool of lipid were not found in 33% of patients whereas they formed greater than 90% of the plaques in 9% of patients. No segments of stenosis > 50% by diameter with a vasospastic potential were found in 44% of the patients but one or more such plaques was present in the the remaining 56%. 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.

Aged↗
PubMed1986

Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death.

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 less than .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 (11/54, 20.4%). Multifocal microscopic necrosis with involvement of the full thickness of the ventricular wall, including the subpericardial zone, was significantly more common (p = less than .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.

Angina Pectoris↗
PubMed1985

The assessment of cardiac hypertrophy at autopsy.

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.

Adult↗