Atrial coronary angiography, tachyarrhythmias and the Ta segment

J. ELECTROCARDIOLOGY 16 (4), 1983, 325-330

Original Communications Atrial Coronary Angiography, Tachyarrhythmias and the Ta Segment BY NANCY J. PICKEItING, M.D.* AND T o n y R. ENGEI., M . D . ~

SUMMARY Electrocardiograms and angiograms were reviewed to determine if atrial Ta segment displacements and atrial flutter or fibrillation indicate atrial coronary disease. Atrial circulation was assessed by angiography in 28 patients with chest pain and normal coronary arteries, 29 patients with significant stenosis of at least one major coronary vessel, and 16 with coronary artery disease and atrial flutter or fibrillation. The prevalence of Ta segment displacement was 71% without coronary disease and 79% with coronary disease. There was no relationship between Ta displacement and segmental atrial coronary insufficiency. Among an additional 28 patients with acute transmural myocardial infarction, 79% had equivalent Ta segment displacement. Half of the patients with atrial flutter/fibrillation had significant mitral regurgitation, in contrast to 3% of coronary patients in sinus r h y t h m (p <0.001), but their atrial coronary circulation was not more severely compromised. Thus, Ta segment displacement did not identify atrial coronary disease and was not more frequent during acute myocardial infarction. Abnormal atrial perfusion did not explain Ta segment displacement or atrial flutter/fibrillation.

MATERIALS AND METHODS

The incidence of atrial infarction at autopsy averages 17%1. However, antemortem diagnosis is infrequent because previously reported electrocardiographic criteria are seldom met and often transient. The Ta IPR) segment represents the time of atrial repolarization. Ligation of atrial branches of the coronary arteries of dogs results in depression or elevation of the Ta segment, changes in P wave form, and supraventricular arrhythmiasl. Although a consistent sequence of such electrocardiographic changes has not been established in humans, they have been recorded in patients with atrial infarction documented by postmortem examination1-3. We systematically examined the relationship between Ta waves, atrial flutter and fibrillation, and angiographically identified atrial coronary disease. Additionally, patients with acute infarction were screened for Ta abnormalities.

Group I formed the basis for characterizing normal atrial coronary circulation and consisted of 28 consecutive catheterized patients without coronary stenoses, normal left ventriculograms, and no evidence of valvular disease. Group II was 29 consecutive patients with >/50% narrowing of the left main coronary artery or i> 70% narrowing of a major coronary artery. Twentyeight consecutive patients with acute transmural myocardial infarction (chest pain, cardiac enzyme elevation, and characteristic evolution of "Q" waves) comprised Group III. Group IV consisted of all patients catheterized at the Medical College of Pennsylvania between 1974 and 1981 who had atrial flutter or fibrillation recorded before catheterization and who had significant coronary disease, as noted above, but not valvular heart disease {excepting mitral regurgitation thought to be secondary to papillary muscle dysfunction). Sixteen such patients were identified among 6028 patients catheterized in these years. Individual leads from ECGs recorded prior to catheterization of patients in Groups I and II were cut from the tracing and one of the authors, unaware of the catheterization results, reviewed the PR segments of leads I, AVF, and Vs separately in random order after their QRS complexes and T waves had been removed (Fig. la). Thus each lead was analyzed without comparison to other leads and without patient identification or bias from knowledge of QRS-T changes. The Ta segment was considered elevated or depressed if it was found to be above or below the baseline inscribed before the P wave by at least the thickness of the inscribed line. In Group III, the uncut ECG demonstrating the greatest

From the Division of Cardiology, Medical College of Pennsylvania, Philadelphia, Pennsylvania 19129. *Instructor of Medicine. j'Professor of Medicine. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "'advertisement" in accordance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Toby R. Engel, M.D., Department of Medicine, Medical College of Pennsylvania, 3300 Henry Avenue, Philadelphia, Pennsylvania 19129.

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ST segment elevation for each individual was chosen to assess the Ta segment (Fig. lb). Angiographic analysis of the atrial coronary circulation was done in the right anterior oblique projection. Normally the major atrial supply originated from the sinus node, right intermediate atrial, and left atrial circumflex arteries. The sinus node artery, seen in every patient, was a large branch originating proximally from either the right or circumflex coronary artery and extending to the junction of the right atrium and superior vena cava to encircle the base of the superior vena cava with distal branches4. The right intermediate atrial arteries originated from the mid-portion of the right coronary artery and traveled toward the right heart border in a direction opposite the right ventricular branches. The left atrial circumflex artery originated from the proximal or middle third of the main circumflex artery and coursed along the atrioventricular groove before traveling opposite the left ventricular branches, sometimes with branches that passed superiorly or inferiorly to the atrial walls9 Occasionally, a second atrial circumflex branch was present 9 Perfusion to each of the superior, middle and inferior thirds of the atria was identified by an atrial coronary branch, regardless of caliber, that traversed at least one-third of the atrial diameter. Inadequate atrial perfusion was suggested by: 1} absence of a vessel traversing at least one-third of the atrial diameter to the appropriate region; 2) >/ 70% luminal narrowing of the right or circumflex coronary artery proximal to that atrial branch; 3) critical luminal narrowing of the atrial branch itself or a ghost-like appearance in the expected

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Fig. 1. This ECG from a Group I I I patient with an acute transmural inferior myocardial infarction demonstrates how the QRS-T complexes were removed from the intact tracing (top panel}, leaving the Ta segment for analysis in leads I, AVF, and V 6. In spite of dramatic ST segment elevation during acute inferior myocardial infarction, this tracing was the most striking example of Ta depression {lead AVF) that was seen in our patients with transmural infarction.

area; or 4) filling of the region only by collateral circulation from a major coronary vessel, itself with at least 70% proximal stenosis. Statistical analysis was performed using a Student's t test and cM-square analysis with Yates' correction, and p<0.05 was considered significant.

RESULTS E i g h t of 28 E C G s f r o m G r o u p I p a t i e n t s w i t h n o r m a l c o r o n a r y a n g i o g r a m s h a d no T a s e g m e n t d i s p l a c e m e n t . A m o n g t h e r e m a i n i n g 71% of E C G s , 11 d e m o n s t r a t e d T a d i s p l a c e m e n t in a single lead, a n d nine s h o w e d t w o or t h r e e leads with displaced Ta segments. Two ECGs had Ta d e p r e s s i o n of one m m in a single lead, b u t all o t h e r T a d i s p l a c e m e n t s w e r e less t h a n one m m . I n 21 of t h e 28 p a t i e n t s , the atrial c o r o n a r y circulation w a s seen to p e r f u s e all t h r e e regions (superior, mid, a n d inferior}. F o u r t e e n of t h e s e 21 p a t i e n t s {67%} h a d T a d i s p l a c e m e n t . Of the remaining seven patients, mid-atrial perfusion was n o t visualized in four, inferior p e r f u s i o n w a s not v i s u a l i z e d in two, a n d in one, the atrial s u p p l y to b o t h m i d a n d inferior r e g i o n s w a s n o t seen. Six of t h e s e s e v e n (86%} h a d T a d i s p l a c e m e n t . E C G s f r o m six of the 29 G r o u p I I p a t i e n t s w h o h a d a n g i o g r a p h i c a l l y d o c u m e n t e d c o r o n a r y arter y d i s e a s e h a d no T a d i s p l a c e m e n t . Of the r e m a i n ing 23 E C G s {79%}, nine h a d T a d i s p l a c e m e n t in

J. ELECTROCARDIOLOGY 16 (4), 1983

ATRIAL Ta SEGM ENT AN D ATRIAL CORONARY DISEASE

one lead, 11 had two of the three with Ta displacement, and three showed three leads with Ta displacement. All Ta displacements were less than one mm. There was no significant difference between the prevalence of Ta displacement in patients with normal (71%) and diseased (79%) coronary arteries (Fig. 2). In Group II, left ventricular ejection fraction averaged 61% _+ 16 (SD) and end diastolic pressure 19 m m H g ___ 8 (SD) in patients with Ta displacement and averaged 62% _+ 20 and 21 m m H g _+ 6, respectively, in patients with isoelectric Ta segments. In eight of 29 patients with corornary artery disease adequate atrial perfusion was not visualized in two atrial regions, and adequate atrial perfusion was not seen at all in three patients. Nine of these 11 patients had at least one Ta segment displaced. Eight additional angiograms showed lack of perfusion to one atrial region (one to the superior, two to the mid, and five to the inferior atrial portions), and seven among this subgroup had Ta displacement. The coronary circulation perfused all three atrial regions without significant proximal stenosis in ten of the 29 coronary patients, but seven in this subgroup with intact atrial circulation had Ta displacement. Thus there was not a relationship between Ta displacement and the angiographic identification of inadequate atrial perfusion. Furthermore, although 84% of the patients with apparently insufficient atrial perfusion had Ta displacement, this was not significantly more frequent than the 71% with Ta displacement and normal coronary arteries. Among the 28 Group III patients with acute transmural myocardial infarction, six sustained anteroseptal infarction. Two ECGs with anteroseptal infarction had no Ta displacement, two had one lead with Ta displacement, one had two, and one had three leads with Ta displacement. Of the 20 patients with inferior infarction, five had no Ta displacement, ten had one lead with Ta displacement, four had two Ta displacements, and one had three Ta displacements. One patient with both anterior and inferior infarctions had a single lead with Ta displacement, and a patient with lateral infarction also had one Ta displacement. All Ta deviations were less than one mm with the exception of one patient with an inferior myocardial infarction who showed one mm Ta depression in lead A V F only (Fig. 1). In summary, of the 28 Group III patients with acute transmural myocardial infarction, 22 had Ta displacements (79%), an incidence similar to the 71% Ta

J. ELECTROCARDIOLOGY 16 (4), 1983

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I "ff Fig. 2. The prevalence of Ta segment displacement in patients with normal coronary arteries (Group I) and in patients with stable coronary disease (Group II). The upslanting lines indicate the percentage of patients with intact atrial perfusion who had Ta displacement. The downslanting lines indicate patients with a segmental defect in atrial perfusion (see text). The horizontal lines represent patients with inadequately visualized perfusion to two-thirds of the atria, and the stippling, patients with inadequate perfusion of the entire atria.

displacements in Group I patients with normal coronary arteries (pNS). Five of the 16 Group IV patients with atrial flutter or fibrillation had adequate coronary perfusion visualized in all three atrial regions. Seven patients lacked angiographically identified adequate perfusion to one atrial region, three to two regions, and one had seemingly jeopardized perfusion to all three regions. All but the last had normal circulation to the superior atria. Thus the extent of disruption in atrial supply that was identified resembled that seen when there was sinus rhythm. Left ventricular ejection fraction averaged 57% _ 16 in these Group IV patients, similar

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to Group II coronary patients with sinus rhythm (61% + 17, pNS). Average left ventricular end diastolic pressure was the same in Groups II and IV (19 mmHg). However, classification of Group II and IV patients on the basis of mitral regurgitation identified b y left ventriculography showed that only one of the 29 with coronary artery disease and sinus rhythm had significant mitral regurgitation whereas eight of 16 with coronary disease and atrial fibrillation had significant mitral regurgitation (p<0.001). Group IV patients with significant mitral regurgitation had a lower left ventricular ejection fraction of 49% __+ 15 and a higher mean left ventricular end diastolic pressure of 25 m m H g _+ 8 than seen in patients without mitral regurgitation (65% _+ 12 [p<0.05] and 15 m m H g _+ 5 [p<0.001]). The atrial coronary circulation was similar in coronary disease patients with atrial fibrillation whether or not significant mitral regurgitation was present.

DISCUSSION Ta segment displacement and atrial flutter or fibrillation have been reported in animal models of atrial infarctionl.~ and from a u t o p s y studies of patients with myocardial infarctionL6. However, other studies have not confirmed these findings7. Animal studies have used either a bolus injection of air into the left ventricle, direct atrial cauterization, or ligation of atrial coronary arteries, b u t these techniques might not reproduce the same injury as sustained in humans with more extensive coronary disease. Recordings obtained by direct placement of leads on injured atria in some of these experiments are not necessarily analogous to those obtained from chest and arm leads in patients. The first patient with atrial infarction identified antemortem was diagnosed in 1948 by electrocardiographic findings similar to the changes previously described in dogss. Liu et al.9 later suggested that Ta segment elevation >0.5 mm associated with reciprocal Ta depression, or depression of >1.2 mm in standard leads or >1.5 mm in precordial leads, associated with any atrial arrhythmias, might indicate atrial infarction at autopsy. Several reports suggested a causal relationship between atrial infarction at autopsy and atrial fibrillation 1.6.1o. Coronary angiography allows characterization of the status of the atrial coronary circulation in the living patient b u t has not previously been used to decide whether the Ta

segment is useful in detecting inadequate atrial coronary perfusion in patients with coronary artery disease. Atrial repolarization {Ta displacement} was seen in the majority (71%) of patients with normal coronary arteries. Even a full one mm deviation of the Ta segment was seen in this group. Patients with stable angina pectoris due to significant coronary artery disease also had minor Ta segment displacements, b u t not more frequently than those with normal coronary arteries. Ta displacement correlated with neither depressed left ventricular ejection fraction or elevated end diastolic pressure. It was not found more frequently in patients with inadequate atrial perfusion by angiography. Patients with acute transmural myocardial infarction also had frequent Ta displacements, b u t not more so than those with normal coronary arteries. Only one of 28 patients had a full one mm of Ta depression (in one lead), and this extent of depression had been noted in two patients with normal coronary arteries. We used clinical tracings, the thickness of the line varied with different recorders, and baseline drift was perhaps exaggerated when we isolated the Ta segment for inspection. Thus, previous autopsy reports have emphasized that there are marked Ta depressions with atrial infarction, b u t we found this electrocardiographic change infrequently and saw it in patients with normal coronary arteries. Although atrial infarction might produce a dramatic Ta abnormality in occasional patients, that is unusual in light of the 17% average incidence of atrial infarction documented by a u t o p s y during ventricular myocardial infarction. Patients with coronary artery disease and atrial flutter or fibrillation in the absence of valvular heart disease constituted a minority of our population of catheterized patients (0.1%), in confirmation of the experience reported by Haddad, et all1. We presume this is explained by the extensive nature of atrial coronary collateral supply. However, angiographic abnormalities of atrial coronary circulation were the same as in patients with stable angina pectoris who were in sinus rhythm, and left ventricular ejection fraction and end diastolic pressure were not different in these two groups. The presence of atrial flutter/fibrillation might be explained in part by mitral regurgitation, found in 50% of coronary patients with these arrhythmias. However, atrial fibrillation and mitral regurgitation were both associated with a very depressed left ventricular

J. ELECTROCARDIOLOGY 16 (4), 1983

ATRIAL Ta SEGMENT AND ATRIAL CORONARY DISEASE

ejection fraction and v e r y e l e v a t e d end diastolic pressure, and the a r r h y t h m i a m i g h t reflect the latter. T h u s , the presence of atrial fibrillation cannot be u s e d to j u d g e the s t a t u s of the atrial coro n a r y circulation, j u s t as sinus node d y s f u n c t i o n does not d i a g n o s e sinus node a r t e r y disease in the p r e s e n c e of c o r o n a r y a r t e r y disease4. In conclusion, identification of atrial repolarization b y T a d i s p l a c e m e n t and atrial flutter/fibrillation c a n n o t be used to p r e d i c t the s t a t u s of the atrial c o r o n a r y circulation in p a t i e n t s w i t h angina p e c t o r i s or a c u t e m y o c a r d i a l infarction. T h e E C G does not diagnose atrial c o r o n a r y disease. Acknowledgement: We express our appreciation to Mr. Scott Bain for help in data collection and to Mrs. Donna Simonds for her excellent secretarial assistance.

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Infarkt. Acta Med Scand 100:136, 1939 3. FREUNDLICII,J ANDSERENO,L R: Auricular infarction.

Am Ileart J 57:654, 1959 d. ENGEL,T R, MEISTER,S G, FEITOSA,G S, Fisclma, H A AND FRANKL,W S: Appraisal of sinus node artery disease. Circulation 52:286, 1975 5. JAMES,T N ANDGEOGHEGAN,T: Sequential electrocardiographic changes following auricular injury. Am Heart J 46:830, 1953 6. McCAIN,F If, KLINE,E M ANDGILSON,J M: A clinical study of 281 autopsy reports on patients with myocardial infarction. Am Heart J 39:263, 1957 7. AmtANsoN,D I, FENICIIEL,N M ANDSHOOKnOFF,C: A study of the electrical activity of the auricles. Am Heart J 15:471, 1938 8. I IELLERSTEIN,H I~ Atrial infarction with diagnostic electrocardiographic findings. Am lleart J 36:422, 1948 9. LIU C K, GREENSPAN,G ANDPICCIRILLO,n T: Atrial infarction of the heart. Circulation 23:331, 1961 10. SODERSTItOM,N: Myocardial infarction and mural thrombosis in the atria of the heart. Acta Med Scand Suppl 217:1, 1948 11. ttADDAD,A H, PRCIIKOV,V K ANDVEAR, D C" Chronic atrial fibrillation and coronary artery disease. Electrocardiol 11:67, 1978

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Few people are capable of expressing with equanimity opinions which differ from the prejudices of their social environment. Most people are even incapable of forming such opinion. --Albert Einstein