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Electrocardiographic atrial complex and acute atrial myocardial infarction
ElectrocardiographicAtrial Complex and Acute Atrial Myocardial Infarction
EGIL SIVERTSSEN. MD BJCiPN HOEL. MD GUNNAR BAY, MD LEIF JtjRGENSEN. MD Osla Norway
From the Department of Medicine (VIII) and Department of Pathology, Ullev& Hospital, University of Oslo, Oslo, Norway. Manuscript received June 20, 1972; revised manuscript received August 24, 1972, accepted September 27, 1972. Address for reprints: Egil Sivertssen, MD, Department of Medicine (VI II), UllevHl Hospital, University of Oslo, Oslo 1, Norway.
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The atrial complex was examined by use of standard and right atrial leads in 59 patients with acute myocardial infarction. Abnormal atrial complexes were found in standard leads in 17 patients, and in the right atrial lead in 29 patients. Abnormal atrial complexes were found more frequently in patients who had arrhythmias in the acute phase than in patients without arrhythmias. Ten patients died during the acute phase. ,lnfarcts in the right atrium were found in all 7 patients whose right atrium was examined microscopically. Abnormal atrial complexes in the right atrial lead were found in patients with atrial infarcts, especially when the lateral atrial wall was involved.
Two types of changes of the electrocardiographic atria1 complex in acute myocardial infarction have been described: (1) changes due to sympathetic stimulation and heart failure, and (2) changes due to atria1 infarction. Sympathetic stimulation results in a downward displacement of the P-R segment and S-T segment in standard leads as normally seen in exercise electrocardiograms.ly2 Left ventricular failure and left atria1 overloading may result in a change of electrical axis and increased negative phase of the P wave in lead V1.3-6 The electrocardiographic signs of atria1 infarction have been described as alterations of the P-R segment and the atria1 recovery wave as well as changes in the P wave itself.4,7-g No systematic study has previously been made of intraatrial electrocardiographic changes of the atria1 complex in myocardial infarction in man. MeerschwamlO reported 1 case of atria1 infarction diagnosed by intracavitary leads showing marked displacement of the P-R segment in the right atrium. James and Geogheganll studied direct atria1 electrocardiograms in experimental atria1 infarction in dogs, and found a consistent sequence of changes in all animals. Immediately after the injury, the P-R segment was displaced, and after a few minutes, it developed into a sharp atria1 T wave. Corsi et al.ls in a similar experimental study found that leads that directly overlay the injury exhibited positive P-R displacement, whereas the remaining leads showed negative displacement. Most experimental lesions of both the right and left atrium resulted in a depression of the P-R segment in the right atria1 lead. No direct relation was found between the size of the lesion and the degree of change. Klepacki and Pedich13 found in an experimental study that the intracavitary leads, in contrast to the epicardial leads, were of little use in the diagnosis of atria1 infarcts. It is well known that injury current may also be produced by pressure of the exploring electrode resulting in marked displacement of the P-R segment.14 Although interest in the electrocardiographic atria1 complex has increased, little attention is usually paid to the P wave of the conventional electrocardiogram during acute myocardial infarction. The clinical diagnosis of atria1 infarction is therefore seldom made. On the other hand, arrhythmia of atria1 origin is frequently encountered
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in acute myocardial ischemia.15 It is an open question whether this arrhythmia reflects manifest or impending ischemic injury to the myocardium of the right atrium. In the present study we examined the configuration of the atria1 complex in standard and right atrial leads in patients with acute myocardial infarction, and related the findings to the occurrence of atria1 arrhythmias during the acute phase of myocardial infarction. We also studied the possible relation between electrocardiographic changes and findings at postmortem examination of the heart.
Material and Methods Fifty-nine patients (43 male and 16 female) admitted to the coronary care unit of Department VIII, Ulleval Hospital, with acute myocardial infarction were studied. The patients were consecutive admissions within 3 periods from February 1969 to February 1970. Their ages ranged from 32 to 82 years (mean 59.8 years). Fifteen patients had previously had one or more episodes of myocardial infarction. Ten patients died during the acute phase, and 1 patient died some months later. The diagnosis of acute myocardial infarction was based on: (1) Electrocardiographic changes characteristic of re-
cent myocardial infarction in addition to two or more of the following criteria: rise in body temperature, increase in sedimentation rate and increase in serum glutamic oxaloacetic transaminase (SGOT) values. (2) Typical history in addition to two or more of the previous criteria cited, even when electrocardiographic changes were atypical or absent. The location of the infarct was determined by serial 12 lead electrocardiograms according to the method of Lipman and Massie.16 Atria1 repolarization was assessed by studying the P-R segment. Depression or elevation of the P-R segment was measured as the difference between the T-P segment and the lowest and highest points of the P-R segment. Abnormal P waves in the standard leads were diagnosed when one or more of the following findings were made: (1) P wave configuration other than the rounded form normally seen (notched, peaked or other abnormal configurations), (2) amplitude in lead II of 0.2 mv or more, and (3) duration in any 1 lead of more than 120 msec. The atria1 complex was also analyzed with regard to the mean frontal axis, the P/P-R ratio, I7 the initial and terminal forces in lead VI r* and elevation or depression of the P-R segment. The unipolar right atria1 intracavitary electrocardiogram was registered with the tip of the electrode placed
near the region of the sinus node in the proximal part of the atrium. This position was achieved by withdrawal of the electrode in a proximal direction from a lower position until the initial positive deflection of the atria1 complex disappeared. The position was determined by frontal radiologic examination. The right atria1 electrocardiogram was recorded on the first and in most patients also on the third hospital day. Abnormal atria1 complexes in the right atria1 lead were diagnosed when one or more of the following findings were present: (1) amplitude in the proximal position of less than 0.7 mv or more than 1.6 mv, (2) width in proximal position of less than 80 msec or more than 110 msec, and (3) intrinsicoid deflection slowly inscribed or ill defined with slurring or secondary spikes.rs In addition, the P-R
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segment elevation was measured. A P-R segment elevation of 0.1 mv or less was regarded as isoelectric. Record-. ings were made at a paper speed of 50 mm/set and 1 mv/cm in standard as well as in intracavitary leads. All patients were continously monitored and supervised by experienced nurses in the coronary care unit for at least 48 hours after admission. Any arrhythmia was recorded on an observation chart. Rhythm strips from bipolar chest leads were taken hourly and whenever arrhythmias occurred. A standard 12 lead electrocardiogram was taken on admission, on the first, third and fifth hospital days, and on discharge. Ten of the 59 patients died in the hospital. Complete autopsy was performed on all. In the first 3 patients the heart was examined fresh. The myocardium was cut parallel to the endocardium’, and sections for histologic examination were taken from obviously or possibly infarcted areas. The atria were not examined. In the other 7 patients the heart was fixed for 1 to 2 weeks in a solution of 4 percent formalin. The ventricles were then cut in multiple sections parallel to the annuli fibrosi. Sections for histologic examination were taken from the anterior and posterior walls, as well as from the interventricular septum. Furthermore, 4 sections were taken from the right atrium, perpendicular to the right annulus fibrosus: 1 each from the anterior, lateral and posterior walls and from the interatrial septum. The sections were embedded in paraffin and stained with hematoxylin-eosin, Lendrum’s martius-scarlet-blue method and Mallory’s phosphotungstic acid-hematoxylin (PTAH). The main coronary arteries were examined before fixation by longitudinal opening and inspection. Calculation of statistical significance was made by a chi-square test.
Results of abnormal atria1 complexes. In the standard leads, abnormal complexes were found on the first examination or during the hospital course in 17 patients (29 percent). In 2 patients the atria1 complex changed from normal to abnormal, and in 4 patients it changed from abnormal to normal during the first 3 days of observation. In the right atrial lead abnormal atria1 complexes were found on the first or second examination in 38 patients (68 percent). In 16 patients the atria1 complex changed from abnormal to normal and in 7 patients it changed from normal to abnormal between the 2 examinations. Slowly inscribed or ill defined intrinsicoid deflections were found in 21 patients on the first examination and in 10 patients on the second. Isoelectric or depressed P-R segments were found in 9 patients on the first examination and in 11 patients on the second. Atria1 complex and location of ventricular infarcts: The site of the ventricular infarcts as determined by standard electrocardiography was mainly inferior in 26, anteroseptal in 17, anterior in 11 and in other locations or undetermined in 5 patients. Abnormal atria1 complexes in the standard leads were found more frequently in patients with inferior and anteroseptal infarcts than in patients with anterior infarcts (Table I). The most common pathologic findings were notching and peaked appearance in the
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TABLE
I
Abnormal
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of Ventricular
Infarct Number of Patients with Abnormal Atrial Complexes Right Atrial (RA) Lead
Total no. of Patients
Location of Ventricular Infarct Anteroseptal
17
Anterior Inferior
I1 26
Others
5
Total
59
P Width .~~~~
Standard Leads Total
<80 msec
>llO msec
5(29%)
4 1 3
1(9%) 1~42%) 0 170%)
Abnormal lntrinsicoid Deflection
Any Abnormality in RA Lead
<0.7 mv
>1.6 mv
1
3
4
4
12(71%)
1 2
2 12
1 1
5 15
6(55%) 18(69%)
0
0
1
1
0
2(40%)
a
4
7
24
limb leads. The mean duration and amplitude in lead II, the mean P-R interval and the mean initial and terminal forces in lead VI were not significantly different among groups. The findings of a P/P-R ratio outside the normal limits of 1.0 to 1.617 showed no constant relation to the site of the infarct. Marked negativity of the P wave in lead VI (terminal force -0.04 or more)18 was found in 8 patients and showed no apparent relation to the site of the infarct. Depression of the P-R segment of more than 0.5 mm (0.05 mv) was found in lead II or in the precordial leads in 7 patients, 6 of whom had anteroseptal or anterior infarcts; the remaining patient had an inferior infarct (21 percent and 4 percent, respectively). Elevation of the P-R segment was not found in any patient. Abnormal atria1 complexes in the right atria1 lead on the first or second examination were frequently found in all types of ventricular infarcts (Table I). Low amplitude of the right atria1 complex and a
TABLE
P Amplitude
ia
38(680/o)
slowly inscribed intrinsicoid deflection were more often found in patients with inferior ventricular infarcts than in the other groups. No significant difference was found between the groups as regards elevation or depression of the P-R segment. Arrhythmias: Of the 59 patients 19 had no arrhythmias during the acute phase except for occasional premature beats. In 40 patients one or more types of arrhythmia occurred either before or after the first intracavitary recording. Arrhythmias, especially of the supraventricular type, occurred more frequently in patients with inferior and anteroseptal infarcts. Atrioventricular (A-V) block, grade II or III, was found in 7 patients, all of whom had inferior ventricular infarcts. Abnormal atria1 complexes in the standard leads were found in only 2 of 19 patients who had no arrhythmias during the acute phase, but in 15 of the 40 patients with arrhythmias (Table II). However, this difference was not statistically significant, (P = 0.07). Abnormal atria1 complexes in the standard
II
Abnormal
Atrial Complex and Occurrence
of Arrhythmia
Number of Patients with Abnormal Atrial Complexes Right Atrial (RA) Lead
Arrhythmia in the Acute Stage of Myocardial Infarction No arrhythmia Arrhythmia Type
P Width
Standard Leads
<80 msec
P Amplitude
>llO msec
<0.7 mv
>1.6 mv
19 40
2(ll%) 15(380/o)
1 7
0 4
5 13
0 7
a
103%) 6(50%) 5(45%) 5(710/o) 4(31%) 2(20%‘0)
1 2 1 1 2 3
2 4 1 1 0 1
3 6 3 4 4 4
1 0 5 1 1 2
Abnormal lntrinsrcoid Deflection 6
ia
Any Abnormality in RA Lead 7(27%)
3mwd
of arrhythmia:
Bradycardia and S-A block Atrial fibrillation and flutter Nodal and idioventricular rhythm A-V block, type III Ventricular ectopic beats Ventricular tachycardia and fibrillation
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6(75%) 10(830/o) 10(91%) 6@6%,) Wl%,) WOO/,)
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I
II
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PR segm.
Pampl.
P width I
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II
II
I
mV
msec
.
2.5
.. 1. --_------00. 3... I%%:’ ,0....
80 FIGURE 1. Width, amplitude (P ampl.) and P-R segment (segm) elevation of the atrial complex in the right atrial lead in 59 patients with acute myocardial infarction. I = on first examination shortly after admission to the hospital, II = on second examination 3 days after admission (not performed in all patients). Open circles denote no arrhythmia; closed circles denote occurrence of arrhythmia in the acute phase.
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.
o.....
2.0
0
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._--_-_---1.5
.. .
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1.0
0.
0.
o......
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0.
0.
0.o.D
00..
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00.
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0.
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.
Autopsy Findings Ventricular infarcts: All 10 patients who died in the hospital had a history of a recent ventricular infarct occurring 9 to 10 hours before admission. The diaphragmatic wall of the left ventricle was infarcted
O-
. . .
. .
000.
00..
0..
. ..”
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-
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leads occurred more often in patients with A-V block, in those with attacks of atria1 fibrillation or flutter, and in those with nodal and idioventricular rhythms. No group difference was found in the mean duration or amplitude of the P wave in lead II, in the mean P-R interval, or in the mean initial and terminal forces in lead VI. Values outside the previously defined normal for P/P-R ratio and terminal force in lead VI were distributed equally among groups. Depression of the P-R segment in lead II or in the precordial leads was found in 1 of the 19 patients who had no arrhythmias and in 6 of the 40 patients who had arrhythmias during the acute phase. Abnormal atria1 complexes in the right atria1 lead were found in 7 of 19 patients who had no arrhythmias and’ in 31 of 40 patients who had arrhythmias during the acute phase. This difference was statistically highly significant (P = 0.006). Abnormal atria1 complexes were frequently seen in patients with supraventricular as well as in those with ventricular arrhythmias. Values outside the previously defined normal limits for width and amplitude of the atria1 complex in the right atria1 lead were found almost exclusively in patients who had one or more types of arrhythmia. However, several patients with arrhythmia had values within normal limits (Fig. 1).
.2-
-.2 0
in 5 patients, 4 of whom had involvement of the interventricular septum as well. In the remaining 5 cases the infarct was located in the interventricular septum alone (3 cases) or combined with involvement of the anterior wall (1 case) or lateral wall (1 case) of the ventricle. Associated coronary arterial thrombi were found in 7 cases, in 5 in the right coronary artery, and in 2 in the descending branch of the left coronary artery. The immediate cause of death was myocardial rupture (3 cases), shock and pump failure (3 cases) and ventricular fibrillation or coma after cardiac arrest (4 cases). Right atria1 infarcts: The right atrium was examined histologically in 7 cases, and recent atria1 infarcts were found in all. In 1 additional case gross examination revealed subepicardial hemorrhages on the surface of the right atrium. In 3 cases the atria1 infarcts were some hours old. In 3 cases the infarcts were thought to be of 6 to 8 days’ duration. In 1 case separate right atria1 infarcts of 2 different ages were found. In all cases there was agreement between the histologic appearance of the atria1 infarct and its duration. The infarcts were located in the lateral wall of the right atrium in 5 cases, in 2 of which they were also found in the anterior wall; 1 patient had an additional infarct in the interatrial septum. One patient had an infarct in the anterior and 1 in the posterior atria1 wall. The atria1 complex in the standard electrocardiogram showed various abnormalities in 5 of the 10 cases. In the right atria1 lead, the atria1 complex was abnormal shortly before death in 9 cases (Fig. 2). In
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Discussion
FIGURE 2. Standard and right atrial lead electrocardiograms and section from the lateral wall of the right atrium (hematoxylineosin X480, reduced by 24 percent). The patient was a 70 year old man-who died from cardiac rupture 9 hours after admission. The standard electrocardiogram showed an inferior myocardial infarction and abnormal atrial complexes with notching in the precordial leads (not illustrated). The right atrial lead (RA) shows split atrial complexes, sinoatrial block and ectopic atrial escape beats. The section from the right atrium shows irregular cross striation and a few granulocytes (arrow) indicating ischemia of some hours’ duration.
the 10th case a change in the P wave had occurred between the 2 recordings, but the pattern before death was considered normal by our criteria. This patient had an infarct in the anterior wall of the right atrium and no involvement of the lateral atria1 wall. In 2 cases the atria1 infarcts were judged to be more recent than the ventricular infarcts (Fig. 3 and 4). In both cases the configuration of the P wave in the right atria1 lead had changed from that on previous recordings shortly before the death of the patient. Arrhythmias occurred in 8 of the patients who died. Two of the 5 patients with histologically confirmed infarction of the lateral wall of the right atrium had atria1 fibrillation, 1 patient had sinoatrial block and 2 patients had A--V block. Two patients with atria1 infarction localized only to the anterior or posterior wall did not have atria1 arrhythmias or atrioventricular conduction disturbances. 454
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Abnormal atria1 complexes were found in the right atria1 lead in 68 percent of patients with acute ventricular infarction, whereas only 29 percent of the patients had abnormal atria1 complexes in the standard leads. This difference suggests that the right atria1 lead may be the more sensitive in detecting atria1 abnormalities in acute myocardial infarction. In 6 cases with abnormal atria1 complexes in the right atria1 lead, the right atrium was examined histologically. In 5 patients the infarct was localized to the lateral wall and in 1 patient to the posterior wall of the right atrium. The seventh patient whose right atrium was examined histologically showed no definite electrocardiographic atria1 abnormalities before death in the standard or right atria1 leads, although there was an infarct in the anterior wall of the right atrium. In 2 cases, histologic findings indicated that the atria1 complex in the right atria1 lead changed pari passu with the development of new lateral atria1 infarcts. These observations suggest that abnormal atria1 complexes reflect atria1 infarction, primarily of the lateral wall, that is, in the region of the sinus node. Changes of the atria1 complex and P-R segment similar to those found in patients with acute myocardial infarction have been found in patients with atria1 disorders due to valvular heart disease.20 Thus, the changes do not seem to be specific. However, it is not established whether the abnormal atrial complex in valvular heart disease is also due to ischemic changes in the atria1 myocardium. Insidence of atria1 infarcts: All 7 patients who died from myocardial infarction and whose right atrium was examined histologically had atria1 infarcts by histologic criteria. According to previous autopsy series, atria1 infarcts occur in 1 to 27 percent of all cases of ventricular myocardial infarcts.21,22 However, the number of reported cases is small in relation to the frequency of ventricular infarction. It may be that atria1 infarction, as several investigators have pointed out, is difficult to recognize even in postmortem examinations if systematic histologic examination is not performed. Our results support the statement by Sbderstrom7 that atria1 infarcts are “overlooked rather than rare.” Atria1 infarction and cardiac arrhythmias: Our study shows that atria1 involvement in acute myocardial infarction, as reflected by changes in the atrial complexes both in standard and in intracavitary leads, are associated with an increased incidence of arrhythmias. The findings suggest that pathologic changes of the atria1 complex in the right atria1 lead may be particularly related to atria1 arrhythmias and sinoatrial or atrioventricular conduction disturbances. However, the significance of this finding is difficult to evaluate because more than one type of arrhythmia occurred in several of the patients, and the number of patients in each group was small. Several factors may cause arrhythmias during acute myocardial infarction: infarction of the sinus node, ischemia of the A-V node, vagal and vagomi-
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atria1 distension and circulating metic reflexes, chronotropic substances. l5 The association found in our study between changes in the atria1 electrocardiographic complex and atria1 infarcts on the one hand, and between changes in the atria1 complex and arrhythmias on the other, is suggestive of a relation between atria1 infarcts and arrhythmias as well. Furthermore, in 6 of 7 cases in which the right atrium was examined histologically various types of arrhythmia were present. All 6 patients had infarcts in
the right atrium, and in 5 of the 6, the infarct was in the lateral wall of the right atrium; 3 of the latter patients had arrhythmias of atria1 origin. These observations agree with the concept that the most frequent cause of cardiac arrhythmias is ischemia due to localized circulatory disturbances. The circulatory disturbance may originate in the main coronary vessel occlusion, which results in the ventricular infarct, or in the appearance of thrombotic material in several small vessels. Experimentally, ar-
FIGURE 3. Standard and right atrial electrocardiograms and section from the anterior wall of the right atrium (hematoxylineosin X480, reduced by 24 percent). The patient was a 59 year old man who collapsed with ventricular fibrillation before hospital admission. Defibrillation was performed by an ambulance team. Shortly after admission he had another attack of ventricular fibrillation which was converted by electroshock. However, he did not regain consciousness and died 7 days later. The standard electrocardiogram showed inferior myocardial infarction and normal atrial complexes. Shortly before death atrioventricular block occurred. The right atrial lead (RA) shows changes of the atrial complexes from the first examination (left) to the second (right), which was performed 5 hours before the patient’s death. On the second examination grade II atrioventricular block was found. In sections from the lateral and anterior watls of the right atrium areas of irregular cross striation and slight accumulation of neutrophils were found (arrows). The appearance indicates an infarct of a few hours’ duration. Section from the left ventricle showed an infarct compatible with a history of 5 days.
FIGURE 4. Standard and right atrial electrocardiograms and sections from the lateral wall of the right atrium (hematoxylineosin X74, reduced by 25 percent). The patient was a 77 year old woman with multiple previous myocardial infarcts. She was discharged from the coronary care unit to the general ward 6 days after an uneventful acute infarct, and died suddenly from ventricular fibrillation on the following day. The atria1 complex iS abnormal in the standard and right atrial (RA) leads on admission (left). On the second examination a few hours before death, the right atrial electrocardiogram has changed and shows depression of the P-R segment [right). Sections from the lateral wall of right atrium show an infarct in the stage of resorption, compatible with 7 days’ duration (A), and small areas of quite recent necrosis (6).
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rhythmia and sudden death from myocardial infarction have been produced in pigs by creating myocardial microcirculatory disturbances by transient platelet aggregation. 23 Autopsy studies of cases of coronary heart disease have revealed the presence of larger and more numerous platelet aggregates in the myocardial circulation of patients who died suddenly, presumably from arrhythmias, than in control subjects.24~25 Platelet-fibrin masses were observed in the atria1 vessels in some patients in our series, but they were not quantified. In favor of a local ischemia-inducing factor such as platelet fibrin masses within the microcirculation was the fact that some of the atria1 infarcts were small and multifocal. Clinical implications: The association between abnormal atria1 complexes and the development of
arrhythmias may be clinically important, since abnormal atria1 complexes should be regarded as a warning signal. The right atria1 electrocardiogram seems to be superior to the standard lead electrocardiogram in detecting atria1 abnormalities, but has the disadvantage of being an invasive method and is therefore less suitable for routine use in patients with acute myocardial infarction. Studies of the atria1 complex in patients with acute myocardial infarction may give information of clinical value especially with regard to atria1 conduction disturbances, arrhythmias and left ventricular failure. The development of a noninvasive electrocardiographic method which allows better analysis of the P wave than that provided by the standard electrocardiogram would therefore be of practical value.
References 1. Scherf D, Schaffer Al: The electrocardiographic exercise test. Amer Heart J 43:927-943, 1952 2. Tranchesi J, Abeiardi V, Oliveira JM: Atrial repolarizationits importance in clinical electrocardiography. Circulation 22:635-644, 1960. 3. Sutnick AJ, Soloff LA: Posterior rotation of the atrial vector. An electrocardiographic sign of left ventricular failure. Circulation 26:913-916, 1962 4. Zimmerman HA, Bersano E, Dicosky C: The Auricular Electrocardiogram. Springfield, Ill, Charles C Thomas, 1968, p 54-64 5. von Gross D: Uber die Veranderungen der Vorhofzacke bei Myokardinfarkten. 2. Krejslaufforsch 59:262-270, 1969 6. Grossman JI, Deiman AJ: Serial P wave changes in acute myocardial infarction. Amer Heart J 77:336-341, 1969 7. Siiderstrom N: Myocardial infarction and mural thrombosis in the atria of the heart (abstr). Acta Med Stand 132: suppl 217:1-114.1948 8. Lepesckin E: Modern Electrocardiography. Baltimore, Williams & Wilkins, 1955, p 409 9. Liu CK, Greenspan G, Piccirillo RT: Atrial Infarction of the heart. Circulation 23:331-338, 1961 10. Meerschwam IS: A case of auricular infarct confirmed by endocavitary leads. Arch Mal Coeur 58:558-563, 1965 11. James TN, Geoghegan T: Sequential electrocardiographic changes following auricular injury. Amer Heart J 46:830843, 1953 12. Corsi V, Sangiorgi M, Coreili D: Contribution to the electrocardiographic localization of auricular myocardial damage. An experimental study. Cardiologia 23:255-273, 1953 13. Kiepacki Z, Pedich W: Intracardiac electrocardiographic leads in experimental atrial necrosis. Kardiol Pol 12:197202, 1969
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14. Kossmann CE, Berger AR, Rader B, et al: Intracardiac and intravascular potentials resulting from electrical activity in the normal human heart. Circulation 2:10-30, 1950 15. James TN: Myocardial infarction and atrial arrhythmias. Circulation 24:761-766, 1961 16. Ltpman, BS, Massie E: Clinical Scalar Electrocardiography, fifth edition. Chicago, Year Book Medical Publishers, 1965, p 250-258 17. Macruz R, Perioff JK, Case RB: A method for the electrocardiographic recognition of atrial enlargement. Circulation 17:882-889, 1958 18. Morris JJ, Estes EH Jr, Whalen RE, et al: P-wave analysis in valvular heart disease. Circulation 29:242-252, 1964 19. Sivertssen E: The atrial complex in right atrial electrocardiography. Angiology, in press 20. Sivertssen E: Right atrial electrocardiography (RA ECG) in the diagnosis of right and left atrial abnormalities. Angiology, in press 21. Cushing EH, Feii HS, Stanton EJ, et al: Infarction of the cardiac auricles (atria): clinical, pathological, and experimental studies. Brit Heart J 4117-34, 1942 22. Wartman WB, Heiierstein HK: The incidence of heart disease in 2000 consecutive autopsies. Ann Intern Med 28:41-65, 1948 23. Jorgensen L, Rowseii HC, Hovig T, et al: Adenosine diphosphate-induced platelet aggregation and myocardial infarction in swine. Lab Invest 17:616-644, 1967 24. Haerem JW: Sudden coronary death: the occurrence of platelet aggregates in the epicardial arteries of man. Atherosclerosis 14:417-432, 1971 25. Haerem JW: Platelet aggregates in intramyocardial vessels in patients dying suddenly and unexpectedly of coronary disease. Atherosclerosis 15:199-213, 1972
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EGIL SIVERTSSEN. MD BJCiPN HOEL. MD GUNNAR BAY, MD LEIF JtjRGENSEN. MD Osla Norway
From the Department of Medicine (VIII) and Department of Pathology, Ullev& Hospital, University of Oslo, Oslo, Norway. Manuscript received June 20, 1972; revised manuscript received August 24, 1972, accepted September 27, 1972. Address for reprints: Egil Sivertssen, MD, Department of Medicine (VI II), UllevHl Hospital, University of Oslo, Oslo 1, Norway.
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The atrial complex was examined by use of standard and right atrial leads in 59 patients with acute myocardial infarction. Abnormal atrial complexes were found in standard leads in 17 patients, and in the right atrial lead in 29 patients. Abnormal atrial complexes were found more frequently in patients who had arrhythmias in the acute phase than in patients without arrhythmias. Ten patients died during the acute phase. ,lnfarcts in the right atrium were found in all 7 patients whose right atrium was examined microscopically. Abnormal atrial complexes in the right atrial lead were found in patients with atrial infarcts, especially when the lateral atrial wall was involved.
Two types of changes of the electrocardiographic atria1 complex in acute myocardial infarction have been described: (1) changes due to sympathetic stimulation and heart failure, and (2) changes due to atria1 infarction. Sympathetic stimulation results in a downward displacement of the P-R segment and S-T segment in standard leads as normally seen in exercise electrocardiograms.ly2 Left ventricular failure and left atria1 overloading may result in a change of electrical axis and increased negative phase of the P wave in lead V1.3-6 The electrocardiographic signs of atria1 infarction have been described as alterations of the P-R segment and the atria1 recovery wave as well as changes in the P wave itself.4,7-g No systematic study has previously been made of intraatrial electrocardiographic changes of the atria1 complex in myocardial infarction in man. MeerschwamlO reported 1 case of atria1 infarction diagnosed by intracavitary leads showing marked displacement of the P-R segment in the right atrium. James and Geogheganll studied direct atria1 electrocardiograms in experimental atria1 infarction in dogs, and found a consistent sequence of changes in all animals. Immediately after the injury, the P-R segment was displaced, and after a few minutes, it developed into a sharp atria1 T wave. Corsi et al.ls in a similar experimental study found that leads that directly overlay the injury exhibited positive P-R displacement, whereas the remaining leads showed negative displacement. Most experimental lesions of both the right and left atrium resulted in a depression of the P-R segment in the right atria1 lead. No direct relation was found between the size of the lesion and the degree of change. Klepacki and Pedich13 found in an experimental study that the intracavitary leads, in contrast to the epicardial leads, were of little use in the diagnosis of atria1 infarcts. It is well known that injury current may also be produced by pressure of the exploring electrode resulting in marked displacement of the P-R segment.14 Although interest in the electrocardiographic atria1 complex has increased, little attention is usually paid to the P wave of the conventional electrocardiogram during acute myocardial infarction. The clinical diagnosis of atria1 infarction is therefore seldom made. On the other hand, arrhythmia of atria1 origin is frequently encountered
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in acute myocardial ischemia.15 It is an open question whether this arrhythmia reflects manifest or impending ischemic injury to the myocardium of the right atrium. In the present study we examined the configuration of the atria1 complex in standard and right atrial leads in patients with acute myocardial infarction, and related the findings to the occurrence of atria1 arrhythmias during the acute phase of myocardial infarction. We also studied the possible relation between electrocardiographic changes and findings at postmortem examination of the heart.
Material and Methods Fifty-nine patients (43 male and 16 female) admitted to the coronary care unit of Department VIII, Ulleval Hospital, with acute myocardial infarction were studied. The patients were consecutive admissions within 3 periods from February 1969 to February 1970. Their ages ranged from 32 to 82 years (mean 59.8 years). Fifteen patients had previously had one or more episodes of myocardial infarction. Ten patients died during the acute phase, and 1 patient died some months later. The diagnosis of acute myocardial infarction was based on: (1) Electrocardiographic changes characteristic of re-
cent myocardial infarction in addition to two or more of the following criteria: rise in body temperature, increase in sedimentation rate and increase in serum glutamic oxaloacetic transaminase (SGOT) values. (2) Typical history in addition to two or more of the previous criteria cited, even when electrocardiographic changes were atypical or absent. The location of the infarct was determined by serial 12 lead electrocardiograms according to the method of Lipman and Massie.16 Atria1 repolarization was assessed by studying the P-R segment. Depression or elevation of the P-R segment was measured as the difference between the T-P segment and the lowest and highest points of the P-R segment. Abnormal P waves in the standard leads were diagnosed when one or more of the following findings were made: (1) P wave configuration other than the rounded form normally seen (notched, peaked or other abnormal configurations), (2) amplitude in lead II of 0.2 mv or more, and (3) duration in any 1 lead of more than 120 msec. The atria1 complex was also analyzed with regard to the mean frontal axis, the P/P-R ratio, I7 the initial and terminal forces in lead VI r* and elevation or depression of the P-R segment. The unipolar right atria1 intracavitary electrocardiogram was registered with the tip of the electrode placed
near the region of the sinus node in the proximal part of the atrium. This position was achieved by withdrawal of the electrode in a proximal direction from a lower position until the initial positive deflection of the atria1 complex disappeared. The position was determined by frontal radiologic examination. The right atria1 electrocardiogram was recorded on the first and in most patients also on the third hospital day. Abnormal atria1 complexes in the right atria1 lead were diagnosed when one or more of the following findings were present: (1) amplitude in the proximal position of less than 0.7 mv or more than 1.6 mv, (2) width in proximal position of less than 80 msec or more than 110 msec, and (3) intrinsicoid deflection slowly inscribed or ill defined with slurring or secondary spikes.rs In addition, the P-R
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segment elevation was measured. A P-R segment elevation of 0.1 mv or less was regarded as isoelectric. Record-. ings were made at a paper speed of 50 mm/set and 1 mv/cm in standard as well as in intracavitary leads. All patients were continously monitored and supervised by experienced nurses in the coronary care unit for at least 48 hours after admission. Any arrhythmia was recorded on an observation chart. Rhythm strips from bipolar chest leads were taken hourly and whenever arrhythmias occurred. A standard 12 lead electrocardiogram was taken on admission, on the first, third and fifth hospital days, and on discharge. Ten of the 59 patients died in the hospital. Complete autopsy was performed on all. In the first 3 patients the heart was examined fresh. The myocardium was cut parallel to the endocardium’, and sections for histologic examination were taken from obviously or possibly infarcted areas. The atria were not examined. In the other 7 patients the heart was fixed for 1 to 2 weeks in a solution of 4 percent formalin. The ventricles were then cut in multiple sections parallel to the annuli fibrosi. Sections for histologic examination were taken from the anterior and posterior walls, as well as from the interventricular septum. Furthermore, 4 sections were taken from the right atrium, perpendicular to the right annulus fibrosus: 1 each from the anterior, lateral and posterior walls and from the interatrial septum. The sections were embedded in paraffin and stained with hematoxylin-eosin, Lendrum’s martius-scarlet-blue method and Mallory’s phosphotungstic acid-hematoxylin (PTAH). The main coronary arteries were examined before fixation by longitudinal opening and inspection. Calculation of statistical significance was made by a chi-square test.
Results of abnormal atria1 complexes. In the standard leads, abnormal complexes were found on the first examination or during the hospital course in 17 patients (29 percent). In 2 patients the atria1 complex changed from normal to abnormal, and in 4 patients it changed from abnormal to normal during the first 3 days of observation. In the right atrial lead abnormal atria1 complexes were found on the first or second examination in 38 patients (68 percent). In 16 patients the atria1 complex changed from abnormal to normal and in 7 patients it changed from normal to abnormal between the 2 examinations. Slowly inscribed or ill defined intrinsicoid deflections were found in 21 patients on the first examination and in 10 patients on the second. Isoelectric or depressed P-R segments were found in 9 patients on the first examination and in 11 patients on the second. Atria1 complex and location of ventricular infarcts: The site of the ventricular infarcts as determined by standard electrocardiography was mainly inferior in 26, anteroseptal in 17, anterior in 11 and in other locations or undetermined in 5 patients. Abnormal atria1 complexes in the standard leads were found more frequently in patients with inferior and anteroseptal infarcts than in patients with anterior infarcts (Table I). The most common pathologic findings were notching and peaked appearance in the
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TABLE
I
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of Ventricular
Infarct Number of Patients with Abnormal Atrial Complexes Right Atrial (RA) Lead
Total no. of Patients
Location of Ventricular Infarct Anteroseptal
17
Anterior Inferior
I1 26
Others
5
Total
59
P Width .~~~~
Standard Leads Total
<80 msec
>llO msec
5(29%)
4 1 3
1(9%) 1~42%) 0 170%)
Abnormal lntrinsicoid Deflection
Any Abnormality in RA Lead
<0.7 mv
>1.6 mv
1
3
4
4
12(71%)
1 2
2 12
1 1
5 15
6(55%) 18(69%)
0
0
1
1
0
2(40%)
a
4
7
24
limb leads. The mean duration and amplitude in lead II, the mean P-R interval and the mean initial and terminal forces in lead VI were not significantly different among groups. The findings of a P/P-R ratio outside the normal limits of 1.0 to 1.617 showed no constant relation to the site of the infarct. Marked negativity of the P wave in lead VI (terminal force -0.04 or more)18 was found in 8 patients and showed no apparent relation to the site of the infarct. Depression of the P-R segment of more than 0.5 mm (0.05 mv) was found in lead II or in the precordial leads in 7 patients, 6 of whom had anteroseptal or anterior infarcts; the remaining patient had an inferior infarct (21 percent and 4 percent, respectively). Elevation of the P-R segment was not found in any patient. Abnormal atria1 complexes in the right atria1 lead on the first or second examination were frequently found in all types of ventricular infarcts (Table I). Low amplitude of the right atria1 complex and a
TABLE
P Amplitude
ia
38(680/o)
slowly inscribed intrinsicoid deflection were more often found in patients with inferior ventricular infarcts than in the other groups. No significant difference was found between the groups as regards elevation or depression of the P-R segment. Arrhythmias: Of the 59 patients 19 had no arrhythmias during the acute phase except for occasional premature beats. In 40 patients one or more types of arrhythmia occurred either before or after the first intracavitary recording. Arrhythmias, especially of the supraventricular type, occurred more frequently in patients with inferior and anteroseptal infarcts. Atrioventricular (A-V) block, grade II or III, was found in 7 patients, all of whom had inferior ventricular infarcts. Abnormal atria1 complexes in the standard leads were found in only 2 of 19 patients who had no arrhythmias during the acute phase, but in 15 of the 40 patients with arrhythmias (Table II). However, this difference was not statistically significant, (P = 0.07). Abnormal atria1 complexes in the standard
II
Abnormal
Atrial Complex and Occurrence
of Arrhythmia
Number of Patients with Abnormal Atrial Complexes Right Atrial (RA) Lead
Arrhythmia in the Acute Stage of Myocardial Infarction No arrhythmia Arrhythmia Type
P Width
Standard Leads
<80 msec
P Amplitude
>llO msec
<0.7 mv
>1.6 mv
19 40
2(ll%) 15(380/o)
1 7
0 4
5 13
0 7
a
103%) 6(50%) 5(45%) 5(710/o) 4(31%) 2(20%‘0)
1 2 1 1 2 3
2 4 1 1 0 1
3 6 3 4 4 4
1 0 5 1 1 2
Abnormal lntrinsrcoid Deflection 6
ia
Any Abnormality in RA Lead 7(27%)
3mwd
of arrhythmia:
Bradycardia and S-A block Atrial fibrillation and flutter Nodal and idioventricular rhythm A-V block, type III Ventricular ectopic beats Ventricular tachycardia and fibrillation
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6(75%) 10(830/o) 10(91%) 6@6%,) Wl%,) WOO/,)
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I
II
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PR segm.
Pampl.
P width I
INFARCTION-SIVERTSSEN
II
II
I
mV
msec
.
2.5
.. 1. --_------00. 3... I%%:’ ,0....
80 FIGURE 1. Width, amplitude (P ampl.) and P-R segment (segm) elevation of the atrial complex in the right atrial lead in 59 patients with acute myocardial infarction. I = on first examination shortly after admission to the hospital, II = on second examination 3 days after admission (not performed in all patients). Open circles denote no arrhythmia; closed circles denote occurrence of arrhythmia in the acute phase.
Es::* St::.. ,o....
.
o.....
2.0
0
cm..... ooo....
oo***m.
g::....
._--_-_---1.5
.. .
o***
.. .
1.0
0.
0.
o......
ooo....
0.
0.
0.o.D
00..
000..
00.
. . . .
. . . . .
. . . .
0.
cmo...
000..
0
. . .
0..
c.oo.... 0000...
.
.5
z37-. .
ocm... o.... . . .. ----cl... 0. . .
.
o...
.
Autopsy Findings Ventricular infarcts: All 10 patients who died in the hospital had a history of a recent ventricular infarct occurring 9 to 10 hours before admission. The diaphragmatic wall of the left ventricle was infarcted
O-
. . .
. .
000.
00..
0..
. ..”
0
0.
-
. .
cl... .
leads occurred more often in patients with A-V block, in those with attacks of atria1 fibrillation or flutter, and in those with nodal and idioventricular rhythms. No group difference was found in the mean duration or amplitude of the P wave in lead II, in the mean P-R interval, or in the mean initial and terminal forces in lead VI. Values outside the previously defined normal for P/P-R ratio and terminal force in lead VI were distributed equally among groups. Depression of the P-R segment in lead II or in the precordial leads was found in 1 of the 19 patients who had no arrhythmias and in 6 of the 40 patients who had arrhythmias during the acute phase. Abnormal atria1 complexes in the right atria1 lead were found in 7 of 19 patients who had no arrhythmias and’ in 31 of 40 patients who had arrhythmias during the acute phase. This difference was statistically highly significant (P = 0.006). Abnormal atria1 complexes were frequently seen in patients with supraventricular as well as in those with ventricular arrhythmias. Values outside the previously defined normal limits for width and amplitude of the atria1 complex in the right atria1 lead were found almost exclusively in patients who had one or more types of arrhythmia. However, several patients with arrhythmia had values within normal limits (Fig. 1).
.2-
-.2 0
in 5 patients, 4 of whom had involvement of the interventricular septum as well. In the remaining 5 cases the infarct was located in the interventricular septum alone (3 cases) or combined with involvement of the anterior wall (1 case) or lateral wall (1 case) of the ventricle. Associated coronary arterial thrombi were found in 7 cases, in 5 in the right coronary artery, and in 2 in the descending branch of the left coronary artery. The immediate cause of death was myocardial rupture (3 cases), shock and pump failure (3 cases) and ventricular fibrillation or coma after cardiac arrest (4 cases). Right atria1 infarcts: The right atrium was examined histologically in 7 cases, and recent atria1 infarcts were found in all. In 1 additional case gross examination revealed subepicardial hemorrhages on the surface of the right atrium. In 3 cases the atria1 infarcts were some hours old. In 3 cases the infarcts were thought to be of 6 to 8 days’ duration. In 1 case separate right atria1 infarcts of 2 different ages were found. In all cases there was agreement between the histologic appearance of the atria1 infarct and its duration. The infarcts were located in the lateral wall of the right atrium in 5 cases, in 2 of which they were also found in the anterior wall; 1 patient had an additional infarct in the interatrial septum. One patient had an infarct in the anterior and 1 in the posterior atria1 wall. The atria1 complex in the standard electrocardiogram showed various abnormalities in 5 of the 10 cases. In the right atria1 lead, the atria1 complex was abnormal shortly before death in 9 cases (Fig. 2). In
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Discussion
FIGURE 2. Standard and right atrial lead electrocardiograms and section from the lateral wall of the right atrium (hematoxylineosin X480, reduced by 24 percent). The patient was a 70 year old man-who died from cardiac rupture 9 hours after admission. The standard electrocardiogram showed an inferior myocardial infarction and abnormal atrial complexes with notching in the precordial leads (not illustrated). The right atrial lead (RA) shows split atrial complexes, sinoatrial block and ectopic atrial escape beats. The section from the right atrium shows irregular cross striation and a few granulocytes (arrow) indicating ischemia of some hours’ duration.
the 10th case a change in the P wave had occurred between the 2 recordings, but the pattern before death was considered normal by our criteria. This patient had an infarct in the anterior wall of the right atrium and no involvement of the lateral atria1 wall. In 2 cases the atria1 infarcts were judged to be more recent than the ventricular infarcts (Fig. 3 and 4). In both cases the configuration of the P wave in the right atria1 lead had changed from that on previous recordings shortly before the death of the patient. Arrhythmias occurred in 8 of the patients who died. Two of the 5 patients with histologically confirmed infarction of the lateral wall of the right atrium had atria1 fibrillation, 1 patient had sinoatrial block and 2 patients had A--V block. Two patients with atria1 infarction localized only to the anterior or posterior wall did not have atria1 arrhythmias or atrioventricular conduction disturbances. 454
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Abnormal atria1 complexes were found in the right atria1 lead in 68 percent of patients with acute ventricular infarction, whereas only 29 percent of the patients had abnormal atria1 complexes in the standard leads. This difference suggests that the right atria1 lead may be the more sensitive in detecting atria1 abnormalities in acute myocardial infarction. In 6 cases with abnormal atria1 complexes in the right atria1 lead, the right atrium was examined histologically. In 5 patients the infarct was localized to the lateral wall and in 1 patient to the posterior wall of the right atrium. The seventh patient whose right atrium was examined histologically showed no definite electrocardiographic atria1 abnormalities before death in the standard or right atria1 leads, although there was an infarct in the anterior wall of the right atrium. In 2 cases, histologic findings indicated that the atria1 complex in the right atria1 lead changed pari passu with the development of new lateral atria1 infarcts. These observations suggest that abnormal atria1 complexes reflect atria1 infarction, primarily of the lateral wall, that is, in the region of the sinus node. Changes of the atria1 complex and P-R segment similar to those found in patients with acute myocardial infarction have been found in patients with atria1 disorders due to valvular heart disease.20 Thus, the changes do not seem to be specific. However, it is not established whether the abnormal atrial complex in valvular heart disease is also due to ischemic changes in the atria1 myocardium. Insidence of atria1 infarcts: All 7 patients who died from myocardial infarction and whose right atrium was examined histologically had atria1 infarcts by histologic criteria. According to previous autopsy series, atria1 infarcts occur in 1 to 27 percent of all cases of ventricular myocardial infarcts.21,22 However, the number of reported cases is small in relation to the frequency of ventricular infarction. It may be that atria1 infarction, as several investigators have pointed out, is difficult to recognize even in postmortem examinations if systematic histologic examination is not performed. Our results support the statement by Sbderstrom7 that atria1 infarcts are “overlooked rather than rare.” Atria1 infarction and cardiac arrhythmias: Our study shows that atria1 involvement in acute myocardial infarction, as reflected by changes in the atrial complexes both in standard and in intracavitary leads, are associated with an increased incidence of arrhythmias. The findings suggest that pathologic changes of the atria1 complex in the right atria1 lead may be particularly related to atria1 arrhythmias and sinoatrial or atrioventricular conduction disturbances. However, the significance of this finding is difficult to evaluate because more than one type of arrhythmia occurred in several of the patients, and the number of patients in each group was small. Several factors may cause arrhythmias during acute myocardial infarction: infarction of the sinus node, ischemia of the A-V node, vagal and vagomi-
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atria1 distension and circulating metic reflexes, chronotropic substances. l5 The association found in our study between changes in the atria1 electrocardiographic complex and atria1 infarcts on the one hand, and between changes in the atria1 complex and arrhythmias on the other, is suggestive of a relation between atria1 infarcts and arrhythmias as well. Furthermore, in 6 of 7 cases in which the right atrium was examined histologically various types of arrhythmia were present. All 6 patients had infarcts in
the right atrium, and in 5 of the 6, the infarct was in the lateral wall of the right atrium; 3 of the latter patients had arrhythmias of atria1 origin. These observations agree with the concept that the most frequent cause of cardiac arrhythmias is ischemia due to localized circulatory disturbances. The circulatory disturbance may originate in the main coronary vessel occlusion, which results in the ventricular infarct, or in the appearance of thrombotic material in several small vessels. Experimentally, ar-
FIGURE 3. Standard and right atrial electrocardiograms and section from the anterior wall of the right atrium (hematoxylineosin X480, reduced by 24 percent). The patient was a 59 year old man who collapsed with ventricular fibrillation before hospital admission. Defibrillation was performed by an ambulance team. Shortly after admission he had another attack of ventricular fibrillation which was converted by electroshock. However, he did not regain consciousness and died 7 days later. The standard electrocardiogram showed inferior myocardial infarction and normal atrial complexes. Shortly before death atrioventricular block occurred. The right atrial lead (RA) shows changes of the atrial complexes from the first examination (left) to the second (right), which was performed 5 hours before the patient’s death. On the second examination grade II atrioventricular block was found. In sections from the lateral and anterior watls of the right atrium areas of irregular cross striation and slight accumulation of neutrophils were found (arrows). The appearance indicates an infarct of a few hours’ duration. Section from the left ventricle showed an infarct compatible with a history of 5 days.
FIGURE 4. Standard and right atrial electrocardiograms and sections from the lateral wall of the right atrium (hematoxylineosin X74, reduced by 25 percent). The patient was a 77 year old woman with multiple previous myocardial infarcts. She was discharged from the coronary care unit to the general ward 6 days after an uneventful acute infarct, and died suddenly from ventricular fibrillation on the following day. The atria1 complex iS abnormal in the standard and right atrial (RA) leads on admission (left). On the second examination a few hours before death, the right atrial electrocardiogram has changed and shows depression of the P-R segment [right). Sections from the lateral wall of right atrium show an infarct in the stage of resorption, compatible with 7 days’ duration (A), and small areas of quite recent necrosis (6).
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rhythmia and sudden death from myocardial infarction have been produced in pigs by creating myocardial microcirculatory disturbances by transient platelet aggregation. 23 Autopsy studies of cases of coronary heart disease have revealed the presence of larger and more numerous platelet aggregates in the myocardial circulation of patients who died suddenly, presumably from arrhythmias, than in control subjects.24~25 Platelet-fibrin masses were observed in the atria1 vessels in some patients in our series, but they were not quantified. In favor of a local ischemia-inducing factor such as platelet fibrin masses within the microcirculation was the fact that some of the atria1 infarcts were small and multifocal. Clinical implications: The association between abnormal atria1 complexes and the development of
arrhythmias may be clinically important, since abnormal atria1 complexes should be regarded as a warning signal. The right atria1 electrocardiogram seems to be superior to the standard lead electrocardiogram in detecting atria1 abnormalities, but has the disadvantage of being an invasive method and is therefore less suitable for routine use in patients with acute myocardial infarction. Studies of the atria1 complex in patients with acute myocardial infarction may give information of clinical value especially with regard to atria1 conduction disturbances, arrhythmias and left ventricular failure. The development of a noninvasive electrocardiographic method which allows better analysis of the P wave than that provided by the standard electrocardiogram would therefore be of practical value.
References 1. Scherf D, Schaffer Al: The electrocardiographic exercise test. Amer Heart J 43:927-943, 1952 2. Tranchesi J, Abeiardi V, Oliveira JM: Atrial repolarizationits importance in clinical electrocardiography. Circulation 22:635-644, 1960. 3. Sutnick AJ, Soloff LA: Posterior rotation of the atrial vector. An electrocardiographic sign of left ventricular failure. Circulation 26:913-916, 1962 4. Zimmerman HA, Bersano E, Dicosky C: The Auricular Electrocardiogram. Springfield, Ill, Charles C Thomas, 1968, p 54-64 5. von Gross D: Uber die Veranderungen der Vorhofzacke bei Myokardinfarkten. 2. Krejslaufforsch 59:262-270, 1969 6. Grossman JI, Deiman AJ: Serial P wave changes in acute myocardial infarction. Amer Heart J 77:336-341, 1969 7. Siiderstrom N: Myocardial infarction and mural thrombosis in the atria of the heart (abstr). Acta Med Stand 132: suppl 217:1-114.1948 8. Lepesckin E: Modern Electrocardiography. Baltimore, Williams & Wilkins, 1955, p 409 9. Liu CK, Greenspan G, Piccirillo RT: Atrial Infarction of the heart. Circulation 23:331-338, 1961 10. Meerschwam IS: A case of auricular infarct confirmed by endocavitary leads. Arch Mal Coeur 58:558-563, 1965 11. James TN, Geoghegan T: Sequential electrocardiographic changes following auricular injury. Amer Heart J 46:830843, 1953 12. Corsi V, Sangiorgi M, Coreili D: Contribution to the electrocardiographic localization of auricular myocardial damage. An experimental study. Cardiologia 23:255-273, 1953 13. Kiepacki Z, Pedich W: Intracardiac electrocardiographic leads in experimental atrial necrosis. Kardiol Pol 12:197202, 1969
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14. Kossmann CE, Berger AR, Rader B, et al: Intracardiac and intravascular potentials resulting from electrical activity in the normal human heart. Circulation 2:10-30, 1950 15. James TN: Myocardial infarction and atrial arrhythmias. Circulation 24:761-766, 1961 16. Ltpman, BS, Massie E: Clinical Scalar Electrocardiography, fifth edition. Chicago, Year Book Medical Publishers, 1965, p 250-258 17. Macruz R, Perioff JK, Case RB: A method for the electrocardiographic recognition of atrial enlargement. Circulation 17:882-889, 1958 18. Morris JJ, Estes EH Jr, Whalen RE, et al: P-wave analysis in valvular heart disease. Circulation 29:242-252, 1964 19. Sivertssen E: The atrial complex in right atrial electrocardiography. Angiology, in press 20. Sivertssen E: Right atrial electrocardiography (RA ECG) in the diagnosis of right and left atrial abnormalities. Angiology, in press 21. Cushing EH, Feii HS, Stanton EJ, et al: Infarction of the cardiac auricles (atria): clinical, pathological, and experimental studies. Brit Heart J 4117-34, 1942 22. Wartman WB, Heiierstein HK: The incidence of heart disease in 2000 consecutive autopsies. Ann Intern Med 28:41-65, 1948 23. Jorgensen L, Rowseii HC, Hovig T, et al: Adenosine diphosphate-induced platelet aggregation and myocardial infarction in swine. Lab Invest 17:616-644, 1967 24. Haerem JW: Sudden coronary death: the occurrence of platelet aggregates in the epicardial arteries of man. Atherosclerosis 14:417-432, 1971 25. Haerem JW: Platelet aggregates in intramyocardial vessels in patients dying suddenly and unexpectedly of coronary disease. Atherosclerosis 15:199-213, 1972
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