Adv. Cardio!., vol. 25, pp. 96-97 (Karger, Basel 1978)
Sudden Coronary Death and Coronary Artery Disease! V.
RISSANEN
Department of Medicine, University of Kuopio, Kuopio
1 This
is a summary of the paper presented. A complete version has been sub-
mitted for publication elsewhere.
Downloaded by: University of Cambridge 131.111.164.128 - 3/17/2019 10:47:20 PM
Understanding of the role of coronary artery disease (CAD) as a cause of sudden death (SD - death within 24 h of onset of symptoms) at the population level is still imperfect. Similarly, it is not clear whether the risk factors for CAD are associated with increased risk of death due to premature, accelerated development of atherosclerosis or because of a different myocardial response to coronary stenosis. Little is known of factors related to individual tolerances of varying degrees of coronary stenosis. The above problems were investigated in postmortem series, (1) 214 male violent deaths [1] and (2) 254 male and 37 female cases of SD due to CAD [2, 3]. It was found, that the mean extent of the coronary raised lesions was significantly higher in the age-matched SD cases than in violent deaths, though marked overlapping was characteristic. Cigarette smoking was associated with increased risks for SD and CAD. CAD at younger ages reaches the threshold level of severity for risk of SD more frequently in smokers than in nonsmokers. Stress factors are known to precipitate acute attacks of CAD. It may then be asked whether stress factors can cause SD even without severe CAD. In the present series, SD seemed to occur only if the involvement of the coronary arteries had reached the critical level of severity. The suddenness of death did not correlate with the severity of CAD. There was evidence suggesting that severe stenosis in the RCA is a major finding in SD, while in AMI deaths at hospital, a major finding tends to be severe occlusion of LADB. The condition of the myocardium also seems to affect the risk for SD. Multiple coronary occlusions were more frequent among patients with
RISSANEN
97
previous myocardial infarction. Previous infarctions have obviously weakened the condition of the heart as a result of both the myocardial damage and the thrombotic obstruction. The mean age of SD patients with single vessel disease was lower than that of those with double or triple vessel disease. The sex ratio (males/ females) in the group of single vessel disease (1.0/0.9) was different from that suffering double and triple vessel disease (3.7/1.0). It thus appears that the lowest range of CAD severity in SD represents a special group of patients in whom the factors contributing to SD may be different from those at work in the groups with more severe CAD. It can be concluded that there is a critical level of severity of CAD which determines the risk of SD. The more severe the CAD within this range, the higher the risk. CAD alone, however, is not a selective factor for sudden or nonsudden death among the critical population. There are factors which determine the age and frequency of persons reaching the critical level of CAD severity (atherogenic factors) which influence the selection of SD victims (precipitating factors) and which determine the individual variation of CAD severity with which CAD and SD manifest themselves (sensitising-protecting factors). Every annual cohort of SD includes many patients (about 1/3) with extremely severe CAD ('bumedout disease'). The majority of SDs can, however, be prevented. For prevention we should (a) minimise the number of people who reach the critical level of CAD severity 'too early' , (b) minimise those factors and events which influence the selection of SD victims from the critical population, and (c) minimise the risk of SD, particularly within the low ranges of CAD severity ('viable patients'). References
2
3
RISSANEN, V.: Coronary atherosclerosis in cases of coronary death as compared with that occurring in the population. A study of a medico-legal autopsy series of coronary deaths and violent deaths. Ann. c1in. Res. 7: 412-425 (1975). RISSANEN, V.; ROMO, M.; SARNA, S., and SILTANEN, P.: Deaths from ischemic heart disease in persons aged 65 or younger in Helsinki in 1970. With special reference to patho-anatomic findings in hearts. Acta med. scand. 197: 51-60 (1975). RISSANEN, V.: Sudden coronary death and coronary artery disease. A clinicopathologic appraisal (in press).
V. RISSANEN, MD, University Central Hospital, University of Kuopio, SF-7021O Kuopio 21 (Finland)
Downloaded by: University of Cambridge 131.111.164.128 - 3/17/2019 10:47:20 PM
1
Sudden Coronary Death and Coronary Artery Disease! V.
RISSANEN
Department of Medicine, University of Kuopio, Kuopio
1 This
is a summary of the paper presented. A complete version has been sub-
mitted for publication elsewhere.
Downloaded by: University of Cambridge 131.111.164.128 - 3/17/2019 10:47:20 PM
Understanding of the role of coronary artery disease (CAD) as a cause of sudden death (SD - death within 24 h of onset of symptoms) at the population level is still imperfect. Similarly, it is not clear whether the risk factors for CAD are associated with increased risk of death due to premature, accelerated development of atherosclerosis or because of a different myocardial response to coronary stenosis. Little is known of factors related to individual tolerances of varying degrees of coronary stenosis. The above problems were investigated in postmortem series, (1) 214 male violent deaths [1] and (2) 254 male and 37 female cases of SD due to CAD [2, 3]. It was found, that the mean extent of the coronary raised lesions was significantly higher in the age-matched SD cases than in violent deaths, though marked overlapping was characteristic. Cigarette smoking was associated with increased risks for SD and CAD. CAD at younger ages reaches the threshold level of severity for risk of SD more frequently in smokers than in nonsmokers. Stress factors are known to precipitate acute attacks of CAD. It may then be asked whether stress factors can cause SD even without severe CAD. In the present series, SD seemed to occur only if the involvement of the coronary arteries had reached the critical level of severity. The suddenness of death did not correlate with the severity of CAD. There was evidence suggesting that severe stenosis in the RCA is a major finding in SD, while in AMI deaths at hospital, a major finding tends to be severe occlusion of LADB. The condition of the myocardium also seems to affect the risk for SD. Multiple coronary occlusions were more frequent among patients with
RISSANEN
97
previous myocardial infarction. Previous infarctions have obviously weakened the condition of the heart as a result of both the myocardial damage and the thrombotic obstruction. The mean age of SD patients with single vessel disease was lower than that of those with double or triple vessel disease. The sex ratio (males/ females) in the group of single vessel disease (1.0/0.9) was different from that suffering double and triple vessel disease (3.7/1.0). It thus appears that the lowest range of CAD severity in SD represents a special group of patients in whom the factors contributing to SD may be different from those at work in the groups with more severe CAD. It can be concluded that there is a critical level of severity of CAD which determines the risk of SD. The more severe the CAD within this range, the higher the risk. CAD alone, however, is not a selective factor for sudden or nonsudden death among the critical population. There are factors which determine the age and frequency of persons reaching the critical level of CAD severity (atherogenic factors) which influence the selection of SD victims (precipitating factors) and which determine the individual variation of CAD severity with which CAD and SD manifest themselves (sensitising-protecting factors). Every annual cohort of SD includes many patients (about 1/3) with extremely severe CAD ('bumedout disease'). The majority of SDs can, however, be prevented. For prevention we should (a) minimise the number of people who reach the critical level of CAD severity 'too early' , (b) minimise those factors and events which influence the selection of SD victims from the critical population, and (c) minimise the risk of SD, particularly within the low ranges of CAD severity ('viable patients'). References
2
3
RISSANEN, V.: Coronary atherosclerosis in cases of coronary death as compared with that occurring in the population. A study of a medico-legal autopsy series of coronary deaths and violent deaths. Ann. c1in. Res. 7: 412-425 (1975). RISSANEN, V.; ROMO, M.; SARNA, S., and SILTANEN, P.: Deaths from ischemic heart disease in persons aged 65 or younger in Helsinki in 1970. With special reference to patho-anatomic findings in hearts. Acta med. scand. 197: 51-60 (1975). RISSANEN, V.: Sudden coronary death and coronary artery disease. A clinicopathologic appraisal (in press).
V. RISSANEN, MD, University Central Hospital, University of Kuopio, SF-7021O Kuopio 21 (Finland)
Downloaded by: University of Cambridge 131.111.164.128 - 3/17/2019 10:47:20 PM
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