Abstract-This document details the procedures and recommendations of the Goals and Metrics Committee of the StrategicPlanning 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 Ͻ25 kg/m 2 , physical activity at goal levels, and pursuit of a diet consistent with current guideline recommendations) and ideal health factors (untreated total cholesterol Ͻ200 mg/dL, untreated blood pressure Ͻ120/Ͻ80 mm Hg, and fasting blood glucose Ͻ100 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. (Circulation. 2010;121:586-613.) Key Words: AHA Special Reports Ⅲ obesity Ⅲ quality of life Ⅲ epidemiology Ⅲ risk factors Ⅲ quality of care

Class III 7. ICD as a standalone therapy is not indicated in an asymptomatic patient with a diagnosis of CPVT. 8. Programmed electrical stimulation is not indicated in CPVT patients.

Background-The extent of the peri-infarct zone by magnetic resonance imaging (MRI) has been related to all-cause mortality in patients with coronary artery disease. This relationship may result from arrhythmogenesis in the infarct border. However, the relationship between tissue heterogeneity in the infarct periphery and arrhythmic substrate has not been investigated. In the present study, we quantify myocardial infarct heterogeneity by contrast-enhanced MRI and relate it to an electrophysiological marker of arrhythmic substrate in patients with left ventricular (LV) systolic dysfunction undergoing prophylactic implantable cardioverter defibrillator placement. Methods and Results-Before implantable cardioverter defibrillator implantation for primary prevention of sudden cardiac death, 47 patients underwent cine and contrast-enhanced MRI to measure LV function, volumes, mass, and infarct size. A method for quantifying the heterogeneous infarct periphery and the denser infarct core is described. MRI indices were related to inducibility of sustained monomorphic ventricular tachycardia during electrophysiological or device testing. For the noninducible versus inducible patients, LV ejection fraction (30Ϯ10% versus 29Ϯ7%, Pϭ0.79), LV end-diastolic volume (220Ϯ70 versus 228Ϯ57 mL, Pϭ0.68), and infarct size by standard contrast-enhanced MRI definitions (PϭNS) were similar. Quantification of tissue heterogeneity at the infarct periphery was strongly associated with inducibility for monomorphic ventricular tachycardia (noninducible versus inducible: 13Ϯ9 versus 19Ϯ8 g, Pϭ0.015) and was the single significant factor in a stepwise logistic regression. Conclusions-Tissue heterogeneity is present and quantifiable within human infarcts. More extensive tissue heterogeneity correlates with increased ventricular irritability by programmed electrical stimulation. These findings support the hypothesis that anatomic tissue heterogeneity increases susceptibility to ventricular arrhythmias in patients with prior myocardial infarction and LV dysfunction.

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Abstract-Patients with heart failure experience a number of changes in the electrical function of the heart that predispose to potentially lethal cardiac arrhythmias. Action potential prolongation, the result of functional downregulation of K currents, and aberrant Ca 2ϩ handling is a recurrent theme. Significant alterations in conduction and activation of a number of initially adaptive but ultimately maladaptive signaling cascades contribute to the generation of a highly arrhythmogenic substrate. We review the changes in active and passive membrane properties, neurohumoral signaling, and genetic determinants that predispose to sudden arrhythmic death in patients with heart failure and highlight the critical unanswered questions that are ripe for future investigation. Key Words: arrhythmia Ⅲ Ca 2ϩ handling Ⅲ cardiac electrophysiology Ⅲ heart failure Ⅲ ionic remodeling N early 5 million Americans experience heart failure (HF) and Ͼ250 000 die annually. The incidence and prevalence has continued to increase with the aging of the US population. 1 Despite remarkable improvements in medical therapy, the prognosis of patients with myocardial failure remains poor, with almost 20% of patients dying within 1 year of initial diagnosis and Ͼ80% 8-year mortality. Of the deaths in patients with HF, up to 50% are sudden and unexpected; indeed, patients with HF have 6-to 9-times the rate of sudden cardiac death (SCD) of the general population. 1 What causes SCD in patients with HF? It is safe to say that in any individual patient, the mechanism of SCD is uncertain. The uncertainty begins with the definition of sudden death, which describes a sequence of events, not a mechanism. The presumption is that SCD is produced by a lethal cardiac arrhythmia, most often ventricular tachycardia or fibrillation.Bradyarrhythmias and pulseless electrical activity occur less frequently, and generally in hearts with more advanced structural disease. Some data suggest that bradyarrhythmias and pulseless electrical activity may account for an increasing percentage of SCDs, because the frequency of ventricular tachycardia and fibrillation (VT/VF) may be decreasing. 2 The World Health Organization definition of sudden death certainly leaves open the possibility that death may result from a precipitous decline in mechanical function of the heart, such as pulseless electrical activity. Even sudden witnessed death may be produced by a sudden mechanical or vascular catastrophe (pulmonary embolus, cardiac, or vascular rupture) rather than a malignant cardiac rhythm abnormality.SCD most likely results from a cascade of "upstream" events that create an electrically unstable heart that most often is manifested by a ventricular tachyarrhythmia. Interestingly, it is the nonantiarrhythmic drugs, ie, those without What is certain about SCD in the setting of HF in particular is that there are a number of structural and functional changes in the heart and genetic predisposition that may contribute to an increased risk of dying suddenly. This review considers so...

ObjectivesWe examined whether the presence and extent of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance (CMR) predict adverse outcomes in nonischemic cardiomyopathy (NICM) patients.