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The heart muscle in acute coronary insufficiency
CORRESPONDENCE literature makes no reference to an increased prevalence o f thyroid cancer in this disease. A published series o f 126 patients with rnyasthenia gravis and concurrent malignant neo9 plasia nmkes no reference to thyroid cancer? However, data are available relating to tile presence o f thyroid carcinoma in thymoma, a condition whose association with myasthenia is well established. A m o n g the 31 patients at the Mayo Clinic who had thymoma and a n o t h e r malignant tumor, three had thyroid c a r c i n o m a ? This represents a prevalence o f about I0 per cent. T h y r o i d cancer accounts for only 0.7 p e r cent ofall cancers, and therefore one would need a very large series o f patients to be able to establish the relative frequency o f this cancer in subjects with myasthenia gravis. T h e presence o f thyroid carcinoma in two o f o u r subjects may be a chance association, but it could also indicate an increase in thyroid carcinoma in this disease. M. VERDY, M.D. J. I'. FANTEUX, M.D. ~1. CADOTTE, M.D. j . CANTIN, M.D. D. BOGIIEN, M.D. Hotel-Dieu Hospital Montreal, Quebec 1. Papatestas, A. E., Osserman, K. E., and Kark, A. E.: The r6lationship between thymus and oncogenesis. A study of the incidence of nonthymic malignancy in myasthenia gravis. Brit. J. Cancer, 25:635-6-t5, 1971. 2. Souadjian, J. v., Enriquez, P., Silverstein, M. N., anti Pepin, J. M.: The spectrum of diseases associated with thymoma. Coincidence or syndrome? Arch. Intern. Med., 134:37.t-379, 197-t. 3. Papatestas, A. E., Genkins, G., th~rnwitz, S. ! I., and Kornfeld, P.:'rh) mectomy in myasthenia gravis: pathologic, clinical, and electrophysiologic correlations. Ann. N.Y. Acad. Sci., 274:555-573, 1976. 4. Souadjian,J. V., Silverstein, M. N., and Titus,J. L.: Thymoma and cancer. Cancer, 22:1211-1225, 1968.
le, in Table 1, it is customary a n d desirable naathematically to use a d e n o m i n a t o r o f N - I , one less than the n u m b e r o f items in tile sample. T h e authors have used N instead. Weibel appears to have used both in different situations, somewhat inconsistently in my opinion. I believe the present authors should have used N -- 1. (Their use o f N can be calculated from their vahles for SE.) 4. In Table 2 it a p p e a r s to me that the probahility, P, has been d e t e r m i n e d from t, calculated from the means and SE's, whereas I believe it is correct to use the means and the standard deviations to calculate t values. Since the number o f items used to obtain the data for acute coronary insufficiency is (by error) not available in Table 1, tile nunaher o f degrees 9 f freedom cannot be d e t e r m i n e d by the reader. However, it is clear that the probability will rise considerably, to a r o u n d 5 p e r cent by my a p p r o x i m a t e calculation. T h u s the significance o f the author's claims approaches being doubtful. Perhaps only a " t r e n d " can be claimed. In summary, I believe that the authors have not established the validity o f using mitral stcnosis biopsies as morphometrically equivalent to normal controls, and I question ' the statistical methods and statistical significance o f their resnhs. I also believe both these problems might have been avokled by better reviewing o f t h e manuscript, since tile data themselves are interesting. Finall)', the attthols might have dealt with an obvious (to me) alternative hypothesis: that tile heart in "acnte coronary insufficiency" has not h a d time to show m o r p h o m e t r i c changes from normal, while the chronically stressed hearts o f mitral stenosis a n d "chronic angina" have had time to hypertrophy, as they usually do, with an "anoxic response" being an increase in mitochondrial substance and possibly a relatively lesser increase o r a loss o f contractile substance, as discussed by Page (authors' ref. 12). Since tiffs was not dealt with, readers like myself with only a passing acquaintance with this field are likely to r e m a i n confused; the conclusions do not fit o u r clinical observations.
J. I)ouc, Lxs LEI'rlI, M.D. Brockton l lospital
THE HEART MUSCLE IN ACUTE CORONARY INSUFFICIENCY T o TIlE EDITOR:
T h e article by l.aguens et al. in ltumrm l'alhologq.' [10: 695-705, 1979] has some problems in it which 1 find confilSing and which affect adversely nay evaluation o f their conclusions. Some o f these a p p e a r to be related to u n i n f o r m e d o r inattentive editorial review. I. In the Results section, it is stated that for the mitral stenosis biopsies "the fine structure o f the ventricular myoc a r d i u m was similar to that r e p o r t e d for normal h u m a n nmscle cells." Since such hearts are usually hypertrophic, I find it dilticult to helieve that this would apply tu the m o r p h o m e t r i c analysis of the heart, and yet although the authors do not explicitly specify this, they use the nlitral stenosis data as their controls; see, for ex:lmple, their headings a n d connnents in their M o r p h o m e t r i c A,mlysis section, and the fact that Table 2 compares "acute coronary insulliciency" with "mitral stenosis," but with no g r o u p labeled "Normal ('ontr,)ls." 2. T a b l e 1 has no category "acute coronary insufficiency," although summary data from this category are shown in Table 2. I cannot j u d g e the quality o f the data in their absence. 3. In calculating the s t a n d a r d deviation o f a small sam-
Brockton, Massachusetts
The foregoing letter was referred to the authors of the article in question. Their reply follows. T o TIIE EDI'I'OR"
We have read Dr. l.eith's letter and we think that several facts should be pointed out, since they did not a p p e a r in o u r article because they were considered too ohvious. 1. Besides the difficulties existing in defining what call be considered as a normal control, we did not dare, for obvious ethical reasons, to ohtain samples from living healthy humans. We agree that material from necropsies is not suitable tbr this kind o f study. W e thought that mitral stenosis patients who u n d e r w e n t o p e n chest surgery were the best cases for comparative purposes, since they usually do not present left ventricular hypertroplly; in o u r article it is well established that the patients used as "controls ~' had n o r m a l coronary arteries as proven by selective coronary arteriography and showed a left ventriculogram that was entirely nornlal.
2. Regarding point 2 o f Dr. Leith's letter, we feel that he has not read carefnlly the whole article, since in the ",X.lcthods" section we describe the clinical entities considered as "acute coronary iusulliciency": intermediate
691
le, in Table 1, it is customary a n d desirable naathematically to use a d e n o m i n a t o r o f N - I , one less than the n u m b e r o f items in tile sample. T h e authors have used N instead. Weibel appears to have used both in different situations, somewhat inconsistently in my opinion. I believe the present authors should have used N -- 1. (Their use o f N can be calculated from their vahles for SE.) 4. In Table 2 it a p p e a r s to me that the probahility, P, has been d e t e r m i n e d from t, calculated from the means and SE's, whereas I believe it is correct to use the means and the standard deviations to calculate t values. Since the number o f items used to obtain the data for acute coronary insufficiency is (by error) not available in Table 1, tile nunaher o f degrees 9 f freedom cannot be d e t e r m i n e d by the reader. However, it is clear that the probability will rise considerably, to a r o u n d 5 p e r cent by my a p p r o x i m a t e calculation. T h u s the significance o f the author's claims approaches being doubtful. Perhaps only a " t r e n d " can be claimed. In summary, I believe that the authors have not established the validity o f using mitral stcnosis biopsies as morphometrically equivalent to normal controls, and I question ' the statistical methods and statistical significance o f their resnhs. I also believe both these problems might have been avokled by better reviewing o f t h e manuscript, since tile data themselves are interesting. Finall)', the attthols might have dealt with an obvious (to me) alternative hypothesis: that tile heart in "acnte coronary insufficiency" has not h a d time to show m o r p h o m e t r i c changes from normal, while the chronically stressed hearts o f mitral stenosis a n d "chronic angina" have had time to hypertrophy, as they usually do, with an "anoxic response" being an increase in mitochondrial substance and possibly a relatively lesser increase o r a loss o f contractile substance, as discussed by Page (authors' ref. 12). Since tiffs was not dealt with, readers like myself with only a passing acquaintance with this field are likely to r e m a i n confused; the conclusions do not fit o u r clinical observations.
J. I)ouc, Lxs LEI'rlI, M.D. Brockton l lospital
THE HEART MUSCLE IN ACUTE CORONARY INSUFFICIENCY T o TIlE EDITOR:
T h e article by l.aguens et al. in ltumrm l'alhologq.' [10: 695-705, 1979] has some problems in it which 1 find confilSing and which affect adversely nay evaluation o f their conclusions. Some o f these a p p e a r to be related to u n i n f o r m e d o r inattentive editorial review. I. In the Results section, it is stated that for the mitral stenosis biopsies "the fine structure o f the ventricular myoc a r d i u m was similar to that r e p o r t e d for normal h u m a n nmscle cells." Since such hearts are usually hypertrophic, I find it dilticult to helieve that this would apply tu the m o r p h o m e t r i c analysis of the heart, and yet although the authors do not explicitly specify this, they use the nlitral stenosis data as their controls; see, for ex:lmple, their headings a n d connnents in their M o r p h o m e t r i c A,mlysis section, and the fact that Table 2 compares "acute coronary insulliciency" with "mitral stenosis," but with no g r o u p labeled "Normal ('ontr,)ls." 2. T a b l e 1 has no category "acute coronary insufficiency," although summary data from this category are shown in Table 2. I cannot j u d g e the quality o f the data in their absence. 3. In calculating the s t a n d a r d deviation o f a small sam-
Brockton, Massachusetts
The foregoing letter was referred to the authors of the article in question. Their reply follows. T o TIIE EDI'I'OR"
We have read Dr. l.eith's letter and we think that several facts should be pointed out, since they did not a p p e a r in o u r article because they were considered too ohvious. 1. Besides the difficulties existing in defining what call be considered as a normal control, we did not dare, for obvious ethical reasons, to ohtain samples from living healthy humans. We agree that material from necropsies is not suitable tbr this kind o f study. W e thought that mitral stenosis patients who u n d e r w e n t o p e n chest surgery were the best cases for comparative purposes, since they usually do not present left ventricular hypertroplly; in o u r article it is well established that the patients used as "controls ~' had n o r m a l coronary arteries as proven by selective coronary arteriography and showed a left ventriculogram that was entirely nornlal.
2. Regarding point 2 o f Dr. Leith's letter, we feel that he has not read carefnlly the whole article, since in the ",X.lcthods" section we describe the clinical entities considered as "acute coronary iusulliciency": intermediate
691