Executive Summary: Heart Disease and Stroke Statistics—2014 Update

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3 1. About These Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e7 2. American Heart Association's 2020 Impact Goals. . . . . . . . . . . . . . . . .e10 3. Cardiovascular Diseases . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . .e21 4. Subclinical Atherosclerosis . . . . . . . . . . . . . . . . . . . . .e45 5. Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris . . . . . . . . .e54 6. Stroke (Cerebrovascular Disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . .e68 7. High Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .e88 8. Congenital Cardiovascular Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . .e97 9. Cardiomyopathy and Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . .e102 10. Disorders …

Executive Summary: Heart Disease and Stroke Statistics—2011 Update

Heart Disease and Stroke Statistics—2009 Update

<i>Circulation</i> Editors’ Picks

Preventable Coronary Heart Disease Events from Control of Cardiovascular Risk Factors in US Adults With Diabetes (Projections from Utilizing the UKPDS Risk Engine)

This statement examines the cardiovascular complications of diabetes mellitus and considers opportunities for their prevention. These complications include coronary heart disease (CHD), stroke, peripheral arterial disease, nephropathy, retinopathy, and possibly neuropathy and cardiomyopathy. Because of the aging of the population and an increasing prevalence of obesity and sedentary life habits in the United States, the prevalence of diabetes is increasing. Thus, diabetes must take its place alongside the other major risk factors as important causes of cardiovascular disease (CVD). In fact, from the point of view of cardiovascular medicine, it may be appropriate to say, “diabetes is a cardiovascular disease.” The most prevalent form of diabetes mellitus is type 2 diabetes. This disorder typically makes its appearance later in life. The underlying metabolic causes of type 2 diabetes are the combination of impairment in insulin-mediated glucose disposal (insulin resistance) and defective secretion of insulin by pancreatic β-cells. Insulin resistance develops from obesity and physical inactivity, acting on a substrate of genetic susceptibility.1 2 Insulin secretion declines with advancing age,3 4 and this decline may be accelerated by genetic factors.5 6 Insulin resistance typically precedes the onset of type 2 diabetes and is commonly accompanied by other cardiovascular risk factors: dyslipidemia, hypertension, and prothrombotic factors.7 8 The common clustering of these risk factors in a single individual has been called the metabolic syndrome. Many patients with the metabolic syndrome manifest impaired fasting glucose (IFG)9 even when they do not have overt diabetes mellitus.10 The metabolic syndrome commonly precedes the development of type 2 diabetes by many years11 ; of great importance, the risk factors that constitute this syndrome contribute independently to CVD risk. Recently, new criteria have been accepted for the diagnosis of diabetes.9 The upper threshold of fasting plasma glucose for the …

C ardiovascular disease (CVD) is a leading cause of morbidity and premature mortality in women and men in the United States, most of the industrialized world, and many developing countries. 1Data accumulated over the past 3 decades indicate that atherosclerotic-CVD processes begin early in childhood and are influenced over the life course by genetic and potentially modifiable risk factors and environmental exposures.Taken together, these data provide compelling evidence for primary prevention of CVD beginning early in childhood.Within the pediatric healthcare community, this evidence has prompted and informed the development of science-based guidelines with recommendations for individual/high-risk and population-based approaches to primary prevention of CVD in children and youth.The purpose of this statement is to provide an overview of the evidence and current science-based recommendations and to emphasize the role of advanced practice nurses in the implementation of strategies consistent with population-based and individual/high-risk approaches to CVD prevention in children and youth.The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel.Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.

As we reach the midpoint of the first decade of the twenty-first century, we are also at the midpoint in the timeline of the American Heart Association (AHA) strategic plan to reduce coronary heart disease, stroke, and risk by 25% by the year 2010.1,2 Encouraging evidence demonstrates important gains toward that goal, with decreases in coronary heart disease and stroke mortality, as well as reductions in certain risk factors such as cigarette consumption and untreated hypercholesterolemia. Still, troubling evidence indicates that other ominous risk factors—physical inactivity, overweight and obesity, diabetes, and hypertension—are on the rise,3 especially among adolescents and young adults, and these may contribute to the next wave of the cardiovascular epidemic. And there is undeniable evidence that not all Americans have shared equally in the improved cardiovascular outcomes. Individuals in specific subgroups defined by race, ethnicity, socioeconomic status, and geography have a disproportionate burden of myocardial infarction, heart failure, stroke, and other cardiovascular events. These individuals also have a worse outcome after these events, including higher mortality rates, and a higher prevalence of unrecognized and untreated risk factors places them at greater likelihood of experiencing these events. Differences such as these arise not only from disparities in access to care and quality of care but also from disparities in awareness and access to knowledge. Disparities in cardiovascular prevention, diagnosis, treatment, and outcomes have been documented in a number of publications from the US Department of Health and Human Services (DHHS),4–6 the Institute of Medicine,7 and the Kaiser Family Foundation,8 and reports of continuing racial and ethnic disparities appear regularly in cardiovascular scientific journals.9,10 If this unacceptable situation fails to be rectified, it is unlikely that the AHA’s 2010 goals or the DHHS Healthy People 2010 goals can be achieved. In the autumn …

At least 25% of coronary patients have sudden death or nonfatal myocardial infarction without prior symptoms.1 Therefore, the search for coronary patients with subclinical disease who could potentially benefit from intensive primary prevention efforts is critically important. The American Heart Association’s (AHA) Prevention V Conference, “Beyond Secondary Prevention: Identifying the High Risk Patient for Primary Prevention,” addressed ways to identify more patients who are asymptomatic and clinically free of coronary heart disease (CHD) but at sufficiently high risk for a future coronary event to justify more intensive risk reduction efforts.2 In this report, we amplify on key findings and recommendations of the AHA Prevention V conference, highlight new research since the conference, and propose an approach to the use of office-based testing and additional noninvasive procedures in selected patients to better define their coronary event risk. The recommendations are concordant with the recently released approach to risk assessment and management from the third report of the Adult Treatment Panel of the National Cholesterol Education Program (ATP-III).3 Enthusiasm for primary prevention and risk assessment in asymptomatic people has been spurred by recent advances in prevention research. Lipid-lowering trials demonstrated that primary prevention of coronary events is feasible, evidenced by the West of Scotland Coronary Primary Prevention Study (WOSCOPS) trial4 of hypercholesterolemic men and by the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) trial5 in average or typical risk men and women with only moderate lipid abnormalities. Aspirin6 or ACE inhibitors7 can also reduce risk in selected asymptomatic, high-risk people. Emerging coronary risk factors have been described including inflammatory, infectious, and thrombotic markers,8 and there has been a steady flow of reports that focus attention on potential new ways of predicting coronary risk.9 In addition, noninvasive tests for subclinical atherosclerotic disease are available …

An Institute of Medicine report titled U.S. Health in International Perspective: Shorter Lives, Poorer Health documents the decline in the health status of Americans relative to people in other high-income countries, concluding that “Americans are dying and suffering from illness and injury at rates that are demonstrably unnecessary.”1 The report blames many factors, “adverse economic and social conditions” among them. In an editorial in Science discussing the findings of the Institute of Medicine report, Bayer et al2 call for a national commission on health “to address the social causes that have put the USA last among comparable nations.” Although mortality from cardiovascular disease (CVD) in the United States has been on a linear decline since the 1970s, the burden remains high. It accounted for 31.9% of deaths in 2010.3 There is general agreement that the decline is the result, in equal measure, of advances in prevention and advances in treatment. These advances in turn rest on dramatic successes in efforts to understand the biology of CVD that began in the late 1940s.4,5 It has been assumed that the steady downward trend in mortality will continue into the future as further breakthroughs in biological science lead to further advances in prevention and treatment. This view of the future may not be warranted. The prevalence of CVD in the United States is expected to rise 10% between 2010 and 2030.6 This change in the trajectory of cardiovascular burden is the result not only of an aging population but also of a dramatic rise over the past 25 years in obesity and the hypertension, diabetes mellitus, and physical inactivity that accompany weight gain. Although there is no consensus on the precise causes of the obesity epidemic, a dramatic change in the underlying biology of Americans is …

<i>Circulation</i> Editors’ Picks

We thank Drs Robert Adams, Gary Friday, Philip Gorelick, and Sylvia Wasserthiel-Smoller, members of Stroke Statistics Subcommittee; Drs Joe Broderick, Brian Eigel, Kimberlee Gauveau, Jane Khoury, Jerry Potts, Jane Newburger, and Kathryn Taubert; and Sean Coady and Michael Wolz for their valuable comments and contributions. We acknowledge Tim Anderson and Tom Schneider for their editorial contributions and Karen Modesitt for her administrative assistance. View this table: Writing Group Disclosures # Summary {#article-title-2} Each year the American Heart Association, in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media, the lay public, and many others who seek the …

European guidelines on cardiovascular disease prevention in clinical practice<SBT>Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of eight societies and by invited experts)

Stroke, the third leading cause of death in the United States, is a leading cause of adult neurological disability and accounts for the greatest number of hospitalizations for neurological disease. Although treatment of acute stroke has the potential of reducing death and disability, it is likely that prevention will more effectively reduce the ravages of stroke. The patient who is recovering from a mild stroke or who has had a recent transient ischemic attack (TIA) is at high risk of stroke recurrence, physical and intellectual disability, long-term institutionalization, and death. There is substantial evidence from observational epidemiological studies and clinical trials that recurrent ischemic stroke can be prevented (Table 1⇓). Control of risk factors is important for prevention of a first stroke and is practical after ischemic stroke and TIA have occurred. Identification of the specific ischemic stroke mechanism, eg, TIA or minor stroke ipsilateral to a moderate or severe internal carotid stenosis, guides decision making with regard to recurrent stroke prevention therapy (Table 2⇓). A patient with symptomatic cerebrovascular disease is likely to have other cardiovascular diseases or is predisposed to develop them. Preventive measures should complement reduction in risk of atherothrombotic events in the coronary arteries and other arterial territories. Certain nonmodifiable characteristics identify persons at high risk of stroke and stroke recurrence. These include advancing age, male sex, and black and Hispanic race-ethnic backgrounds. Some risk factors, however, such as elevated blood pressure, cigarette smoking, obesity, impaired glucose tolerance, and physical inactivity, are modifiable. Other conditions, ie, prior cardiovascular diseases such as coronary heart disease with angina or prior myocardial infarction, valvular heart disease, congestive heart failure, atrial fibrillation, increased left ventricular mass, and certain other echocardiographic abnormalities, identify persons at increased risk who may be treated with antithrombotic therapy. More recently, other modifiable risk …

Multifactorial risk factor modification and control, especially interventions designed to reduce total cholesterol, systolic blood pressure, smoking prevalence, overweight/obesity, diabetes mellitus, and physical inactivity, can have a profound and favorable impact on decreasing the incidence of initial and recurrent cardiovascular events. Between 1980 and 2000, mortality rates from coronary heart disease (CHD) fell by >40%. Using a previously validated statistical model (IMPACT), researchers attempted to determine how much of this decrease could be explained by the use of medical and surgical treatments as opposed to changes in risk factors among US adults aged 25 to 84 years. Approximately half of the decline in cardiovascular deaths was attributed to reductions in major risk factors (obesity and diabetes mellitus were notable exceptions), and approximately half was attributed to evidence-based medical therapies (eg, secondary prevention medications, rehabilitation, and initial treatments for acute myocardial infarction [AMI]).1 In contrast, emergent and elective revascularization accounted for only 7% of the overall decline in deaths from CHD. Recently, similar results were reported in a Canadian study that evaluated the decrease in CHD mortality between 1994 and 2005.2 Over the past decade, mortality rates from CHD and stroke in the United States decreased by >25% (Figure 1).3 Although there were also impressive reductions in the prevalence of uncontrolled high blood pressure, elevated blood cholesterol, and, to a lesser extent, cigarette smoking, there was only limited impact on other risk factors, including increases in the prevalence of obesity and diabetes mellitus, and a small reduction in those not engaged in moderate or vigorous physical activity.3 These indicators represent major challenges to achieving future goals for cardiovascular health promotion and disease reduction. Figure 1. Mortality rates from coronary heart disease and stroke, rate of uncontrolled blood pressure, and prevalence of high cholesterol from 2004 to 2008. Reproduced …