1004 the controls. The data revealed a trend of increasing s.c.B.R. values with increasing serum concentrations of cholesterol and triglycerides among the controls, but this trend was virtually lost among the patients. This suggests that the controls could expand their S.C.B.R. in response to increased serum-lipid concentrations, while the patients could not. This difference in the relationship of s.c.B.R. to triglyceride and cholesterol may have significance in the aetiology of atherosclerosis, and may provide a new means to assess the risk of premature myocardial infarction among individuals with raised serum-lipid levels. It seems that a balance of opposing forces is operating in atherogenesis: the process is accelerated by increased serum-lipid levels but retarded by
expanded s.c.B.R. The patients were being treated with one or more drugs, including clofibrate, diazepam, warfarin, antihypertensives, digitalis, diuretics, and glyceryl trinitrate. The observed decrease in s.c.B.R. and the loss of correlation between S.C.B.R. and lipid levels among the patients might have been the result of drug therapy, but this seems unlikely since if the decreased s.c.B.R. among the
patients were drug induced, a pharmacologically diverse group of drugs would have to share a common effect in lowering S.C.B.R. Furthermore, if drugs such as clofibrate do lower serum-lipids in some patients, the ratio of s.c.B.R. to cholesterol or to triglyceride should increase, resulting in higher slopes of the regression lines: fig. 3 shows the opposite to be the case. Thus, any effect of hypolipaemic drugs would be masking, rather than contributing to the observed relationship between S.C.B.R. and serum-lipids. The specific effects of each of these drugs on s.c.B.R. is unknown. Further studies on larger patient populations are necessary to resolve any possible influence of drugs or diet on S.C.B.R., s.F.v., and S.F.H. Our findings, although preliminary, do provide a working hypothesis for further investigation into the mechanism of atherogenesis. It may be possible in the future to develop therapeutic measures designed to raise the levels of S.C.B.R., s.F.v., and S.F.H. in the prevention and treatment
of coronary heart-disease.
We thank Dr Mary Jane Jesse, Dr Barbara Klein, Dr Benjamin Befeler, Dr Lee Bricker, and Dr Doyle Campbell for assistance in recruiting patients and controls; Dr Franklin Briese and Dr Paul Bergstresser for useful suggestions; Mrs Janet Cassady and Miss Iris Kiem for assistance with the statistical analysis. This work was supported in part by grant N.I.H. HL 14141 from the National Heart and Lung In-
stitute, U.S. Public Health Service.
Requests for reprints should be addressed to S. L. H., Department Dermatology, University of Miami School of Medicine, P.O. Box 520875, Biscayne Annex, Miami, Florida 33152, U.S.A.
of
REFERENCES
1. Miller, G. J., Miller, N. E. Lancet, 1975, i, 16. 2. Bailey, J. M. in Atherogenesis: Initiation Factors
(edited by
PERICARDITIS IN ACUTE MYOCARDIAL INFARCTION K. L. LIEM D. DURRER
K. I. LIE H.
J. J. WELLENS
University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, Netherlands. a prospective study of 300 consecutive patients who survived the first 24 h of acute myocardial infarction, pericarditis was present in 44 patients (14·7%). The only factors independently associated with pericarditis were transmural myocardial infarction, extent of myocardial damage, atrial fibrillation, and longer duration of fever. Pericarditis did not affect immediate prognosis or incidence of cardiac rup-
Summary
In
These findings and the high incidence of atrial fibrillation suggest that anticoagulant therapy should not be discontinued in patients with pericarditis complicating acute myocardial infarction. ture.
Introduction WHEN pericarditis complicates acute myocardial infarction it is usually associated with transmural myocardial injury due to extension of infarction to the epicardial surface.’ A high incidence of arrhythmias and extensive myocardial damage have been reported under these circumstances.2-5 However, from retrospective studies2-6 it is not clear if these features are the consequence of a transmural myocardial infarction or a characteristic of pericarditis per se. We therefore designed a prospective study in which we evaluated the incidence, clinical setting, and prognosis of pericarditis complicating acute myocardial infarction. And, in the setting of transmural myocardial infarction, we compared the clinical course of subgroups with and without
pericarditis. Patients and Methods 312 patients admitted consecutively to the coronary-care unit within 24 h of infarction from November, 1974, to August, 1975, were studied prospectively. The diagnosis of acute myocardial infarction was based on a characteristic history of chest pain correlated with typical electrocardiographic (E.c.G.) changes and a serial rise in serum enzymes. Continuous E.c.G. monitoring was performed in all patients during their stay in the coronary-care unit. A twelve-lead E.c.G. was obtained at least twice a day during the first week after infarction. The size of infarction was estimated by sampling serum enzymes (S.G.o.T.) 6-hourly until the peak value was reached.’ Infarct location was defined according to the criteria proposed by the New York Heart Association.s A transmural
R. Porter and
J. Knight); p. 63. Amsterdam, 1973. 3. Bondjers, G., Bjorkerud, S. Artery, 1974, 1, 3. 4. Artery, 1975, 1, 165. 5. Walten, K. W., Williamson, N. J. Atheroscler. Res. 1968, 8, 599. 6. Kao, V. C. Y., Wissler, R. W. Expl. mol. Path. 1965, 4, 465. 7. Smith, E. B., Slater, R. S. Biochem. J. 1971, 123, 39. 8. Stein, O., Stein, Y. Circulation, Res. 1975, 36, 436. 9. Bailey, J. M., Butler, J. Archs Biochem. Biophys. 1973, 159, 580. 10. Day, A. J., Wahlquist, M. L., Campbell, D. J. Atherosclerosis, 1970, 11, 301. 11. Kramsch, D. M., Hollander, W. J. clin. Invest. 1973, 52, 236. 12. Nestel, P. J. Adv. Lipid Res. 1970, 8, 1. 13. Stein, O., Stein, Y. Biochim. biophys. Acta, 1973, 326, 232. 14. Loeper, M., Lemaire, A., Lesure, A. C. r. Soc. Biol. 1928, 98, 103. 15. Avigan, J. J. biol. Chem. 1958, 234, 787.
16. 17. 18.
T. C., Chen, C. P., Wefler, V., Raftery, A. Analyt. Chem 1961, 33, 1405. Havel, R. J., Eder, H. A., Bragdon, J. H. J. clin Invest. 1955, 34, 1345. Rudel, L. L., Lee, J. A., Morris, M. D., Fills, J. M. Biochem. J. 1974, 139,
19.
Lowry, O. H., Rosebrough, N. J., Farr, A. L., Randall, R. J. J
Chuang,
89. biol Chem.
1951, 193, 265. 20. Ischæmic Heart Disease Registers: report of the 5th working group World Health Organisation, Copenhagen, 1971. 21. Haberland, M. E., Reynolds, J. A. Proc. nat Acad. Sci. U.S.A. 1973, 70, 2313. 22. Stein, Y., Stein, O. in Atherogenesis: Initiation Factors (edited by R. Porter and J. Knight); p. 165. Amsterdam, 1973. 23. Iverius, P. H. ibid. p. 185.
1005 TABLE III-RELATION OF ATRIAL FIBRILLATION, ATRIOVENTRICUi.AR BLOCK, AND FEVER TO PERICARDITIS IN PATIENTS WITH TRANSMURAI. INFARCTION, MATCHED FOR SIZE OF INFARCTION
TABLE I-PATIENT CHARACTERISTICS
Figures in italic type indicate %.
agulant therapy because of hypertension. Patients with and without pericarditis were comparable with respect to sex, number of previous infarction, site of infarction, incidence of heart-failure, and subsequent hospital mortality (table i). Patients with pericarditis had a lower mean age, a higher mean peak S.G.O.T., a higher inci’Excluded those who died within 24 h of onset of infarction. dence of transmural infarction and major arrhythmias, italic in indicate %. type Figures N.S. = not significant. and a longer duration of fever. Table n relates factors of age, size of infarction, major arrhythmias, and fever to the presence or absence myocardial infarction was diagnosed by the development of times waves. three Patients were examined of pericarditis in patients with and without transmural pathological Q daily, Pericarditis was diagnosed when a two-component or myocardial infarction. In the subgroup with transmural three-component pericardial rub was heard by at least two myocardial infarction pericarditis was associated only physicians. Anticoagulant therapy was instituted routinely on with a higher mean peak S.G.O.T., a higher incidence of admission unless contraindicated and was continued irrespecatrial fibrillation, atrioventricular block, and a longer tive of the absence or presence of pericarditis. 12 patients withwere
who died within the first 24 h of infarction were excluded from this study. The immediate prognosis was considered to include only the 28-day hospital mortality. The significance of differences in incidence and mortality rate were tested by use of chi-square test. Differences in mean ages and mean peak S.G.O.T. were tested by Student’s t test.
out
pericarditis
Results
Pericarditis developed in 44 patients, 9 of whom had pain characteristic for pericarditis. Pericarditis occurred 12 h to 5 days after onset of acute myocardial infarction. 35 patients (80%) developed pericarditis within 48 h and 15 patients within 24 h of acute myocardial infarction. The pericarditis lasted for 6-9 days. In 1 pericarditis recurred 2 weeks later. Anticoagulant therapy was instituted on admission in 41 patients and continued during the period that pericardial rub was present. The remaining 3 patients received no antico-
duration of fever. Table in shows the relation of atrial fibrillation, atrioventricular block, and fever to pericarditis in patients with transmural myocardial infarction matched for size of infarction. In these patients pericarditis was associated with a higher incidence of atrial fibrillation and a longer period of fever. None of the patients with pericarditis developed cardiac rupture. The 2 deaths in the subgroup of pericarditis were due to heart-failure.
no
TABLE F II-RFI ATION OF
Discussion
prospective study we found pericarditis in patients who survived the first 24 h of acute myocardial infarction. This figure is slightly higher than that found in retrospective studies, in which pericarditis was associated with extensive myocardial damage and a high incidence of both atrial and ventricular arrhythmias as well as a longer period offever.2-s In this
14.7% of
AGE, SIZE OF INFARCTION, FEVER, AND MAJOR ARRHYTHMIAS TO PERICARDITIS IN PATIENTS WITH AND WITHOUT TRANSMURAL INFARCTION
Figures in italic type indicate %.
1006 In our study atrial fibrillation, size of infarction, and fever were the only factors which were independently associated with pericarditis. The incidence of atrial fibrillation and the longer duration of fever are more probably due to inflammation localised to the area overlying the myocardial infarct. Our data also suggest that transmural infarction is correlated with the appearance of pericarditis. In contrast, ventricular
arrhythmias, atrioventricular block, and age were related to transmural myocardial infarction or size of infarction. Like others2-5 we also found that the immediate mortality is not affected by pericarditis. However, this does not mean that pericarditis does not affect the long-term prognosis after discharge since the eventual outcome may be related to the size of infarction.9 Are
patients with pericarditis at higher risk of cardiac rupture? This question is controversial2-5and raises the problem of whether anticoagulant therapy should be discontinued in these patients. None of our patients developed cardiac rupture despite continuation of anticoagulant therapy, and these were patients at higher risk of thromboembolic complications since our data revealed that in 43% of our patients pericarditis was associated with atrial fibrillation. We therefore feel that anticoagulant therapy should not be discontinued in patients who develop pericarditis associated with acute myocardial infarction.
Patients Patients
regarded as having bird-fancier’s lung if they satisfied all the following criteria: recent history of avian exposure; serum avian precipitins; diffuse shadowing on chest radiograph; a significant reduction (less than 70 % predicted value) of carbon-monoxide transfer factor (single breath); and improvement or no deterioration when
to
K. L. L.
REFERENCES
Parkinson, J., Bedford, D. R. Lancet, 1928, i, 4. Thadani, U., Chopra, M. P., Aber, C. P., Portal, R. W. Br. med. J. 1971, ii, 135. 3. Niarchos, A. P., McKendrick, C S. Br Heart J 1973, 35, 49 4. Lichtstein, E., Liu, H. M., Gupta, P. Am. Heart J. 1974, 87, 246. 5. Toole, J. G., Silverman, M. E Chest. 1975, 67, 647 6. Rosenbaum, F. F., Levine, S. A. Archs intern. Med. 1941, 68, 913. 7. West, M., Eschar, J., Zimmerman, H. J. Med. Clins N. Am. 1966, 50, 171.
1. 2.
8. The Criteria Committee of the New York Heart Association Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis; p. 98.
Boston, 1973. Kibe, O., Nilsson, N. J. Acta med. scand. 1967, 182, 597.
BIRD-FANCIER’S LUNG AND JEJUNAL VILLOUS ATROPHY W. T. BERRILL P. F. FITZPATRICK W. M. MACLEOD
O. E. EADE I. HYDE RALPH WRIGHT
Southampton University Hospitals Sixteen patients with bird-fancier’s lung screened for evidence of cœliac disease by assessing their clinical features, red-bloodcell or serum folate levels, and serum for reticulin antibodies. Five of nine patients selected for jejunal biopsy showed villous atrophy, and in some this seemed to be a true gluten-sensitive enteropathy.
Summary
were
Introduction patient with diffuse radiographic pulmonary shadowing, a history of contact with birds, and serum avian precipitins was found by chance to have jejunal villous atrophy. A second such patient was seen in 1969, and both case-reports were pubIN 1968
a
were
exposure to birds and their excreta ceased. Twenty-four patients, presumed to have bird-fancier’s lung, seen by one of us (W.M.M.) between 1958 and 1975, were reviewed. Sixteen of these who satisfied the above criteria were available for study. Of the remaining patients, one had died, one refused to attend for follow-up, and six did not satisfy all the above criteria. None of the sixteen continued to deteriorate, but two patients relapsed after a remission of 4 and 9 years. Methods recalled for review to look for clinical or laboratory evidence of coeliac disease. Specific laboratory screening tests included examination of a peripheral film for Howell-Jolly bodies as an index of splenic atrophy,4 serum and/or red-blood-cell folate,5 and serum for reticulin antibodies. s Patients with any clinical evidence to suggest malabsorption or in whom any screening test was positive were further investigated with barium studies of the small intestine and jejunal biopsy.
Patients
Requests for reprints should be addressed
9.
lished.1 An account of another patient with a similar combination of diseases appeared in 1970.2 In 1971, in a study of twenty-four patients with coeliac disease, three were found with diffuse interstitial lung disease and serum avian precipitins, although they had not apparently had contact with birds.3 A group of patients diagnosed as having bird-fancier’s lung were therefore investigated for evidence of coeliac disease. They had all been seen in one centre, and included the two cases originally reported by Hood and Mason)
were
Results Of the sixteen patients who fulfilled the criteria for bird-fancier’s lung, eight had clinical or laboratory features which led us to suspect malabsorption, and they were selected for further investigation including jejunal biopsy. A biopsy specimen was taken in one patient purely because we had found that the two conditions were often associated. The results in these patients are summarised in the accompanying table. This shows that five patients had jejunal villous atrophy, and brief summaries are given below. Cases 1 and 2 have been described elsewhere.1 Case 1 Presented with signs and symptoms of diffuse pulmonary disease at the age of 54 years in 1958, and relapsed 10 years later. The investigation of coincident anaemia included a barium-meal examination, during which the small bowel was noted to be dilated, and this was confirmed by progress films. Jejunal biopsy showed subtotal villous atrophy. There was a good clinical and laboratory response to a gluten-free diet, which has been maintained, but her pulmonary symptoms at the time of recall for review in May, 1975, had deteriorated, with severe respiratory insufficiency and extensive pulmonary shadowing, despite no known further contact with birds. Serum avian precipitins persist and she is reticulin antibody negative; however, she is too ill for a repeat jejunal biopsy. Despite her recent deterioration, the initial clinical course and persistent serum avian precipitins fulfil our criteria for bird-fancier’s lung.
expanded s.c.B.R. The patients were being treated with one or more drugs, including clofibrate, diazepam, warfarin, antihypertensives, digitalis, diuretics, and glyceryl trinitrate. The observed decrease in s.c.B.R. and the loss of correlation between S.C.B.R. and lipid levels among the patients might have been the result of drug therapy, but this seems unlikely since if the decreased s.c.B.R. among the
patients were drug induced, a pharmacologically diverse group of drugs would have to share a common effect in lowering S.C.B.R. Furthermore, if drugs such as clofibrate do lower serum-lipids in some patients, the ratio of s.c.B.R. to cholesterol or to triglyceride should increase, resulting in higher slopes of the regression lines: fig. 3 shows the opposite to be the case. Thus, any effect of hypolipaemic drugs would be masking, rather than contributing to the observed relationship between S.C.B.R. and serum-lipids. The specific effects of each of these drugs on s.c.B.R. is unknown. Further studies on larger patient populations are necessary to resolve any possible influence of drugs or diet on S.C.B.R., s.F.v., and S.F.H. Our findings, although preliminary, do provide a working hypothesis for further investigation into the mechanism of atherogenesis. It may be possible in the future to develop therapeutic measures designed to raise the levels of S.C.B.R., s.F.v., and S.F.H. in the prevention and treatment
of coronary heart-disease.
We thank Dr Mary Jane Jesse, Dr Barbara Klein, Dr Benjamin Befeler, Dr Lee Bricker, and Dr Doyle Campbell for assistance in recruiting patients and controls; Dr Franklin Briese and Dr Paul Bergstresser for useful suggestions; Mrs Janet Cassady and Miss Iris Kiem for assistance with the statistical analysis. This work was supported in part by grant N.I.H. HL 14141 from the National Heart and Lung In-
stitute, U.S. Public Health Service.
Requests for reprints should be addressed to S. L. H., Department Dermatology, University of Miami School of Medicine, P.O. Box 520875, Biscayne Annex, Miami, Florida 33152, U.S.A.
of
REFERENCES
1. Miller, G. J., Miller, N. E. Lancet, 1975, i, 16. 2. Bailey, J. M. in Atherogenesis: Initiation Factors
(edited by
PERICARDITIS IN ACUTE MYOCARDIAL INFARCTION K. L. LIEM D. DURRER
K. I. LIE H.
J. J. WELLENS
University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, Netherlands. a prospective study of 300 consecutive patients who survived the first 24 h of acute myocardial infarction, pericarditis was present in 44 patients (14·7%). The only factors independently associated with pericarditis were transmural myocardial infarction, extent of myocardial damage, atrial fibrillation, and longer duration of fever. Pericarditis did not affect immediate prognosis or incidence of cardiac rup-
Summary
In
These findings and the high incidence of atrial fibrillation suggest that anticoagulant therapy should not be discontinued in patients with pericarditis complicating acute myocardial infarction. ture.
Introduction WHEN pericarditis complicates acute myocardial infarction it is usually associated with transmural myocardial injury due to extension of infarction to the epicardial surface.’ A high incidence of arrhythmias and extensive myocardial damage have been reported under these circumstances.2-5 However, from retrospective studies2-6 it is not clear if these features are the consequence of a transmural myocardial infarction or a characteristic of pericarditis per se. We therefore designed a prospective study in which we evaluated the incidence, clinical setting, and prognosis of pericarditis complicating acute myocardial infarction. And, in the setting of transmural myocardial infarction, we compared the clinical course of subgroups with and without
pericarditis. Patients and Methods 312 patients admitted consecutively to the coronary-care unit within 24 h of infarction from November, 1974, to August, 1975, were studied prospectively. The diagnosis of acute myocardial infarction was based on a characteristic history of chest pain correlated with typical electrocardiographic (E.c.G.) changes and a serial rise in serum enzymes. Continuous E.c.G. monitoring was performed in all patients during their stay in the coronary-care unit. A twelve-lead E.c.G. was obtained at least twice a day during the first week after infarction. The size of infarction was estimated by sampling serum enzymes (S.G.o.T.) 6-hourly until the peak value was reached.’ Infarct location was defined according to the criteria proposed by the New York Heart Association.s A transmural
R. Porter and
J. Knight); p. 63. Amsterdam, 1973. 3. Bondjers, G., Bjorkerud, S. Artery, 1974, 1, 3. 4. Artery, 1975, 1, 165. 5. Walten, K. W., Williamson, N. J. Atheroscler. Res. 1968, 8, 599. 6. Kao, V. C. Y., Wissler, R. W. Expl. mol. Path. 1965, 4, 465. 7. Smith, E. B., Slater, R. S. Biochem. J. 1971, 123, 39. 8. Stein, O., Stein, Y. Circulation, Res. 1975, 36, 436. 9. Bailey, J. M., Butler, J. Archs Biochem. Biophys. 1973, 159, 580. 10. Day, A. J., Wahlquist, M. L., Campbell, D. J. Atherosclerosis, 1970, 11, 301. 11. Kramsch, D. M., Hollander, W. J. clin. Invest. 1973, 52, 236. 12. Nestel, P. J. Adv. Lipid Res. 1970, 8, 1. 13. Stein, O., Stein, Y. Biochim. biophys. Acta, 1973, 326, 232. 14. Loeper, M., Lemaire, A., Lesure, A. C. r. Soc. Biol. 1928, 98, 103. 15. Avigan, J. J. biol. Chem. 1958, 234, 787.
16. 17. 18.
T. C., Chen, C. P., Wefler, V., Raftery, A. Analyt. Chem 1961, 33, 1405. Havel, R. J., Eder, H. A., Bragdon, J. H. J. clin Invest. 1955, 34, 1345. Rudel, L. L., Lee, J. A., Morris, M. D., Fills, J. M. Biochem. J. 1974, 139,
19.
Lowry, O. H., Rosebrough, N. J., Farr, A. L., Randall, R. J. J
Chuang,
89. biol Chem.
1951, 193, 265. 20. Ischæmic Heart Disease Registers: report of the 5th working group World Health Organisation, Copenhagen, 1971. 21. Haberland, M. E., Reynolds, J. A. Proc. nat Acad. Sci. U.S.A. 1973, 70, 2313. 22. Stein, Y., Stein, O. in Atherogenesis: Initiation Factors (edited by R. Porter and J. Knight); p. 165. Amsterdam, 1973. 23. Iverius, P. H. ibid. p. 185.
1005 TABLE III-RELATION OF ATRIAL FIBRILLATION, ATRIOVENTRICUi.AR BLOCK, AND FEVER TO PERICARDITIS IN PATIENTS WITH TRANSMURAI. INFARCTION, MATCHED FOR SIZE OF INFARCTION
TABLE I-PATIENT CHARACTERISTICS
Figures in italic type indicate %.
agulant therapy because of hypertension. Patients with and without pericarditis were comparable with respect to sex, number of previous infarction, site of infarction, incidence of heart-failure, and subsequent hospital mortality (table i). Patients with pericarditis had a lower mean age, a higher mean peak S.G.O.T., a higher inci’Excluded those who died within 24 h of onset of infarction. dence of transmural infarction and major arrhythmias, italic in indicate %. type Figures N.S. = not significant. and a longer duration of fever. Table n relates factors of age, size of infarction, major arrhythmias, and fever to the presence or absence myocardial infarction was diagnosed by the development of times waves. three Patients were examined of pericarditis in patients with and without transmural pathological Q daily, Pericarditis was diagnosed when a two-component or myocardial infarction. In the subgroup with transmural three-component pericardial rub was heard by at least two myocardial infarction pericarditis was associated only physicians. Anticoagulant therapy was instituted routinely on with a higher mean peak S.G.O.T., a higher incidence of admission unless contraindicated and was continued irrespecatrial fibrillation, atrioventricular block, and a longer tive of the absence or presence of pericarditis. 12 patients withwere
who died within the first 24 h of infarction were excluded from this study. The immediate prognosis was considered to include only the 28-day hospital mortality. The significance of differences in incidence and mortality rate were tested by use of chi-square test. Differences in mean ages and mean peak S.G.O.T. were tested by Student’s t test.
out
pericarditis
Results
Pericarditis developed in 44 patients, 9 of whom had pain characteristic for pericarditis. Pericarditis occurred 12 h to 5 days after onset of acute myocardial infarction. 35 patients (80%) developed pericarditis within 48 h and 15 patients within 24 h of acute myocardial infarction. The pericarditis lasted for 6-9 days. In 1 pericarditis recurred 2 weeks later. Anticoagulant therapy was instituted on admission in 41 patients and continued during the period that pericardial rub was present. The remaining 3 patients received no antico-
duration of fever. Table in shows the relation of atrial fibrillation, atrioventricular block, and fever to pericarditis in patients with transmural myocardial infarction matched for size of infarction. In these patients pericarditis was associated with a higher incidence of atrial fibrillation and a longer period of fever. None of the patients with pericarditis developed cardiac rupture. The 2 deaths in the subgroup of pericarditis were due to heart-failure.
no
TABLE F II-RFI ATION OF
Discussion
prospective study we found pericarditis in patients who survived the first 24 h of acute myocardial infarction. This figure is slightly higher than that found in retrospective studies, in which pericarditis was associated with extensive myocardial damage and a high incidence of both atrial and ventricular arrhythmias as well as a longer period offever.2-s In this
14.7% of
AGE, SIZE OF INFARCTION, FEVER, AND MAJOR ARRHYTHMIAS TO PERICARDITIS IN PATIENTS WITH AND WITHOUT TRANSMURAL INFARCTION
Figures in italic type indicate %.
1006 In our study atrial fibrillation, size of infarction, and fever were the only factors which were independently associated with pericarditis. The incidence of atrial fibrillation and the longer duration of fever are more probably due to inflammation localised to the area overlying the myocardial infarct. Our data also suggest that transmural infarction is correlated with the appearance of pericarditis. In contrast, ventricular
arrhythmias, atrioventricular block, and age were related to transmural myocardial infarction or size of infarction. Like others2-5 we also found that the immediate mortality is not affected by pericarditis. However, this does not mean that pericarditis does not affect the long-term prognosis after discharge since the eventual outcome may be related to the size of infarction.9 Are
patients with pericarditis at higher risk of cardiac rupture? This question is controversial2-5and raises the problem of whether anticoagulant therapy should be discontinued in these patients. None of our patients developed cardiac rupture despite continuation of anticoagulant therapy, and these were patients at higher risk of thromboembolic complications since our data revealed that in 43% of our patients pericarditis was associated with atrial fibrillation. We therefore feel that anticoagulant therapy should not be discontinued in patients who develop pericarditis associated with acute myocardial infarction.
Patients Patients
regarded as having bird-fancier’s lung if they satisfied all the following criteria: recent history of avian exposure; serum avian precipitins; diffuse shadowing on chest radiograph; a significant reduction (less than 70 % predicted value) of carbon-monoxide transfer factor (single breath); and improvement or no deterioration when
to
K. L. L.
REFERENCES
Parkinson, J., Bedford, D. R. Lancet, 1928, i, 4. Thadani, U., Chopra, M. P., Aber, C. P., Portal, R. W. Br. med. J. 1971, ii, 135. 3. Niarchos, A. P., McKendrick, C S. Br Heart J 1973, 35, 49 4. Lichtstein, E., Liu, H. M., Gupta, P. Am. Heart J. 1974, 87, 246. 5. Toole, J. G., Silverman, M. E Chest. 1975, 67, 647 6. Rosenbaum, F. F., Levine, S. A. Archs intern. Med. 1941, 68, 913. 7. West, M., Eschar, J., Zimmerman, H. J. Med. Clins N. Am. 1966, 50, 171.
1. 2.
8. The Criteria Committee of the New York Heart Association Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis; p. 98.
Boston, 1973. Kibe, O., Nilsson, N. J. Acta med. scand. 1967, 182, 597.
BIRD-FANCIER’S LUNG AND JEJUNAL VILLOUS ATROPHY W. T. BERRILL P. F. FITZPATRICK W. M. MACLEOD
O. E. EADE I. HYDE RALPH WRIGHT
Southampton University Hospitals Sixteen patients with bird-fancier’s lung screened for evidence of cœliac disease by assessing their clinical features, red-bloodcell or serum folate levels, and serum for reticulin antibodies. Five of nine patients selected for jejunal biopsy showed villous atrophy, and in some this seemed to be a true gluten-sensitive enteropathy.
Summary
were
Introduction patient with diffuse radiographic pulmonary shadowing, a history of contact with birds, and serum avian precipitins was found by chance to have jejunal villous atrophy. A second such patient was seen in 1969, and both case-reports were pubIN 1968
a
were
exposure to birds and their excreta ceased. Twenty-four patients, presumed to have bird-fancier’s lung, seen by one of us (W.M.M.) between 1958 and 1975, were reviewed. Sixteen of these who satisfied the above criteria were available for study. Of the remaining patients, one had died, one refused to attend for follow-up, and six did not satisfy all the above criteria. None of the sixteen continued to deteriorate, but two patients relapsed after a remission of 4 and 9 years. Methods recalled for review to look for clinical or laboratory evidence of coeliac disease. Specific laboratory screening tests included examination of a peripheral film for Howell-Jolly bodies as an index of splenic atrophy,4 serum and/or red-blood-cell folate,5 and serum for reticulin antibodies. s Patients with any clinical evidence to suggest malabsorption or in whom any screening test was positive were further investigated with barium studies of the small intestine and jejunal biopsy.
Patients
Requests for reprints should be addressed
9.
lished.1 An account of another patient with a similar combination of diseases appeared in 1970.2 In 1971, in a study of twenty-four patients with coeliac disease, three were found with diffuse interstitial lung disease and serum avian precipitins, although they had not apparently had contact with birds.3 A group of patients diagnosed as having bird-fancier’s lung were therefore investigated for evidence of coeliac disease. They had all been seen in one centre, and included the two cases originally reported by Hood and Mason)
were
Results Of the sixteen patients who fulfilled the criteria for bird-fancier’s lung, eight had clinical or laboratory features which led us to suspect malabsorption, and they were selected for further investigation including jejunal biopsy. A biopsy specimen was taken in one patient purely because we had found that the two conditions were often associated. The results in these patients are summarised in the accompanying table. This shows that five patients had jejunal villous atrophy, and brief summaries are given below. Cases 1 and 2 have been described elsewhere.1 Case 1 Presented with signs and symptoms of diffuse pulmonary disease at the age of 54 years in 1958, and relapsed 10 years later. The investigation of coincident anaemia included a barium-meal examination, during which the small bowel was noted to be dilated, and this was confirmed by progress films. Jejunal biopsy showed subtotal villous atrophy. There was a good clinical and laboratory response to a gluten-free diet, which has been maintained, but her pulmonary symptoms at the time of recall for review in May, 1975, had deteriorated, with severe respiratory insufficiency and extensive pulmonary shadowing, despite no known further contact with birds. Serum avian precipitins persist and she is reticulin antibody negative; however, she is too ill for a repeat jejunal biopsy. Despite her recent deterioration, the initial clinical course and persistent serum avian precipitins fulfil our criteria for bird-fancier’s lung.
