1. About These Statistics…e70

2. Cardiovascular Diseases…e72

3. Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris…e89

4. Stroke…e99

5. High Blood Pressure…e111

6. Congenital Cardiovascular Defects…e116

7. Heart Failure…e119

8. Other Cardiovascular Diseases…e122 

9. Risk Factor: Smoking/Tobacco Use…e128

10. Risk Factor: High Blood Cholesterol and Other Lipids…e132

11. Risk Factor: Physical Inactivity…e136

12. Risk Factor: Overweight and Obesity…e139

13. Risk Factor: Diabetes Mellitus…e143

14. End-Stage Renal Disease and Chronic Kidney Disease…e149

15. Metabolic Syndrome…e151

16. Nutrition…e153

17. Quality of Care…e155

18. Medical Procedures…e159

19. Economic Cost of Cardiovascular Diseases…e162

20. At-a-Glance Summary Tables…e164 

21. Glossary and Abbreviation Guide…e168
    Writing Group Disclosures…e171



Appendix I: List of Statistical Fact Sheets:

http://www.americanheart.org/presenter.jhtml?identifier=2007

We thank Drs Robert Adams, Philip Gorelick, Matt Wilson, and Philip Wolf (members of the Statistics Committee or Stroke Statistics Subcommittee); Brian Eigel; Gregg Fonarow; Kathy Jenkins; Gail Pearson; and Michael Wolz for their valuable comments and contributions. We would like to acknowledge Tim Anderson and Tom Schneider for their editorial contributions and Karen Modesitt for her administrative assistance.

# 1. About These Statistics {#article-title-2}

The American Heart Association (AHA) works with the Centers for Disease Control and Prevention’s National Center for Health Statistics (CDC/NCHS); the National Heart, Lung, and Blood Institute (NHLBI); the National Institute of Neurological Disorders and Stroke (NINDS); and other government agencies to derive the annual statistics in this Update. This chapter describes the most important sources and the types of data we use from them. For more details and an alphabetical list of abbreviations, see Chapter 21 of this document, the Glossary and Abbreviation Guide.

The surveys used are:

Heart Disease and Stroke Statistics—2007 Update A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee

1. About These Statistics

2. Cardiovascular Diseases

3. Coronary Heart Disease, Acute Coronary Syndrome and Angina Pectoris

4. Stroke and Stroke in Children

5. High Blood Pressure (and End-Stage Renal Disease)

6. Congenital Cardiovascular Defects

7. Heart Failure

8. Other Cardiovascular Diseases 

9. Risk Factors 

10. Metabolic Syndrome

11. Nutrition

12. Quality of Care

13. Medical Procedures

14. Economic Cost of Cardiovascular Diseases

15. At-a-Glance Summary Tables 

16. Glossary and Abbreviation Guide

17. Acknowledgment

18. References



Appendix I: List of Statistical Fact Sheets. URL: http://www.americanheart.org/presenter.jhtml?identifier=2007

The American Heart Association works with the Centers for Disease Control and Prevention’s National Center for Health Statistics (CDC/NCHS), the National Heart, Lung, and Blood Institute (NHLBI), the National Institute of Neurological Disorders and Stroke (NINDS), and other government agencies to derive the annual statistics in this update. This section describes the most important sources we use. For more details and an alphabetical list of abbreviations, see the Glossary and Abbreviation Guide.

All statistics are for the most recent year available. Prevalence, mortality and hospitalizations are computed for 2003 unless otherwise noted. Mortality as an underlying or contributing cause of death is for 2002. Economic cost estimates are for 2006. Due to late release of data, some disease mortality are not updated to 2003. Mortality for 2003 are underlying preliminary data, obtained from the NCHS publication National Vital Statistics Report: Deaths: Preliminary Data for 2003 (NVSR, 2005;53:15) and from unpublished tabulations furnished by Robert Anderson of NCHS. US and state death rates and prevalence rates are age-adjusted per 100 000 population (unless otherwise specified) using the 2000 …

Heart Disease and Stroke Statistics—2006 Update A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Authors Jan L. Brozek, MD, PhD – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada Jean Bousquet, MD, PhD – Service des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Montpellier, France, INSERM, CESP U1018, Respiratory and Environmental Epidemiology Team, France, and WHO Collaborating Center for Rhinitis and Asthma Carlos E. Baena-Cagnani, MD – Faculty of Medicine, Catholic University of Cordoba, Cordoba, Argentina Sergio Bonini, MD – Institute of Neurobiology and Molecular Medicine – CNR, Rome, Italy and Department of Medicine, Second University of Naples, Naples, Italy G. Walter Canonica, MD – Allergy & Respiratory Diseases, DIMI, Department of Internal Medicine, University of Genoa, Genoa, Italy Thomas B. Casale, MD – Division of Allergy and Immunology, Department of Medicine, Creighton University, Omaha, Nebraska, USA Roy Gerth van Wijk, MD, PhD – Section of Allergology, Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, the Netherlands Ken Ohta, MD, PhD – Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan Torsten Zuberbier, MD – Department of Dermatology and Allergy, Charite Universitatsmedizin Berlin, Berlin, Germany Holger J. Schunemann, MD, PhD, MSc – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada

/pdf/allergic-rhinitis-and-its-impact-on-asthma-20b4c7y0pr.pdf

Allergic Rhinitis and Its Impact on Asthma

Objective To attempt to determine the relative value of preclinical cardiac electrophysiology data (in vitro and in vivo) for predicting risk of torsade de pointes (TdP) in clinical use. Methods Published data on hERG (or I(Kr)) activity, cardiac action potential duration (at 90% repolarisation; APD(90)), and QT prolongation in dogs were compared against QT effects and reports of TdP in humans for 100 drugs. These data were set against the free plasma concentrations attained during clinical use (effective therapeutic plasma concentrations; ETPC(unbound)). The drugs were divided into five categories: (1) Class Ia and III antiarrhythmics; (2) Withdrawn from market due to TdP; (3) Measurable incidence/numerous reports of TdP in humans; (4) Isolated reports of TdP in humans; (5) No reports of TdP in humans. Results Data from hERG (or I(Kr)) assays in addition to ETPC(unbound) data were available for 52 drugs. For Category 1 drugs, data for hERG/I(Kr) IC(50), APD(90), QTc in animals and QTc in humans were generally close to or superimposed on the ETPC(unbound) values. This relationship was uncoupled in the other categories, with more complex relationships between the data. In Category 1 (except amiodarone), the ratios between hERG/I(Kr) IC(50) and ETPC(unbound) (max) ranged from 0.1- to 31-fold. Similar ranges were obtained for drugs in Category 2 (0.31- to 13-fold) and Category 3 (0.03- to 35-fold). A large spread was found for Category 4 drugs (0.13- to 35700-fold); this category embraced an assortment of mechanisms ranging from drugs which may well be affecting I(Kr) currents in clinical use (e.g. sparfloxacin) to others such as nifedipine (35700-fold) where channel block is not involved. Finally, for the majority of Category 5 drugs there was a >30-fold separation between hERG/I(Kr) activity and ETPC(unbound) values, with the notable exception of verapamil (1.7-fold), which is free from QT prolongation in man; this is probably explained by its multiple interactions with cardiac ion channels. Conclusions The dataset confirms the widely-held belief that most drugs associated with TdP in humans are also associated with hERG K(+) channel block at concentrations close to or superimposed upon the free plasma concentrations found in clinical use. A 30-fold margin between C(max) and hERG IC(50) may suffice for drugs currently undergoing clinical evaluation, but for future drug discovery programmes, pharmaceutical companies should consider increasing this margin, particularly for drugs aimed at non-debilitating diseases. However, interactions with multiple cardiac ion channels can either mitigate or exacerbate the prolongation of APD and QT that would ensue from block of I(Kr) currents alone, and delay of repolarisation per se is not necessarily torsadogenic. Clearly, an integrated assessment of in vitro and in vivo data is required in order to predict the torsadogenic risk of a new candidate drug in humans.

Relationships between preclinical cardiac electrophysiology, clinical QT interval prolongation and torsade de pointes for a broad range of drugs : Evidence for a provisional safety margin in drug development

Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.

https://heart.bmj.com/content/heartjnl/63/6/342.full.pdf

QT dispersion: an indication of arrhythmia risk in patients with long QT intervals.

Fifty patients with precordial pain were evaluated by 24 hour ambulatory ECG monitoring during normal everyday activities, and by coronary arteriography. The monitoring was regarded as positive if deviation of the ST segment of 1 mm or more from the resting pattern was observed, or if major T wave inversion occurred. Comparison of the results of the two tests showed a good correlation. Among the 32 patients with positive abnormalities on ECG monitoring, 28 had severe coronary disease (greater than 60% obstruction). Among the 18 patients with negative monitoring, only three had severe coronary disease. All seven patients with major T inversion had significant coronary obstruction. The type of chest pain and the resting ECG were less indicative of coronary pathology. The good correlation demonstrated between the ambulatory ECG monitoring and coronary arteriograms validates the monitoring as a reliable tool for uncovering latent ischemic heart disease (IHD) and for evaluation of patients with established IHD.

Diagnostic accuracy of ambulatory ECG monitoring in ischemic heart disease.

• Recurrent ventricular tachycardia (torsade de pointes) is a serious and sometimes fatal arrhythmia occurring usually with quinidine therapy. Four patients experienced ventricular tachycardia after receiving conventional doses of disopyramide phosphate (600 mg/day) for recurrent atrial fibrillation—two of them in combination with amiodarone hydrochloride. Isoproterenol hydrochloride infusion was effective in three patients, while ventricular pacing promptly abolished ventricular ectopic beats and the ventricular tachycardia in the fourth patient.Torsade de pointesis more likely to occur in patients with severe repolarization delay and sinus bradycardia or atrioventricular block, and its appearance in four patients within a period of nine months after the introduction of disopyramide treatment in our service raises the possibility that this is not a rare complication of this drug, especially if used in combination with other QT interval-prolonging agents. (Arch Intern Med1981;141:946-947)

Disopyramide-induced Torsade de Pointes.

Complete heart block following therapeutic irradiation of the left side of the chest.

Ventricular pacing in atypical ventricular tachycardia

The ability of left ventricular angiography to detect regional ischemic dysfunction was assessed in 10 closed-chest dogs during the course of acute balloon occlusion of the anterior descending coronary artery. During the 2-minute period of occlusion, serial cineangiography revealed a sequence of wall motion abnormalities over the anteroapical region almost identical to that observed using directly implanted gauges. This sequence consisted of progressive reduction in regional systolic shortening with eventual replacement by systolic expansion. These changes preceded both electrocardiographic ST-segment and hemodynamic alterations, and were readily observed by gross subjective inspection of the cineangiograms, but with an intraobserver variability of 22%. Frame-by-frame motional analysis of the ventricular perimeter relative to its centroid of mass allowed more precise characterization of regional dysfunction. These data are consistent with previous studies demonstrating that regional wall motion abnormalities are both sensitive and specific markers of acute ischemia, and support the use of computerized left ventricular angiography for the quantitative assessment of clinical ischemic dysfunction.

Analysis of regional ischemic left ventricular dysfunction by quantitative cineangiography.

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