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Lessons from curbing the coronary artery disease epidemic for confronting the impending epidemic of heart failure
Med Clin N Am 88 (2004) 1129–1133
Lessons from curbing the coronary artery disease epidemic for confronting the impending epidemic of heart failure William B. Kannel, MD, MPH* Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, MA, USA
Five decades of epidemiologic research, which was initiated to investigate a perceived national epidemic of coronary heart disease (CHD), have contributed to an explosive expansion of knowledge of the causes and evolution of cardiovascular disease. This research provided vital information to public health workers, physicians, scientists, and basic researchers about modifiable factors that predispose to the occurrence of cardiovascular disease (CVD), which have come to be known as risk factors, a term coined by the Framingham study [1]. Identification of these major, modifiable risk factors stimulated a greater interest in the prevention of cardiovascular disease around the world and has made cardiovascular epidemiology the basic science of preventive cardiology. The focus changed from a preoccupation with diagnosis and management of overt, symptomatic CVD to an increased interest in preventive cardiology. Corroboration of the Framingham study findings by subsequent epidemiologic investigations stimulated national public health initiatives against smoking, beginning in the 1960s, hypertension in the 1970s, and cholesterol in the 1980s [2]. The identification of major modifiable risk factors also stimulated pharmacologic development of agents to control hypertension and dyslipidemia and controlled trials that demonstrated the efficacy of treating them [2,3,4]. Epidemiologic research exploring the evolution of CHD was initiated to seek out the causes of the mounting epidemic of coronary disease, which
Framingham Study Research is supported by National Institutes of Health/National Heart, Lung, and Blood Institute Contract NO1-HC-38038, and the Framingham Visiting Scientist Program is supported by Servier Amerique. * Boston University School of Medicine/Framingham Heart Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702-5827. E-mail address: [email protected] (W.B. Kannel). 0025-7125/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.mcna.2004.02.002
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occurred between 1930 and 1950, and was found to be the leading cause of death in the United States. At the time, CHD was considered an inevitable degenerative consequence of aging and genetic make up. The longitudinal prospective epidemiologic approach that was used was considered an unproven, novel concept, but it did disclose that at any age in either sex there were possibly correctable predisposing factors [5]. The populationbased approach also provided a less distorted appraisal of the evolution of CHD than that derived from clinical studies that were subject to selection bias. It became apparent that CHD attacks one in five people before they attain 60 years of age, that women lag behind men in incidence by 10 years, and that sudden death and unrecognized or silent myocardial infarctions are prominent features of the disease. Because the disease can be lethal, occur without warning, and is asymptomatic in its most severe form, a preventive approach was deemed essential [6,7]. Fortunately, multivariable risk profiles made up of modifiable risk factors were devised, making it possible to readily identify high-risk CHD candidates for effective preventive measures, long in advance of symptoms [8,9]. The use of risk profiles has been recommended to stratify persons with dyslipidemic and hypertensive conditions as candidates for CHD evaluation and treatment [3,4]. A preventive approach is crucial because once clinically manifest, CHD is often abruptly lethal; and if not immediately lethal, it is progressive, and the heart is seldom cured or restored to full function. As a result of preventive measures directed against the identified predisposing risk factors, applied on a population and individual basis, and aggressive implementation of therapeutic innovations, CHD mortality has taken a dramatic downturn [10]. The CHD death rate increased 10% from 1950 to a peak in 1968 and then took a steep downturn, so that by 2000 it was 58% lower than it was in 1950, whereas non-CVD mortality has declined only 12% since 1950. Heart failure, with a prevalence of 5 million cases, is also a major public health problem in the United States because approximately 500,000 people are newly afflicted each year [11]. Approximately 6% to 10% of the population over the age of 65 experience heart failure [12]. In 1991, heart failure cost the economy $38.1 billion, or approximately 5.4% of the health care budget [11]. As for CHD, epidemiologic research determined that heart failure also is highly lethal, with a survival experience little better than cancer [13]. As late as 1993, it was found that once CHD is clinically overt, heart failure had a median survival rate of only 1.7 and 3.2 years in men and women, respectively. In fact, sudden death was found to be a common feature of heart failure mortality in CHD. Recent examination of long-term trends found by the Framingham study in the incidence of and survival with heart failure indicates that the incidence has declined by 30% to 40% in women but not at all in men. National hospitalization data indicate that between 1971 and 2000 heart failure discharge rates have more than tripled [14]. Demographic studies anticipate a progressive increase in the segment of
W.B. Kannel / Med Clin N Am 88 (2004) 1129–1133
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the population over age 65, from which the bulk of heart failure arises. Given the high incidence of heart failure in the elderly, a dramatic decrease in heart failure incidence would be required to prevent further increase in the number of persons with heart failure. There is, therefore, little hope for an end to the heart failure epidemic by improving survival of those already afflicted. Survival can only be achieved by controlling the predisposing causes of heart failure. In the Framingham study, between 1990 and 1999 the 5-year heart failure mortality rate for men declined by 59% and 45% for women. Overall, the survival rate improved by 12% per decade [15]. Despite favorable trends in survival, heart failure remains highly prevalent and lethal; among persons who were diagnosed with heart failure in the 1990s, more than 50% died within 5 years [15]. Clearly this condition needs to be detected while it is happening and dealt with at that stage. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for evaluation and management of chronic heart failure in adults identify four stages based on risk factors, structural disorder of the heart, and symptoms of heart failure [16]. This classification recognizes established risk factors, structural prerequisites for heart failure development, and that treatment initiated before left ventricular dysfunction or symptoms appear can reduce heart failure morbidity and mortality. This approach postulates that patients are expected to advance from one stage of severity to the next unless progression is slowed or stopped by treatment. Thus, the guidelines focus on prevention of heart failure as well as on evaluation and treatment of chronic heart failure associated with left ventricular systolic or diastolic dysfunction. The staging recognizes that heart failure, like CHD, has established risk factors, structural prerequisites, asymptomatic and symptomatic phases, and that preventive measures applied at each stage can reduce morbidity and mortality [16]. Specific to CHD, major independent contributors to the occurrence of heart failure are being identified and quantified by epidemiologic, population-based research. Using some of these factors, a multivariable heart failure risk profile was formulated by the Framingham study that can efficiently predict events and quantify risk factors [17]. The profile includes deteriorating left ventricular function, such as a rapid resting heart rate, reduced vital capacity, cardiomegaly, and left ventricular hypertrophy as shown by electrocardiography or echocardiography. Persons with any combination of these indicators were shown to be high-risk candidates for heart failure [18]. Risk of heart failure in persons with hypertension, cardiac conditions, or diabetes varies over a 10-fold range depending on the associated burden of modifiable risk factors and indicators of deteriorating left ventricular function [19]. Those in the upper quintile of multivariate risk would appear to be good candidates for vigorously applied preventive measures. CHD and its risk factors are intertwined with the predisposition to the occurrence of heart failure. Hypertension, diabetes, and dyslipidemia
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predispose to both. Hypertension predominates as a predisposing risk factor for women more than men, in whom myocardial infarction is responsible for a greater fraction of the events [20]. Improvement in the treatment of myocardial infarction has led to more patients surviving with residual myocardial damage and high susceptibility to heart failure, which may explain the lack of decline in incidence of heart failure for men, as found in the Framingham study [15]. Increased use of antihypertensive medication has led to a decline in the prevalence of high blood pressure [21], virtually eliminated severe grades of hypertension, and appears to have favorably affected the incidence of heart failure, particularly in women. The high prevalence and poor survival outlook of heart failure in the general population, despite more aggressive and effective treatment of the overt condition, predisposing valve disease, and CHD, remain unacceptable. In CHD, preventive strategies for heart failure require early and vigorous control of elevated blood pressure, left ventricular hypertrophy, dyslipidemia, cigarette smoking, and obesity. ACC/AHA guidelines endorse control of systolic and diastolic hypertension and treatment of dyslipidemia. Guidelines also recommend avoidance of behaviors that may increase risk of heart failure (such as smoking, and consumption of alcohol and illicit drugs) and the use of angiotensin-converting enzyme inhibitors for patients with hypertension, diabetes, and CVD [16]. Control of obesity, which promotes most of the predisposing risk factors for CHD, and heart failure are unfortunately absent from the ACC/AHA recommendations. The high population attributable to risk for heart failure caused by hypertension and CHD indicates where the priorities need to be. Measures available to minimize the adverse effects of these predisposing conditions are not being fully used. Elevated blood pressure is not being adequately controlled, and antiplatelet agents, b-blockers, lipid altering drugs, and ACE-inhibitors are not optimally prescribed [21,22]. Clearly, vigorous control of risk factors not only reduces the risk of CHD, the potential to delay or prevent onset of heart failure is a bonus. Overt heart failure is regarded better as a medical failure rather than as the first indication for treatment.
References [1] Kannel WB, Dawber TR, Kagan A, Revotskie N, Stokes J 3rd. Factors of risk in the development of coronary heart disease-six years follow-up experience: the Framingham Study. Ann Intern Med 1961;55:33–50. [2] Report of the Intersociety Commission for Heart Disease. Resources for primary prevention of atherosclerotic disease. Circulation 1984;70:155A–205A. [3] Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001;285:2486–509. [4] Sixth report of the joint national committee on prevention. detection, evaluation and treatment of high blood pressure. Arch Intern Med 1997;157:2413–44.
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[5] Dawber TR. The Framingham Study: The epidemiology of atherosclerotic disease. Cambridge, MA: Harvard University Press; 1980. pp. 14–29. [6] Gordon T, Kannel WB. Premature mortality from coronary heart disease: the Framingham study. JAMA 1971;215:1617–25. [7] Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction: an update on the Framingham study. N Engl J Med 1984;311:1144–7. [8] Kannel WB, Mcgee DL, Gordon T. A general cardiovascular risk profile; the Framingham study. Am J Cardiol 1976;38:46–51. [9] Anderson KM, Wilson FWF, Odell PM, Kannel WB. An updated coronary risk profile: a statement for health professionals. Circulation 1991;83:357–63. [10] Minino AM, Smith BL. Preliminary data for 2000: National Center for Health Statistics. National Vital Statistics Reports. 49, no.12. Hyattsville, MD; 2000. [11] O’Connell JB, Bristow M. Economic impact of heart failure in the United States: time for a different approach. J Heart Lung Transplant 1993;(Suppl):S107–12. [12] Kannel WB. Epidemiology and prevention of cardiac failure: Framingham study insights. Eur Heart J 1987;8(Suppl F):S23–6. [13] Ho KK, Anderson KM, Kannel WB, Grossman D, Levy D. Survival after the onset of congestive heart failure in Framingham heart study subjects. Circulation 1993;88:107–15. [14] National Center for Health Statistics. National hospital discharge survey. Vital Health Stat 13 1970–2002. [15] Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, Ho KK, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med 2002;347:1397–402. [16] American College of Cardiology/American Heart Association Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. A report of the ACC/AHA Task Force on Practice Guidelines. 2001. Available at: http://www.acc.org/ clinical/guidelines/failure/hf_index.htm. [17] Kannel WB, D’Agostino RB, Silbershatz H, Belanger A, Wilson PW, Levy D. Profile for estimating risk of heart failure. Arch Intern Med 1999;159:1197–204. [18] Kannel WB. Need and prospects for prevention of heart failure. Eur J Clin Pharmacol 1996;49:S3–9. [19] Kannel WB. Incidence and epidemiology of heart failure. Heart Fail Rev 2000;5:167–73. [20] Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996;275:1557–62. [21] Burt VL, Cutler JA, Higgins M, Horan MJ, Labarthe D, Whelton P, et al. Trends in the prevalence, awareness and treatment of hypertension in the adult US population: data from the health examination surveys, 1960 to 1991. Hypertension 1995;26:60–9. [22] Nieto FJ, Alonso J, Chambliss LE, Zhong M, Ceraso M, Romm FJ, et al. Population awareness and control of hypertension and hypercholesterolemia in the atherosclerosis in communities study. Arch Intern Med 1995;155:677–84.
Lessons from curbing the coronary artery disease epidemic for confronting the impending epidemic of heart failure William B. Kannel, MD, MPH* Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, MA, USA
Five decades of epidemiologic research, which was initiated to investigate a perceived national epidemic of coronary heart disease (CHD), have contributed to an explosive expansion of knowledge of the causes and evolution of cardiovascular disease. This research provided vital information to public health workers, physicians, scientists, and basic researchers about modifiable factors that predispose to the occurrence of cardiovascular disease (CVD), which have come to be known as risk factors, a term coined by the Framingham study [1]. Identification of these major, modifiable risk factors stimulated a greater interest in the prevention of cardiovascular disease around the world and has made cardiovascular epidemiology the basic science of preventive cardiology. The focus changed from a preoccupation with diagnosis and management of overt, symptomatic CVD to an increased interest in preventive cardiology. Corroboration of the Framingham study findings by subsequent epidemiologic investigations stimulated national public health initiatives against smoking, beginning in the 1960s, hypertension in the 1970s, and cholesterol in the 1980s [2]. The identification of major modifiable risk factors also stimulated pharmacologic development of agents to control hypertension and dyslipidemia and controlled trials that demonstrated the efficacy of treating them [2,3,4]. Epidemiologic research exploring the evolution of CHD was initiated to seek out the causes of the mounting epidemic of coronary disease, which
Framingham Study Research is supported by National Institutes of Health/National Heart, Lung, and Blood Institute Contract NO1-HC-38038, and the Framingham Visiting Scientist Program is supported by Servier Amerique. * Boston University School of Medicine/Framingham Heart Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702-5827. E-mail address: [email protected] (W.B. Kannel). 0025-7125/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.mcna.2004.02.002
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occurred between 1930 and 1950, and was found to be the leading cause of death in the United States. At the time, CHD was considered an inevitable degenerative consequence of aging and genetic make up. The longitudinal prospective epidemiologic approach that was used was considered an unproven, novel concept, but it did disclose that at any age in either sex there were possibly correctable predisposing factors [5]. The populationbased approach also provided a less distorted appraisal of the evolution of CHD than that derived from clinical studies that were subject to selection bias. It became apparent that CHD attacks one in five people before they attain 60 years of age, that women lag behind men in incidence by 10 years, and that sudden death and unrecognized or silent myocardial infarctions are prominent features of the disease. Because the disease can be lethal, occur without warning, and is asymptomatic in its most severe form, a preventive approach was deemed essential [6,7]. Fortunately, multivariable risk profiles made up of modifiable risk factors were devised, making it possible to readily identify high-risk CHD candidates for effective preventive measures, long in advance of symptoms [8,9]. The use of risk profiles has been recommended to stratify persons with dyslipidemic and hypertensive conditions as candidates for CHD evaluation and treatment [3,4]. A preventive approach is crucial because once clinically manifest, CHD is often abruptly lethal; and if not immediately lethal, it is progressive, and the heart is seldom cured or restored to full function. As a result of preventive measures directed against the identified predisposing risk factors, applied on a population and individual basis, and aggressive implementation of therapeutic innovations, CHD mortality has taken a dramatic downturn [10]. The CHD death rate increased 10% from 1950 to a peak in 1968 and then took a steep downturn, so that by 2000 it was 58% lower than it was in 1950, whereas non-CVD mortality has declined only 12% since 1950. Heart failure, with a prevalence of 5 million cases, is also a major public health problem in the United States because approximately 500,000 people are newly afflicted each year [11]. Approximately 6% to 10% of the population over the age of 65 experience heart failure [12]. In 1991, heart failure cost the economy $38.1 billion, or approximately 5.4% of the health care budget [11]. As for CHD, epidemiologic research determined that heart failure also is highly lethal, with a survival experience little better than cancer [13]. As late as 1993, it was found that once CHD is clinically overt, heart failure had a median survival rate of only 1.7 and 3.2 years in men and women, respectively. In fact, sudden death was found to be a common feature of heart failure mortality in CHD. Recent examination of long-term trends found by the Framingham study in the incidence of and survival with heart failure indicates that the incidence has declined by 30% to 40% in women but not at all in men. National hospitalization data indicate that between 1971 and 2000 heart failure discharge rates have more than tripled [14]. Demographic studies anticipate a progressive increase in the segment of
W.B. Kannel / Med Clin N Am 88 (2004) 1129–1133
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the population over age 65, from which the bulk of heart failure arises. Given the high incidence of heart failure in the elderly, a dramatic decrease in heart failure incidence would be required to prevent further increase in the number of persons with heart failure. There is, therefore, little hope for an end to the heart failure epidemic by improving survival of those already afflicted. Survival can only be achieved by controlling the predisposing causes of heart failure. In the Framingham study, between 1990 and 1999 the 5-year heart failure mortality rate for men declined by 59% and 45% for women. Overall, the survival rate improved by 12% per decade [15]. Despite favorable trends in survival, heart failure remains highly prevalent and lethal; among persons who were diagnosed with heart failure in the 1990s, more than 50% died within 5 years [15]. Clearly this condition needs to be detected while it is happening and dealt with at that stage. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for evaluation and management of chronic heart failure in adults identify four stages based on risk factors, structural disorder of the heart, and symptoms of heart failure [16]. This classification recognizes established risk factors, structural prerequisites for heart failure development, and that treatment initiated before left ventricular dysfunction or symptoms appear can reduce heart failure morbidity and mortality. This approach postulates that patients are expected to advance from one stage of severity to the next unless progression is slowed or stopped by treatment. Thus, the guidelines focus on prevention of heart failure as well as on evaluation and treatment of chronic heart failure associated with left ventricular systolic or diastolic dysfunction. The staging recognizes that heart failure, like CHD, has established risk factors, structural prerequisites, asymptomatic and symptomatic phases, and that preventive measures applied at each stage can reduce morbidity and mortality [16]. Specific to CHD, major independent contributors to the occurrence of heart failure are being identified and quantified by epidemiologic, population-based research. Using some of these factors, a multivariable heart failure risk profile was formulated by the Framingham study that can efficiently predict events and quantify risk factors [17]. The profile includes deteriorating left ventricular function, such as a rapid resting heart rate, reduced vital capacity, cardiomegaly, and left ventricular hypertrophy as shown by electrocardiography or echocardiography. Persons with any combination of these indicators were shown to be high-risk candidates for heart failure [18]. Risk of heart failure in persons with hypertension, cardiac conditions, or diabetes varies over a 10-fold range depending on the associated burden of modifiable risk factors and indicators of deteriorating left ventricular function [19]. Those in the upper quintile of multivariate risk would appear to be good candidates for vigorously applied preventive measures. CHD and its risk factors are intertwined with the predisposition to the occurrence of heart failure. Hypertension, diabetes, and dyslipidemia
1132
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predispose to both. Hypertension predominates as a predisposing risk factor for women more than men, in whom myocardial infarction is responsible for a greater fraction of the events [20]. Improvement in the treatment of myocardial infarction has led to more patients surviving with residual myocardial damage and high susceptibility to heart failure, which may explain the lack of decline in incidence of heart failure for men, as found in the Framingham study [15]. Increased use of antihypertensive medication has led to a decline in the prevalence of high blood pressure [21], virtually eliminated severe grades of hypertension, and appears to have favorably affected the incidence of heart failure, particularly in women. The high prevalence and poor survival outlook of heart failure in the general population, despite more aggressive and effective treatment of the overt condition, predisposing valve disease, and CHD, remain unacceptable. In CHD, preventive strategies for heart failure require early and vigorous control of elevated blood pressure, left ventricular hypertrophy, dyslipidemia, cigarette smoking, and obesity. ACC/AHA guidelines endorse control of systolic and diastolic hypertension and treatment of dyslipidemia. Guidelines also recommend avoidance of behaviors that may increase risk of heart failure (such as smoking, and consumption of alcohol and illicit drugs) and the use of angiotensin-converting enzyme inhibitors for patients with hypertension, diabetes, and CVD [16]. Control of obesity, which promotes most of the predisposing risk factors for CHD, and heart failure are unfortunately absent from the ACC/AHA recommendations. The high population attributable to risk for heart failure caused by hypertension and CHD indicates where the priorities need to be. Measures available to minimize the adverse effects of these predisposing conditions are not being fully used. Elevated blood pressure is not being adequately controlled, and antiplatelet agents, b-blockers, lipid altering drugs, and ACE-inhibitors are not optimally prescribed [21,22]. Clearly, vigorous control of risk factors not only reduces the risk of CHD, the potential to delay or prevent onset of heart failure is a bonus. Overt heart failure is regarded better as a medical failure rather than as the first indication for treatment.
References [1] Kannel WB, Dawber TR, Kagan A, Revotskie N, Stokes J 3rd. Factors of risk in the development of coronary heart disease-six years follow-up experience: the Framingham Study. Ann Intern Med 1961;55:33–50. [2] Report of the Intersociety Commission for Heart Disease. Resources for primary prevention of atherosclerotic disease. Circulation 1984;70:155A–205A. [3] Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001;285:2486–509. [4] Sixth report of the joint national committee on prevention. detection, evaluation and treatment of high blood pressure. Arch Intern Med 1997;157:2413–44.
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[5] Dawber TR. The Framingham Study: The epidemiology of atherosclerotic disease. Cambridge, MA: Harvard University Press; 1980. pp. 14–29. [6] Gordon T, Kannel WB. Premature mortality from coronary heart disease: the Framingham study. JAMA 1971;215:1617–25. [7] Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction: an update on the Framingham study. N Engl J Med 1984;311:1144–7. [8] Kannel WB, Mcgee DL, Gordon T. A general cardiovascular risk profile; the Framingham study. Am J Cardiol 1976;38:46–51. [9] Anderson KM, Wilson FWF, Odell PM, Kannel WB. An updated coronary risk profile: a statement for health professionals. Circulation 1991;83:357–63. [10] Minino AM, Smith BL. Preliminary data for 2000: National Center for Health Statistics. National Vital Statistics Reports. 49, no.12. Hyattsville, MD; 2000. [11] O’Connell JB, Bristow M. Economic impact of heart failure in the United States: time for a different approach. J Heart Lung Transplant 1993;(Suppl):S107–12. [12] Kannel WB. Epidemiology and prevention of cardiac failure: Framingham study insights. Eur Heart J 1987;8(Suppl F):S23–6. [13] Ho KK, Anderson KM, Kannel WB, Grossman D, Levy D. Survival after the onset of congestive heart failure in Framingham heart study subjects. Circulation 1993;88:107–15. [14] National Center for Health Statistics. National hospital discharge survey. Vital Health Stat 13 1970–2002. [15] Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, Ho KK, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med 2002;347:1397–402. [16] American College of Cardiology/American Heart Association Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. A report of the ACC/AHA Task Force on Practice Guidelines. 2001. Available at: http://www.acc.org/ clinical/guidelines/failure/hf_index.htm. [17] Kannel WB, D’Agostino RB, Silbershatz H, Belanger A, Wilson PW, Levy D. Profile for estimating risk of heart failure. Arch Intern Med 1999;159:1197–204. [18] Kannel WB. Need and prospects for prevention of heart failure. Eur J Clin Pharmacol 1996;49:S3–9. [19] Kannel WB. Incidence and epidemiology of heart failure. Heart Fail Rev 2000;5:167–73. [20] Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996;275:1557–62. [21] Burt VL, Cutler JA, Higgins M, Horan MJ, Labarthe D, Whelton P, et al. Trends in the prevalence, awareness and treatment of hypertension in the adult US population: data from the health examination surveys, 1960 to 1991. Hypertension 1995;26:60–9. [22] Nieto FJ, Alonso J, Chambliss LE, Zhong M, Ceraso M, Romm FJ, et al. Population awareness and control of hypertension and hypercholesterolemia in the atherosclerosis in communities study. Arch Intern Med 1995;155:677–84.