Russell S. Fisher

Epidemiological Study of Sudden and Unexpected Deaths due to Arteriosclerotic Heart Disease

A study of sudden unexpected nontraumatic deaths was begun on June 1, 1964. A sample of all nontraumatic deaths in Baltimore residents between the ages of 20 and 64 from June 15, 1964, to June 14, 1965, was obtained. The deaths were then studied by reviewing all available medical information in order to determine: (1) whether the death was possibly sudden or not and (2) the accuracy of the diagnosis reported on the death certificate. The next of kin or other relative or friend of each deceased person who died suddenly was then interviewed.For comparison, information was obtained on (1) a probability sample of the Baltimore population, and (2) deaths due to arteriosclerotic heart disease (ASHD deaths) that were found to be “not-sudden.”There were 1,857 deaths in the original sample, of which 589 were sudden according to the definition of sudden death. After adjustment for sampling, it was estimated that 1,178 (32%) of the total 3,648 deaths in Baltimore were sudden. Arteriosclerotic heart disease (ASHD) accounted for 58% and the cardiovascular group together for 69% of the sudden deaths.Sixty per cent of all ASHD deaths were sudden. Of the 1,030 ASHD deaths in Baltimore City between the ages of 40 and 64, 20.6% occurred outside of a hospital and 46.2% represented deaths on arrival at a hospital. Only 18.9% of all ASHD deaths occurred after the first 24 hours of hospitalization.By use of data provided in several crosssectional and prospective studies, it was estimated that 22% of new coronary events were sudden deaths and that the case-fatality rate was 31%.In approximately half of the ASHD sudden deaths the deceased had a history of heart disease prior to death and in 24% the deceased had seen a physician within the week prior to death. Unfortunately we were not able to determine the reasons for these visits.In considering the implications of these findings with regard to the prevention of ASHD deaths, it would appear that prevention of only a comparatively small percentage (8.2%) of ASHD deaths is completely dependent on primary prevention. For the remaining ASHD deaths a combination of both primary and secondary prevention may be effective. Because of the rapidity of death and the high frequency of these deaths either occurring outside of a hospital or being called deaths on arrival, hospital treatment may well have little effect on reducing the ASHD mortality, while, on the other hand, the combination of better and earlier diagnosis and intensive treatment in a hospital could conceivably re- duce the mortality.

Alcohol and motorcycle fatalities.

A series of 99 fatal motorcycle crashes in Maryland was studied retrospectively, using police and medical examiner records. Blood alcohol concentrations were determined for 62 motorcycle drivers; measurable amounts of alcohol were found in two-thirds (41), and one-half (31) had illegally high concentrations of 100 mg/100 ml or more. The police report mentioned alcohol in only 9 instances. High blood alcohol concentrations were found most commonly among drivers age 20-34.

Carbon monoxide and heart attacks.

A study of the relationship between carbon monoxide exposure and heart attacks was conducted in Baltimore. There was no evidence of clustering of either myocardial infarction or sudden ASHD on a specific day, nor was there correlation between the number of cases per day and ambient CO levels. Postmortem HbCO levels were slightly higher in ASHD sudden deaths than in sudden deaths due to other causes. Any differences were probably primarily due to cigarette smoking. Cigarette smokers who died suddenly due to ASHD had substantially higher postmortem HbCO levels than nonsmokers. Practically all of the elevated HbCO levels could be related to cigarette smoking or specific environmental exposure. There were no differences between HbCO levels in ASHD sudden death patients and in living controls. There was also no relationship between cardiac pathologic findings and postmortem HbCO levels among patients dying suddenly of ASH.

An epidemic of deaths attributed to fatty liver in Baltimore.

Abstract Death rates due to cirrhosis of the liver have increased substantially in the past 20 years. Previous studies have noted that sudden deaths in which a fatty liver was the major pathological finding accounted for a large part of the increase in death rates. The current study of sudden nontraumatic deaths in Baltimore noted that 40% of the “cirrhosis” deaths were sudden. Fatty liver sudden deaths accounted for 25% of the total nontraumatic sudden deaths. Cirrhosis and fatty liver death rates were much higher in men than women and in blacks as compared to whites. Most fatty liver sudden deaths were unwitnessed. The majority of those dying did not have high blood alcohol levels. At postmortem examination, the liver was usually enlarged. Microscopic examination revealed extensive fatty change often with increased eosinophilia of hepatocytes and the presence of Mallory bodies in about 20%. In about half of the fatty liver sudden deaths there was also some degree of periportal fibrosis.

Epidemiological and Ecological Study of Risk Factors for Narcoties Overdose

Histopathological study of lungs in cases of fatal narcotism, addicts with death due to other causes, nonaddict controls, nonnarcotic drug overdose-hypersensitivity deaths, and nonaddicts with fatal liver disease, was made to (1) determine possible meehanism(s) involved in heroin-induced pulmonary edema, and (2) identify risk factors. Maximum number of narcotics overdose deaths in Maryland during 1968 to 1971 occurred from June to October. Allergic diathesis was considered, but rates of such allergies as asthma and those related to food and drugs were not significant for overdose cases. Significant lung abnormalities differentiated cases of fatal narcotism from fatal bronchial asthma, drug-anaphylaxis, and nonnarcotic drug overdose. Acute inflammatory response was apparent in overdose cases, but in the absence of vasculitis, an Arthus-fike reaction seemed unlikely. Anaphylactic-like response in overdose cases also appeared unlikely.