Cardiovascular Diseases: Genetic Susceptibility, Environmental Factors and Their Interaction covers the special heritability characteristics and identifying genetic and environmental contributions to cardiovascular health. This important reference provides an overview of the genetic basis of cardiovascular disease and its risk factors. Included are important topics, ranging from lifestyle choices, risk factors, and exposure, to pollutants and chemicals. Also covered are the influences of Mendelian traits and familial aggregation and the interactions and interrelationships between genetics and environmental factors which, when compared, provide a sound understanding of the interplay between inherited and acquired risk factors. The book provides a much needed reference for this rapidly growing field of study. By combining the latest research within the structured chapters of this reference, a better understanding of genetic and environmental contribution to cardiovascular disease is found, helping to substantiate further investigations in the field and design prevention and treatment strategies. Provides an overview of the genetic basis of cardiovascular disease and its risk factors Reviews several large population-based studies which indicate that exposure to several environmental factors may increase CVD morbidity and mortality, exploring the plausibility of this association by data from animal studies Reflects on future studies to help understanding the role of genes and environmental factors in the development and progression of cardiovascular disease

Annotation Although it is widely recognized that environmental factors such as smoking, diet, exercise, and socioeconomic status affect the risk of cardiovascular disease, recent work showing the effects of other environmental factors provides a more complete assessment of the situation. This view has emerged from three developments. Firstly, there has been a sudden explosion in the prevalence of diabetes and obesity which indicates a strong environmental component. Secondly, there is an accumulation of evidence suggesting that most cases of these diseases could be prevented by healthy lifestyle choices. Finally, studies have shown that exposure to environmental pollutants has a significant effect on heart disease risk. This book is the first to provide a comprehensive account of the effects of pollutants on heart disease and to integrate this area of research within the overall theme of environmental cardiology. The introductory chapter outlines the effects of different aspects of the environment on heart disease and provides a context for the discussion that follows. Subsequent chapters give an overview of the effects of particulate matter and discuss the epidemiological studies supporting the link. The book then goes on to cover the effects of pollution on different aspects of cardiovascular disease (hypertension, stroke, heart failure, ischemic heart disease and atherogenesis). Because of a close association between diabetes and heart disease, a discussion of the effects of particulate matter on diabetes is also included. Later chapters discuss the effects of individual pollutants such as vehicular emissions, metals and aldehydes. A review on manufactured nanoparticles is incorporated because these particles represent an important new threat to cardiovascular health. The understanding that emerges from this monograph suggests that we must be more alert to the effects of the environment and develop strategies that target, not only the diseased individual, but also the unhealthy, disease-causing environment. It is essential reading for cardiologists, epidemiologists, urban planners and pollution control specialists.

This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.

This book provides an introduction to the principles of both cardiovascular epidemiology and molecular pathophysiology; as a unique aspect, it also outlines and discusses the molecular concepts underlying epidemiological observations. This first volume is focused on the genetic and molecular basis of pathogenesis and the role of environmental factors triggering cardiovascular dysfunctions. The book promotes the use of interdisciplinary approaches in the field of preventive medicine based on recent advances in molecular and cellular pathophysiology. The book offers a valuable resource for researchers in basic biomedical fields and clinical scientists alike, as well as guidelines for novel avenues of research in both basic pathophysiology and cardiovascular therapy and prevention.

Annotation This book addresses one major question: Why do men get more heart disease than women? Recent global trends in heart disease show that traditional coronary risk factors, such as elevated blood pressure and cholesterol are poor candidates in explaining the gender gap in heart disease. Changes in these risk factors also cannot explain the recent cardiovascular disease epidemic among middle-aged men in Eastern Europe. This book will focus on environmental, behavioral, and psychosocial variables, as well as new risk factors of a biological nature in an attempt to understand the gender gap in heart disease. It combines perspectives from numerous disciplines, such as demography, epidemiology, medicine, sociology, and psychology. This book features the work of a distinguished group of international researchers appearing in Richard Stone's report on "Stress: the invisible hand in Eastern Europe's death rates" (Science, vol. 288, June 9, 2000, pp. 1732-33). It combines perspectives from numerous disciplines, such as demography, epidemiology, medicine, nutrition, sociology, and psychology to explore the environmental, behavioral, and psychosocial influences on men's greater susceptibility to heart disease

Cardiovascular disease is the main cause of death in Sweden and other developed countries. The purpose of this thesis is to assess the role of certain environmental factors in the etiology of cardiovascular disease, expressed as hypertension and myocardial infarction, focusing on aircraft noise, environmental tobacco smoke, drinking water hardness, and ambient air pollution. The thesis is based on two epidemiological materials, i.e. an Environmental Health Survey (EHsurvey) in Stockholm county during 1997 and the Stockholm Heart Epidemiology Program (SHEEP), which is a county-wide case-control study of myocardial infarction 19921994. Aircraft noise exposure was assessed for 266 residents in the vicinity of Arlanda airport and 2693 inhabitants in other parts or the county who answered the EH-survey. The SHEEPstudy, comprising 2246 cases of myocardial infarction and 3206 population controls, was used to investigate the importance of exposure to environmental tobacco smoke, intake of drinking water magnesium and calcium, and exposure to source-specific residential air pollution. Exposure to energy-averaged aircraft noise above 55 dBA was associated with an adjusted odds ratio for hypertension of 1.59 (95% Cl 1.00-2.53), and maximum aircraft noise above 72 dBA was associated with an adjusted odds ratio of 1.76 (95% Cl 1. 12-2.77). A dose-response relation between aircraft noise and hypertension prevalence was suggested. Exposure to environmental tobacco smoke at home and work was associated with an increased risk of nonfatal myocardial infarction among never-smokers, both with regard to intensity, duration, time since last exposure, and cumulative dose. For example, spousal exposure of 20 cigarettes per day or more was associated with an adjusted odds ratio of 1.58 (95% Cl 0.97-2.56), and cumulative combined exposure at home and work was associated with an adjusted odds ratio of 1.55 (95% Cl 1.022.34) in the top decile of exposure. An inter-quartile range increase in th