Rose Marie Robertson

Defining and Setting National Goals for Cardiovascular Health Promotion and Disease Reduction The American Heart Association’s Strategic Impact Goal Through 2020 and Beyond

This document details the procedures and recommendations of the Goals and Metrics Committee of the Strategic Planning Task Force of the American Heart Association, which developed the 2020 Impact Goals for the organization. The committee was charged with defining a new concept, cardiovascular health, and determining the metrics needed to monitor it over time. Ideal cardiovascular health, a concept well supported in the literature, is defined by the presence of both ideal health behaviors (nonsmoking, body mass index <25 kg/m2, physical activity at goal levels, and pursuit of a diet consistent with current guideline recommendations) and ideal health factors (untreated total cholesterol <200 mg/dL, untreated blood pressure <120/<80 mm Hg, and fasting blood glucose <100 mg/dL). Appropriate levels for children are also provided. With the use of levels that span the entire range of the same metrics, cardiovascular health status for the whole population is defined as poor, intermediate, or ideal. These metrics will be monitored to determine the changing prevalence of cardiovascular health status and define achievement of the Impact Goal. In addition, the committee recommends goals for further reductions in cardiovascular disease and stroke mortality. Thus, the committee recommends the following Impact Goals: “By 2020, to improve the cardiovascular health of all Americans by 20% while reducing deaths from cardiovascular diseases and stroke by 20%.” These goals will require new strategic directions for the American Heart Association in its research, clinical, public health, and advocacy programs for cardiovascular health promotion and disease prevention in the next decade and beyond.

Preventing Cancer, Cardiovascular Disease, and Diabetes A Common Agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association

Collectively, cardiovascular disease (including stroke), cancer, and diabetes account for approximately two thirds of all deaths in the United States and about

2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery

700 billion in direct and indirect economic costs each year. Current approaches to health promotion and prevention of cardiovascular disease, cancer, and diabetes do not approach the potential of the existing state of knowledge. A concerted effort to increase application of public health and clinical interventions of known efficacy to reduce prevalence of tobacco use, poor diet, and insufficient physical activity—the major risk factors for these diseases—and to increase utilization of screening tests for their early detection could substantially reduce the human and economic cost of these diseases. In this article, the ACS, ADA, and AHA review strategies for the prevention and early detection of cancer, cardiovascular disease, and diabetes, as the beginning of a new collaboration among the three organizations. The goal of this joint venture is to stimulate substantial improvements in primary prevention and early detection through collaboration between key organizations, greater public awareness about healthy lifestyles, legislative action that results in more funding for and access to primary prevention programs and research, and reconsideration of the concept of the periodic medical checkup as an effective platform for prevention, early detection, and treatment.

Comparative assessment of stimuli that release neuronal and adrenomedullary catecholamines in man.

Alice K. Jacobs, MD, FACC, FAHA, Chair Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect Nancy Albert, PhD, CCNS, CCRN, FAHA Mark A. Creager, MD, FACC, FAHA Steven M. Ettinger, MD, FACC Robert A. Guyton, MD, FACC Jonathan L. Halperin, MD, FACC, FAHA Judith S. Hochman, MD, FACC, FAHA

Preventing Cardiovascular Disease and Diabetes A Call to Action From the American Diabetes Association and the American Heart Association

We assessed the release of neuronal and adrenomedullary catecholamines in response to various stimuli of the sympathetic nervous system in normal subjects. Plasma catecholamines and their urinary metabolites, normetanephrine and metanephrine, were measured. Sodium restriction increased supine plasma norepinephrine by 37% and ambulatory plasma norepinephrine by 22%, with urinary normetanephrine excretion increased 29%. The sodium restriction did not elevate plasma epinephrine or urinary metanephrine. The most potent stimuli of norepinephrine were treadmill exercise, orthostasis, caffeine, the cold pressor test, sodium restriction and handgrip exercise, in descending order. Plasma epinephrine was increased by caffeine, treadmill exercise, the cold pressor test, handgrip exercise and the Valsalva maneuver, in that order. Syncope resulted in profound changes in plasma epinephrine but only modest changes in plasma norepinephrine. We conclude that in man, there is frequent dissociation between the effects of different stimuli on neuronal and adrenomedullary catecholamine release

The Impact of Prevention on Reducing the Burden of Cardiovascular Disease

Excess body weight has become a major public health problem in the U.S., with nearly two-thirds of adults either overweight or obese.1 The steady gain in the prevalence of obesity over the last 25 years has affected our entire population—no racial or ethnic group, no region of the country, and no socioeconomic group has been spared.2 Perhaps most worrisome is the observation that the rise in the rate of obesity has been greatest in children and minorities, which suggests that future generations of Americans, and our fastest growing populations, may bear the ultimate burden of this condition.3 Overweight or obesity results in a wide range of elevated risk factors and many fatal and nonfatal conditions.4 Paradoxically, although we have witnessed decades in which heart disease and stroke have steadily declined and cancer mortality has at worse remained stable,5 the prevalence of diabetes has soared.6 The increase in diabetes can largely be attributed to weight gain,7,8 and it threatens the enormous advances in disease prevention we have seen.3,9,10 Among individuals with diabetes, cardiovascular disease (CVD) is the leading cause of morbidity and mortality9,11; adults with diabetes have a two- to fourfold higher risk of CVD compared with those without diabetes.12,13 Diabetes is also accompanied by a significantly increased prevalence of hypertension and dyslipidemia.14 It is reasonable to postulate that in many individuals, excess weight gives rise to diabetes, hypertension, and dyslipidemia, thereby leading to frank CVD.15–17 This seemingly simple algorithm is undoubtedly more complex because (1) many studies …

The Neuropathic Postural Tachycardia Syndrome

Objective— Cardiovascular disease (CVD) is prevalent and expensive. While many interventions are recommended to prevent CVD, the potential effects of a comprehensive set of prevention activities on CVD morbidity, mortality, and costs have never been evaluated. We therefore determined the effects of 11 nationally recommended prevention activities on CVD-related morbidity, mortality, and costs in the United States. Research Design and Methods— We used person-specific data from a representative sample of the US population (National Health and Nutrition Education Survey IV) to determine the number and characteristics of adults aged 20-80 years in the United States today who are candidates for different prevention activities related to CVD. We used the Archimedes model to create a simulated population that matched the real US population, person by person. We then used the model to simulate a series of clinical trials that examined the effects over the next 30 years of applying each prevention activity one by one, or altogether, to those who are candidates for the various activities and compared the health outcomes, quality of life, and direct medical costs to current levels of prevention and care. We did this under two sets of assumptions about performance and compliance: 100% success for each activity and lower levels of success considered aggressive but still feasible. Results— Approximately 78% of adults aged 20-80 years alive today in the United States are candidates for at least one prevention activity. If everyone received the activities for which they are eligible, myocardial infarctions and strokes would be reduced by 63% and 31%, respectively. If more feasible levels of performance are assumed, myocardial infarctions and strokes would be reduced 36% and 20%, respectively. Implementation of all prevention activities would add ≈221 million life-years and 244 million quality-adjusted life-years to the US adult population over the coming 30 years, or an average of 1.3 years of life expectancy for all adults. Of the specific prevention activities, the greatest benefits to the US population come from providing aspirin to high-risk individuals, controlling pre-diabetes, weight reduction in obese individuals, lowering blood pressure in people with diabetes, and lowering LDL cholesterol in people with existing coronary artery disease (CAD). As currently delivered and at current prices, most prevention activities are expensive when considering direct medical costs; smoking cessation is the only prevention strategy that is cost-saving over 30 years. Conclusions— Aggressive application of nationally recommended prevention activities could prevent a high proportion of the CAD events and strokes that are otherwise expected to occur in adults in the United States today. However, as they are currently delivered, most of the prevention activities will substantially increase costs. If preventive strategies are to achieve their full potential, ways must be found to reduce the costs and deliver prevention activities more efficiently.

Atherosclerotic Vascular Disease Conference Writing Group III: Pathophysiology

BACKGROUND The postural tachycardia syndrome is a common disorder that is characterized by chronic orthostatic symptoms and a dramatic increase in heart rate on standing, but that does not involve orthostatic hypotension. Several lines of evidence indicate that this disorder may result from sympathetic denervation of the legs. METHODS We measured norepinephrine spillover (the rate of entry of norepinephrine into the venous circulation) in the arms and legs both before and in response to exposure to three stimuli (the cold pressor test, sodium nitroprusside infusion, and tyramine infusion) in 10 patients with the postural tachycardia syndrome and in 8 age- and sex-matched normal subjects. RESULTS At base line, the mean (+/-SD) plasma norepinephrine concentration in the femoral vein was lower in the patients with the postural tachycardia syndrome than in the normal subjects (135+/-30 vs. 215+/-55 pg per milliliter [0.80+/-0.18 vs. 1.27+/-0.32 nmol per liter], P=0.001). Norepinephrine spillover in the arms increased to a similar extent in the two groups in response to each of the three stimuli, but the increases in the legs were smaller in the patients with the postural tachycardia syndrome than in the normal subjects (0.001+/-0.09 vs. 0.12+/-0.12 ng per minute per deciliter of tissue [0.006+/-0.53 vs. 0.71+/-0.71 nmol per minute per deciliter] with the cold pressor test, P=0.02; 0.02+/-0.07 vs. 0.23+/-0.17 ng per minute per deciliter [0.12+/-0.41 vs. 1.36+/-1.00 nmol per minute per deciliter] with nitroprusside infusion, P=0.01; and 0.008+/-0.09 vs. 0.19+/-0.25 ng per minute per deciliter [0.05+/-0.53 vs. 1.12+/-1.47 nmol per minute per deciliter] with tyramine infusion, P=0.04). CONCLUSIONS The neuropathic postural tachycardia syndrome results from partial sympathetic denervation, especially in the legs.

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

The existence of atherosclerosis has been recognized for >500 years; as a pathological condition, it has been recognized for >150 years. Understanding of atherosclerotic vascular disease (AVD) has evolved most dramatically over the past 25 years with the growth of the field of vascular biology.1 Numerous studies have described this disease as a diffuse and progressive process with a variable distribution and clinical presentation that is dependent on the regional circulation involved. Factors that may influence these differences include the size and structure of the affected artery, local and regional flow, changes in microcirculatory alterations, and end-organ damage. This report discusses the general concepts of atherosclerosis, pathophysiology, microcirculatory disturbances, regional responses to atherosclerosis and ischemia, and recommendations for future research, programs, and advocacy. Atherosclerosis involves several highly interrelated processes, including lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, vascular smooth cell activation, altered matrix metabolism, remodeling, and genetic factors.2 This sequence is shown schematically in Figure 1 and described in detail below. Figure 1. The 7 stages of development of an atherosclerotic plaque. First LDL moves into the subendothelium and is oxidized by macrophage and SMCs (1 and 2). Release of growth factors and cytokines attracts additional monocytes (3 and 4). Foam cell accumulation and SMC proliferation result in growth of the plaque (6, 7, and 8). Risk factors play an important role in initiating and accelerating the complex process of atherosclerosis. Risk factors for atherosclerosis are also the primary method of risk assessment and the target for therapeutic intervention in the prevention of premature vascular disease. Interestingly, the impact of these risk factors on disease development and progression in the peripheral vasculature are not the same as those in the coronary vessels and may represent an avenue of investigation to explain variations in clinical presentation …

Exacerbation of vasotonic angina pectoris by propranolol.

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5+/-1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS+ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope.