Trends and disparities in coronary heart disease, stroke, and other cardiovascular diseases in the United States: findings of the national conference on cardiovascular disease prevention.

A workshop was held September 27 through 29, 1999, to address issues relating to national trends in mortality and morbidity from cardiovascular diseases; the apparent slowing of declines in mortality from cardiovascular diseases; levels and trends in risk factors for cardiovascular diseases; disparities in cardiovascular diseases by race/ethnicity, socioeconomic status, and geography; trends in cardiovascular disease preventive and treatment services; and strategies for efforts to reduce cardiovascular diseases overall and to reduce disparities among subpopulations. The conference concluded that coronary heart disease mortality is still declining in the United States as a whole, although perhaps at a slower rate than in the 1980s; that stroke mortality rates have declined little, if at all, since 1990; and that there are striking differences in cardiovascular death rates by race/ethnicity, socioeconomic status, and geography. Trends in risk factors are consistent with a slowing of the decline in mortality; there has been little recent progress in risk factors such as smoking, physical inactivity, and hypertension control. There are increasing levels of obesity and type 2 diabetes, with major differences among subpopulations. There is considerable activity in population-wide prevention, primary prevention for higher risk people, and secondary prevention, but wide disparities exist among groups on the basis of socioeconomic status and geography, pointing to major gaps in efforts to use available, proven approaches to control cardiovascular diseases. Recommendations for strategies to attain the year 2010 health objectives were made.

Pancreatic elastase activation as a possible indicator of the relative hazard of different cigarettes.

Levels of elastase activity in homogenates of pancreas from beagle dogs exposed to cigarette smoke on a daily basis for 600 d were previously reported. Elastase activity in pancreatic homogenates from animals exposed to smoke from high-nicotine cigarettes was significantly greater than in sham-exposed controls or in animals smoking low-nicotine cigarettes. In the study described here, dogs were exposed on an acute basis to smoke from high-nicotine and from nicotine-free cigarettes. Anesthetized animals were prepared by laparotomy, duodenotomy, and pancreatic duct cannulation. Pancreatic fluid was collected and preexposure elastase levels were determined. Samples were then taken during exposure to smoke from cigarettes of both types. There was no measurable elastase activity in the baseline samples. Similarly, no activity was found in fluids collected before and during exposure to smoke from nicotine-free cigarettes. Enzyme activity was detected, however, in samples collected during exposure to smoke from high-nicotine cigarettes once blood levels of nicotine reached 50-70 ng/ml. The results suggest that cigarette smoke may provoke activation of elastase and indicate the need for further study of any association of cigarette smoking with pancreatic disease.

Lifestyle factors and cancer of the pancreas: a hypothetical mechanism.

The interaction of a genetically determined protease inhibitor, the enzymes whose functions are modified by that inhibitor and lifestyle factors, such as cigarette smoking, high lipid diet and alcohol consumption, are considered key factors in a proposed protease-antiprotease imbalance mechanism for pancreatic oncogenesis. Epidemiologic and experimental laboratory evidence in support of the mechanism is presented along with a discussion of suggested research initiatives to further test the hypothesis.

Pancreatic elastase and serum alpha 1-antitrypsin levels in beagle dogs smoking high- and low-nicotine cigarettes: possible mechanism of pancreatic cancer in cigarette smokers.

Beagle dogs exposed to cigarette smoke for 600 d experience a significant change in pancreatic elastase levels, as measured in tissue homogenates, compared with their sham-exposed controls. Greater elastase activity was found in the high-nicotine cigarette smokers than in the low-nicotine cigarette smokers. Levels of serum alpha 1-antitrypsin, an antiprotease capable of complexing the excess elastase, were also investigated. Animals smoking high-nicotine cigarettes had significantly lower serum alpha 1-antitrypsin activities than controls. Low-nicotine smokers showed alpha 1-antitrypsin activities that were not significantly different from those of controls. The importance of these observations is reinforced by a number of studies suggesting that proteases, their inhibitors, and an imbalance thereof may be related to the onset of neoplastic lesions. Studies have indicated that antiprotease levels follow the patterns of Mendelian inheritance. Severe deficiency states predispose human subjects to emphysema. A similar relationship may exist between antiprotease levels and susceptibility or resistance to neoplasms of the pancreas, a concept that deserves investigation in light of the findings reported here.