Postmortem coronary angiography and histological investigation of the conduction system of the heart in sudden unexpected death due to coronary heart disease.

This study has been performed applying postmortem coronary angiography and histological investigation of the conduction system of the heart in 21 persons who died suddenly and unexpectedly because of coronary sclerosis. This "coronary group" is compared with a sex and age matched control group of 24 persons. Acute vascular lesions were found in 20 persons (95.2%), fresh infarctions in 10 (45%), heart rupture in 2 (9.5%) and old infarctions (indicated by localized fibrosis) in 7 (33.3%). The coronary arteries were graded using WHO's recommendations from 1958. Arteriosclerosis of the major coronary arteries was significantly more extensive in the "coronary group". The origin and course of the arteries to the conduction system were located by postmortem coronary angiography. The right coronary artery supplied these arteries in the majority of cases (sinus node artery 77%, a.-v. node artery 85%). A significantly greater degree of arteriosclerosis could be demonstrated histologically in the sinus node artery in the "coronary group". In both groups the degree of arteriosclerosis was greater in the a.-v. node artery than in the sinus node artery. The conduction system was investigated using Hudson's method. There were only 3 cases of infarction in the conduction system, possibly due to its greater resistance to damage from anoxia. In all patients "non-specific changes" (hemorrhage, small cellular infiltrations and/or degeneration) were found and these changes can, therefore, be of no pathophysiological importance in this group of patients. The degree of fibrosis and the amount of fat was semiquantified. Six patients in the "coronary group" had moderate fibrosis around the left sided fibres of the bundle of His. This leads to the conclusion that these changes might play a role in the fatal course, and that some cases of sudden, unexpected cardiac death can be explained by pre-existing fibrosis in the conduction system.