DURING the past several decades, it has become very apparent that a person's risk of developing clinical complications from atherothrombotic arterial disease (cardiovascular disease, CVD) is determined by interactions among a variety of environmental and hereditary factors. For a small percentage of the population, a high-risk genetic profile (eg, low-density lipoprotein cholesterol [LDL-C] receptor deficiency) is the major determinant of early-onset CVD. For most of the population, it is their environmental exposure or their lifestyle that is the major determinant of their CVD risk. If heredity is the major determinant of CVD risk, then mortality rates would not change as rapidly as they did in the United States during the 20th century. Nor, we would not see a rapid increase in CVD risk when a low-risk population adopts the culture of a high-risk population. 1 The enormous difference in CVD risk observed between selected cultures throughout the world, such as the more than 10-fold greater coronary heart disease death rate in American versus Japanese men aged 45 to 65 years, is more a function of how people interact with their environment than selection of parents. 2 With a low CVD risk lifestyle, “bad genes” frequently will not be expressed and cause clinical CVD until very late in life, if ever. In other words, most “bad genes” usually act only in “bad” or high-risk environments. This does not mean that heredity is unimportant or that gene therapy will not be useful in the prevention or management of CVD. What it does mean is that there are great opportunities to substantially reduce clinical CVD events by effective and sustained lifestyle modification.
Data supporting the role that lifestyle plays in CVD prevention have come from cross-sectional and prospective observational studies, basic science investigations of the disease process, and clinical trials with biological and clinical outcomes. Taken in total, studies demonstrate that there are a number of lifestyle risk factors that can act individually or in a synergistic fashion with one another, influencing disease initiation and/or progression and triggering clinical events. Modest but sustained changes in lifestyle can lead to rapid and substantial decreases in risk. Furthermore, larger changes in lifestyle result in greater reductions in CVD events. However, for many people to successfully achieve and maintain a low-risk profile, knowledgeable and sustained support needs to be provided by the health care system. One approach that has demonstrated effectiveness in helping patients to successfully reduce their CVD risk has been a nurse-centered team approach of care or case management. This article will provide the rationale for including lifestyle interventions in a comprehensive program of CVD prevention and management and a commentary on an integrative or multifactor case management approach that can produce major reductions in CVD risk and clinical events.
LIFESTYLE AND CARDIOVASCULAR DISEASE
Many of the actions a person takes in daily life, starting as a child, combine to establish much of their lifetime risk for developing CVD. In fact, it appears that even in uteri exposure to the mother's environment or lifestyle can influence the future CVD risk of the embryo or fetus. 3 Many of these lifestyle factors are prevalent in Westernized or technologically advanced cultures in which required daily physical activity is low because of widespread automation, calorie-dense but nutrient-poor food is readily available at a relatively low cost, psychological stress and social isolation is common, and chronic exposure to cigarette smoke is still a too common occurrence. While various lifestyle factors can initiate the atherosclerotic process early in life, 4 it is the long-term exposure that leads to the clinical manifestations of coronary artery disease (CHD), peripheral vascular disease, and stroke. In the 1950s and 60s, cross-sectional and prospective observational studies began to identify major risk factors for CVD and in the 1970s and 80s early clinical trials demonstrated clinical benefit from single risk factor modification. Since the 1980s numerous intervention trials involving lifestyle and/or medications achieved highly significant reductions in both disease progression as defined by coronary arteriography and in clinical events in patients assigned to special treatment versus usual care or placebo. In addition to epidemiological and clinical trial data, basic science, especially the field of vascular wall biology, has documented the multifactor nature of the CVD process and supported the need to implement multifactor-based strategies to maximize risk reduction. 5,6
Cigarette smoke exposure
Cigarette smoking, along with hypertension and hypercholesterolemia, was the first major risk factor for CVD designated by the American Heart Association (AHA). Cigarette smoke contains a number of constituents that contribute to the initiation or progression of atherosclerosis or trigger clinical events. Carbon monoxide reduces the oxygen carrying capacity of the blood while nicotine increases myocardial oxygen demand via increases in heart rate and blood pressure as well as some increase in myocardial electrical instability. Also, various chemicals, including nicotine, appear to have a direct effect on the initiation and/or progression of the atherosclerotic progress and contribute to increased platelet aggregation. Smokers have lower high-density lipoprotein cholesterol (HDL-C) concentrations, which tend to increase by about 10% soon after smoking cessation. As with lung cancer and chronic obstructive lung disease, the increased risk for CVD contributed by cigarette smoke exposure is dose-dependent. When never smokers are compared to current smokers, those smoking 10 to 20 cigarettes per day typically have a 2-fold increase in risk of CHD and a 5-fold risk of sudden cardiac death. 7 The magnitude of the increase in CHD risk resulting from smoking is similar in men and women and continues into older ages.
While smoking can be a highly addictive behavior, many people have been successful in stopping. In the United States, 22.1% of all adults are current smokers while 18.9% report being former smokers. Thus, about 46% of people who once were smokers have successfully stopped. 8 Approaches to helping patients to stop smoking have been developed and evaluated. 9 Recently the US Public Health Service published Treating Tobacco Use and Dependence: A Clinical Practice Guideline, a comprehensive set of materials for use by health professionals and their patients in the implementation of a smoking cessation program. 10 Some of the key recommendations are summarized in Table 1. Cigarette smoking status and exposure to second-hand smoke should be evaluated at the initial contact with each patient and a plan developed to minimize these exposures. In addition to individual counseling, referrals should be made to “stop smoking programs” provided by various health care or community organizations.
What a person routinely eats appears to play a central role in their long-term risk of CVD. While much of the focus from the 1950s to the 1990s was on the contribution diet made to the blood levels of total cholesterol or LDL-C, it is now realized that this relationship is only one aspect of the diet's role contributing to CVD risk. Beneficial components in the diet include dietary fiber (especially water-soluble fiber), a wide range of antioxidants, B vitamins (B6, B12, and Niacin), folic acid, omega-3 fatty acids, calcium, and potassium while minimizing intake of foods high in saturated fat, trans-fatty acids, calories, and sodium. 11 An eating pattern that contains a high proportion of calories from a wide variety of vegetables, whole grains, fruits, and nuts and frequent consumption of fatty fish, with limited intake of high-fat animal products and processed foods containing trans-fats, is an important foundation for CVD prevention and management.
Men and women in the US population who consume a more “plant based diet” versus those who have a higher intake of foods prepared from animal products experience a significantly lower mortality due to CVD. 12 The general pattern of eating is a much better indicator of CVD risk than the intake of any one food or nutrient despite the numerous reports in the scientific and lay literature of individual foods or nutrients increasing either benefit or risk. 13,14 A well-designed randomized controlled trial (RCT) to test the hypothesis that dietary changes can prevent CVD seems warranted; however, the enormous logistical and cost issues involved have prevented implementation of such a trial. Two RCTs comparing diets in patients following myocardial infraction have been reported, both with highly favorable results. 15,16 Both studies randomized patients following acute myocardial infarction to 1 of 2 diets and then followed them for up to 3 years. Patients assigned to a Mediterranean diet 16 or a plant-based diet 15 had significantly fewer clinical CVD events than did patients assigned to a usual care diet 16 or to a diet that focused on the restriction of saturated fat. 15 These studies had significant design problems but the results are of major interest given the increasing evidence that various micronutrients (antioxidant vitamins, omega-3 fatty acids or niacin and nonnutrients like fiber and phytoestrogens) when taken as food might have a highly favorable effect on the atherosclerotic-thrombotic process. 5
Ready access to low-cost foods high in saturated fat and trans-fat that are good tasting increases the challenge of switching to a more plant-based diet. Components of the food industry vigorously promote the consumption of large portions of high-calorie, low-nutrient-containing foods for profit reasons. 17 Many patients with CVD have grown up consuming such foods as a major part of their diet and require sustained assistance in converting to a heart healthy diet. Our experience has been that a well-trained registered dietitian is a critical member of the case management team to work with the substantial dietary issues faced by many patients.
In addition to not smoking and good nutrition, maintaining a physically active lifestyle appears to be a core component of an effective CVD prevention program. Numerous prospective observational studies have reported that more physically active or fit men and women have a substantially lower risk of CHD, CVD, and all-cause mortality than do their less active counterparts. 18–20 In many of these studies, the relative risk of CHD mortality for the more fit or active groups range from 20% to 40% less than for the least active or fit groups. The benefits from being more active or fit appear to occur at all ages and are largely independent of other major risk factors. The exercise component of cardiac rehabilitation contributes to the secondary prevention of clinical events 21 and improvement in coronary artery vasodilation and blood flow. 22
An endurance-based exercise program performed on a regular basis can favorably change a variety of CVD risk factors. Beneficial effects include increases in aerobic capacity, HDL-C, insulin-mediated glucose uptake, and fibrinolysis while decreasing arterial blood pressure, triglycerides, and adiposity. Sustained endurance exercise can increase stroke volume and decrease heart rate, blood pressure, and myocardial oxygen demand at a given exercise intensity. These changes can lead to a reduced risk of myocardial infarction or cardiac arrest and decrease the need for antiangina medications in patients with myocardial ischemia. 23 Many of these exercise-induced changes are enhanced by even modest improvements in dietary intake, emphasizing a plant-based diet with some restriction of calorie intake.
Over the past decade it has been well documented that the amount and intensity of physical activity required to provide some protection against CVD mortality is well within the capability of most ambulatory adults. The core recommendation for health-promoting physical activity is to perform at least 30 minutes of moderate intensity activity on most, preferably all, days of the week. 24 Moderate intensity has been benchmarked to brisk walking (3–4 mph) for most adults and most days is defined as 5 or more. It is important to communicate to patients that this is a general guide but can be modified to meet the needs, interests, and resources of the individual. For example, duration can be traded off with frequency so that if three 60-minute sessions per week of brisk walking fits the patient's schedule better than six 30-minute sessions, then this program should be encouraged. The 30+ minutes per day can also be accumulated by performing multiple shorter duration bouts as long as each bout is of moderate intensity or higher and is at least 8 minutes in duration. 25 These guidelines benefit most health outcomes but some special attention needs to be given to the issue of obesity prevention, weight loss, and weight loss maintenance. When using increased energy expenditure via physical activity to achieve healthy weight goals, promoting activity at every opportunity throughout the day is an important goal. Here is where walking several flights of stairs a few times a day, walking more around the home or office, or parking at the back of the parking lot can provide some benefit. To achieve as much CVD protection from physical activity as possible, these short bouts need to be in addition to the 30+ minutes per day of more sustained activity.
The rapid increase in the number of overweight (body mass index [BMI] = 25.0–29.9) and obese (BMI ≥ 30) youth and adults in the United States over the past 2 decades appears to be due to both an increase in calorie intake and a decrease in energy expenditure. 26 Reliable scientific data on both of these issues is limited. Some estimates put the recent increase in food intake by American adults to be in the range of 200 to 300 calorie/day. Speculation is that a number of trends in the food industry as well as our fast-paced environment account for much of this increase. Included here are the rapid increase of eating at fast food restaurants with low-cost but high-fat and high-calorie meals (supersizing), the more general increase in portion sizes (diameter of typical restaurant plate increased by 25% between 1980 and 2000), and the confusion among the public about foods that are low fat but not low calorie. The decline in activity-induced calorie expenditure is related to the expanded use of labor saving technologies at work, in the home, and for transportation and increased use of computer and video-based technologies for recreation.
Sustained obesity increases long-term CVD risk in men and women and complicates attempts to control a number of other key CVD risk factors. Obesity contributes to increases in blood pressure, abnormal lipoprotein profile (lower HDL-C and higher triglycerides and LDL-C), insulin resistance, and platelet aggregation. Also, it tends to make performance of many physical activities more difficult and increases the risk of injury caused by weight-bearing activities.
Type II diabetes—A lifestyle disease
The rapid increase in the prevalence of type II diabetes in the United States and its occurrence at a younger age is primarily due to increased calorie intake and reduced energy expenditure and the resulting increase in adiposity. 27 While heredity can influence a person's susceptibility to development of the disease, a sedentary lifestyle and long-term obesity are key triggering events for most people. Adults with a BMI of ≥30 have a 5-fold greater risk of developing diabetes than do people with a normal BMI of 25 or less. 28 Diabetes and the related metabolic syndrome are major risk factors for CVD, especially in persons older than 60, with a higher relative risk imposed on women than on men. The NCEP Adult Treatment Panel Guidelines 29 consider diabetes to be a cardiac equivalent, with the risk of a patient with diabetes having an initial heart attack being similar to the risk of a patient who has CVD (but not diabetes) having a second heart attack. Patients who have CVD and diabetes have twice the risk of a heart attack as patients having only one of these conditions.
Patients at high risk of developing type II diabetes because of obesity, inactivity, and moderately elevated fasting blood glucose levels (100–125 mg/dL) are prime candidates for participation in a multifactor lifestyle intervention program. Three recent RCTs in these high risk patients have demonstrated that moderate changes in diet, exercise, and obesity can reduce the development of diabetes by 50% to 60% over 3 years compared to patients assigned to usual care. 30–32 For example, in the Diabetes Prevention Program, 32 3234 high-risk men and women were randomly assigned to usual care, Metformin, or a lifestyle group. The goals of the lifestyle program were moderate-intensity physical activity for 150 minutes per week, a healthy low-calorie and low-saturated fat diet, and a weight loss of 7% of body weight. The average length of time in the study was 2.8 years (range 1.8–4.6). The patients in the lifestyle group lost an average of 12.6 lb, reduced their calorie intake by about 200 calories per day, and decreased their percentage of calories from fat from 34.1% to 27.5%. These participants exercised, primarily brisk walking, about 100 to 120 minutes per week. As compared to the control group, the decrease in the development of diabetes was 58% in the lifestyle group and 31% in patients assigned to the Metformin group. The decrease in diabetes in the 2 treatment groups began the first year and continued throughout the study. Benefit was seen in men and women, in younger and older patients, and in ethnic minority patients. These studies clearly demonstrated that a multifactor intervention program that includes lifestyle interventions is effective.
Patients reporting higher levels of psychological stress experience a higher frequency of initial clinical cardiac events 33 as well as repeat events 34 than do patients reporting minimal stress. A number of biological mechanisms have been investigated as possible mechanisms by which stress increases CVD clinical events, including a chronic increase in sympathetic drive resulting in increased myocardial work, increases in blood pressure and heart rate, ectopic ventricular activity, and platelet aggregation. Some earlier RCTs have shown a reduction in clinical CVD events in patients receiving stress reduction, 35 but the recently completed large multisite trial (ENRICHED) of stress reduction during and following hospitalization for acute myocardial infarction was negative. 36 However, it might be unrealistic to expect that a brief stress reduction intervention delivered during hospitalization in post myocardial infarction patients can significantly reduce clinical events or hospitalization rate over the next 3 to 6 months.
Chronic depression is a risk factor for developing initial CHD clinical events 37 as well as disease progression in patients with existing CHD. 38 Approximately 1 in 6 patients experience major depression following a myocardial infarction and at least twice as many have significant symptoms of depression soon after the event. In a meta-analysis of 11 studies, clinical depression was a stronger predictor of CHD (RR = 1.64: 95% CI = 1.29–2.08, p < .001) than was a depressed mood (RR = 1.49; 96% CI = 1.16–1.92; p = .02). 39 While the mechanisms responsible for this association have not yet been established, depression is clearly associated with poor adherence with risk-reducing behaviors, with abnormalities in autonomic tone and increased platelet activation. 40
Lack of sustained social support (expressing positive affect, agreement and acknowledgment, encouraging the expression of feeling, and providing aid and information) appears to be an independent risk factor for CVD clinical events, especially in patients with established CVD or other chronic disorders. 41 As with other psychosocial factors, lack of social support may act on the autonomic nervous system to increase the risk of atherosclerosis, thrombosis, and cardiac arrhythmias as well as reduce adherence to other risk-related behaviors such as cigarette smoking, lack of physical activity, and poor nutrition. Many patients and family members overlook the importance of providing social support as patients become depressed and isolated.
Spirituality and religion include a system of beliefs an individual has about the world, which can influence all aspects of their life, including their health behaviors. Spirituality has been described as the need for meaning, purpose, and fulfillment, something that transcends the individual and therefore acts as a common bond between individuals. People with greater spiritual awareness appear to display less distress, anxiety, and depression during times of personal turmoil, which may have both direct and indirect effects on CVD risk. Several studies have shown that persons scoring higher on a scale of spirituality or religious participation have lower mortality due to CHD 42 or following cardiac surgery. 43
One important goal of an integrated risk reduction program is to treat the patient as well as the disease. That is, an improved health-related quality of life, independent of specific disease outcomes, should be an objective for every patient. Assessment of psychological factors and the inclusion of interventions that improve psychological profiles and quality of life should be a part of multifactor risk reduction programs.
Integrative or multifactor approaches to CVD risk reduction
Since the atherosclerotic-thrombotic process leading to CVD events is influenced by a number of factors, a multifactor approach to CVD prevention and management is the basis for current national guidelines. 43–45 Most of the RCTs investigating risk factor modification using lifestyle and/or medications have been limited to a single factor. This is due, in part, to a prevalent reductionistic approach to research. In the 1990s, several studies evaluated the effects of multiple lifestyle changes or lifestyle plus medical management on disease progression using coronary arteriography or clinical events. Lifestyle-only studies included the Lifestyle Heart Trial by Ornish 46 and the diet and exercise intervention by investigators in Heidelberg. 47 Studies using lifestyle and medications included 2 conducted at Stanford University, the Stanford Coronary Risk Intervention Project (SCRIP) 48 and the Multifit Trial, 49 and 1 by Watts and colleagues in England. 50 All of these studies reported significant reductions in the rate of epicardial coronary artery lumen narrowing in the treatment versus the control group, with more patients in the treatment groups demonstrating disease regression and less progression. It is interesting to note that in 3 of these 4 studies, 46,47,50 the treatment groups had an increase in lumen size (regression) while the control groups had a decrease in lumen size (progression).
SCRIP 48 was the first large-scale randomized trial to determine the effects of a multifactor risk reduction program using both multiple lifestyle changes plus cholesterol lowering medications on the progression and regression of coronary atherosclerosis and clinical cardiac events in men and women with established heart disease. This study was unique compared to other trials in that it (1) included attempts to manage all of the major risk factors for atherosclerosis, (2) included both men and women with risk factor profiles that represent most adults who present with CHD, and (3) retained more than 90% of randomized patients (N = 300) in the study for 4 years. The risk reduction program consisted of lifestyle interventions including a low-fat, low-cholesterol, and low-sodium diet, regular exercise, stress management, smoking cessation, and weight loss and a combination drug regimen to lower LDL-C and triglycerides and increase HDL-C. The risk reduction program was based on a physician supervised, nurse-managed model using other health professionals to assist with the intervention. Treatment patients visited the clinic approximately once every 2 months over the 4 years for an average of slightly less than 6 visits per year and the intervention program required no special facilities.
The intervention was very successful with highly significant reductions occurring in many major risk factors in the risk reduction group but not in the usual care group. Significant improvements were seen in dietary intake of saturated fat and cholesterol, all the lipid and lipoprotein measurements, fasting glucose, body weight, exercise capacity, and Framingham risk score. Most risk factors were significantly improved by the end of the first year and this improvement was retained or enhanced over the next 3 years. The rate of coronary plaque progression was reduced by approximately 50% with a reduction in new lesion formation. The number of hospitalizations for primary cardiac events was significantly less in the risk reduction patients (n = 25) compared to those assigned to usual care (n = 44, p < .05).
Recently 2 multifactor risk reduction projects in patients with CVD or at high risk of developing clinical CVD events have been reported. 51,52 In Denmark, 80 patients with type II diabetes and microalbuminuria were randomly assigned to usual care following national treatment guidelines or an intensive multifactor intervention involving lifestyle and medical management. Major outcome were fatal and nonfatal cardiovascular events and amputation. 51 The special intervention targeted hyperglycemia, hypertension, dyslipidemia, and microalbuminuria and the use of aspirin to reduce CVD events. Over the mean follow-up of 7.8 years, significant improvements in glucose control, blood pressure, cholesterol and triglyceride concentrations, and urinary albumin excretion were achieved in the intensive intervention versus the usual care group. The intensive intervention patients experienced a 53% lower CVD and amputation rate (p = .007), a 62% lower rate of nephropathy (p = .003), and a 58% lower rate of retinopathy (p = .02) than did usual care patients. Key elements of the special risk reduction program included individualized risk assessment, strict risk reduction targets, a focused multifactor intervention, reasonably frequent patient contact, and continued patient education and motivation.
In another study, evaluating the effects of combined CVD intensive lifestyle management and pharmacologic lipid treatment on coronary atherosclerosis progression and CVD clinical events, 326 patients who had myocardial perfusion imaging at baseline were followed for more than 1 year and up to 5 years with repeat perfusion imaging. 52 Primary outcomes included cardiac death, nonfatal myocardial infarction, percutaneous transluminal coronary angioplasty, and bypass surgery. Patients were categorized for the level of CVD risk management they received during the 5-year follow-up: poor = treatment without diet, lipid-lowering drugs, or smoking cessation, moderate = AHA diet and lipid-lowering drugs or on strict lipid-lowering diet (<10% of calories from fat) but not on lipid-lowering medications, or maximal = low-fat diet (<10% of calories from fat), regular exercise, and lipid treatment to LDL-C < 90 mg/dL, HDL-C > 45 mg/dL, and triglycerides < 100 mg/dL. Over 5 years, coronary events occurred in 6.6%, 20.3%, and 30.6% of patients on maximal, moderate, and poor treatments, respectively (p = .001). Also, myocardial perfusion abnormalities significantly decreased for patients receiving maximal treatment and increased for patients receiving moderate and poor treatment (p = .003 and .0001, respectively). The maximum intervention group had the greatest weight reduction (p < .0001), more regular exercisers (p = .01), a much better lipid profile, and greater use of various medications for lowering CVD risk. This maximum intervention group included highly motivated patients and health care providers, highlighting the role of the health care provider.
The above RCTs clearly demonstrate the effectiveness of CVD multifactor risk reduction programs. The research models using a nurse-managed approach to risk reduction have been successfully disseminated to several community settings. For example, Kaiser Permanente Hospitals in California have implanted outpatient home-based programs for myocardial infarction patients in most of their outpatient clinics. 53 Other institutions have disseminated such models into low income, underserved populations, and adapted the model for stroke and heart failure patients. 54,55 Components of successful programs include utilizing a multidisciplinary team with a nurse case-manager, establishing individualized goals for optimal risk factor status, carefully instructing the patient on what will need to be done to achieve these goals, education of the patient on how to achieve the behavior change required, identifying resources to be used, and frequent monitoring of progress. 56 The failure of many CVD risk reduction programs is due to the lack of mutual goal setting, commitment to the process on the part of all of the staff and patient, and lack of frequent patient contact or follow-up.
Substantial experience has been gained in how to utilize case management approaches to reduce CVD morbidity and mortality in high risk patients. The implementation of such programs in a wide range of clinical settings would have an enormous impact on reducing CVD morbidity and mortality and improving the health-related quality of life of many patients.
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