Behavioral Medicine Approaches to Cardiovascular Disease Prevention

Kristina Orth-Gom‚r, Neil Schneiderman, Kristina Orth-Gomer, Kristina Orth-Gom'r

• Publisher: Psychology Press
• Year: 2013
• Topic: Psychology
• eBook ISBN:
  9781134791774
• Subtopic: Applied Psychology
• Index: Psychology

Cardiovascular disease (CVD) is the number one killer of men and women in industrialized countries. In older age groups, CVD is also the most important cause for hospitalization, and, in many countries, it is the basis of early retirement from work. Thus, CVD is associated with enormous costs for care and loss of productivity, as well as for disabilities, pensions, etc. All this has motivated clinicians and scientists to develop and implement new methodologies and technologies to better care for patients who are hospitalized for heart disease.

Efforts to improve care in the acute phases of coronary heart disease (CHD) have been successful. During the last decade, the immediate mortality risk of a patient admitted to coronary care for a suspected myocardial infarction or other acute coronary syndrome has decreased to less than 10%. Despite these achievements, CVD continues to represent a major threat to the health of middle-aged and elderly men and women.

This volume addresses myriad aspects of CHD prevention, including biobehavioral and psychosocial factors, behavioral epidemiology, behavioral intervention models, and policy. The first section of the text provides an introduction to CVD prevention and behavioral medicine. The second section introduces two theoretically different approaches to preventive action, high-risk and population-based strategies. The third section describes and discusses the important questions of how behavioral sciences can be conceptually integrated into traditional, medically based, preventive efforts. The fourth section presents both population and high-risk behavioral intervention approaches.

In summary, this volume examines the social environment and its potentials for preventive actions, reviews the psychosocial and biobehavioral mechanisms involved in these effects, and describes concrete and practical implementations of behavioral medicine knowledge as they have been applied to CHD prevention.

Part I

INTRODUCTION TO CARDIOVASCULAR DISEASE PREVENTION AND BEHAVIORAL MEDICINE

Chapter 1

Concepts and Theories of Prevention: Reasons for Soliciting Behavioral Medicine Knowledge

Kristina Orth-Gomér
Karolinska Institute

Cardiovascular disease (CVD) is the number-one killer of men and women in industrialized countries. In men above age forty and in women above age sixty CVD is the most important cause of death (1). In older age groups, CVD is also the most important cause for hospitalization. Furthermore, in many countries, heart disease is an important cause of early retirement from work. Thus, CVD is associated with enormous costs for care and loss of productivity, as well as for disabilities, pensions, and so on. Furthermore, it is the cause of acute and prolonged suffering in many people. All this has motivated clinicians and scientists to develop and implement new methodologies and technologies to better care for patients who are hospitalized for heart disease.

Efforts to improve care in the acute phases of coronary heart disease (CHD), the most common CVD, have been very successful. In the 1960s and 1970s, the initiation of intensive coronary care units (ICCUs) with continuous monitoring of cardiac activity and prompt therapy of life-threatening complications substantially reduced mortality rates. In an early Swedish trial, patients were randomized to intensive coronary care or traditional inpatient care without continuous surveillance. Mortality fell by 50% in the former group (2).

During the last decade, the immediate mortality risk of a patient admitted to coronary care for a suspected myocardial infarction (MI) or other acute coronary syndrome has further decreased to less than 10%. This can be ascribed to various attempts to limit infarct size before the full development of the myocardial damage has occurred. Thrombolysis, beta blockade, angiotensin converting enzyme inhibitors for patients with early signs of heart failure, and acute surgery have all contributed to these remarkable gains in human lives and well-being (3).

Despite these achievements, CVD continues to represent a major threat to the health of middle-aged and elderly men and women. This is particularly true for middle-aged men in high-risk groups. In men under 65, more than half of deaths from CHD are sudden cardiac deaths. This usually means that they occur before the patient has had a chance to be admitted to a hospital and benefit from the technological advancements of modem acute care. Sudden cardiac deaths often come as a complete surprise, without any known or noticed premonitory symptoms. In a few fortunate cases, the patient happens to be in a place where resuscitation competence and equipment are available. Most often, however, these deaths are medically unattended (4). Therefore, to prevent or postpone these deaths, it seems necessary to address the underlying process before it becomes symptomatic. Sudden cardiac death is less frequent in women than in men, and with increasing age its frequency decreases in both genders. However, the total number of sudden deaths is so large that powerful actions and measures are necessary to deal with the problem. Thus, many facts speak in the favor of prevention (5).

It is often said that there is no cure for CHD once it has occurred, and that the lifelong development of atherosclerosis in the coronary arteries—as well as in other organ vessels such as the brain, kidneys, legs, and aorta—needs to be controlled. It has become known through a variety of pathological studies that this process starts early in life, perhaps in adolescence or early childhood. Thus, it seems necessary to influence this atherosclerotic process at an early stage, and to maintain the effects over a long period of time—indeed, throughout the life span.

These and other facts are the basis for a growing public interest in the epidemiology and prevention of CVD. The insight has become widespread that, even if acute care becomes sufficiently successful that it saves the life of almost every admitted patient, this approach will never be efficient enough from a public health viewpoint. So it becomes evident that efforts in acute care have to be complemented by population-based attempts to prevent or at least slow down the atherosclerotic process. In that way, it has been argued, many more people would be able to lead healthy lives until their seventies or eighties, many unnecessary premature deaths would be postponed, productivity would be increased, and the costs of care, disabilities, and pensions would decrease. Most important, perhaps, the quality of many lives would considerably improve.

CAUSALITY AND THE RISK-FACTOR CONCEPT

How could this goal of preventing a considerable number of disease cases in the population be most efficiently approached? If the true causes of the accelerated atherosclerotic process were recognized, it is conceivable that these could be eliminated and the unhealthy development stopped. If CHD, like some other major diseases and threats to humankind, was caused by a single infectious agent that could be identified, modified, or eradicated, its prevention would be technically possible. In the case of many widespread infectious diseases in Third World populations, it has been estimated, for example, that infant mortality might be reduced by as much as 40% if only proper immunization programs were implemented. In diseases caused by the atherosclerotic process, however, it has proved impossible to identify single causes. Instead, multiple factors associated with an increased risk of an accelerated disease process have been recognized. These factors are referred to as risk factors. This does not imply causality, but only that the factors have been identified as related to the disease process.

It is reasonable to question the extent to which one can rely on evidence derived from statistical associations without having complete scientific control over the entire disease process. Therefore, certain criteria have been postulated that may increase the plausibility of a risk factor being a causal factor. If several of these criteria of the risk factor are met (6), the likelihood of a causal relationship is increased. The eight criteria are:

1. Temporality of events. If it can be demonstrated in prospective studies that the exposure to the risk factor precedes the disease outcome, the likelihood of causality increases.

2. Strength of association. How much of the variance in the outcome variable is explained by the exposure variable? How great is the relative risk associated with the exposure? The greater the risk and the narrower the confidence limits, the more certain is the association.

3. Consistency of associations. If several studies demonstrate similar results, the conclusiveness of results is increased.

4. Biological gradient. If there is an increased risk of adverse outcome with an increase of exposure to the risk factor, likelihood of causality increases.

5. Biological plausibility. Is there evidence of a plausible pathogenic mechanism linking the exposure to the outcome variable? If such mechanisms are identified, associations become understandable and the results are more readily accepted as support for causality.

6. Coherence. If several kinds of studies (e.g., animal, human population, human patient) point in the same direction in their conclusions, the likelihood of causality is increased.

7. Specificity of outcome. If the effects of risk-factor exposure are specific for a particular disease, the likelihood of causality is increased.

8. Experimental/intervention evidence. If there is evidence from intervention studies that the disease can be prevented, more support is provided that the association is based on causality.

Most commonly, the identification of behavioral factors associated with an increased cardiovascular risk has been based on observations of real-life processes. Evidence from experimental studies, in which the entire disease process is kept under control, is usually not provided. Such demonstrations from truly experimental conditions have been carried out using animal models, which are difficult to apply directly to the human situation. Thus, one cannot be entirely sure that the risk factor is a causal factor. Rather, it may be associated with an underlying cause that was not recognized in the observation, but just happened to be associated with both the hypothesized risk factor and the disease outcome. This phenomenon—often encountered in epidemiology and referred to as confounding—causes multiple problems in the interpretation of results. In particular, the results from behavioral epidemiology need to be scrutinized as to various possible sources of confounding.

THE APPLICATION OF BEHAVIORAL MEDICINE IN PREVENTION

Ample evidence has been gathered that the rates of chronic diseases, such as CHD, can be reduced. Often, however, it has been found that net preventive effects on disease incidence or mortality have not been as strong as expected. Even if the effects in the intervention group are satisfactory, the net gain of preventive efforts can become small because favorable changes begin to occur in the control group as well. Usually the mechanisms of these effects have been poorly understood. They may have involved unintended dissemination of health knowledge and health practices to the control group as well as the target group. They may involve a change of therapeutic principles and treatment modalities by health professionals, which were not intended in the prevention project. Finally, they may have affected the health concepts of an entire population, although they were only aimed at specific target groups.

In other cases, unexpected adverse effects have occurred, which may unfavorably influence the disease outcome. An example is official policies against cigarette smoking in public places and workplaces. In some groups under specific conditions, this has led to an increased consumption of snuff tobacco because its use is not as visible and it is believed to be less health damaging. A further complication has been noted when preventive measures have led to the decrease in CHD expected, but other concomitant effects of the treatment were so unfavorable that the decrease in CHD became secondary in importance (7). This has been experienced with pharmacological lipid lowering, which in some cases has led to a decrease in CHD incidence, but also a concomitant rise in mortality from violent causes. Consequently, the net gain for patients has become questionable. The reasons for these effects are not known, but behavioral mechanisms cannot be ruled out (8). It is possible that some of these ambiguities in the conclusions about preventive efforts can be explained by the fact that behavioral factors usually have not been considered to any major extent in prevention projects.

It is quite obvious that any traditional preventive program, primary or secondary, that tries to influence CVD incidence will need to include knowledge and techniques for behavior change, and consider the interactions between physiological and behavioral effects that are so commonly present.

HIGH-RISK AND POPULATION-BASED STRATEGIES IN PREVENTION

Two theoretically different approaches to preventive action have been introduced. With the high-risk approach, the preventive efforts are only directed toward individuals or patients identified through screening or health care registers as being at high risk for CHD. Special efforts are directed toward these persons, mostly on an individual or group basis. Behavior change and behavior modification are crucial components among the preventive tools. It is assumed that if one is able to correctly identify the persons at risk in the population and significantly modify their risk-factor profile, a net and substantial reduction of CHD morbidity and mortality will occur in the target population.

The other approach is based on a different assumption—namely, that changing habits of an entire population, including those who are not recognized as high-risk individuals, but make up the majority of that population, will be highly effective in preventing CHD. The preventive techniques are different. They rely on media, community actions, political and community bodies, and institutions to communicate health-promoting knowledge and practices.

Most modem disease-prevention projects use both approaches in combination. However, to disentangle specific effects and possible mechanisms of behavioral methodologies, one needs to make the distinction between the two different concepts. The high-risk strategy was successfully applied in the Oslo Heart Study. It was a study of high-risk men, in whom smoking cessation and dietary change were managed by means of highly skilled dietitians and doctors. The behavioral interventions were quite effective, with strong and convincing effects on lipids, smoking, and CHD incidence. Unfortunately, the behavioral interventions were not described in great detail in that study, so it may be difficult for other groups to replicate the findings (9). Another successful disease-prevention study that has used a traditional risk-factor model, but more consciously applied behavioral techniques to lifestyle change, is the North Karelia Study (see chap. 15, this volume). In contrast to the Oslo Heart Study, this project used a population-based approach, in which it attempted to change lifestyles toward more healthy habits in the entire target population of eastern Finland (North Karelia). These two examples—the Oslo Heart Study and North Karelia Study—refer to primary prevention projects, in which attempts were made to prevent people from acquiring heart disease. In secondary prevention, a field where behavioral methodologies have been extensively used, the target group is patients who are already diseased.

Part 1 of this volume is intended to provide an introduction to CVD prevention (chap. 1) and behavioral medicine (chap. 2). In this chapter, attention is called to the multiple risk factors associated with the acceleration of CHD. Both high-risk and population-based disease-prevention strategies are described, as is the need for attending to the social environment, biobehavioral and psychosocial factors, and behavioral intervention models in CVD prevention. In chapter 2, by Stephen Weiss, the many interfaces and possible interactions between the behavioral and biomedical sciences are explored. These range from epidemiology and public health to clinical patient-oriented approaches, and invoke biomedical, biobehavioral, and psychosocial mechanisms.

THE SOCIAL ENVIRONMENT

Cardiovascular preventive efforts have traditionally focused on the three well-established and major risk factors for CVD: smoking, diet, and blood pressure. Large-scale epidemiological trials have attempted to influence these factors in such a way that incidence and mortality rates would be significantly and substantially decreased. However, it is often found that preventive effects are unevenly distributed in the target groups or populations. Often the necessity to consider the social settings and social environments in preventive projects is overlooked. These aspects have only recently been recognized as relevant for prevention. They are widely described and discussed in Part 2 of this volume, “Behavioral Epidemiology and Public Health in Cardiovascular Disease Prevention.”

The important potentials of new models for preventive efforts and projects become particularly evident when one considers the uneven basic distributions of disease among social groups and in social hierarchies. Within industrialized countries, social epidemiologists are almost unanimo...

Table of contents

• Cover Page
• Half Title Page
• Title Page
• Copyright Page
• Contents
• Acknowledgments
• Part 1 Introduction to Cardiovascular Disease Prevention and Behavioral Medicine
• Part 2 Behavioral Epidemiology and Public Health in Cardiovascular Disease Prevention
• Part 3 Biobehavioral and Psychosocial Factors in Cardiovascular Disease Prevention
• Part 4 Behavioral Intervention Models in Cardiovascular Disease Prevention
• Part 5 Summary and Conclusions
• Author Index
• Subject Index