specific death rates (Fig. 2). Most striking is that, from young adulthood, death rates from cancer have scarcely increased, and this must seem at variance with current experience. After having been similar at birth, the rates diverge throughout childhood; this may, in part, result from underdiagnosis of cancer in 1931, with some deaths ascribed incorrectly to infectious diseases, whereas the more stable higher rates in 1971 may reflect an increase in leukemia. With current improvements in the diagnosis and treatment of cancer, and with decreases in the incidence of certain forms, such as cancers of the cervix .nd stomach, we might expect mortality rates to' decrease. However, any progress has been largely offset
by increases in the incidence of other cancers (for example, of the lung in men and, perhaps, of the breast in women) and by better diagnosis and more complete case-finding. The inescapable fact is that 20% of Canadians are currently dying from cancer and it is estimated that those who die from it lose, on average, 18 years of life.3 In addition to teaching everyone to recognize the early signs and symptoms of cancer, and encouraging them to seek earlier diagnosis and treatment, we must place increasing emphasis on prevention and on the elimination of causal factors. What better place to start than through reduction in smoking, as recently advocated by Miller,4 which Reir has estimated would alone
-. .-
20
-
o . C
/
El / /
0)
. 10
/
/
//
0. --U -
5
-
- -w
0 50
40
30
20
10
0
W
70
80+
Age (yrs) FIG. 1-Proportion of deaths from cancer (including benign tumours and those of unspecified nature) among all deaths, Canada, 1931 and 1971 1200 -- -
1000 C0 **.
500
.
200
.-.1971 . 1931
/
-
.
100 /
to
.. to 0)
.U
/
50
/
// /
20 10 /
@1
/
5 2 1'
60 50 40 Age (yrs) FIG. Z-A.e-specific death rates for cancer, Canada, 1931 and 1971. 0
10
ADEN C. IRWIN, MD, DPH Department of sreventive medicine ousie University Halifax, NS
References 1. Dominion Bureau of Statistics: Vital Statistics, 1931, Ottawa, King's Printer, 1933 2. Causes of Death, Canada, 1971, Ottawa, Information Canada, 1972 3. DOLL R: The prevention of cancer. I R Coil Physicians Lond 11: 125, 1977 4. MILLER AB: Recent trends in lung cancer mortality. Can Med Assoc J 116: 28, 1977 5. Ran' AE: Public information on smoking: an urgent responsibility for cancer research workers (E). I Nati Cancer Inst 57: 1207, 1976
Technetium pyrophosphate scanning in acute myocardial infarction
.-. 1971
30
reduce cancer mortality by nearly 25%?
20
30
70
80+
To the editor: The most interesting report on the use of technetium pyrophosphate scanning to detect acute myocardial infarcts, by Ko, Kostuk and Deatrich (Can Med Assoc J 116: 260, 1977), demonstrates the danger of making sweeping statistical conclusions from scanty data. I fear the authors are reading more into the elegant statistical analysis than the small series of observations warrants. In relating the scintigraphic area of myocardial uptake of technetium-99mstannous pyrophosphate (ssmTc.PYP) to the peak value of serum creatine phosphokinase (CPK) in 17 patients, Ko and colleagues find what they consider to be good correlation between the two sets of values and quote a correlation coefficient of 0.74 to back up this contention, stating that there is less than a 1000 to 1 chance of no such correlation. This is unintentional sleight of hand. Simple inspection of their Fig. 4 shows clearly that there is substantial scatter of the values and really very little correlation at all. I believe the fallacy arises largely because of the "outlier" - the CPK value of 6000 U/i. If this is omitted, as .1 believe it should be, the slope of the regression line changes from the present value of about 100 to a value of 46, the intercept on the Y axis from -1500 to -200 and the correlation coefficient from 0.74 to 0.51. Except for the correlation coefficient these figures are meaningless, though the decrease in "r" is probably important. The reason for this strange situation is clearly that the one very high value is receiving undue weight; the cloud of CPK values between 0 and 2500 U/i becomes effectively a single point lying at the mean of the 16 lesser values, and the outlier becomes the sec-
CMA JOURNAL/MAY 21, 1977/VOL. 116 1119
Indodd
(indomethacin, MSD Std.) Indications INDOCID (indomethacin, MSD Std.) has been found effective in the symptomatic treatment of se/ected cases of rheumatoid arthritis, ankylosing (rheumatoid) spondy/itis, gout, se/ected cases of severe osteoarthritis including degenerative disease of the hip. INDOCID should be used in those cases of severe osteoarthritis which do not respond to treatment with other drugs such as the salicylates. In these conditions it may on occasion replace other commonly used agents such as corticosteroids, salicylates, phenylbutazone-like compounds, and colchicine. Dosage Summary For Adults In chronic rheumatoid arthritis and ankylosing (rheumatoid) spondylitis: Start with 25 mg b.i.d. or tid. If response is inadequate, add 25 mg daily each week until an adequate response is obtained or a dosage of 150 to 200 mg is reached. In acute rheumatoid arthritis and acute flares of chronic rheumatoid arthritis: Start with 25mg bid. or tid. If response is inadequate, add 25 mg each day until an' adequate response is obtained or until a total daily dose of 150-200 mg is reached. Maintenance corticosteroids can often gradually be reduced 25 to 50 percent and completely discontinued over several weeks or months in some patients. In severe osteoarthritis and degenerative disease of the hip: Start with 25 mg bid. or tid. If response is inadequate, increase the daily dosage by 25 mg at about weekly intervals until an adequate response is obtained or until a dosage of 150 to 200 mg is reached. In acute gout: 50 mg t.i.d. until all signs and symptoms subside. INDOCID Suppositories: 100 mg to 200 mg a day. May be administered one at bedtime, and if necessary one the following morning. Also may be used in combined administration with Capsules: 100 mg suppository at bedtime, supplemented the following day by 25 mg capsules as needed up to a total of 150 to 200 mg (capsules and suppositories) of indomethacin. Note: In chronic disorders, it is important to start with low dosage and increase gradually for best results with fewer adverse reactions. Always give INDOCID* with food or immediately after meals or with antacid to reduce gastric irritation. As with all drugs, the lowest possible effective dose should be utilized for each individual patient. ContraIndications Active peptic ulcer, gastritis, regional enteritis, ulcerative colitis, divert iculit is and if there is a recurrent history of GI. lesions. Also contraindicated in patients allergic to ass. or indomethacin. Safety of indomethacin for use in pregnancy or lactation has not been established. Indomethacin suppositories are contraindicated in subjects with a history of recent rectal bleeding. SHOULD NOT BE ADMINISTERED TO PEDIATRIC AGE GROUPS. Warning Patients who experience dizziness, lightheadedness, or feelings of detachment on indomethacin should be cautioned against operating motor vehicles, machinery, climbing ladders, etc. Use cautiously in patients with psychiatric disturbances, epilepsy, or parkinsonism. PrecautIons Indomethacin should be used with caution because of the possible occurrence of gastrointestinal reactions, the incidence of which may be decreased by glying the drug immediately after meals, with food or antacids. The risk of continuing therapy with indomethacin in the face of such symptoms must be weighed against the possible benefits to the individual patient. Indomethacin suppositories should be given with caution to patients with any anal or rectal pathology. Discontinue if GI. bleeding occurs. Peptic ulcer has been reported. Hemorrhage and perforation have occurred in patients with history of peptic ulcer (see Contralndlcatlons) or in patients receiving steroids or salicylates concomitantly. In some patients there was no history of peptic ulcer or of other drugs being given. As a result of GI. bleeding some patients may manifest anemia and, for this reason, appropriate blood determinations are recommended periodically. Headache may occur, usually early in treatment. Discontinue therapy if headache persists despite dosage reduction. In common with other drugs which have anti-inflamma-
tory, analgesic and antipyretic properties, indomethacin possesses the potential of masking the signs and symptoms which ordinarily accompany infectious disease. The physician must be alert to this possibility to avoid undue delay in initiating appropriate treatment of the infection. Indomethacin should be used with caution in patients with existing, but controlled infections. Where therapy is prolonged, ophthalmological examinations are desirable at periodic intervals (see Eye Reactions). Since advancing years appear to increase the possibility of adverse reactions, indomethacin should be used with greater care in the elderly. As with any drug, patients should be followed carefully to detect unusual manifestations of drug sensitivity.
Adverse Reactions Central Nervous System: Commonly seen, headache (usually more severe in morning), dizziness, and lightheadedness. Infrequently observed: mental confusion, syncope, drowsiness, convulsions, coma, depression which may be severe, and other psychic disturbances, such as depersonalization. The severity of these effects may occasionally require cessation of therapy and rarely, admission to hospital. Gastrointestinal: include nausea, anorexia, vomiting, epigastric distress, abdominal pain, and diarrhea, which are not uncommon. Single or multiple ulceration of esophagus, stomach, duodenum orsmall intestine, perforation and hemorrhage have occurred. A few fatalities have been reported. Hemorrhage wit hout obvious ulceration. Increased abdominal pain in patients with ulcerative colitis. Indomethacin has been suspected of precipitating the symptoms of ulcerative colitis or regional ileitis but causal relationship not proven. Rarely reported, intestinal ulceration followed by stenosis and obstruction. Least frequent reactions: ulcerative stomatitis, bleeding from sigmoid colon or divert iculi, perforation of pre-existing sigmoid lesions, e.g., diverticuli or carcinoma. With the use of indomethacin suppositories, pruritus ani, tenesmus, and irritation of the rectal mucosa reported occasionally; rectal bleeding rarely. However, sigmoidoscopic examination in a number of patients did not reveal any significant changes of rectal mucosa. Hepatic: Toxic hepatitis and jaundice of uncertain etiology, including se-
vere and fatal cases. Cardiovascular-Renal: Infrequently, edema, elevation of blood pressure,
and hematuria.
Dermatologic-Hypersensitivity:
Infrequently, pruritus, urticaria, angioneurotic edema, angiitis, erythema nodosum, skin rashes, loss of hair, and acute respiratory distress including sudden dyspnea and asthma. Hematologic Reactions: Infrequently leukopenia, purpura and thrombocytopenia. Rarely agranulocytosis, hemolytic anemia, but definite relationship to drug not established. Anemia secondary to obvious or occult gastrointestinal bleeding. It is advisable to perform periodic blood counts (including platelet) in patients on long term therapy. If signs or symptoms of above reactions appear, discontinue drug and institute appropriate hematological investigations. Ear Reactions: Tinnitus infrequently, and deafness rarely. Eye Reactions: Retinal disturbances, including those of the macula, and corneal deposits have been observed. Some of these changes regressed after discontinuation of therapy. Infrequently, blurred vision, orbital and penorbital pain. Miscellaneous: Rarely, vaginal bleeding, hyperglycemia, glycosuria and peripheral neuropathy, and epistaxis.
DETAILED INFORMATION AVAILABLE ON REQUEST. How Supplied Ca 8662-lNDOClD. Capsules 25 mg each, are opaque, blue and white, imprinted with an MSD trademarkand potency, and are supplied in bottles of 100 and 1000. Ca 8663-lNDOClD. Capsules 50 mg each, are opaque, blue and white, imprinted with an MSD trademarkand potency, and are supplied in bottles of 100 and 500. Ca 8711-lNDOClD. Suppositories 100 mg each, are white opaque suppositories, supplied in boxes of 12 and 30. Trademark
C
ERCK I SHARP I & DOHME CANADA LIMITED POINTE CLAIRE, 0uEeEc H9R 4P7
(MC-941 b)
1122 CMA JOURNAL/MAY 21, 1977/VOL. 116
ond point of what is now a two-point regression with an inflated coefficient of "correlation" that decreases greatly when one point is omitted. There is a second fallacy. In the attempted correlation of scintigraphic area of myocardial uptake of .mTc. PYP with peak serum CPK value the mean CPK value for infarcts of 15 cm2 (that is, 3 x 5 cm) appears, from Fig. 4, to be zero, and if there is no infarct at all the prospective value is of the order of -1500 U/i - clearly a ridiculous situation. The terms "good correlation.., "significant" and the like, when applied in a statistical context, are by no means synonymous with "meaningful" and they must 'be interpreted in clinical or diagnostic contexts only with common sense. The most that can be said, in common-sense terms, about the correlation between radioactive technetium uptake and peak serum CPK value is that there is a trend towards agreement, but this is very different from suggesting that "scintigraphy can achieve the same results as serum enzyme studies". IAN MAXWELL, MB, FRCP[C] 6239 Watt St. Halifax, N5
To the editor: We appreciate Dr. Maxwell's interest and comments. We do not propose to make "sweeping statistical conclusions" from our data. At present, the enzyme method described 'by Sobel and . is perhaps the best technique for assessing myocardial infarct size in man. This method, however, depends on serial measurement of serum CPK concentration, for which blood samples must be taken every 2 to 4 hours for 48 hours; this prevents its routine clinical use. One of the goals of our study was to assess whether a single myocardial scan with 99mTcPYP might achieve the same result - that is, an assessment of infarct size. Our simple approach was to study the relation between the "peak" serum CPK value (based on values from samples taken only once every 24 hours) and the scintigraphic area of myocardial uptake of .mTc.PYP within 72 hours of onset of the acute pain of transmural infarction. Values for the 17 patients in whom this relation could be studied are plotted in our Fig. 4. ,We appreciate the scatter; it did not particularly surprise us since the peak serum CPK value was likely missed in many instances. We noted several bothersome points - not only that one infarct was unusually large (peak CPK value, 6000 U/i; area of uptake, 50.7 cm2), as Dr. Maxwell points out, but also that two infarcts with a large area of "mTc-PYP uptake (35 cm2) had disproportionately low peak serum CPK
by increases in the incidence of other cancers (for example, of the lung in men and, perhaps, of the breast in women) and by better diagnosis and more complete case-finding. The inescapable fact is that 20% of Canadians are currently dying from cancer and it is estimated that those who die from it lose, on average, 18 years of life.3 In addition to teaching everyone to recognize the early signs and symptoms of cancer, and encouraging them to seek earlier diagnosis and treatment, we must place increasing emphasis on prevention and on the elimination of causal factors. What better place to start than through reduction in smoking, as recently advocated by Miller,4 which Reir has estimated would alone
-. .-
20
-
o . C
/
El / /
0)
. 10
/
/
//
0. --U -
5
-
- -w
0 50
40
30
20
10
0
W
70
80+
Age (yrs) FIG. 1-Proportion of deaths from cancer (including benign tumours and those of unspecified nature) among all deaths, Canada, 1931 and 1971 1200 -- -
1000 C0 **.
500
.
200
.-.1971 . 1931
/
-
.
100 /
to
.. to 0)
.U
/
50
/
// /
20 10 /
@1
/
5 2 1'
60 50 40 Age (yrs) FIG. Z-A.e-specific death rates for cancer, Canada, 1931 and 1971. 0
10
ADEN C. IRWIN, MD, DPH Department of sreventive medicine ousie University Halifax, NS
References 1. Dominion Bureau of Statistics: Vital Statistics, 1931, Ottawa, King's Printer, 1933 2. Causes of Death, Canada, 1971, Ottawa, Information Canada, 1972 3. DOLL R: The prevention of cancer. I R Coil Physicians Lond 11: 125, 1977 4. MILLER AB: Recent trends in lung cancer mortality. Can Med Assoc J 116: 28, 1977 5. Ran' AE: Public information on smoking: an urgent responsibility for cancer research workers (E). I Nati Cancer Inst 57: 1207, 1976
Technetium pyrophosphate scanning in acute myocardial infarction
.-. 1971
30
reduce cancer mortality by nearly 25%?
20
30
70
80+
To the editor: The most interesting report on the use of technetium pyrophosphate scanning to detect acute myocardial infarcts, by Ko, Kostuk and Deatrich (Can Med Assoc J 116: 260, 1977), demonstrates the danger of making sweeping statistical conclusions from scanty data. I fear the authors are reading more into the elegant statistical analysis than the small series of observations warrants. In relating the scintigraphic area of myocardial uptake of technetium-99mstannous pyrophosphate (ssmTc.PYP) to the peak value of serum creatine phosphokinase (CPK) in 17 patients, Ko and colleagues find what they consider to be good correlation between the two sets of values and quote a correlation coefficient of 0.74 to back up this contention, stating that there is less than a 1000 to 1 chance of no such correlation. This is unintentional sleight of hand. Simple inspection of their Fig. 4 shows clearly that there is substantial scatter of the values and really very little correlation at all. I believe the fallacy arises largely because of the "outlier" - the CPK value of 6000 U/i. If this is omitted, as .1 believe it should be, the slope of the regression line changes from the present value of about 100 to a value of 46, the intercept on the Y axis from -1500 to -200 and the correlation coefficient from 0.74 to 0.51. Except for the correlation coefficient these figures are meaningless, though the decrease in "r" is probably important. The reason for this strange situation is clearly that the one very high value is receiving undue weight; the cloud of CPK values between 0 and 2500 U/i becomes effectively a single point lying at the mean of the 16 lesser values, and the outlier becomes the sec-
CMA JOURNAL/MAY 21, 1977/VOL. 116 1119
Indodd
(indomethacin, MSD Std.) Indications INDOCID (indomethacin, MSD Std.) has been found effective in the symptomatic treatment of se/ected cases of rheumatoid arthritis, ankylosing (rheumatoid) spondy/itis, gout, se/ected cases of severe osteoarthritis including degenerative disease of the hip. INDOCID should be used in those cases of severe osteoarthritis which do not respond to treatment with other drugs such as the salicylates. In these conditions it may on occasion replace other commonly used agents such as corticosteroids, salicylates, phenylbutazone-like compounds, and colchicine. Dosage Summary For Adults In chronic rheumatoid arthritis and ankylosing (rheumatoid) spondylitis: Start with 25 mg b.i.d. or tid. If response is inadequate, add 25 mg daily each week until an adequate response is obtained or a dosage of 150 to 200 mg is reached. In acute rheumatoid arthritis and acute flares of chronic rheumatoid arthritis: Start with 25mg bid. or tid. If response is inadequate, add 25 mg each day until an' adequate response is obtained or until a total daily dose of 150-200 mg is reached. Maintenance corticosteroids can often gradually be reduced 25 to 50 percent and completely discontinued over several weeks or months in some patients. In severe osteoarthritis and degenerative disease of the hip: Start with 25 mg bid. or tid. If response is inadequate, increase the daily dosage by 25 mg at about weekly intervals until an adequate response is obtained or until a dosage of 150 to 200 mg is reached. In acute gout: 50 mg t.i.d. until all signs and symptoms subside. INDOCID Suppositories: 100 mg to 200 mg a day. May be administered one at bedtime, and if necessary one the following morning. Also may be used in combined administration with Capsules: 100 mg suppository at bedtime, supplemented the following day by 25 mg capsules as needed up to a total of 150 to 200 mg (capsules and suppositories) of indomethacin. Note: In chronic disorders, it is important to start with low dosage and increase gradually for best results with fewer adverse reactions. Always give INDOCID* with food or immediately after meals or with antacid to reduce gastric irritation. As with all drugs, the lowest possible effective dose should be utilized for each individual patient. ContraIndications Active peptic ulcer, gastritis, regional enteritis, ulcerative colitis, divert iculit is and if there is a recurrent history of GI. lesions. Also contraindicated in patients allergic to ass. or indomethacin. Safety of indomethacin for use in pregnancy or lactation has not been established. Indomethacin suppositories are contraindicated in subjects with a history of recent rectal bleeding. SHOULD NOT BE ADMINISTERED TO PEDIATRIC AGE GROUPS. Warning Patients who experience dizziness, lightheadedness, or feelings of detachment on indomethacin should be cautioned against operating motor vehicles, machinery, climbing ladders, etc. Use cautiously in patients with psychiatric disturbances, epilepsy, or parkinsonism. PrecautIons Indomethacin should be used with caution because of the possible occurrence of gastrointestinal reactions, the incidence of which may be decreased by glying the drug immediately after meals, with food or antacids. The risk of continuing therapy with indomethacin in the face of such symptoms must be weighed against the possible benefits to the individual patient. Indomethacin suppositories should be given with caution to patients with any anal or rectal pathology. Discontinue if GI. bleeding occurs. Peptic ulcer has been reported. Hemorrhage and perforation have occurred in patients with history of peptic ulcer (see Contralndlcatlons) or in patients receiving steroids or salicylates concomitantly. In some patients there was no history of peptic ulcer or of other drugs being given. As a result of GI. bleeding some patients may manifest anemia and, for this reason, appropriate blood determinations are recommended periodically. Headache may occur, usually early in treatment. Discontinue therapy if headache persists despite dosage reduction. In common with other drugs which have anti-inflamma-
tory, analgesic and antipyretic properties, indomethacin possesses the potential of masking the signs and symptoms which ordinarily accompany infectious disease. The physician must be alert to this possibility to avoid undue delay in initiating appropriate treatment of the infection. Indomethacin should be used with caution in patients with existing, but controlled infections. Where therapy is prolonged, ophthalmological examinations are desirable at periodic intervals (see Eye Reactions). Since advancing years appear to increase the possibility of adverse reactions, indomethacin should be used with greater care in the elderly. As with any drug, patients should be followed carefully to detect unusual manifestations of drug sensitivity.
Adverse Reactions Central Nervous System: Commonly seen, headache (usually more severe in morning), dizziness, and lightheadedness. Infrequently observed: mental confusion, syncope, drowsiness, convulsions, coma, depression which may be severe, and other psychic disturbances, such as depersonalization. The severity of these effects may occasionally require cessation of therapy and rarely, admission to hospital. Gastrointestinal: include nausea, anorexia, vomiting, epigastric distress, abdominal pain, and diarrhea, which are not uncommon. Single or multiple ulceration of esophagus, stomach, duodenum orsmall intestine, perforation and hemorrhage have occurred. A few fatalities have been reported. Hemorrhage wit hout obvious ulceration. Increased abdominal pain in patients with ulcerative colitis. Indomethacin has been suspected of precipitating the symptoms of ulcerative colitis or regional ileitis but causal relationship not proven. Rarely reported, intestinal ulceration followed by stenosis and obstruction. Least frequent reactions: ulcerative stomatitis, bleeding from sigmoid colon or divert iculi, perforation of pre-existing sigmoid lesions, e.g., diverticuli or carcinoma. With the use of indomethacin suppositories, pruritus ani, tenesmus, and irritation of the rectal mucosa reported occasionally; rectal bleeding rarely. However, sigmoidoscopic examination in a number of patients did not reveal any significant changes of rectal mucosa. Hepatic: Toxic hepatitis and jaundice of uncertain etiology, including se-
vere and fatal cases. Cardiovascular-Renal: Infrequently, edema, elevation of blood pressure,
and hematuria.
Dermatologic-Hypersensitivity:
Infrequently, pruritus, urticaria, angioneurotic edema, angiitis, erythema nodosum, skin rashes, loss of hair, and acute respiratory distress including sudden dyspnea and asthma. Hematologic Reactions: Infrequently leukopenia, purpura and thrombocytopenia. Rarely agranulocytosis, hemolytic anemia, but definite relationship to drug not established. Anemia secondary to obvious or occult gastrointestinal bleeding. It is advisable to perform periodic blood counts (including platelet) in patients on long term therapy. If signs or symptoms of above reactions appear, discontinue drug and institute appropriate hematological investigations. Ear Reactions: Tinnitus infrequently, and deafness rarely. Eye Reactions: Retinal disturbances, including those of the macula, and corneal deposits have been observed. Some of these changes regressed after discontinuation of therapy. Infrequently, blurred vision, orbital and penorbital pain. Miscellaneous: Rarely, vaginal bleeding, hyperglycemia, glycosuria and peripheral neuropathy, and epistaxis.
DETAILED INFORMATION AVAILABLE ON REQUEST. How Supplied Ca 8662-lNDOClD. Capsules 25 mg each, are opaque, blue and white, imprinted with an MSD trademarkand potency, and are supplied in bottles of 100 and 1000. Ca 8663-lNDOClD. Capsules 50 mg each, are opaque, blue and white, imprinted with an MSD trademarkand potency, and are supplied in bottles of 100 and 500. Ca 8711-lNDOClD. Suppositories 100 mg each, are white opaque suppositories, supplied in boxes of 12 and 30. Trademark
C
ERCK I SHARP I & DOHME CANADA LIMITED POINTE CLAIRE, 0uEeEc H9R 4P7
(MC-941 b)
1122 CMA JOURNAL/MAY 21, 1977/VOL. 116
ond point of what is now a two-point regression with an inflated coefficient of "correlation" that decreases greatly when one point is omitted. There is a second fallacy. In the attempted correlation of scintigraphic area of myocardial uptake of .mTc. PYP with peak serum CPK value the mean CPK value for infarcts of 15 cm2 (that is, 3 x 5 cm) appears, from Fig. 4, to be zero, and if there is no infarct at all the prospective value is of the order of -1500 U/i - clearly a ridiculous situation. The terms "good correlation.., "significant" and the like, when applied in a statistical context, are by no means synonymous with "meaningful" and they must 'be interpreted in clinical or diagnostic contexts only with common sense. The most that can be said, in common-sense terms, about the correlation between radioactive technetium uptake and peak serum CPK value is that there is a trend towards agreement, but this is very different from suggesting that "scintigraphy can achieve the same results as serum enzyme studies". IAN MAXWELL, MB, FRCP[C] 6239 Watt St. Halifax, N5
To the editor: We appreciate Dr. Maxwell's interest and comments. We do not propose to make "sweeping statistical conclusions" from our data. At present, the enzyme method described 'by Sobel and . is perhaps the best technique for assessing myocardial infarct size in man. This method, however, depends on serial measurement of serum CPK concentration, for which blood samples must be taken every 2 to 4 hours for 48 hours; this prevents its routine clinical use. One of the goals of our study was to assess whether a single myocardial scan with 99mTcPYP might achieve the same result - that is, an assessment of infarct size. Our simple approach was to study the relation between the "peak" serum CPK value (based on values from samples taken only once every 24 hours) and the scintigraphic area of myocardial uptake of .mTc.PYP within 72 hours of onset of the acute pain of transmural infarction. Values for the 17 patients in whom this relation could be studied are plotted in our Fig. 4. ,We appreciate the scatter; it did not particularly surprise us since the peak serum CPK value was likely missed in many instances. We noted several bothersome points - not only that one infarct was unusually large (peak CPK value, 6000 U/i; area of uptake, 50.7 cm2), as Dr. Maxwell points out, but also that two infarcts with a large area of "mTc-PYP uptake (35 cm2) had disproportionately low peak serum CPK
