312
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
JULY, 1976
Prevalence of Hemoglobinopathies in Patients with Ischemic Heart Disease* JOSEPH BORNHEIMER, M.D. and L. JULIAN HAYWOOD, M.D., Los Angeles County-University of Southern California Medical Center, Los Angeles, California
OMOZYGOUS hemoglobinopathies affect thousands of people yearly. Many more individuals are heterozygotes without clearly defined increased risk of mortality and morbidity except under certain specific circumstances.1 Patients with sickle cell disease may die in young adulthood or early middle age, while patients with sickle cell trait (hemoglobin AS) in general are not known to have an altered life expectany.24 It is not known whether or not the presence of abnormal hemoglobin without primary anemia is associated with increased or decreased risk for the development of complications of common clinical diseases. This pilot study was undertaken to determine whether there was an increased prevalence of abnormal hemoglobins in patients with ischemic heart disease, possibly indicating a role of abnormal hemoglobins in precipitating clinical manifestations of this syndrome. This report combines a prospective survey of patients with suspected ischemic heart disease with a retrospective survey of previously admitted patients to determine the prevalence of hemoglobinopathies in such patients. This initial survey involves coronary artery disease as this is known to be the most common cause of death in the United States. An important question is whether or not hemoglobinopathies represent a potential risk factor for the development of coronary occlusive disease.
H
METHODS
Two hundred and five consecutive patients admitted to the coronary care unit for suspected myocardial infarction had blood taken *Supported in part by Comprehensive Sickle Cell Center Grant No. HL 15162.
for Hb type and percent of A2 by cellulose acetate electrophoresis and percent of F as determined by alkali denaturation procedure. The hemoglobin type was then correlated with the subsequent clinical cardiac diagnosis at the time of discharge from the hospital. Patients were classed as Caucasian, Spanish surnamed, black and Oriental, and were subdivided into male and female. In addition, 65 black patients, already in follow-up in our coronary care unit follow-up clinic, had determination of Hb type by the same methods; these blood samples were taken at the time of routine clinic appearance and were not consecutive according to previous hospital admission. All charts were reviewed and the clinical cardiac diagnosis of arteriosclerotic heart disease manifested by typical myocardial infarction was confirmed in all of them. Some inpatients, although admitted for suspected ischemic episodes, had a final clinical cardiac diagnosis of valvular heart disease (rheumatic heart disease, prolapsing mitral valve, luetic aortitis), congenital heart disease, cardiomyopathy, arrhythmias, hypertension, pulmonary embolism, and chest pain of unknown cause. Diagnostic cardiac catheterization was subsequently performed in some patients. The diagnosis of arteriosclerotic heart disease was based on old or recent clinically documented myocardial infarction, diagnostic electrocardiographic changes or a typical history of angina pectoris. The diagnosis of valvular heart disease was based on history and characteristic cardiac ausculatory findings. Cardiomyopathy was based on the lack of confirmation of myocardial infarction, presence of generalized cardiomegaly, S3 gallop and congestive heart failure without
Prevalence of Hemoglobinopathies
Vol. 68, No. 4
other apparent etiology. Primary arrhythmias were similarly diagnosed when heart block or other arrhythmias occurred without a definite etiology. Cardiac catheritization established the diagnosis of congenital heart disease in one patient. RESULTS
One hundred and 98 inpatients had satisfactory laboratory reports on blood samples taken after admission to the coronary care Table 1. INPATIENTS Valvular Heart Cardio- ArrhythASHD Disease CHDmyopathy mia Other
313
listed in Table 1. As expected, arteriosclerotic heart disease was the most frequent confirmed diagnosis. Fifty-eight black outpatients were satisfactorily screened (Table 2). Hb AS occurred in five (8.6%), while Hb AC was found in two (3.4%). All outpatients had a clinical diagnosis of arteriosclerotic heart disease. The overall incidence of Hb AS in black patients was 12/130 (9.2%) and of Hb AC was 8/130 (6.2%) while the incidence of Hb AS and AC in black patients with arteriosclerotic heart disease was 11/108 (10.2%) and 6/108 (5.6%); the incidence of Hb AC in black patients without arteriosclerotic heart disease was 2/22 (8%). The mean ages for black patients with Hb AA was 58 years and for patients with Hb AS and AC was 59.6 years and 54.4 years, respectively.
HB AA M (85) C* F (40)
67
4
0
6
2
6
29
2
0
1
1
7
M (43)
29
2
1
5
1
5
Table 2. OUTPATIENTS
F(16)
11
2
0
0
2
1
ASHD
% of Total
HB AS M(1)
1
0
0
0
0
0
HB AA M
23
87.9
F(O)
0
0
0
0
0
0
Black F
28
M(4)
4
0
0
0
0
0
HB AS
F(3)
2
0
0
0
0
1
M
3
Black F
2
M
1
F
1
B
C
B
HB AC M (0) C
0
0
0
0
0
0
F(0)
0
0
0
0
0
0
M(3)
2
0
0
0
0
1
F(3)
2
1
0
0
0
0
B
8.6
HB AC 3.4
Black Total
58
100
Total-(198)
DISCUSSION *C
=
Caucasian combined with spanish surnamed and oriental.
unit for suspected myocardial infarction; 72 (36.4%) were black, 84 (42.4%) were Caucasian, 39 (19.7%) were Spanish surnamed and 3 (1.5%) were Oriental. Hb AA occurred in all the non-black patients except for one Caucasian with Hb AS. Repeat studies could not be obtained on this patient as he was lost to follow-up. No patient had a Hb less than 10 gms. % and none of the patients with abnormal Hb were anemic. Hb AS occurred in 7/72 (9.7%) of the black inpatients and Hb AC in 6/72 (8.3%). Clinical diagnoses for all inpatients are
Previous work in regard to sickle cell heart disease has noted the presence of hemodynamic changes presumably related to chronic anemia, often with subsequent development of congestive heart failure and possibly a cardiomyopathic state.58 The latter may be secondary to sludging of red blood cells in the coronary vessels leading to ischemic fibrosis.9 Endarteritis of the intramyocardial coronary arteries has also been suggested as a cause of the myopathy.5 However, ischemic myocardial changes due to red cell sludging were not confirmed in 53 patients with Hb SS studied by Baroldi at autopsy.10 Some
314
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
authors have noted difficulty in differentiating cardiac findings related to crises in patients with Hb SS from those of acute rheumatic fever. 11 Patients with Hb AS have not been reported to demonstrate significant cardiac pathology 12 Certain precipitating factors such as high altitude, severe exercise, intra and postoperative states, drug reactions such as with alcohol, and direct injection of contrast material have been reported to lead to vaso-occlusive crises with involvement of any or all organs. 13-15 Cardiomyopathy has been reported in children, and adults with Hb AS, though no proof exists as to whether they are incidental findings or directly related. 15"16 Epidemiological studies in Jamaica sponsored by the World Health Organization revealed a history suggestive of angina in a higher percentage of patients with abnormal Hb as compared to those with normal Hb.4'17'18 In view of the relative rarity of myocardial infarction and coronary artery disease in that population, this observation needs further evaluation.17 Our data do not suggest an increased incidence of Hb AS in patients with myocardial infarction or clinically suspected arteriosclerotic heart disease. The overall frequency with which we found abnormal Hb AS (9.2%) was similar to that expected in the general population.19 The 5.6% incidence of Hb AC in black patients with arteriosclerotic heart disease was significantly higher than the 2.3% that has been reported in the literature, however.19'20 There were no unusual features to the clinical course of these patients. On the basis of this preliminary data, it seems likely that in the absence of precipitating factors for acute vascular occlusion, patients with Hb AS are not at either increased or decreased risk for the development of clinical signs of arteriosclerotic heart disease. The finding of a higher than expected percentage of patients with hemoglobin AC in the black patients with arteriosclerotic and non-arteriosclerotic heart disease deserves further investigation. SUMMARY
One hundred and 98 patients admitted to a
JULY, 1976
coronary care unit were screened for abnormal hemoglobins by electrophoresis. Fiftyeight additional black patients with known ASHD were screened. No abnormal homozygous Hb's were found. The incidence of Hb AS in black inpatients was 9.7% and in black outpatients 8.6%; Hb AC occurred in 8.3% of black inpatients and 3.4% of black outpatients, respectively. The overall incidence of Hb AS and Hb AC in black patients was 12/130 (9.2%) and 8/130 (6.2%) respectively. Black patients with ASHD had an incidence of Hb AS of 10. 2% and of Hb AC of 5.6%. Hemoglobin AS does not appear to be an added risk factor for the development of clinical signs of ischemic heart disease in black patients. The increased prevalence of Hb AC deserves further study. LITERATURE CITED
1. CHARACHE, S. The Treatment of Sickle Cell Anemia. Arch. Intern. Med., 133:698-705, 1974. 2. WINTROBE, M. M. Clinical Hematology. Lea and Febiger, Philadelphia, 1974, pp. 822-855. 3. WILLIAMS, W. J. Hematology. McGraw-Hill Book Co., New York, 1972, pp. 413-434. 4. ASHCROFT, M. T. and W. E. MIALL, and P. F. MILNER. Comparison Between the Characteristics of Jamaican Adults with Normal Hemoglobin and Those With Sickle Cell Trait. Am. J. Epidemiology, 90:236-243, 1969. 5. WINSOR, T. and G. E. BURCH. The Electrocardiogram and Cardiac State in Active Sickle Cell Anemia. Amer. Heart Jour., 29:685-696, 1945. 6. SHUBIN, H. and R. KAUFMAN, M. SHAPIRO, and D. C. LEVINSON. Cardiovascular Findings in Children with Sickle Cell Anemia. Amer. Jour. Cardiology, 6:875-885, 1960. 7. NG, M. L. and J. LIEBMAN, J. ANSLOVAR, and S. GROSS. Cardiovascular Findings in Children with Sickle Cell Anemia. Dis. Chest,
52:788-799, 1967. 8. UZSAY, N. K. Cardiovascular Findings in Patients with Sickle Cell Anemia. Amer. Jour. Cardiology, 13:320, 328, 1964. 9. OLIVIERA, E. and N. GOMEZ-PATRUO. Ischemic Cardiopathy. Amer. Jour. Cardiology,
11:686-688, 1963. 10. BAROLDI, G. High Resistance of Human Myocardium to Shock and Red Blood Cell Aggregation (Sludge). Cardiology, 54:271-277, 1969. 11. KLINEFELTER, H. F. The Heart in Sickle Cell Anemia. Am. J. of Med. Sci., 203:34-51, 1942.
(Concluded on page 288)
288
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
ability of program operation and performance. We have all heard the horror stories about abuses of the Medicaid and Medicare programs, much of which has involved black patients. A knowledgeable public with higher expectations of the health care delivery system will make accountability possible.
JULY, 1976
sources and availability of services. 5. Be administered for maximum benefit to the consumer and provider. 6. Be accountable to the public. 7. Represent the interest of the consumer.
Responding to the special interests of blacks will, in all likelihood, result in the greater benefit to all Americans.
SUMMARY
These six major items represent a perspective for viewing a NHI proposal. In addition to an adequate financing bill, matters of policy determination and implementation are important. The representation of the minority consumer and provider viewpoints at this level will make a worthy NHI bill a workable instrument to address our health needs. Black consumers and providers must take part in the decision-making process at all levels. There is no question about whether blacks represent a large and special group with special problems which must be addressed. NHI must take cognizance of this group and provide the means to alleviate the health problems unique to this group. In sum, National Health Insurance proposals are now the first order of business for the legislative branch of government. In order that NHI answer the health problems of blacks, a bill must: 1. Be universal for all American residents. 2. Have broad benefits with emphasis on preventive care and cover routine and catastrophic illness. 3. Be equably financed. 4. Promote the development of health care delivery re-
LITERATURE CITED
1. FALK, I. S. National Health Insurance: A Review of Policies and Proposals. Duke University Law School., 35:670, 1970. 2. CORNELY, P. B. There is More to Health Than Just Paying Bills (Editorial), J. Amer. Pub. Health Assoc., 64:845, 1974. 3. FEIN, R. The New National Policy, New EngI. J. Med., 290:37, 1974. 4. National Association of Household Workers, Inc., Silver Spring, Maryland. 5. SOMMERS, H. H. and R. ANNE. Doctors, Patients and Health Insurance. Brookings Institutions, Washington, D.C. 1961, p.518. 6. FALK, I. S. National Health Insurance: A Review of Policies and Proposals. Duke University Law School., 35:671, 1970. 7. Health Maintenance Organization Assistance Act of 1973. (P.L. 93-222). 8. ROBERTSON, W., Health Educator. Howard University College of Medicine, Washington, D.C. 20059. (Personal communication). 9. Committee on the Cost of Medical Care. Publication #5. 1932. Roanoke Rapids (20) and Union Health Services (19). 10. LORENSEN, L. C. Journal of International Health Services. Vol. 4, No. 1, 1974, pp. 49-57. 11. NEWHOUSE, J. P. et al. Policy Options and Impact of National Health Insurance. New Engl. J. Med., 290:1345, 1974.
(Bornheimer and Havwood from Dage 314) 12. LINDSAY, JR., J. and J. C. MESHEL, and R. 56:1443-1444, 1963. H. PATTERSON. The Cardiovascular Manifes17. FODOR, J. and W. E. MIALL, K. L. STANtations of Sickle Cell Disease. Arch. Int. Med., DARD, Z. FEJFAR, and K. L. STUART, 133:643-651, 1974. Myocardial Disease in a Rural Population in 13. GREEN, R. L. and R. G. HUNTSMAN, and Jamaica. Bull. W.H.O., 31:321-325, 1964. G. R. SERJEANT. Sickle Cell Altitude. Brit. 18. ROSE, G. A. The Diagnosis of Ischemic Heart Med. J., 4:593-594, 1971. Pain and Intermittent Claudication in Field Sur14. JONES, S. R. and R. A. BINDER, and E. M. veys. Bull. W.H.O., 27:645-658, 1962. DNOWHO, JR. Sudden Death in Sickle Cell 19. MOTULSKY, A. G. Frequency of Sickling DisTrait. New Engl. J. Med., 282:323-325, 1970. orders in U.S. Blacks. New Engl. J. Med., 15. RUBLER, S. and R. A. FLEISCHER. Sickle 288:31, 1973. Cell States and Cardiomyopathy. Amer. Jour. 20. SCHNEIDER, R. G. Incidence of Hb C Trait in Cardiology, 19:867-873, 1967. 505 Normal Negroes: A Family with Homo16. BRINSFIELD, G. and F. K. EDWARDS, and zygous Hb C and Sickle-cell Trait Union. Jour. W. L. WATKINS. Sickle Cell Trait and AbnorLab. Clin. Med., 44:133, 1954. mal Cardiovascular Findings. South. Med. Jour.,
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
JULY, 1976
Prevalence of Hemoglobinopathies in Patients with Ischemic Heart Disease* JOSEPH BORNHEIMER, M.D. and L. JULIAN HAYWOOD, M.D., Los Angeles County-University of Southern California Medical Center, Los Angeles, California
OMOZYGOUS hemoglobinopathies affect thousands of people yearly. Many more individuals are heterozygotes without clearly defined increased risk of mortality and morbidity except under certain specific circumstances.1 Patients with sickle cell disease may die in young adulthood or early middle age, while patients with sickle cell trait (hemoglobin AS) in general are not known to have an altered life expectany.24 It is not known whether or not the presence of abnormal hemoglobin without primary anemia is associated with increased or decreased risk for the development of complications of common clinical diseases. This pilot study was undertaken to determine whether there was an increased prevalence of abnormal hemoglobins in patients with ischemic heart disease, possibly indicating a role of abnormal hemoglobins in precipitating clinical manifestations of this syndrome. This report combines a prospective survey of patients with suspected ischemic heart disease with a retrospective survey of previously admitted patients to determine the prevalence of hemoglobinopathies in such patients. This initial survey involves coronary artery disease as this is known to be the most common cause of death in the United States. An important question is whether or not hemoglobinopathies represent a potential risk factor for the development of coronary occlusive disease.
H
METHODS
Two hundred and five consecutive patients admitted to the coronary care unit for suspected myocardial infarction had blood taken *Supported in part by Comprehensive Sickle Cell Center Grant No. HL 15162.
for Hb type and percent of A2 by cellulose acetate electrophoresis and percent of F as determined by alkali denaturation procedure. The hemoglobin type was then correlated with the subsequent clinical cardiac diagnosis at the time of discharge from the hospital. Patients were classed as Caucasian, Spanish surnamed, black and Oriental, and were subdivided into male and female. In addition, 65 black patients, already in follow-up in our coronary care unit follow-up clinic, had determination of Hb type by the same methods; these blood samples were taken at the time of routine clinic appearance and were not consecutive according to previous hospital admission. All charts were reviewed and the clinical cardiac diagnosis of arteriosclerotic heart disease manifested by typical myocardial infarction was confirmed in all of them. Some inpatients, although admitted for suspected ischemic episodes, had a final clinical cardiac diagnosis of valvular heart disease (rheumatic heart disease, prolapsing mitral valve, luetic aortitis), congenital heart disease, cardiomyopathy, arrhythmias, hypertension, pulmonary embolism, and chest pain of unknown cause. Diagnostic cardiac catheterization was subsequently performed in some patients. The diagnosis of arteriosclerotic heart disease was based on old or recent clinically documented myocardial infarction, diagnostic electrocardiographic changes or a typical history of angina pectoris. The diagnosis of valvular heart disease was based on history and characteristic cardiac ausculatory findings. Cardiomyopathy was based on the lack of confirmation of myocardial infarction, presence of generalized cardiomegaly, S3 gallop and congestive heart failure without
Prevalence of Hemoglobinopathies
Vol. 68, No. 4
other apparent etiology. Primary arrhythmias were similarly diagnosed when heart block or other arrhythmias occurred without a definite etiology. Cardiac catheritization established the diagnosis of congenital heart disease in one patient. RESULTS
One hundred and 98 inpatients had satisfactory laboratory reports on blood samples taken after admission to the coronary care Table 1. INPATIENTS Valvular Heart Cardio- ArrhythASHD Disease CHDmyopathy mia Other
313
listed in Table 1. As expected, arteriosclerotic heart disease was the most frequent confirmed diagnosis. Fifty-eight black outpatients were satisfactorily screened (Table 2). Hb AS occurred in five (8.6%), while Hb AC was found in two (3.4%). All outpatients had a clinical diagnosis of arteriosclerotic heart disease. The overall incidence of Hb AS in black patients was 12/130 (9.2%) and of Hb AC was 8/130 (6.2%) while the incidence of Hb AS and AC in black patients with arteriosclerotic heart disease was 11/108 (10.2%) and 6/108 (5.6%); the incidence of Hb AC in black patients without arteriosclerotic heart disease was 2/22 (8%). The mean ages for black patients with Hb AA was 58 years and for patients with Hb AS and AC was 59.6 years and 54.4 years, respectively.
HB AA M (85) C* F (40)
67
4
0
6
2
6
29
2
0
1
1
7
M (43)
29
2
1
5
1
5
Table 2. OUTPATIENTS
F(16)
11
2
0
0
2
1
ASHD
% of Total
HB AS M(1)
1
0
0
0
0
0
HB AA M
23
87.9
F(O)
0
0
0
0
0
0
Black F
28
M(4)
4
0
0
0
0
0
HB AS
F(3)
2
0
0
0
0
1
M
3
Black F
2
M
1
F
1
B
C
B
HB AC M (0) C
0
0
0
0
0
0
F(0)
0
0
0
0
0
0
M(3)
2
0
0
0
0
1
F(3)
2
1
0
0
0
0
B
8.6
HB AC 3.4
Black Total
58
100
Total-(198)
DISCUSSION *C
=
Caucasian combined with spanish surnamed and oriental.
unit for suspected myocardial infarction; 72 (36.4%) were black, 84 (42.4%) were Caucasian, 39 (19.7%) were Spanish surnamed and 3 (1.5%) were Oriental. Hb AA occurred in all the non-black patients except for one Caucasian with Hb AS. Repeat studies could not be obtained on this patient as he was lost to follow-up. No patient had a Hb less than 10 gms. % and none of the patients with abnormal Hb were anemic. Hb AS occurred in 7/72 (9.7%) of the black inpatients and Hb AC in 6/72 (8.3%). Clinical diagnoses for all inpatients are
Previous work in regard to sickle cell heart disease has noted the presence of hemodynamic changes presumably related to chronic anemia, often with subsequent development of congestive heart failure and possibly a cardiomyopathic state.58 The latter may be secondary to sludging of red blood cells in the coronary vessels leading to ischemic fibrosis.9 Endarteritis of the intramyocardial coronary arteries has also been suggested as a cause of the myopathy.5 However, ischemic myocardial changes due to red cell sludging were not confirmed in 53 patients with Hb SS studied by Baroldi at autopsy.10 Some
314
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
authors have noted difficulty in differentiating cardiac findings related to crises in patients with Hb SS from those of acute rheumatic fever. 11 Patients with Hb AS have not been reported to demonstrate significant cardiac pathology 12 Certain precipitating factors such as high altitude, severe exercise, intra and postoperative states, drug reactions such as with alcohol, and direct injection of contrast material have been reported to lead to vaso-occlusive crises with involvement of any or all organs. 13-15 Cardiomyopathy has been reported in children, and adults with Hb AS, though no proof exists as to whether they are incidental findings or directly related. 15"16 Epidemiological studies in Jamaica sponsored by the World Health Organization revealed a history suggestive of angina in a higher percentage of patients with abnormal Hb as compared to those with normal Hb.4'17'18 In view of the relative rarity of myocardial infarction and coronary artery disease in that population, this observation needs further evaluation.17 Our data do not suggest an increased incidence of Hb AS in patients with myocardial infarction or clinically suspected arteriosclerotic heart disease. The overall frequency with which we found abnormal Hb AS (9.2%) was similar to that expected in the general population.19 The 5.6% incidence of Hb AC in black patients with arteriosclerotic heart disease was significantly higher than the 2.3% that has been reported in the literature, however.19'20 There were no unusual features to the clinical course of these patients. On the basis of this preliminary data, it seems likely that in the absence of precipitating factors for acute vascular occlusion, patients with Hb AS are not at either increased or decreased risk for the development of clinical signs of arteriosclerotic heart disease. The finding of a higher than expected percentage of patients with hemoglobin AC in the black patients with arteriosclerotic and non-arteriosclerotic heart disease deserves further investigation. SUMMARY
One hundred and 98 patients admitted to a
JULY, 1976
coronary care unit were screened for abnormal hemoglobins by electrophoresis. Fiftyeight additional black patients with known ASHD were screened. No abnormal homozygous Hb's were found. The incidence of Hb AS in black inpatients was 9.7% and in black outpatients 8.6%; Hb AC occurred in 8.3% of black inpatients and 3.4% of black outpatients, respectively. The overall incidence of Hb AS and Hb AC in black patients was 12/130 (9.2%) and 8/130 (6.2%) respectively. Black patients with ASHD had an incidence of Hb AS of 10. 2% and of Hb AC of 5.6%. Hemoglobin AS does not appear to be an added risk factor for the development of clinical signs of ischemic heart disease in black patients. The increased prevalence of Hb AC deserves further study. LITERATURE CITED
1. CHARACHE, S. The Treatment of Sickle Cell Anemia. Arch. Intern. Med., 133:698-705, 1974. 2. WINTROBE, M. M. Clinical Hematology. Lea and Febiger, Philadelphia, 1974, pp. 822-855. 3. WILLIAMS, W. J. Hematology. McGraw-Hill Book Co., New York, 1972, pp. 413-434. 4. ASHCROFT, M. T. and W. E. MIALL, and P. F. MILNER. Comparison Between the Characteristics of Jamaican Adults with Normal Hemoglobin and Those With Sickle Cell Trait. Am. J. Epidemiology, 90:236-243, 1969. 5. WINSOR, T. and G. E. BURCH. The Electrocardiogram and Cardiac State in Active Sickle Cell Anemia. Amer. Heart Jour., 29:685-696, 1945. 6. SHUBIN, H. and R. KAUFMAN, M. SHAPIRO, and D. C. LEVINSON. Cardiovascular Findings in Children with Sickle Cell Anemia. Amer. Jour. Cardiology, 6:875-885, 1960. 7. NG, M. L. and J. LIEBMAN, J. ANSLOVAR, and S. GROSS. Cardiovascular Findings in Children with Sickle Cell Anemia. Dis. Chest,
52:788-799, 1967. 8. UZSAY, N. K. Cardiovascular Findings in Patients with Sickle Cell Anemia. Amer. Jour. Cardiology, 13:320, 328, 1964. 9. OLIVIERA, E. and N. GOMEZ-PATRUO. Ischemic Cardiopathy. Amer. Jour. Cardiology,
11:686-688, 1963. 10. BAROLDI, G. High Resistance of Human Myocardium to Shock and Red Blood Cell Aggregation (Sludge). Cardiology, 54:271-277, 1969. 11. KLINEFELTER, H. F. The Heart in Sickle Cell Anemia. Am. J. of Med. Sci., 203:34-51, 1942.
(Concluded on page 288)
288
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
ability of program operation and performance. We have all heard the horror stories about abuses of the Medicaid and Medicare programs, much of which has involved black patients. A knowledgeable public with higher expectations of the health care delivery system will make accountability possible.
JULY, 1976
sources and availability of services. 5. Be administered for maximum benefit to the consumer and provider. 6. Be accountable to the public. 7. Represent the interest of the consumer.
Responding to the special interests of blacks will, in all likelihood, result in the greater benefit to all Americans.
SUMMARY
These six major items represent a perspective for viewing a NHI proposal. In addition to an adequate financing bill, matters of policy determination and implementation are important. The representation of the minority consumer and provider viewpoints at this level will make a worthy NHI bill a workable instrument to address our health needs. Black consumers and providers must take part in the decision-making process at all levels. There is no question about whether blacks represent a large and special group with special problems which must be addressed. NHI must take cognizance of this group and provide the means to alleviate the health problems unique to this group. In sum, National Health Insurance proposals are now the first order of business for the legislative branch of government. In order that NHI answer the health problems of blacks, a bill must: 1. Be universal for all American residents. 2. Have broad benefits with emphasis on preventive care and cover routine and catastrophic illness. 3. Be equably financed. 4. Promote the development of health care delivery re-
LITERATURE CITED
1. FALK, I. S. National Health Insurance: A Review of Policies and Proposals. Duke University Law School., 35:670, 1970. 2. CORNELY, P. B. There is More to Health Than Just Paying Bills (Editorial), J. Amer. Pub. Health Assoc., 64:845, 1974. 3. FEIN, R. The New National Policy, New EngI. J. Med., 290:37, 1974. 4. National Association of Household Workers, Inc., Silver Spring, Maryland. 5. SOMMERS, H. H. and R. ANNE. Doctors, Patients and Health Insurance. Brookings Institutions, Washington, D.C. 1961, p.518. 6. FALK, I. S. National Health Insurance: A Review of Policies and Proposals. Duke University Law School., 35:671, 1970. 7. Health Maintenance Organization Assistance Act of 1973. (P.L. 93-222). 8. ROBERTSON, W., Health Educator. Howard University College of Medicine, Washington, D.C. 20059. (Personal communication). 9. Committee on the Cost of Medical Care. Publication #5. 1932. Roanoke Rapids (20) and Union Health Services (19). 10. LORENSEN, L. C. Journal of International Health Services. Vol. 4, No. 1, 1974, pp. 49-57. 11. NEWHOUSE, J. P. et al. Policy Options and Impact of National Health Insurance. New Engl. J. Med., 290:1345, 1974.
(Bornheimer and Havwood from Dage 314) 12. LINDSAY, JR., J. and J. C. MESHEL, and R. 56:1443-1444, 1963. H. PATTERSON. The Cardiovascular Manifes17. FODOR, J. and W. E. MIALL, K. L. STANtations of Sickle Cell Disease. Arch. Int. Med., DARD, Z. FEJFAR, and K. L. STUART, 133:643-651, 1974. Myocardial Disease in a Rural Population in 13. GREEN, R. L. and R. G. HUNTSMAN, and Jamaica. Bull. W.H.O., 31:321-325, 1964. G. R. SERJEANT. Sickle Cell Altitude. Brit. 18. ROSE, G. A. The Diagnosis of Ischemic Heart Med. J., 4:593-594, 1971. Pain and Intermittent Claudication in Field Sur14. JONES, S. R. and R. A. BINDER, and E. M. veys. Bull. W.H.O., 27:645-658, 1962. DNOWHO, JR. Sudden Death in Sickle Cell 19. MOTULSKY, A. G. Frequency of Sickling DisTrait. New Engl. J. Med., 282:323-325, 1970. orders in U.S. Blacks. New Engl. J. Med., 15. RUBLER, S. and R. A. FLEISCHER. Sickle 288:31, 1973. Cell States and Cardiomyopathy. Amer. Jour. 20. SCHNEIDER, R. G. Incidence of Hb C Trait in Cardiology, 19:867-873, 1967. 505 Normal Negroes: A Family with Homo16. BRINSFIELD, G. and F. K. EDWARDS, and zygous Hb C and Sickle-cell Trait Union. Jour. W. L. WATKINS. Sickle Cell Trait and AbnorLab. Clin. Med., 44:133, 1954. mal Cardiovascular Findings. South. Med. Jour.,
