EDITORIAL
Racial Differences in Coronary Heart Disease Incidence and Mortality Methodologic Mythology?
In this issue of Annuls of Ep’1d emiolog-y, Lee and colleagues provide valuable data, obtained from community surveillance, on the incidence of fatal and nonfatal coronary heart disease (CHD) in blacks compared with whites (1). Comparing data from community surveillance with those from death certificates and hospital discharge indices in 12 selected US communities in 1981, the investigators conclude that the annual age-adjusted mortality rates for definite myocardial infarction (MI) were higher in blacks than in whites of both sexes but that rates for nonfatal and total MI were higher among whites. The authors propose that a higher case/fatality ratio and some misclassification of cause of death could explain their results. These findings raise at least three major issues. First, if the racial differential in MI mortality and case fatality is real, what factors account for it? What are the relative contributions of black-white differences in coronary risk factor status and susceptibility to coronary disease, on the one hand, and differential access to and utilization of medical care, on the other? Second, are the lower incidence rates for nonfatal events an artifact of underdiagnosis of nonfatal CHD among blacks? Finally, what are the reasons for the differential misclassification of MI in the death certification process? Is the diagnostic accuracy of death certificates poorer for blacks than for whites or does the application of stringent criteria for defining MI systematically reduce verification rates in one group more than in the other! A large body of evidence addresses the question of black-white differences in the prevalence of traditional coronary risk factors. Several studies indicate a higher level of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-l in blacks than in whites, although other lipoproteins appear to be negligibly different (2, 3). An excess frequency of rest and exercise-induced hypertension, as well as a greater prevalence of left ventricular hypertrophy, however, has been demonstrated in blacks (2, 4). In addition, despite a similar prevalence of obesity in white and black men, black women have a striking excess of obesity compared to other sex-race groups; the prevalence of obesity in data from the National Health and Nutrition Examination Survey (NHANES) of 1976 to 1980 was 60% among black women aged 45 to 74 years, nearly double the prevalence among white women in the same age groups (5). Not unexpectedly, the prevalence of diabetes mellitus among black females is also markedly elevated (2). Cigarette smoking, the primary reversible behavioral determinant of CHD, appears to be more common among black men than among white men, while smoking prevalence among black and white women is similar (2, 6, 7). In NHANES data from 1976 to 1980, the percent current smokers was 50.4 in black men, 39.3 in white men, 3 1.1 in black women, and 33.1 in white women, although heavy smoking (greater than 25 cigarettes per day) was more common among whites of both sexes (2, 6). Social, economic, and behavioral factors play a major role in influencing coronary risk. In the Evans County study (8), in which a simple dichotomization of social status was employed, the lower social stratum among whites had a 20-year survival curve almost identical to that of blacks, and markedly less favorable than that of whites in a 0 1490Elsev~er SciencePuhllshing Co.. Inc. 1047.2797/90/$03.50
98
Manson and Ridker EDITORIAL
higher
AEP Vol. I, No. 1 Octoberf990: 97- 100
social stratum.
ton heart blacks
of lotier
whites, influence
class
comparative
These
excess
factors,
fatality, evidence blacks
heart four
major
whether
that
events.
Further,
importance
race-sex
groups
the strides
term
trends
Carolina,
to arrival
Thus
it is apparent
and,
even
Of particular elevated
the four sex-race comparably Multicenter mortality
(13),
there
Discharge these
considerably
from those
have been only half
influencing
accounted
the decline
for approximately
(15).
three
one-
Delay time from onset of both shortin blacks
of
and long-
compared
times as great)
suggest
(17).
with
Further,
a racial bias in the referral
as their
are less likely to receive
they are hospitalized,
as to
1975. From
revascularization,
procedures
in all
since
women
increased
Survey
ischemic
is controversy
in whites
determinant
mean delay,
rates in blacks
In a study from the rural Pee Dee
in blacks
an important
with white
early medical
are likely to receive
blacks
approxi-
( 18).
counterparts
a different
attention
for MI
quality
of care
by whites. concern
in the report
this group groups,
by Lee and colleagues
black women
had the highest almost
MI mortality
(140/100,000
markedly based on
population)
of
times the rate in white women and higher than and white men (1101100,000). In the (1141100,000)
men of the Limitation
MI among
women
of Infarct
Size (MILIS),
stresses
the poorer
was found to be primarily attributable higher (48%), which was significantly
black women sex-race subgroups ( 19). Th e excess mortality by their greater prevalence of obesity and
socioenvironmental
(1) is the
aged 55 to 74 years. Although
three
rate among
the other influenced
MI deaths
and coronary
to undergo
aged black Investigation
nosis following
unique
Hospital
rate of fatal MI among
small numbers,
between
the past two decades
that the factors
to be markedly
that blacks
received
&ring
groups equally.
twice as great;
arteriography
half as likely once
men,
or autopsy
differs
care. Although
men have diverged
and two-thirds
was found
data from the National
from that
disease
of case fatality
States
indicating
out-of-hospital
delay,
rate for coronary mately
attrib-
among
angiographic
of health
for blacks and white
at the hospital,
(16),
(median
and quality
for white
groups; declines
all the demographic
survival
is little
have been as great as those
of total cases in whites
whites
and smoking
as determinants
United
as steep as those for white men (14), are not affecting
symptoms
and
may also
blacks could be partially
of coronary
dramatically
in the
in blacks
sex-race
area of South
there
severity
utilization,
has declined
1976 to 1985, the secular
third
metabolism,
(10). among
such as hypertension
the underlying
to access,
mortality
of the other
with
blacks
obesity, and diabetes among women. are more likely to increase the incidence, rather than the case
greater
related
disease
between
(2, 11, 12).
Of potentially are factors
intake
and electrolyte
disease
in the Charles-
in comparison
of hypertension,
ischemic
to suggest
status
in dietary
for MI observed
risk factors
however,
and whites
Differences
rates of coronary
prevalence
of acute
have also been observed socioeconomic
to hypertension
case fatality
to accompanying the
(9).
as it relates
The elevated and
rates of CHD
black males of higher
social
especially
utable
Reduced
study among
and differences
among
black women
diabetes,
in health
prog-
to the high than that of may be
as well as by their
care.
In view of major differences by race in medical care access, quality, and utilization, the findings of lower incidence rates for nonfatal MI events among blacks are difficult to interpret. In addition, Lee and colleagues apply stringent criteria for the diagnosis of MI, including documentation of serial enzyme changes, Q wave or major ST evolution, and prolonged chest pain. Given these criteria, the possibility that nonfatal
events
among
blacks are underdiagnosed
appears
quite
likely.
If blacks have a
AEP Vol. I, No. I October1990: 97-100
Manson and Ridker EDITORIAL
99
greater time delay to hospitalization, enzyme elevations may be missed more frequently and failure to satisfy the stringent standardized criteria for MI may be more common. Further, the relative frequency of Q and non-Q wave infarction in blacks compared with whites is unknown, as are relative differences in silent MI and nondiagnostic creatine kinase elevations. It is even possible that many nonfatal events are missed entirely and that this underdiagnosis reflects social and economic restrictions to medical care more than it reflects any true racial difference. Finally, Lee and associates suggest that differential misclassification in vital records may explain some of the observed differences in CHD mortality rates. This may indeed be possible if, for instance, blacks have higher out-of-hospital mortality than do whites, especially if the diagnostic accuracy of death certificates is lower for deaths at home than for those in the hospital. The authors confirm that black men and women over age 55 were in fact more likely to die at home than were whites. The authors also demonstrate that the coding of CHD on death certificates and hospital discharge records is less specific for blacks than for whites, particularly among black women. Finally, changes in the International Classification of Disease coding practices since the Eighth Revision in 1968, when hypertensive heart disease was assigned to the codes for CHD, may have produced additional misclassification (15). The sobering finding by Lee and colleagues that only 13.6% of all cases coded as fatal MI by state nosologists could be confirmed with the use of strict clinical criteria and chart review casts serious doubt on the use of this data source alone in any study of absolute or comparative rates of disease. In conclusion, the most compelling finding of the present study is the elevated MI mortality rates observed among blacks, particularly black women. Although likely to be multifactorial in etiology, the difference in rates appears to be largely explained by socioenvironmental factors influencing susceptibility to infarction, medical care access and utilization, as well as by methodologic issues in data acquisition. Carefully designed and executed prospective studies in a variety of locations among socioeconomitally heterogeneous populations will be mandatory to assess any true differential in health status. Of particular importance will be an improved understanding of the causes of sudden death among blacks, of the marked excess in MI mortality among black women, and of methods to improve access to health care. Without such additional data, the gaps in mortality between blacks and whites are not likely to narrow and may even broaden. JoAnn E. Manson, MD, DrPH Department of Medicine Paul M. Ridker, MD Division of Cardiology
Brigham and Women’s Hospital Harvard Medical School Boston, MA 02115
REFERENCES 1. Lee MH, Borhani NO, Kuller LH. Validating reported myocardial infarction mortality in blacks and whites: A report from the Community Cardiovascular Surveillance Program. Ann Epidemiol. 1990;1:1-12. 2. Curry CL, Oliver J, Mumtaz FB. Coronary artery disease in blacks: Risk factors. Am Heart J. 1984;108:653-7. 3. Tyroler HA, Hames CC, Krishan I, Heyden S, Cooper G, Cassel JC. Black-white differences in serum lipids and lipoproteins in Evans County. Prev Med. 1975;4:541-9.
100
Manson and Ridker EDITORIAL
AEP Vol. 1, No. 1 October 1990: 97- IO0
4. Ekelund LG, Suchindran CM, K aron JM, McMahan RP, Tyroler HA. Black-white differences in exercise blood pressure. Circulation 1990;81:1568-74. 5. National Center for Health Statistics. Plan and operation of the National Health and Examination Survey, 1976-80. Washington, DC.: US Public Health Services; 1981. Department of Health and Human Services publication no. (PHS) 8 1-13 17. (Vital Health Stat [l], no. 15.) 6. Rowland M, Roberts J. Blood pressure levels and hypertension in persons ages 6-74 years: United States, 1976-80. National Center for Health Statistics Advance Data, no. 84, Hyattsville, MD., 1982. 7. Kleinman JC, Feldman JJ, Mond MA. The effects of changes in smoking habits on coronary heart disease mortality. Am J Public Health 1979;69:795-802. 8. Tyroler HA, Knowles MG, Wing SB, et al. Ischemic heart disease risk factors and twenty-year mortality in middle-age Evans County black males. Am Heart J. 1984;108:738-46. 9. Keil JE, Loadholt CB, Weinrich MC, Sandifer SH, Boyle E. Incidence of coronary heart disease in blacks in Charleston, South Carolina. Am Heart J. 1984;108:779-86. 10. Frisancho AR, Leonard WR, Bollettino LA. Blood pressure in blacks and whites and its relationship to dietary sodium and potassium intake. J Chronic Dis. 1984;37:515-9. 11. Cooper R, Castaner A, Campo A, Islam N, Simmons B. Severity of coronary artery disease among blacks with acute myocardial infarction. Am J Cardiol. 1989;63:788-91. 12. Strong JP, Restrepo C, Guzman MA. Coronary and aortic atherosclerosis in New Orleans. II. Comparison of lesions by age, sex, and race. Lab Invest. 1978;39:364-9. 13. Gillum RF, Liu KC. Coronary heart disease mortality in United States blacks, 19401978: Trends and unanswered questions. Am Heart J. 1984;108:728-32. 14. Sempos C, Cooper R, Kovar MG, McMillen M. Divergence of the recent trends in coronary mortality for the four major race-sex groups in the United States. Am J Public Health 1988;78:1422-27. 15. Keil JE, Saunders DE, Lackland DT, et al. Acute myocardial infarction: Period prevalence, case fatality, and comparison of black and white cases in urban and rural areas of South Carolina. Am Heart J. 1985;109:776-84. 16. Turi ZG, Stone PH, Muller JE, et al. Implications for acute intervention related to time of hospital arrival in acute myocardial infarction. Am J Cardiol. 1986;58:203-9. 17. Cooper RS, Simmons B, Castaner A, Prasad R, Franklin C, Ferlinz J. Survival rates and prehospital delay during myocardial infarction among black persons. Am J Cardiol. 1986;208- 11. 18. Ford E, Cooper R, Castaner A, Simmons B, Mar M. Coronary arteriography and coronary bypass surgery among whites and other racial groups relative to hospital-based incidence rates for coronary artery disease: Findings from NHDS. Am J Public Health 1989;79:437-40. 19. Tofler GH, Stone PH, Muller JE, et al. Effects of gender and race on prognosis after myocardial infarction: Adverse prognosis for women, particularly black women. J Am Co11 Cardiol. 1987;9:473-82.
Racial Differences in Coronary Heart Disease Incidence and Mortality Methodologic Mythology?
In this issue of Annuls of Ep’1d emiolog-y, Lee and colleagues provide valuable data, obtained from community surveillance, on the incidence of fatal and nonfatal coronary heart disease (CHD) in blacks compared with whites (1). Comparing data from community surveillance with those from death certificates and hospital discharge indices in 12 selected US communities in 1981, the investigators conclude that the annual age-adjusted mortality rates for definite myocardial infarction (MI) were higher in blacks than in whites of both sexes but that rates for nonfatal and total MI were higher among whites. The authors propose that a higher case/fatality ratio and some misclassification of cause of death could explain their results. These findings raise at least three major issues. First, if the racial differential in MI mortality and case fatality is real, what factors account for it? What are the relative contributions of black-white differences in coronary risk factor status and susceptibility to coronary disease, on the one hand, and differential access to and utilization of medical care, on the other? Second, are the lower incidence rates for nonfatal events an artifact of underdiagnosis of nonfatal CHD among blacks? Finally, what are the reasons for the differential misclassification of MI in the death certification process? Is the diagnostic accuracy of death certificates poorer for blacks than for whites or does the application of stringent criteria for defining MI systematically reduce verification rates in one group more than in the other! A large body of evidence addresses the question of black-white differences in the prevalence of traditional coronary risk factors. Several studies indicate a higher level of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-l in blacks than in whites, although other lipoproteins appear to be negligibly different (2, 3). An excess frequency of rest and exercise-induced hypertension, as well as a greater prevalence of left ventricular hypertrophy, however, has been demonstrated in blacks (2, 4). In addition, despite a similar prevalence of obesity in white and black men, black women have a striking excess of obesity compared to other sex-race groups; the prevalence of obesity in data from the National Health and Nutrition Examination Survey (NHANES) of 1976 to 1980 was 60% among black women aged 45 to 74 years, nearly double the prevalence among white women in the same age groups (5). Not unexpectedly, the prevalence of diabetes mellitus among black females is also markedly elevated (2). Cigarette smoking, the primary reversible behavioral determinant of CHD, appears to be more common among black men than among white men, while smoking prevalence among black and white women is similar (2, 6, 7). In NHANES data from 1976 to 1980, the percent current smokers was 50.4 in black men, 39.3 in white men, 3 1.1 in black women, and 33.1 in white women, although heavy smoking (greater than 25 cigarettes per day) was more common among whites of both sexes (2, 6). Social, economic, and behavioral factors play a major role in influencing coronary risk. In the Evans County study (8), in which a simple dichotomization of social status was employed, the lower social stratum among whites had a 20-year survival curve almost identical to that of blacks, and markedly less favorable than that of whites in a 0 1490Elsev~er SciencePuhllshing Co.. Inc. 1047.2797/90/$03.50
98
Manson and Ridker EDITORIAL
higher
AEP Vol. I, No. 1 Octoberf990: 97- 100
social stratum.
ton heart blacks
of lotier
whites, influence
class
comparative
These
excess
factors,
fatality, evidence blacks
heart four
major
whether
that
events.
Further,
importance
race-sex
groups
the strides
term
trends
Carolina,
to arrival
Thus
it is apparent
and,
even
Of particular elevated
the four sex-race comparably Multicenter mortality
(13),
there
Discharge these
considerably
from those
have been only half
influencing
accounted
the decline
for approximately
(15).
three
one-
Delay time from onset of both shortin blacks
of
and long-
compared
times as great)
suggest
(17).
with
Further,
a racial bias in the referral
as their
are less likely to receive
they are hospitalized,
as to
1975. From
revascularization,
procedures
in all
since
women
increased
Survey
ischemic
is controversy
in whites
determinant
mean delay,
rates in blacks
In a study from the rural Pee Dee
in blacks
an important
with white
early medical
are likely to receive
blacks
approxi-
( 18).
counterparts
a different
attention
for MI
quality
of care
by whites. concern
in the report
this group groups,
by Lee and colleagues
black women
had the highest almost
MI mortality
(140/100,000
markedly based on
population)
of
times the rate in white women and higher than and white men (1101100,000). In the (1141100,000)
men of the Limitation
MI among
women
of Infarct
Size (MILIS),
stresses
the poorer
was found to be primarily attributable higher (48%), which was significantly
black women sex-race subgroups ( 19). Th e excess mortality by their greater prevalence of obesity and
socioenvironmental
(1) is the
aged 55 to 74 years. Although
three
rate among
the other influenced
MI deaths
and coronary
to undergo
aged black Investigation
nosis following
unique
Hospital
rate of fatal MI among
small numbers,
between
the past two decades
that the factors
to be markedly
that blacks
received
&ring
groups equally.
twice as great;
arteriography
half as likely once
men,
or autopsy
differs
care. Although
men have diverged
and two-thirds
was found
data from the National
from that
disease
of case fatality
States
indicating
out-of-hospital
delay,
rate for coronary mately
attrib-
among
angiographic
of health
for blacks and white
at the hospital,
(16),
(median
and quality
for white
groups; declines
all the demographic
survival
is little
have been as great as those
of total cases in whites
whites
and smoking
as determinants
United
as steep as those for white men (14), are not affecting
symptoms
and
may also
blacks could be partially
of coronary
dramatically
in the
in blacks
sex-race
area of South
there
severity
utilization,
has declined
1976 to 1985, the secular
third
metabolism,
(10). among
such as hypertension
the underlying
to access,
mortality
of the other
with
blacks
obesity, and diabetes among women. are more likely to increase the incidence, rather than the case
greater
related
disease
between
(2, 11, 12).
Of potentially are factors
intake
and electrolyte
disease
in the Charles-
in comparison
of hypertension,
ischemic
to suggest
status
in dietary
for MI observed
risk factors
however,
and whites
Differences
rates of coronary
prevalence
of acute
have also been observed socioeconomic
to hypertension
case fatality
to accompanying the
(9).
as it relates
The elevated and
rates of CHD
black males of higher
social
especially
utable
Reduced
study among
and differences
among
black women
diabetes,
in health
prog-
to the high than that of may be
as well as by their
care.
In view of major differences by race in medical care access, quality, and utilization, the findings of lower incidence rates for nonfatal MI events among blacks are difficult to interpret. In addition, Lee and colleagues apply stringent criteria for the diagnosis of MI, including documentation of serial enzyme changes, Q wave or major ST evolution, and prolonged chest pain. Given these criteria, the possibility that nonfatal
events
among
blacks are underdiagnosed
appears
quite
likely.
If blacks have a
AEP Vol. I, No. I October1990: 97-100
Manson and Ridker EDITORIAL
99
greater time delay to hospitalization, enzyme elevations may be missed more frequently and failure to satisfy the stringent standardized criteria for MI may be more common. Further, the relative frequency of Q and non-Q wave infarction in blacks compared with whites is unknown, as are relative differences in silent MI and nondiagnostic creatine kinase elevations. It is even possible that many nonfatal events are missed entirely and that this underdiagnosis reflects social and economic restrictions to medical care more than it reflects any true racial difference. Finally, Lee and associates suggest that differential misclassification in vital records may explain some of the observed differences in CHD mortality rates. This may indeed be possible if, for instance, blacks have higher out-of-hospital mortality than do whites, especially if the diagnostic accuracy of death certificates is lower for deaths at home than for those in the hospital. The authors confirm that black men and women over age 55 were in fact more likely to die at home than were whites. The authors also demonstrate that the coding of CHD on death certificates and hospital discharge records is less specific for blacks than for whites, particularly among black women. Finally, changes in the International Classification of Disease coding practices since the Eighth Revision in 1968, when hypertensive heart disease was assigned to the codes for CHD, may have produced additional misclassification (15). The sobering finding by Lee and colleagues that only 13.6% of all cases coded as fatal MI by state nosologists could be confirmed with the use of strict clinical criteria and chart review casts serious doubt on the use of this data source alone in any study of absolute or comparative rates of disease. In conclusion, the most compelling finding of the present study is the elevated MI mortality rates observed among blacks, particularly black women. Although likely to be multifactorial in etiology, the difference in rates appears to be largely explained by socioenvironmental factors influencing susceptibility to infarction, medical care access and utilization, as well as by methodologic issues in data acquisition. Carefully designed and executed prospective studies in a variety of locations among socioeconomitally heterogeneous populations will be mandatory to assess any true differential in health status. Of particular importance will be an improved understanding of the causes of sudden death among blacks, of the marked excess in MI mortality among black women, and of methods to improve access to health care. Without such additional data, the gaps in mortality between blacks and whites are not likely to narrow and may even broaden. JoAnn E. Manson, MD, DrPH Department of Medicine Paul M. Ridker, MD Division of Cardiology
Brigham and Women’s Hospital Harvard Medical School Boston, MA 02115
REFERENCES 1. Lee MH, Borhani NO, Kuller LH. Validating reported myocardial infarction mortality in blacks and whites: A report from the Community Cardiovascular Surveillance Program. Ann Epidemiol. 1990;1:1-12. 2. Curry CL, Oliver J, Mumtaz FB. Coronary artery disease in blacks: Risk factors. Am Heart J. 1984;108:653-7. 3. Tyroler HA, Hames CC, Krishan I, Heyden S, Cooper G, Cassel JC. Black-white differences in serum lipids and lipoproteins in Evans County. Prev Med. 1975;4:541-9.
100
Manson and Ridker EDITORIAL
AEP Vol. 1, No. 1 October 1990: 97- IO0
4. Ekelund LG, Suchindran CM, K aron JM, McMahan RP, Tyroler HA. Black-white differences in exercise blood pressure. Circulation 1990;81:1568-74. 5. National Center for Health Statistics. Plan and operation of the National Health and Examination Survey, 1976-80. Washington, DC.: US Public Health Services; 1981. Department of Health and Human Services publication no. (PHS) 8 1-13 17. (Vital Health Stat [l], no. 15.) 6. Rowland M, Roberts J. Blood pressure levels and hypertension in persons ages 6-74 years: United States, 1976-80. National Center for Health Statistics Advance Data, no. 84, Hyattsville, MD., 1982. 7. Kleinman JC, Feldman JJ, Mond MA. The effects of changes in smoking habits on coronary heart disease mortality. Am J Public Health 1979;69:795-802. 8. Tyroler HA, Knowles MG, Wing SB, et al. Ischemic heart disease risk factors and twenty-year mortality in middle-age Evans County black males. Am Heart J. 1984;108:738-46. 9. Keil JE, Loadholt CB, Weinrich MC, Sandifer SH, Boyle E. Incidence of coronary heart disease in blacks in Charleston, South Carolina. Am Heart J. 1984;108:779-86. 10. Frisancho AR, Leonard WR, Bollettino LA. Blood pressure in blacks and whites and its relationship to dietary sodium and potassium intake. J Chronic Dis. 1984;37:515-9. 11. Cooper R, Castaner A, Campo A, Islam N, Simmons B. Severity of coronary artery disease among blacks with acute myocardial infarction. Am J Cardiol. 1989;63:788-91. 12. Strong JP, Restrepo C, Guzman MA. Coronary and aortic atherosclerosis in New Orleans. II. Comparison of lesions by age, sex, and race. Lab Invest. 1978;39:364-9. 13. Gillum RF, Liu KC. Coronary heart disease mortality in United States blacks, 19401978: Trends and unanswered questions. Am Heart J. 1984;108:728-32. 14. Sempos C, Cooper R, Kovar MG, McMillen M. Divergence of the recent trends in coronary mortality for the four major race-sex groups in the United States. Am J Public Health 1988;78:1422-27. 15. Keil JE, Saunders DE, Lackland DT, et al. Acute myocardial infarction: Period prevalence, case fatality, and comparison of black and white cases in urban and rural areas of South Carolina. Am Heart J. 1985;109:776-84. 16. Turi ZG, Stone PH, Muller JE, et al. Implications for acute intervention related to time of hospital arrival in acute myocardial infarction. Am J Cardiol. 1986;58:203-9. 17. Cooper RS, Simmons B, Castaner A, Prasad R, Franklin C, Ferlinz J. Survival rates and prehospital delay during myocardial infarction among black persons. Am J Cardiol. 1986;208- 11. 18. Ford E, Cooper R, Castaner A, Simmons B, Mar M. Coronary arteriography and coronary bypass surgery among whites and other racial groups relative to hospital-based incidence rates for coronary artery disease: Findings from NHDS. Am J Public Health 1989;79:437-40. 19. Tofler GH, Stone PH, Muller JE, et al. Effects of gender and race on prognosis after myocardial infarction: Adverse prognosis for women, particularly black women. J Am Co11 Cardiol. 1987;9:473-82.
