Editorial
Inferences from Secular Trend Analysis of Hypertension Control Hypertension is one ofthe most prevalent vascular diseases worldwide. In the United States of America it is one of the most powerful contributors to cardiovascular morbidity and mortality. It is the chief factor contributing to the 500 000 strokes that occur each year, the most dreaded of its cardiovascular sequela. It is also a major factor in the 1.25 million annual coronary attacks, now the most common and most lethal consequence of hypertension.",2 In 1989, hypertension was the main cause of the 147 000 stroke deaths, 35 000 cardiac failures, many of the 498 000 coronary deaths, and the 22 000 renal deaths that occurred.2 Yet, each year hypertension is identified as the underlying disease in only about 32 000 deaths. Thus hypertension appears to account for only 3% of cardiovascular deaths. This is a gross underestimate of its impact on mortality. Hypertension is associated with a two- to fourfold increase in the development of major cardiovascular events, including strokes, coronary attacks, cardiac failure, and peripheral arterial disease.3 Mortality from hypertensive disease is now largely due to atherosclerotic cardiovascular sequelae such as coronary disease, stroke, and cardiac failure. It is in deaths from these cardiovascular sequelae that hypertension takes its toll. Secular trends in hypertension and its cardiovascular sequelae are of great public health importance because of the insights provided about their determinants and continuing contribution to national morbidity and mortality. The trend in mortality has been downwards. Around 1940 steady declines began in stroke, hypertensive diseases, and rheumatic heart disease. For coronary disease, a decline began in the mid-1960s.2 It accelerated in
the 1970s to 3% per year so that about 62% of the decline occurred after 1972. The overall age-adjusted decline is 50%. The decline continues at 3% to 4% per year from the peak of the epidemic in 1963. For stroke mortality the rate of decline has exceeded 6% per year although it has lessened in recent years.2 The declines in both stroke and coronary mortality predate effective antihypertensive and thrombolytic therapy for reasons that remain unclear. Nonetheless, a striking feature of the declines in the United States is their universal nature. All races, both sexes, all age groups, and all geographic areas are involved. However, they are greatest in young adults and higher socioeconomic groups.2,4 Together with geographic variation in the rate of decline these facts suggest a role for such socioeconomic factors as access to medical care, health education, and life-styles. The decline in cardiovascular mortality indicates that this major force of mortality is not an inevitable burden of aging or genetic makeup and should be controllable. Which class of factors is most responsible for the changes is uncertain. Unfortunately, there is a paucity of uniform statistics on trends in morbidity. Reduced mortality without a decline in the attack rate would imply that either better medical care or milder attacks are responsible. Reduction in both morbidity and mortality would suggest that environmental influences or preventive measures are chiefly responsible. Some investigations, but not
all, suggest that cardiovascular disease incidence, including stroke, has declined.4,5 In the Framingham Study, however, uniform tracking of stroke incidence over 4 Editor's Note. See related article by Casper et al. (p 1600) in this issue.
American Journal of Public Health 1593
EdMoral
decades did not reveal much change in either incidence or variety of stroke.6 The decline in mortality appears to have resulted from milder strokes and lower case fatality rates. Rather than attnbute improved survival following completed stroke to more effective treatment of the cerebral infarction, which is difficult to do, one should perhaps attribute it to the better general management of acute stroke patients. Uniformity of stroke mortality assessment from death certificates over time is uncertain. Death certification practices change over time as has the diagnostic precision with the advent of computerized axial tomography (CAT) scans. Stroke mortality may well have declined despite little change in incidence owing to milder strokes allowing victims to survive and die of other causes. There are about 10 stroke patients per 1000 people in the United States, constituting a total of 2.6 million persons,5 and 41% of these are signiicantly disabled.6 After the age of 75 years prevalence rises to almost 80 strokes per 1000 people.7 About 85% of all strokes are ischemic infarctions (thrombotic or embolic), and fewer than 15% are hemorrhagic. The chance of having a stroke before the age of 70 years, in the Framingham Study data, is 1 in 20 for either sex.8 Despite the remarkable decline in the stroke death rate, this disease still accounts for 1 in 14 deaths.2 For persons under the age of 65 years the stroke mortality rate is three times greater in Blacks than Whites, a fact widely attributed to a higher prevalence and increased severity of hypertension in Blacks. Hypertension has been shown to be a major contributor to stroke incidence and mortality in all the major epidemiologic investigations of factors related to occurrence of cardiovascular disease.3 Furthermore, controlled trials have consistently shown that lowering blood pressure reduces stroke incidence and mortality.9 This reduction in stroke events has been noted with a variety of antihypertensive agents, despite the absence of convincing benefit against coronary heart disease. There has been a major improvement in the detection and treatment of hypertension over the past 3 decades. From the foregoing it is reasonable to conclude that the decline in stroke mortality has been largely a result of a reduction in the prevalence of untreated hypertension in the general population. However, it has been evident frm national vital statistics that stroke mortalitywas on the decline for decades prior to the implementation of 1594 American Journal of Public Health
effective antihypertensive therapy. This suggests some other reason for the decline except that the rate of decline greatly accelerated around 1972 when the National High Blood Pressure Education Program was implemented. Can this be taken as an unrelated coincidence? In a paper published in this issue of the Journal, Casper et al. question whether the rate of decline observed is related to antihypertensive treatment because they observed the rate of stroke mortality change to be unrelated to the rate of change in controlled hypertension.10 Unfortunately, this kind ofanalysis cannot be taken at face value. It is difficult to prove guilt by association. Observational studies are seldom conclusive in evaluating therapy because of the strong possibility of selection bias. Otherwise there would be no need for tedious, expensive and time-consuming controlled trials. In this case it is quite possible that those selected for treatment by physicians were more ill and stroke-prone than those left untreated. In the Franiingham Study, those who received antihypertensive treatment had higherblood pressure, were diabetic and showed left ventricular hypertrophy in an electrocardiogram more frequently than those receiving no antihypertensive treatment. It is no surprise, therefore, that persons with treated hypertension had a higher risk ofcardiovascular sequelae, including stroke, than those untreated.11 Of course, this result does not mean that antihypertensive therapy was detrimental. A clinical trial is the appropriate way to determine the efficacy of treatment, and the trials indicate effective prevention of stroke through antihypertensive therapy. Again, this result does not necessarily mean that the rate of decline in stroke mortality is entirely attributable to the treatment of hypertension. Trials are often conducted in highly selected populations and therapies administered under strict protocols. In the general population compliance is less certain, supervision less stringent, and other vexing conditions are commonly present. It is rather difficult to explain trends in mortality from any sort of data available. Many alternative explanations, such as a reduction in the prevalence of cigarette smoking, are difficult to exclude. However, the change in smoking does not seem large enough, particularly in women, to account for the rate of decline in stroke mortality. The evidence linking education, income, and occupation to stroke incidence is also notvery convincing. More-
over, a direct biological connection between these socioeconomic factors and stroke mortality seems unlikely. Some other factors, such as access to medical care or health education, or some unknown noxious agent, would have to be involved. Diet as a possible explanation does not seem promising because the stroke-lipid connection is weak; but a connection to salt, potassium, magnesium, fish oil, or calcium intake might be relevant. The fact that declines in stroke have occurred in all sociodemographic subgroups of the population also undermines the diet hypothesis. Once again, the groups with the largest increases in treatment and control of hypertension may have had the highest pressures, the most left ventricular hypertrophy, and more associated cardiovascular and metabolic conditions given the likelihood that the presence ofdiabetes prompts selection for therapy and more vigorous treatment. Hence, an increase in treatment cannot be taken at face value in relation to accompanying declines in stroke mortality. Few diseases have been controlled in populations solely because they were detected and treated. Effective control has interrupted the chain of circumstances leading to disease occurrence. The ultimate eradication of hypertensive cardiovascular disease requires the primary prevention of hypertension. Trends in hypertension prevalence are difficult to assess because of a massive increase in antihypertensive treatment.'2 Over the past 3 decades in the Framingham Study cohort, mean blood pressure has declined and elevated blood pressure came to be only one third as prevalent. However, if those on treatment with normalized blood pressures are added, hypertension prevalence has increased. For hypertension incidence no consistent trend was noted over 3 decades, but two thirds of the Framingham Study cohort eventually developed high blood pressure.13 Blood pressure in the normotensive segment of the population has been quite stable.13 To clarify this issue, one study examined the trend in mean blood pressure. Among normotensive subjects only a 1 mm Hg decline in mean systolic and diastolic pressure over each of the 3 decades was noted. Thus, the decline in mean blood pressure in the general population appears to be chiefly due to widespread drug treatment of a major proportion of the population. The high incidence of hypertension poses an urgent need for primary prevention targeted at the upper December 1992, Vol. 82, No. 12
Editorbl
end of the nonnal blood pressure distribution from which most future hypertension arises.14 Consideration should be given to particular preventive measures such as weight control, exercise, and the avoidance of salt and alcohol. Adiposity stands out as the major controllable contributor to new onset of hypertension.13 Every 10 lb weight gain results in a 4.5 mm Hg average rise in systolic blood pressure. Because of the high prevalence of obesity and its strong association with hypertension, 70%o of hypertension in men and 61% in women appear directly attributable to excess adiposity (i.e., subscapular skinfold of 1 cm or greater). Patients with hypertension who control their weight and restrict their use of salt have been shown to stay in remission and off drugs. These measures, along with avoidance of alcohol, the use of exercise, and the adoption of a low-fat diet could help prevent or delay the onset of hypertension in susceptible persons. [J Wuliam B. Kwme4 MD, FACC Philip A. Wolf, MD The authors are with the Department of Medicine, Section of Preventive Medicine and Epidemiology, Evans Memorial Research Foundation, Boston University School of Medicine. Requests for reprints should be sent to William B. Kannel, MD, BU/Framingham Heart Study, 5 Thurber St, Framingham, MA 01701.
Acknowledgments The authors are supported by Pfizer; Merck, Sharpe & Dohme; and ICI, as weil as by NIH grants N01-HV-92922 and N01-HV-52971.
References 1. Health, United States, 1990. Hyattsville, MD: National Center for Health Statistics; 1991, DHHS publication PHS 91-1232. 2. Morbidity and mortality chartbook on cardiovascular, lung and blood diseases1990. Bethesda, Md: National Heart, Lung and Blood Institute; 1990. 3. Kannel WB. Epidemiology of essential hypertension: the Framingham experience. In:TPrcR CoiPhys. Edinburgh, Scotland: 1991;21:273-287. 4. Thom TJ, Kannel WB. Factors in the decline of coronary disease mortality. In: Connor WE, Bristow JD, eds. Coronary Heart Disease: Prevention, Complications and Treatment. Philadelphia, Pa: JB Lippincott; 1985:5-20. 5. Higgins MW, Luepker RV, eds. Trends in coronary heart disease mortality: the influence ofmedical care. New York, NY: Oxford University Press; 1988:302. 6. Wolf PA, D'Agostino RB, O'Neal M, et al. Secular trends in stroke incidence and mortality. The Framingham Study. Stmke. In press. 7. Adams PF, Benson V. Current estimates from the National Health Interview Survey, United States, 1989. Vital Health Stat [10]. 1990; no. 176. DHHS publication PHS 90-1504. 8. Gresham GE, Fitzpatrick TE, Wolf PA, et al. Residual disability in survivors of stroke: The Framingham Study. New Eng JMed. 1985;293:954.
9. Moser M. Management of hypertension in the elderly. Am J Genatr CardioL 1992;1: 22-35. 10. Casper M, Wing S, Strogatz D, Davis CE, Tyroler HA. Antihypertensive treatment and US trends in stroke mortality, 1962 to 1980. Am J Public Health. 1992;82:16001606. 11. Cupples LA, D'Agostino RB. Some risk factors related to the annual incidence of cardiovascular disease and death using pooled repeated biennial measurements: Framingham Heart Study, 30-year followup. In: Kannel WB, Wolf PA, Garrison RJ, eds. 7he Framirgham Study. An Epidemiological Investigation of Cardiovasular Disease. Bethesda, Md: National Heart, Lung and Blood Institute; 1987; section 34. DHHS publication PHS 87-2703. (Available from National Technical Information Service, Springfield, VA 22161.) 12. Drisd T, Dannenberg A, Engel A. Blood pressure levels in persons 18-74 years of age in 1976-80 and trends in blood pressure from 1960-1980. Vaal Health Stat [111. 1986; no. 234. DHHS publication PHS 861684. 13. Garrison RJ, Kannel WB, Stokes JS IH, Casteili WP. Incidence and precursors of hypertension in young adults. The Framingham offspring study. P,ev MedL
1987;16:235-251. 14. Leitschuh M, Cupples LA, Kannel WB, Gagnon D, Chobanian A. High normal blood pressure progression to hypertension in the Framingham Study. Hypetension.
1991;17:22-27.
AMERICAN PUBLIC HEALTH ASSOCIATION Announcement of Searchfor New Executive Director The American Public Health Association (APHA) has begun a national search to find an Executive Director to replace our current Executive Director, who is retiring in1993. We are seeking a proven public health professional who will share the national leadership of our Association with strong volunteer leadership and who will plan and direct the supporting activities of approximately 70 APHA staff persons. Our search committee plans to present finalist candidates to the APHA Executive Board in early April 1993. This position is based in Washington, DC. Strong candidates will have the education and experience necessaly for defining and planning the success of APHA during the late 20th and early 21st centuly and the demonstrated ability to combine volunteer and staff resources to ensure that success. Finalists will meet the following criteria: * An advanced degree in public health, medicine, or another health discipline * A demonstrated commitment to and knowledge of public health * A comprehensive understanding of public health issues, system components, and opportunities * At least 10 to 12 years of progressive and highly relevant experience * Experience in the management, leadership, or administration of a large organization * Demonstrated ability to create and direct the implementation of long-term strategic plans * Demonstrated administrative success, including the development and control of financial resources * Strong evidence of ability in leading large diverse groups, especially those with strong volunteer leadership * Demonstrated ability to use modern business and communication tools and systems * A background that includes both line and staff responsibility (especially desirable) The APHA Executive Board, to whom the Executive Director reports, and its search committee are working closely with the consulting firm of Kimball Shaw Associates, which has the staff responsibility for this search. If you are qualified and interested in this position, or if you can recommend qualified candidates, please write to Mr. Kimball Shaw at the following address: Kimball Shaw Associates, Attn: Martha Nevill, 3 Pleasant St., Hingham, MA 02043.
December 1992, Vol. 82, No. 12
American Journal of Public Health 1595
Inferences from Secular Trend Analysis of Hypertension Control Hypertension is one ofthe most prevalent vascular diseases worldwide. In the United States of America it is one of the most powerful contributors to cardiovascular morbidity and mortality. It is the chief factor contributing to the 500 000 strokes that occur each year, the most dreaded of its cardiovascular sequela. It is also a major factor in the 1.25 million annual coronary attacks, now the most common and most lethal consequence of hypertension.",2 In 1989, hypertension was the main cause of the 147 000 stroke deaths, 35 000 cardiac failures, many of the 498 000 coronary deaths, and the 22 000 renal deaths that occurred.2 Yet, each year hypertension is identified as the underlying disease in only about 32 000 deaths. Thus hypertension appears to account for only 3% of cardiovascular deaths. This is a gross underestimate of its impact on mortality. Hypertension is associated with a two- to fourfold increase in the development of major cardiovascular events, including strokes, coronary attacks, cardiac failure, and peripheral arterial disease.3 Mortality from hypertensive disease is now largely due to atherosclerotic cardiovascular sequelae such as coronary disease, stroke, and cardiac failure. It is in deaths from these cardiovascular sequelae that hypertension takes its toll. Secular trends in hypertension and its cardiovascular sequelae are of great public health importance because of the insights provided about their determinants and continuing contribution to national morbidity and mortality. The trend in mortality has been downwards. Around 1940 steady declines began in stroke, hypertensive diseases, and rheumatic heart disease. For coronary disease, a decline began in the mid-1960s.2 It accelerated in
the 1970s to 3% per year so that about 62% of the decline occurred after 1972. The overall age-adjusted decline is 50%. The decline continues at 3% to 4% per year from the peak of the epidemic in 1963. For stroke mortality the rate of decline has exceeded 6% per year although it has lessened in recent years.2 The declines in both stroke and coronary mortality predate effective antihypertensive and thrombolytic therapy for reasons that remain unclear. Nonetheless, a striking feature of the declines in the United States is their universal nature. All races, both sexes, all age groups, and all geographic areas are involved. However, they are greatest in young adults and higher socioeconomic groups.2,4 Together with geographic variation in the rate of decline these facts suggest a role for such socioeconomic factors as access to medical care, health education, and life-styles. The decline in cardiovascular mortality indicates that this major force of mortality is not an inevitable burden of aging or genetic makeup and should be controllable. Which class of factors is most responsible for the changes is uncertain. Unfortunately, there is a paucity of uniform statistics on trends in morbidity. Reduced mortality without a decline in the attack rate would imply that either better medical care or milder attacks are responsible. Reduction in both morbidity and mortality would suggest that environmental influences or preventive measures are chiefly responsible. Some investigations, but not
all, suggest that cardiovascular disease incidence, including stroke, has declined.4,5 In the Framingham Study, however, uniform tracking of stroke incidence over 4 Editor's Note. See related article by Casper et al. (p 1600) in this issue.
American Journal of Public Health 1593
EdMoral
decades did not reveal much change in either incidence or variety of stroke.6 The decline in mortality appears to have resulted from milder strokes and lower case fatality rates. Rather than attnbute improved survival following completed stroke to more effective treatment of the cerebral infarction, which is difficult to do, one should perhaps attribute it to the better general management of acute stroke patients. Uniformity of stroke mortality assessment from death certificates over time is uncertain. Death certification practices change over time as has the diagnostic precision with the advent of computerized axial tomography (CAT) scans. Stroke mortality may well have declined despite little change in incidence owing to milder strokes allowing victims to survive and die of other causes. There are about 10 stroke patients per 1000 people in the United States, constituting a total of 2.6 million persons,5 and 41% of these are signiicantly disabled.6 After the age of 75 years prevalence rises to almost 80 strokes per 1000 people.7 About 85% of all strokes are ischemic infarctions (thrombotic or embolic), and fewer than 15% are hemorrhagic. The chance of having a stroke before the age of 70 years, in the Framingham Study data, is 1 in 20 for either sex.8 Despite the remarkable decline in the stroke death rate, this disease still accounts for 1 in 14 deaths.2 For persons under the age of 65 years the stroke mortality rate is three times greater in Blacks than Whites, a fact widely attributed to a higher prevalence and increased severity of hypertension in Blacks. Hypertension has been shown to be a major contributor to stroke incidence and mortality in all the major epidemiologic investigations of factors related to occurrence of cardiovascular disease.3 Furthermore, controlled trials have consistently shown that lowering blood pressure reduces stroke incidence and mortality.9 This reduction in stroke events has been noted with a variety of antihypertensive agents, despite the absence of convincing benefit against coronary heart disease. There has been a major improvement in the detection and treatment of hypertension over the past 3 decades. From the foregoing it is reasonable to conclude that the decline in stroke mortality has been largely a result of a reduction in the prevalence of untreated hypertension in the general population. However, it has been evident frm national vital statistics that stroke mortalitywas on the decline for decades prior to the implementation of 1594 American Journal of Public Health
effective antihypertensive therapy. This suggests some other reason for the decline except that the rate of decline greatly accelerated around 1972 when the National High Blood Pressure Education Program was implemented. Can this be taken as an unrelated coincidence? In a paper published in this issue of the Journal, Casper et al. question whether the rate of decline observed is related to antihypertensive treatment because they observed the rate of stroke mortality change to be unrelated to the rate of change in controlled hypertension.10 Unfortunately, this kind ofanalysis cannot be taken at face value. It is difficult to prove guilt by association. Observational studies are seldom conclusive in evaluating therapy because of the strong possibility of selection bias. Otherwise there would be no need for tedious, expensive and time-consuming controlled trials. In this case it is quite possible that those selected for treatment by physicians were more ill and stroke-prone than those left untreated. In the Franiingham Study, those who received antihypertensive treatment had higherblood pressure, were diabetic and showed left ventricular hypertrophy in an electrocardiogram more frequently than those receiving no antihypertensive treatment. It is no surprise, therefore, that persons with treated hypertension had a higher risk ofcardiovascular sequelae, including stroke, than those untreated.11 Of course, this result does not mean that antihypertensive therapy was detrimental. A clinical trial is the appropriate way to determine the efficacy of treatment, and the trials indicate effective prevention of stroke through antihypertensive therapy. Again, this result does not necessarily mean that the rate of decline in stroke mortality is entirely attributable to the treatment of hypertension. Trials are often conducted in highly selected populations and therapies administered under strict protocols. In the general population compliance is less certain, supervision less stringent, and other vexing conditions are commonly present. It is rather difficult to explain trends in mortality from any sort of data available. Many alternative explanations, such as a reduction in the prevalence of cigarette smoking, are difficult to exclude. However, the change in smoking does not seem large enough, particularly in women, to account for the rate of decline in stroke mortality. The evidence linking education, income, and occupation to stroke incidence is also notvery convincing. More-
over, a direct biological connection between these socioeconomic factors and stroke mortality seems unlikely. Some other factors, such as access to medical care or health education, or some unknown noxious agent, would have to be involved. Diet as a possible explanation does not seem promising because the stroke-lipid connection is weak; but a connection to salt, potassium, magnesium, fish oil, or calcium intake might be relevant. The fact that declines in stroke have occurred in all sociodemographic subgroups of the population also undermines the diet hypothesis. Once again, the groups with the largest increases in treatment and control of hypertension may have had the highest pressures, the most left ventricular hypertrophy, and more associated cardiovascular and metabolic conditions given the likelihood that the presence ofdiabetes prompts selection for therapy and more vigorous treatment. Hence, an increase in treatment cannot be taken at face value in relation to accompanying declines in stroke mortality. Few diseases have been controlled in populations solely because they were detected and treated. Effective control has interrupted the chain of circumstances leading to disease occurrence. The ultimate eradication of hypertensive cardiovascular disease requires the primary prevention of hypertension. Trends in hypertension prevalence are difficult to assess because of a massive increase in antihypertensive treatment.'2 Over the past 3 decades in the Framingham Study cohort, mean blood pressure has declined and elevated blood pressure came to be only one third as prevalent. However, if those on treatment with normalized blood pressures are added, hypertension prevalence has increased. For hypertension incidence no consistent trend was noted over 3 decades, but two thirds of the Framingham Study cohort eventually developed high blood pressure.13 Blood pressure in the normotensive segment of the population has been quite stable.13 To clarify this issue, one study examined the trend in mean blood pressure. Among normotensive subjects only a 1 mm Hg decline in mean systolic and diastolic pressure over each of the 3 decades was noted. Thus, the decline in mean blood pressure in the general population appears to be chiefly due to widespread drug treatment of a major proportion of the population. The high incidence of hypertension poses an urgent need for primary prevention targeted at the upper December 1992, Vol. 82, No. 12
Editorbl
end of the nonnal blood pressure distribution from which most future hypertension arises.14 Consideration should be given to particular preventive measures such as weight control, exercise, and the avoidance of salt and alcohol. Adiposity stands out as the major controllable contributor to new onset of hypertension.13 Every 10 lb weight gain results in a 4.5 mm Hg average rise in systolic blood pressure. Because of the high prevalence of obesity and its strong association with hypertension, 70%o of hypertension in men and 61% in women appear directly attributable to excess adiposity (i.e., subscapular skinfold of 1 cm or greater). Patients with hypertension who control their weight and restrict their use of salt have been shown to stay in remission and off drugs. These measures, along with avoidance of alcohol, the use of exercise, and the adoption of a low-fat diet could help prevent or delay the onset of hypertension in susceptible persons. [J Wuliam B. Kwme4 MD, FACC Philip A. Wolf, MD The authors are with the Department of Medicine, Section of Preventive Medicine and Epidemiology, Evans Memorial Research Foundation, Boston University School of Medicine. Requests for reprints should be sent to William B. Kannel, MD, BU/Framingham Heart Study, 5 Thurber St, Framingham, MA 01701.
Acknowledgments The authors are supported by Pfizer; Merck, Sharpe & Dohme; and ICI, as weil as by NIH grants N01-HV-92922 and N01-HV-52971.
References 1. Health, United States, 1990. Hyattsville, MD: National Center for Health Statistics; 1991, DHHS publication PHS 91-1232. 2. Morbidity and mortality chartbook on cardiovascular, lung and blood diseases1990. Bethesda, Md: National Heart, Lung and Blood Institute; 1990. 3. Kannel WB. Epidemiology of essential hypertension: the Framingham experience. In:TPrcR CoiPhys. Edinburgh, Scotland: 1991;21:273-287. 4. Thom TJ, Kannel WB. Factors in the decline of coronary disease mortality. In: Connor WE, Bristow JD, eds. Coronary Heart Disease: Prevention, Complications and Treatment. Philadelphia, Pa: JB Lippincott; 1985:5-20. 5. Higgins MW, Luepker RV, eds. Trends in coronary heart disease mortality: the influence ofmedical care. New York, NY: Oxford University Press; 1988:302. 6. Wolf PA, D'Agostino RB, O'Neal M, et al. Secular trends in stroke incidence and mortality. The Framingham Study. Stmke. In press. 7. Adams PF, Benson V. Current estimates from the National Health Interview Survey, United States, 1989. Vital Health Stat [10]. 1990; no. 176. DHHS publication PHS 90-1504. 8. Gresham GE, Fitzpatrick TE, Wolf PA, et al. Residual disability in survivors of stroke: The Framingham Study. New Eng JMed. 1985;293:954.
9. Moser M. Management of hypertension in the elderly. Am J Genatr CardioL 1992;1: 22-35. 10. Casper M, Wing S, Strogatz D, Davis CE, Tyroler HA. Antihypertensive treatment and US trends in stroke mortality, 1962 to 1980. Am J Public Health. 1992;82:16001606. 11. Cupples LA, D'Agostino RB. Some risk factors related to the annual incidence of cardiovascular disease and death using pooled repeated biennial measurements: Framingham Heart Study, 30-year followup. In: Kannel WB, Wolf PA, Garrison RJ, eds. 7he Framirgham Study. An Epidemiological Investigation of Cardiovasular Disease. Bethesda, Md: National Heart, Lung and Blood Institute; 1987; section 34. DHHS publication PHS 87-2703. (Available from National Technical Information Service, Springfield, VA 22161.) 12. Drisd T, Dannenberg A, Engel A. Blood pressure levels in persons 18-74 years of age in 1976-80 and trends in blood pressure from 1960-1980. Vaal Health Stat [111. 1986; no. 234. DHHS publication PHS 861684. 13. Garrison RJ, Kannel WB, Stokes JS IH, Casteili WP. Incidence and precursors of hypertension in young adults. The Framingham offspring study. P,ev MedL
1987;16:235-251. 14. Leitschuh M, Cupples LA, Kannel WB, Gagnon D, Chobanian A. High normal blood pressure progression to hypertension in the Framingham Study. Hypetension.
1991;17:22-27.
AMERICAN PUBLIC HEALTH ASSOCIATION Announcement of Searchfor New Executive Director The American Public Health Association (APHA) has begun a national search to find an Executive Director to replace our current Executive Director, who is retiring in1993. We are seeking a proven public health professional who will share the national leadership of our Association with strong volunteer leadership and who will plan and direct the supporting activities of approximately 70 APHA staff persons. Our search committee plans to present finalist candidates to the APHA Executive Board in early April 1993. This position is based in Washington, DC. Strong candidates will have the education and experience necessaly for defining and planning the success of APHA during the late 20th and early 21st centuly and the demonstrated ability to combine volunteer and staff resources to ensure that success. Finalists will meet the following criteria: * An advanced degree in public health, medicine, or another health discipline * A demonstrated commitment to and knowledge of public health * A comprehensive understanding of public health issues, system components, and opportunities * At least 10 to 12 years of progressive and highly relevant experience * Experience in the management, leadership, or administration of a large organization * Demonstrated ability to create and direct the implementation of long-term strategic plans * Demonstrated administrative success, including the development and control of financial resources * Strong evidence of ability in leading large diverse groups, especially those with strong volunteer leadership * Demonstrated ability to use modern business and communication tools and systems * A background that includes both line and staff responsibility (especially desirable) The APHA Executive Board, to whom the Executive Director reports, and its search committee are working closely with the consulting firm of Kimball Shaw Associates, which has the staff responsibility for this search. If you are qualified and interested in this position, or if you can recommend qualified candidates, please write to Mr. Kimball Shaw at the following address: Kimball Shaw Associates, Attn: Martha Nevill, 3 Pleasant St., Hingham, MA 02043.
December 1992, Vol. 82, No. 12
American Journal of Public Health 1595
