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Precordial T wave vectors in the detection of coronary heart disease. The Framingham study
Precordial T wave vectors in the detection of coronary heart disease. The Framingham Study John F, Schneider, M.D. H. Emerson Thomas Jr., M.D. William B. Kannel, M.D. Framingham and Boston, Mass.
It is well known t h a t resting electrocardiographic aberrancy is often absent in persons soon to develop clinically Overt coronary heart disease. In addition, a significant percentage of people diagnosed as having angina pectoriS have entirely normal resting electrocardiographic tracings. 1 It would, therefore, be of great value if some pattern within the "normal" resting electrocardiographic tracing could be identified t h a t would either aid in detecting impending clinical coronary heart disease, or in confirming coronary heart disease in the presence of clinical symptoms. Several reports have claimed an association between an anteriorly Oriented precordial T wave vector and various anatomic and clinical parameters of coronary heart disease. 2~ In these reports, a T wave amplitude in V1 greater than t h a t in V~ (TV1 > TV,,) was utilized as the electrocardiographic expression of an anteriorly oriented precordial T wave vector. If the pattern of TV~ > TV~ in an otherwise normal electrocardiographic tracing is truly an indicator of ischemic changes in the myocardium, it might then be a reliable detector of the presence of impending clinical coronary heart disease. It might also prove to be a useful adjunct in the di~ignostic evalUation of patients with chest pain. A case-control study utilizing the epidemiologic data of the Framingham Heart Study was designed to test this hypothesis.
From the Framingham Epidemiology Study, Framingham, Massachusstts, and The Departments of Medicine and Epidemiology, Boston University Medical Center, Boston, Mass. Received for publication June 7, 1976. Accepted for publication July 16, 1976. Reprint requests: John F. Schneider, M.D., Framingham Heart Study, 123 Lincoln St., Framingham, Mass. 01701.
568
Material and methods
The case population consisted of 518 people (323 males, 195 females) who had developed coronary heart disease between 1948 and 1968 while under observation by the Framingham Heart Study Program. Each was characterized according to the initial clinical manifestation of the disease as defined by Framingham criteria, i.e:, angina pectoris, coronary insufficiency, myocardial infarction, sudden death, and non-sudden d e a t h / E a c h case was matched with a control by age, sex, and Framingham exam number on which the case's diagnosis of coronary heart disease was first made. Each control was drawn from the Framingham Heart Study cohort t h a t had never manifested any clinical evidence of coronary heart disease from 1948 through 1968. Data from the routine Framingham Heart Study biennial exams which immediately preceded and followed the initial clinical manifestations of coronary disease were evaluated for each member of the case population. Data from corresponding exam numbers were evaluated for each m a t c h e d control. All electrocardiographic tracings were recorded on a standard twelve-lead Sanborn visocardiette with the subject in the recumbent position. Criteria used to designate the tracing as normal or abnormal were consistent with those previously o u t l i n e d / T h e amplitudes of TV1 and TV~ were determined with a standard electrocardiographic caliper by measuring on a line perpendicular to a cohtinuation of the TP segment, the vertical distance between the T P segment and the peak of the T wave. TV1 h a d to be at least onehalf millimeter greater in amplitude than TV6 before a designation of TV1 > TV~ could be made. In order to be considered within the category of normal T waves, the T wave in V6 had to be
November, 1977, Vol. 94, No. 5, pp. 568-572
Precordial T wave vectors in CHD
Table I. Prevalence of TV1 > TV~ in an otherwise n o r m a l e l e c t r o c a r d i o g r a m in cases a n d controls on the exam before the initial onset of clinical m a n i f e s t a t i o n of c o r o n a r y h e a r t disease
Females
Males
Diagnosis Angina pectoris Coronary insufficiency Anterior myocardial infarction True posterior myocardial infarction Inferior myocardial infarction Myocardial infarction without electrocardiographic evidence Non-suddendeath Sudden death Totals
Prevalence in matched controls
Prevalence in cases 18/64 6/i3 8/33 2/7 9/29 8/21
= 28% = 46% = 24% --- 28% --- 31% = 38%
17/69 7/20 9/35 0/5 1!/32 8/21
5/19 = 26% 9/28 = 32% 65/214
= 24% = 35% --25% = 0% -- 34% = 38%
2/24 -~ 8% 13/36 = 36% 67/242~27%
30%
Prevalence in matched controls
Prevalence in cases 6/82 0/11 1/13 .0/1 1[7 1/5
- 7% = 0% -- 7% = 0% = 14% = 20%
10/90 = 11% 0/11 = 0% 1/14 = 7% None 0/6 = 0% 0/6 ~- 0%
1/6 0/6
= 16% = 0%
0/11 = 0% 0 / 6 -- 0%
10/130= 7%
li/144
7%
Table II. Prevalence of TV1 > TV6 in an otherwise n o r m a l e l e c t r o c a r d i o g r a m in cases a n d c o n t r o l s on the exam after the initial onset of clinica| m a n i f e s t a t i o n s of c o r o n a r y h e a r t disease
Males Prevalence in cases
Prevalence in matghed controls
Prevalence in cases
Prevalence in matched controls
12/58 --- 21% 3/6 --- 50% 8/14 = 57%
13/65 = 20% 7/17 = 41% 6/21 = 28%
9/62 = 14% 0/7 -- 0% 0/4 = 0%
10/85 -- 12% !/12 -- 8% 0/6 ~- 0%
23/78 -- 29%
26/103 --' 25%
9/73 = i2%
I Diagnosis Angina pectoris Coronary insufficiency Myocardial infarction without electrocardiographic evidence Totals
upright while the T wave in V, could either be upright, fiat, or inverted. Since certain non-cardiac characteristics such as blood pressure level, relative weight, a n d cigarette smoking s t a t u s m a y play a role' in predisposing to c o r o n a r y h e a r t diseas e as well as in producing this electrocardiographic pattern, i n f o r m a t i o n regarding these factors was recorded for all cases and controls.
Results A m o n g all those who would go on to develop a clinical m a n i f e s t a t i o n of c o r o n a r y h e a r t disease, 214 of 323 (66 per cent) of the males, and 131 of 195 (67 per cent) of the females h a d n o r m a l electrocardiographic tracings on the F r a m i n g h a m exam immediately preceding its onset. Of t h e controls, 72 per cent had a n o r m a l tracing on the corresponding exam. D a t a concerning the ability
American Heart Journal
Females I
11/103 = 11%
of TV1 > TV6 in an otherwise n o r m a l electrocardiogram to detect impending clinical c o r o n a r y h e a r t disease are given in T a b l e I, As h a d been previously reported by Teichholz and associates, 6 TV1 > TV~ was fou.nd to be far m o r e p r e v a l e n t in males t h a n in females. C o n s e q u e n t l y , all t h e analyses were done separately for males a n d females. I n individuals with otherwise n o r m a l electrocardiograms, there was no significant difference between the cases a n d the controls i n the prevalence of TV1 > TV6 on the exam before the onset of clinical disease. This was true for all five designated categories of c o r o n a r y disease in b o t h males and females. A m o n g individuals diagnosed as having a n g i n a pectoris or c o r o n a r y insufficiency, 64 of 123 (52 per cent) of the males, and 69 of 137 (50 per cent) Of the females h a d n o r m a l e l e c t r o c a r d i o g r a m s on the first F r a m i n g h a m exam after t h e initial onset
569
Schneider, Thomas, and Kannel
Table III. Percentage of cases and Controls with normal electrocardiograms on both the exam before and the exam after t h e initial onset of clinical manifestations of coronary heart disease that go from a TV1 < TV6 on the first exam to a TV~ > TV~ on the second exam Males
I 7/43
Females
Finding
Cases
Controls
Cases
TV~ < TV6 to TVI > TV~
ffi i6%
12/137 = 9%
4/57 ffi 7%
IControls 5/109 ffi 5%
of clinical disease. Of the individuals who developed clinically documented myocardial infarctions, 18 of 155 (12 per cent) had electrocardiographic tracings that were entirely normal on the first Framingham exam after the event. Table II shows t h a t in individuals with otherwise normal electrocardiograms there was again no significant difference between the cases and the controls in the prevalence of TV~ > TV~ on the exam after the initial clinical manifestations of coronary disease appeared. From Table II it can be calculated t h a t in males, T V , > TV~ had a sensitivity of only 29 per cent, a specificity of 47 per cent, and a false positivity of 25 per cent in detecting the presence of overt coronary heart disease. These values differ markedly from/ those reported by Okomoto and colleagues~ and by Teichholz and associates2 The incidence of conversion from a TV, < TV8 on the exam preceding the onset of clinical coronary heart disease to a TV~ > TV6 on the exam following the development of disease in cases and controls with normal electrocardiograms on both exams is illustrated in Table III. In both males and females, conversion from TV1 < TV6 on the first exam to a TV~ > TV6 on the second exam, although almost twice as common in cases than in controls, was not significant to p < 0.05. TV ! > TV6 was far m o r e prevalent among people listed as having non-specific or possible non-specific T wave changes than among people with otherwise normal electrocardiograms. However, among people with definite, or possible, nonspecific T wave changes on the exam before the onset Of clinical disease, the ratio of the number of people with TV~ > TV6 to the number Of people with TVi < TV~ was not significantly different in the cases than in the controls. Like-
570
wise, among people with definite or possible nonspecific T wave changes on the exam after overt disease first appeared, the ratio of the number of people with TV1 > TV6 to the number of people with TV1 < TV~ was again not significantly different in the cases than in the controls. In neither cases nor controls with normal electrocardiograms was there a relationship between the prevalence of TV~ > TV6 and the individuals' age, relative weight, cigarette smoking habits, or electrocardiographic frontal plane axis. This was true for both males and females. In male controls, there was an increasing prevalence of TV, > TV6 with increasing blood pressure levels (p < 0.05). There was no correlation, however, between the prevalence of TV~ > TV6 and blood pressure levels in male cases, or in female cases or controls. Discussion
The absence Of resting electrocardiographic aberrancy in two-thirds of the Framingham subjects soon to develop clinical coronary heart disease and in half of the Framingham subjects with documented angina attests to the insensitivity of the standard electrocardiographic abnormalities in detecting incipient or o v e r t clinical coronary disease. These observations justify the search for other electrocardiographic patterns within the "normal" tracing which might indicate the presence of ventricular ischemia. Meyer and Herr 2 and Arustamov, 3 associated a finding of TV, > TV,, with various causes of delayed left ventricular repolarization such as left ventricular hypertrophy or coronary insufficiency. Weyn and Marriott 4 stated t h a t the importance of TV~ > TV~ lay in its potential to indicate ischemic or hypertensive myocardial abnormalities in the presence of an otherwise normal electrocardiogram. Okomoto and colleagues ~ examined the electrocardiograms of 500 males diagnosed a s having angina pectoris, myocardial infarction, hypertensive, pulmonary, or valvular heart disease and 960 unmatched controls without clinical evidence of heart disease. When they considered only subjects with otherwise normal electrocardiograms with positive T waves in V1, TV1 > TV~ was approximately 60 per cent sensitive i n detecting the presence of cardiac disease with 22 per cent false positives. Teichholz and associhtes ~ studied the relevance Of
November, 1977, VoL 94, No. 5
Precordial T wave vectors in C H D
TV, > TV~ angiographically in 179 patients with chest pain syndromes and otherwise normal electrocardiograms. Their results in males indicated a 46 per cent sensitivity and a 90 per cent specificity in the ability of TV1 > TV6 to diagnose coronary artery disease in the presence of chest pain syndromes. Grant 8 has stated t h a t delayed left ventricular repolarization will tend to rotate the precordial T wave vector anteriorly. This is the mechanism he invokes to explain how left ventricular ischemia might lead to an anteriorly oriented T wave vector. Previous investigators chose TV1 > TV6 simply as a reference point which they believed defined a T wave vector sufficiently anteriorly oriented to indicate the presence of left ventricular ischemia. To the best of our knowledge, this is the first report that presents data t h a t run contrary to previous data concerning the diagnostic significance of an anteriorly oriented precordial T wave vector in an otherwise normal electrocardiogram. The presence of generalized non-specific ST and T abnormalities on an individual's electrocardiogram has been shown by the Framingham Heart Study to impart approximately a twofold increased risk for the subsequent development of clinical coronary heart disease. 9 However, the accuracy of utilizing changes in T wave morphology as a diagnostic tool in the detection of coronary heart disease is limited by the large number of physiologic c o n d i t i o n s other than ischemia t h a t can alter the amplitude and direction of the T wave. 1~Some of these factors might have contributed both to the low prevalence of an anterior T wave vector in the case population in this study, and to the high prevalence in the controls. The results of this study, however, indicate that subsequent development of clinical coronary disease in people with normal electrocardiograms is unrelated tO TV~ > TV~ as an antecedent finding. Furthermore, this study demonstrates t h a t in people with clinical evidence of coronary heart disease and normal electrocardiograms, TV~ > TV~ fulfills neither the criterion for a good screening test {high sensitivity) nor the criterion for a good diagnostic test (high specificity). In addition, TV1 > TV8 was not able to add to the specificity of generalized non-specific T wave changes in detecting the people with either preclinical or overt coronary heart disease.
American Heart Journal
Methodological differences between this study and the others, such as the patient selection, definition of disease, and the composition of the control groups, can be invoked to account for the divergent findings. All the previous studies utilized various selective processes t o a s s e m b l e their patient populations. This study drew its cases and controls from a representative population sample which contained within it all the people who developed coronary heart disease and all the people with the TV~ > TV,~ phenomenon. It is certain t h a t if a T wave amplitude in V1 greater than t h a t in V6 in an otherwise normal electrocardiogram was truly a result of coronary heart disease, its prevalence should have been significantly greater in a large group of people with clinical coronary heart disease t h a n in a control group of people known to be free from clinical coronary heart disease, matched for age and sex, and drawn from the same unselected general population sample.
Summary An anteriorly oriented precordial T wave vector manifested by a T wave amplitude in V1 greater than that in V,~ (TV1 > TV6) has been reported to be a useful criterion for the detection of coronary heart disease in people with otherwise normal electrocardiograms. In an effort to confirm this observation, a prospective case-control study based on 518 subjects who developed clinical coronary heart disease while under observation by the Framingham Heart Study and 518 age- and sex-matched controls free from coronary heart disease was carried out. Analysis of electrocardiograms considered to be normal and obtained at routine biennial exams revealed t h a t on the exam prior to the onset of clinical coronary heart disease there was no significant difference in the prevalence of TV, > TV~, between people who subsequently went on to develop disease and the controls. Furthermore, no significant difference in the prevalence of TV, > TV,~ was noted between cases and controls on the first exam following the initial clinical manifestations of coronary heart disease. When studied prospectively in the general population, the data indicate t h a t TV1 > TV~ in an otherwise normal electrocardiogram is not sufficiently specific a discriminator to be utilized as a reliable criterion for the detection of coronary heart disease.
571
Schneider, Thomas, and Kannel
We would like to thank Dr. Herbert Kayne for his help with the statistical analysis of the data and Patricia McNamara for her over-all assistance. REFERENCES
1. Hurst, J. W., and Logue, R. B:: The clinical recognition and medical management of coronary atherosclerotic heart disease, in, The heart: Arteries and veins, 3rd ed., Hurst, J. W., Logue, R. B., Schlant, R. C., and Wenger, N. K., eds., New York, 1974, McGraw-Hill Book Company, pp. 1038-1132. 2. Meyer, P., and Herr, R.: L'interet du syndrome electrocardiographique TV, > TV,~pour le depostage precoce de troubles de la repolarisation ventriculaire gauche, Arch. Mal. Coeur 52:753, 1959. 3. Arustamov, A. S.: The TV, > TV,, syndrome in the diagnosis of myocardial repolarization disorders, Ter. Arkh. 32:37, 1960 (Abstracted in Excerpta Medica 5:535, 1961). 4. Weyn, A. S., and Marriott, H. J. L.: The TV~ taller thaa TV,, pattern, its potential value in the early recognition
572
of myocardial disease, Am. J. Cardiol. 10:764, 1962. 5. Okomoto, N. O., Simonson, E., and Blackburn, H.: The T-V1 > T-V,, pattern for electrocardiographic diagnosis of left ventricular hypertrophy and ischemia, sensitivity and specificity, Circulation 31:719, 1965. 6. Teichholz, L. E., Young, E., and Gorlin, R.: T wave in V, greater than T wave in V, in coronary artery disease (Abstr.), Am. J. Cardiol. 31:161, 1973. 7. Shurtleff, D.: Some characteristics related to the incidence of cardiovascular disease and death: Framingham Study, 16 year follow-up, in, The Framingham Study, Kannel, W. B., and Gordon, T., eds., Washington D.C., 1970. U.S. Government Printing Office, Section 26. 8. Beckwith, J. R.: Grant's Clinical Electrocardiography: The spatial vector approach, 2nd ed., New York, 1970, McGraw-Hill Book Company, p. 85. 9. Kannel, W. B.: Some lessons in cardiovascular epidemiology from Framingham, Am. J. Cardiol. 37:269, 1976. 10. Marriott, H. J. L.: Coronary mimicry: normal variants, and physiologic, pharmacologic and pathologic influences that simulate coronary patterns in the electrocardiogram, Ann. Intern. Med. 52:411, 1960.
November, 1977, Vol. 94, No. 5
It is well known t h a t resting electrocardiographic aberrancy is often absent in persons soon to develop clinically Overt coronary heart disease. In addition, a significant percentage of people diagnosed as having angina pectoriS have entirely normal resting electrocardiographic tracings. 1 It would, therefore, be of great value if some pattern within the "normal" resting electrocardiographic tracing could be identified t h a t would either aid in detecting impending clinical coronary heart disease, or in confirming coronary heart disease in the presence of clinical symptoms. Several reports have claimed an association between an anteriorly Oriented precordial T wave vector and various anatomic and clinical parameters of coronary heart disease. 2~ In these reports, a T wave amplitude in V1 greater than t h a t in V~ (TV1 > TV,,) was utilized as the electrocardiographic expression of an anteriorly oriented precordial T wave vector. If the pattern of TV~ > TV~ in an otherwise normal electrocardiographic tracing is truly an indicator of ischemic changes in the myocardium, it might then be a reliable detector of the presence of impending clinical coronary heart disease. It might also prove to be a useful adjunct in the di~ignostic evalUation of patients with chest pain. A case-control study utilizing the epidemiologic data of the Framingham Heart Study was designed to test this hypothesis.
From the Framingham Epidemiology Study, Framingham, Massachusstts, and The Departments of Medicine and Epidemiology, Boston University Medical Center, Boston, Mass. Received for publication June 7, 1976. Accepted for publication July 16, 1976. Reprint requests: John F. Schneider, M.D., Framingham Heart Study, 123 Lincoln St., Framingham, Mass. 01701.
568
Material and methods
The case population consisted of 518 people (323 males, 195 females) who had developed coronary heart disease between 1948 and 1968 while under observation by the Framingham Heart Study Program. Each was characterized according to the initial clinical manifestation of the disease as defined by Framingham criteria, i.e:, angina pectoris, coronary insufficiency, myocardial infarction, sudden death, and non-sudden d e a t h / E a c h case was matched with a control by age, sex, and Framingham exam number on which the case's diagnosis of coronary heart disease was first made. Each control was drawn from the Framingham Heart Study cohort t h a t had never manifested any clinical evidence of coronary heart disease from 1948 through 1968. Data from the routine Framingham Heart Study biennial exams which immediately preceded and followed the initial clinical manifestations of coronary disease were evaluated for each member of the case population. Data from corresponding exam numbers were evaluated for each m a t c h e d control. All electrocardiographic tracings were recorded on a standard twelve-lead Sanborn visocardiette with the subject in the recumbent position. Criteria used to designate the tracing as normal or abnormal were consistent with those previously o u t l i n e d / T h e amplitudes of TV1 and TV~ were determined with a standard electrocardiographic caliper by measuring on a line perpendicular to a cohtinuation of the TP segment, the vertical distance between the T P segment and the peak of the T wave. TV1 h a d to be at least onehalf millimeter greater in amplitude than TV6 before a designation of TV1 > TV~ could be made. In order to be considered within the category of normal T waves, the T wave in V6 had to be
November, 1977, Vol. 94, No. 5, pp. 568-572
Precordial T wave vectors in CHD
Table I. Prevalence of TV1 > TV~ in an otherwise n o r m a l e l e c t r o c a r d i o g r a m in cases a n d controls on the exam before the initial onset of clinical m a n i f e s t a t i o n of c o r o n a r y h e a r t disease
Females
Males
Diagnosis Angina pectoris Coronary insufficiency Anterior myocardial infarction True posterior myocardial infarction Inferior myocardial infarction Myocardial infarction without electrocardiographic evidence Non-suddendeath Sudden death Totals
Prevalence in matched controls
Prevalence in cases 18/64 6/i3 8/33 2/7 9/29 8/21
= 28% = 46% = 24% --- 28% --- 31% = 38%
17/69 7/20 9/35 0/5 1!/32 8/21
5/19 = 26% 9/28 = 32% 65/214
= 24% = 35% --25% = 0% -- 34% = 38%
2/24 -~ 8% 13/36 = 36% 67/242~27%
30%
Prevalence in matched controls
Prevalence in cases 6/82 0/11 1/13 .0/1 1[7 1/5
- 7% = 0% -- 7% = 0% = 14% = 20%
10/90 = 11% 0/11 = 0% 1/14 = 7% None 0/6 = 0% 0/6 ~- 0%
1/6 0/6
= 16% = 0%
0/11 = 0% 0 / 6 -- 0%
10/130= 7%
li/144
7%
Table II. Prevalence of TV1 > TV6 in an otherwise n o r m a l e l e c t r o c a r d i o g r a m in cases a n d c o n t r o l s on the exam after the initial onset of clinica| m a n i f e s t a t i o n s of c o r o n a r y h e a r t disease
Males Prevalence in cases
Prevalence in matghed controls
Prevalence in cases
Prevalence in matched controls
12/58 --- 21% 3/6 --- 50% 8/14 = 57%
13/65 = 20% 7/17 = 41% 6/21 = 28%
9/62 = 14% 0/7 -- 0% 0/4 = 0%
10/85 -- 12% !/12 -- 8% 0/6 ~- 0%
23/78 -- 29%
26/103 --' 25%
9/73 = i2%
I Diagnosis Angina pectoris Coronary insufficiency Myocardial infarction without electrocardiographic evidence Totals
upright while the T wave in V, could either be upright, fiat, or inverted. Since certain non-cardiac characteristics such as blood pressure level, relative weight, a n d cigarette smoking s t a t u s m a y play a role' in predisposing to c o r o n a r y h e a r t diseas e as well as in producing this electrocardiographic pattern, i n f o r m a t i o n regarding these factors was recorded for all cases and controls.
Results A m o n g all those who would go on to develop a clinical m a n i f e s t a t i o n of c o r o n a r y h e a r t disease, 214 of 323 (66 per cent) of the males, and 131 of 195 (67 per cent) of the females h a d n o r m a l electrocardiographic tracings on the F r a m i n g h a m exam immediately preceding its onset. Of t h e controls, 72 per cent had a n o r m a l tracing on the corresponding exam. D a t a concerning the ability
American Heart Journal
Females I
11/103 = 11%
of TV1 > TV6 in an otherwise n o r m a l electrocardiogram to detect impending clinical c o r o n a r y h e a r t disease are given in T a b l e I, As h a d been previously reported by Teichholz and associates, 6 TV1 > TV~ was fou.nd to be far m o r e p r e v a l e n t in males t h a n in females. C o n s e q u e n t l y , all t h e analyses were done separately for males a n d females. I n individuals with otherwise n o r m a l electrocardiograms, there was no significant difference between the cases a n d the controls i n the prevalence of TV1 > TV6 on the exam before the onset of clinical disease. This was true for all five designated categories of c o r o n a r y disease in b o t h males and females. A m o n g individuals diagnosed as having a n g i n a pectoris or c o r o n a r y insufficiency, 64 of 123 (52 per cent) of the males, and 69 of 137 (50 per cent) Of the females h a d n o r m a l e l e c t r o c a r d i o g r a m s on the first F r a m i n g h a m exam after t h e initial onset
569
Schneider, Thomas, and Kannel
Table III. Percentage of cases and Controls with normal electrocardiograms on both the exam before and the exam after t h e initial onset of clinical manifestations of coronary heart disease that go from a TV1 < TV6 on the first exam to a TV~ > TV~ on the second exam Males
I 7/43
Females
Finding
Cases
Controls
Cases
TV~ < TV6 to TVI > TV~
ffi i6%
12/137 = 9%
4/57 ffi 7%
IControls 5/109 ffi 5%
of clinical disease. Of the individuals who developed clinically documented myocardial infarctions, 18 of 155 (12 per cent) had electrocardiographic tracings that were entirely normal on the first Framingham exam after the event. Table II shows t h a t in individuals with otherwise normal electrocardiograms there was again no significant difference between the cases and the controls in the prevalence of TV~ > TV~ on the exam after the initial clinical manifestations of coronary disease appeared. From Table II it can be calculated t h a t in males, T V , > TV~ had a sensitivity of only 29 per cent, a specificity of 47 per cent, and a false positivity of 25 per cent in detecting the presence of overt coronary heart disease. These values differ markedly from/ those reported by Okomoto and colleagues~ and by Teichholz and associates2 The incidence of conversion from a TV, < TV8 on the exam preceding the onset of clinical coronary heart disease to a TV~ > TV6 on the exam following the development of disease in cases and controls with normal electrocardiograms on both exams is illustrated in Table III. In both males and females, conversion from TV1 < TV6 on the first exam to a TV~ > TV6 on the second exam, although almost twice as common in cases than in controls, was not significant to p < 0.05. TV ! > TV6 was far m o r e prevalent among people listed as having non-specific or possible non-specific T wave changes than among people with otherwise normal electrocardiograms. However, among people with definite, or possible, nonspecific T wave changes on the exam before the onset Of clinical disease, the ratio of the number of people with TV~ > TV6 to the number Of people with TVi < TV~ was not significantly different in the cases than in the controls. Like-
570
wise, among people with definite or possible nonspecific T wave changes on the exam after overt disease first appeared, the ratio of the number of people with TV1 > TV6 to the number of people with TV1 < TV~ was again not significantly different in the cases than in the controls. In neither cases nor controls with normal electrocardiograms was there a relationship between the prevalence of TV~ > TV6 and the individuals' age, relative weight, cigarette smoking habits, or electrocardiographic frontal plane axis. This was true for both males and females. In male controls, there was an increasing prevalence of TV, > TV6 with increasing blood pressure levels (p < 0.05). There was no correlation, however, between the prevalence of TV~ > TV6 and blood pressure levels in male cases, or in female cases or controls. Discussion
The absence Of resting electrocardiographic aberrancy in two-thirds of the Framingham subjects soon to develop clinical coronary heart disease and in half of the Framingham subjects with documented angina attests to the insensitivity of the standard electrocardiographic abnormalities in detecting incipient or o v e r t clinical coronary disease. These observations justify the search for other electrocardiographic patterns within the "normal" tracing which might indicate the presence of ventricular ischemia. Meyer and Herr 2 and Arustamov, 3 associated a finding of TV, > TV,, with various causes of delayed left ventricular repolarization such as left ventricular hypertrophy or coronary insufficiency. Weyn and Marriott 4 stated t h a t the importance of TV~ > TV~ lay in its potential to indicate ischemic or hypertensive myocardial abnormalities in the presence of an otherwise normal electrocardiogram. Okomoto and colleagues ~ examined the electrocardiograms of 500 males diagnosed a s having angina pectoris, myocardial infarction, hypertensive, pulmonary, or valvular heart disease and 960 unmatched controls without clinical evidence of heart disease. When they considered only subjects with otherwise normal electrocardiograms with positive T waves in V1, TV1 > TV~ was approximately 60 per cent sensitive i n detecting the presence of cardiac disease with 22 per cent false positives. Teichholz and associhtes ~ studied the relevance Of
November, 1977, VoL 94, No. 5
Precordial T wave vectors in C H D
TV, > TV~ angiographically in 179 patients with chest pain syndromes and otherwise normal electrocardiograms. Their results in males indicated a 46 per cent sensitivity and a 90 per cent specificity in the ability of TV1 > TV6 to diagnose coronary artery disease in the presence of chest pain syndromes. Grant 8 has stated t h a t delayed left ventricular repolarization will tend to rotate the precordial T wave vector anteriorly. This is the mechanism he invokes to explain how left ventricular ischemia might lead to an anteriorly oriented T wave vector. Previous investigators chose TV1 > TV6 simply as a reference point which they believed defined a T wave vector sufficiently anteriorly oriented to indicate the presence of left ventricular ischemia. To the best of our knowledge, this is the first report that presents data t h a t run contrary to previous data concerning the diagnostic significance of an anteriorly oriented precordial T wave vector in an otherwise normal electrocardiogram. The presence of generalized non-specific ST and T abnormalities on an individual's electrocardiogram has been shown by the Framingham Heart Study to impart approximately a twofold increased risk for the subsequent development of clinical coronary heart disease. 9 However, the accuracy of utilizing changes in T wave morphology as a diagnostic tool in the detection of coronary heart disease is limited by the large number of physiologic c o n d i t i o n s other than ischemia t h a t can alter the amplitude and direction of the T wave. 1~Some of these factors might have contributed both to the low prevalence of an anterior T wave vector in the case population in this study, and to the high prevalence in the controls. The results of this study, however, indicate that subsequent development of clinical coronary disease in people with normal electrocardiograms is unrelated tO TV~ > TV~ as an antecedent finding. Furthermore, this study demonstrates t h a t in people with clinical evidence of coronary heart disease and normal electrocardiograms, TV~ > TV~ fulfills neither the criterion for a good screening test {high sensitivity) nor the criterion for a good diagnostic test (high specificity). In addition, TV1 > TV8 was not able to add to the specificity of generalized non-specific T wave changes in detecting the people with either preclinical or overt coronary heart disease.
American Heart Journal
Methodological differences between this study and the others, such as the patient selection, definition of disease, and the composition of the control groups, can be invoked to account for the divergent findings. All the previous studies utilized various selective processes t o a s s e m b l e their patient populations. This study drew its cases and controls from a representative population sample which contained within it all the people who developed coronary heart disease and all the people with the TV~ > TV,~ phenomenon. It is certain t h a t if a T wave amplitude in V1 greater than t h a t in V6 in an otherwise normal electrocardiogram was truly a result of coronary heart disease, its prevalence should have been significantly greater in a large group of people with clinical coronary heart disease t h a n in a control group of people known to be free from clinical coronary heart disease, matched for age and sex, and drawn from the same unselected general population sample.
Summary An anteriorly oriented precordial T wave vector manifested by a T wave amplitude in V1 greater than that in V,~ (TV1 > TV6) has been reported to be a useful criterion for the detection of coronary heart disease in people with otherwise normal electrocardiograms. In an effort to confirm this observation, a prospective case-control study based on 518 subjects who developed clinical coronary heart disease while under observation by the Framingham Heart Study and 518 age- and sex-matched controls free from coronary heart disease was carried out. Analysis of electrocardiograms considered to be normal and obtained at routine biennial exams revealed t h a t on the exam prior to the onset of clinical coronary heart disease there was no significant difference in the prevalence of TV, > TV~, between people who subsequently went on to develop disease and the controls. Furthermore, no significant difference in the prevalence of TV, > TV,~ was noted between cases and controls on the first exam following the initial clinical manifestations of coronary heart disease. When studied prospectively in the general population, the data indicate t h a t TV1 > TV~ in an otherwise normal electrocardiogram is not sufficiently specific a discriminator to be utilized as a reliable criterion for the detection of coronary heart disease.
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Schneider, Thomas, and Kannel
We would like to thank Dr. Herbert Kayne for his help with the statistical analysis of the data and Patricia McNamara for her over-all assistance. REFERENCES
1. Hurst, J. W., and Logue, R. B:: The clinical recognition and medical management of coronary atherosclerotic heart disease, in, The heart: Arteries and veins, 3rd ed., Hurst, J. W., Logue, R. B., Schlant, R. C., and Wenger, N. K., eds., New York, 1974, McGraw-Hill Book Company, pp. 1038-1132. 2. Meyer, P., and Herr, R.: L'interet du syndrome electrocardiographique TV, > TV,~pour le depostage precoce de troubles de la repolarisation ventriculaire gauche, Arch. Mal. Coeur 52:753, 1959. 3. Arustamov, A. S.: The TV, > TV,, syndrome in the diagnosis of myocardial repolarization disorders, Ter. Arkh. 32:37, 1960 (Abstracted in Excerpta Medica 5:535, 1961). 4. Weyn, A. S., and Marriott, H. J. L.: The TV~ taller thaa TV,, pattern, its potential value in the early recognition
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of myocardial disease, Am. J. Cardiol. 10:764, 1962. 5. Okomoto, N. O., Simonson, E., and Blackburn, H.: The T-V1 > T-V,, pattern for electrocardiographic diagnosis of left ventricular hypertrophy and ischemia, sensitivity and specificity, Circulation 31:719, 1965. 6. Teichholz, L. E., Young, E., and Gorlin, R.: T wave in V, greater than T wave in V, in coronary artery disease (Abstr.), Am. J. Cardiol. 31:161, 1973. 7. Shurtleff, D.: Some characteristics related to the incidence of cardiovascular disease and death: Framingham Study, 16 year follow-up, in, The Framingham Study, Kannel, W. B., and Gordon, T., eds., Washington D.C., 1970. U.S. Government Printing Office, Section 26. 8. Beckwith, J. R.: Grant's Clinical Electrocardiography: The spatial vector approach, 2nd ed., New York, 1970, McGraw-Hill Book Company, p. 85. 9. Kannel, W. B.: Some lessons in cardiovascular epidemiology from Framingham, Am. J. Cardiol. 37:269, 1976. 10. Marriott, H. J. L.: Coronary mimicry: normal variants, and physiologic, pharmacologic and pathologic influences that simulate coronary patterns in the electrocardiogram, Ann. Intern. Med. 52:411, 1960.
November, 1977, Vol. 94, No. 5