miological studies have reported positive associations between the risk of coronary heart disease (CHD) and plasma fibrinogen levels. Fibrinogen is the major coagulation protein in blood by mass, the precursor of fibrin, and an important determinant of blood viscosity and platelet aggregation. [38][39][40][41] Because fibrinogen levels can be reduced considerably by lifestyle interventions that also affect levels of established risk factors (such as regular exercise, smoking cessation, and moderate alcohol consumption), there is interest in the possibility that measurement (or modification) of fibrinogen may help in disease prediction or prevention. [38][39][40]42 A meta-analysis of published data from 18 such studies, involving about 4000 CHD cases, indicated a relative risk of 1.8 (95% confidence interval [CI], 1.6-2.0) per 1-g/L increase in plasma fibrinogen level. 43 However, such analyses are not able to provide detailed assessments of the nature of any independent association of fibrinogen level with CHD or with other vascular and nonvascular outcomes. [43][44][45] This meta-analysis differs from previous analyses in several ways that should increase its reliability and scientific value. First, it is large and comprehensive: the data comprise 6944 first nonfatal myocardial infarction (MI) or stroke events and 13 210 deaths (cause-*The Authors/Writing Committee, Authors/Members, and Other Members of the Fibrinogen Studies Collaboration are listed at the end of this article.

A central database has been established containing data on plasma fibrinogen, sex and other potential confounding factors, age at baseline fibrinogen measurement, age at event or at last follow-up, major vascular morbidity and cause-specific mortality. Information about any repeat measurements of fibrinogen and potential confounding factors is being sought to allow study-specific correction for regression dilution. The analyses will involve age-specific regression models. Synthesis of the available prospective studies of plasma fibrinogen will yield information on more than 10000 incident cardiovascular deaths and events among the approximately 200000 total participants who have been monitored, on average, for about 10 years.

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Background/Introduction There is scant information on the geographic variability in the rate of stroke incidence as it relates to the demographics, comorbidities, risk factors, and insurance type. Purpose/Methods County-level data on four modifiable groups of health factors including healthy behaviors, clinical care, physical environment, and socioeconomic conditions were obtained from the Robert Wood Johnson Foundation. The percentage of persons 65 years or older, smokers, physically inactive, obese, diabetics, heavy drinkers, college graduates, low income, unemployed, uninsured heads of single parent households, and residence in areas of violent crime was used in predicting fatal or non-fatal stroke. The counties were lumped into 5 categories based on similarities of the above characteristics. The incidence of fatal and non-fatal stroke was compared among the 5 county clusters using a mixed-effects regression model. Results The incidence of fatal and non-fatal stroke was significantly lower (p<0.0001) in cluster 3, where residents had higher income, were better educated, and were less likely to be unemployed, to live in single parent households, to have diabetes, to be obese, to smoke, to be physically inactive, or to live in communities with violent crime. The percentage of persons older than 65, violent crime rate, and obesity were identified as significant predictors of stroke using a mixed-effects regression model. Conclusions This study indicates that the incidence of stroke is higher in areas with older population, higher rate of obesity, and in regions with more violent crime. In order to improve health outcomes, preventive measures for stroke should address environmental factors in addition to the known cardiovascular risk factors. Acknowledgement/Funding Robert Wood Johnson Foundation

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Summary:Full recovery occurred after 15 months of severe congestive heart failure in a patient with peripartum cardiomyopathy. Clinical improvement was noted when propranolol was added to conventional therapy.