- Email: [email protected]
Morphologic significance of left atrial involvement
Morphologic
si~dicance
of left atrial
invdvement
Donald W. Romhilt, M.D. Kevin E. Bove, M.D. Sandra Conradi, M.D. Ralph C. Scott, M.D. Cincinnati, Ohio
I
n 1964 Morris and colleagues’ reported that in many forms of left-sided heart disease a terminal negative deflection of the P wave in Lead Vr of 1 mm. or more in depth with a duration of 0.04 second or more was observed in the electrocardiogram (ECG). This electrocardiographic finding was termed “left atria1 involvement.” Although anatomic studies were not available, they noted that electrocardiographic evidence of left atria1 involvement sometimes occurred in patients with left-sided heart disease with normal mean left atria1 pressure and normal left atria1 size by radiologic examination. Despite the obvious limitations this type of P wave abnormality has commonly been equated with left atria1 enlargement or hypertrophy. In the following study Morris’s electrocardiographic sign of left atria1 involvement was correlated with anatomic evidence of atria1 and ventricular hypertrophy in 270 autopsied cases employing a chamber dissection technique for the determination of atria1 and ventricular hypertrophy.2
Methods Cases were selected for the chamber dissection technique at random from autopsies performed at the University of Cincinnati Medical Center from 1962 to 1968, provided at least one technically satisfactory 12 lead ECG taken within three months of death was available. Those cases with ECG’s displaying atria1 fibrillation or atria1 flutter on all available ECG’s within the three months prior to death were excluded. Cases with ECG’s having both atria1 fibrillation or flutter and sinus rhythm within three months of death were included. In these cases, only those ECG’s with normal sinus rhythm were evaluated for terminal negativity of the P wave in Lead Vr. The criteria used for the pathologic determination of atria1 and ventricular hypertrophy have been reported by Bove, Rowlands, and Scott.2 After removal of epicardial fat, each atrium, the ventricular septum, and each ventricle were isolated for the identification of hypertrophy. In hearts with normal ventricular weight, the
From the Division of Cardiology, Departments of Internal Medicine and Pathology, University of Cincinnati Medical Center, Cincinnati. Ohio 45229. Supported by United States Public Health Service Grants HE-08578, HE-6307, HE-5445 and HE-5776, and also in part by the Heart Association of Southwestern Ohio, Inc. Received for publication May 28, 1971. Reprint requests to: Donald W. Romhilt, M.D., Dept. of Internal Medicine, College of Medicine, University of Cincinnati, Cincinnati. Ohio 45229.
322
American
Heart
Journal
March, 1972
Vol. 83, No. 3, bp. 322-327
Volume Number
83 3
Left atria1 involvement
323
Table I* 1. Normal LV + S < 175 grams (< 200 grams if individual > 70 inches tall) RV < 65 grams (< 75 grams if individual > 70 inches tall) (LV + S)/RV = 2.1 to 3.6 2. Right ventricular hypertrophy A. Small heart LV + S = normal range RV = normal range (LV + S)/RV < 2.1 B. Large heart LV + S = normal range RV > 75 grams (LV+ S)/RV < 2.1 C. Combined ventricular hypertrophy with right ventricular predominance LV + S > 220 grams RV > 75 grams (LV + S)/RV < 2.1 3. Left ventricular hypertrophy A. Isolated left ventricular hypertrophy; small heart LV + S = normal range RV = normal range (LV + S),‘RV > 3.6 B. Isolated left ventricular hypertrophy; large heart LV + S > 200 grams RV < 75 grams (LV + S)/RV > 3.6 C. Combined ventricular hypertrophy with left ventricular predominance; LV + S = 175 to 220 grams (individuals < 70 inches tall) RV > 60 grams (individuals < 70 inches tall) (LV + S)/RV = normal D. Combined ventricular hypertrophy with left ventricular predominance; LV + S > 220 grams RV > 75 grams (LV + S)/RV = normal or high *Abbreviations:
LV.
left ventricle;
RV, right
ventricle;
LV + S. left ventricle
upper limit of observed weight for each atrium was 28 grams.2 The breadth of the range of normal values (11 to 28 grams) was attributed to variation in atria1 weight with body size, the considerable contribution of nondissectable atria1 adipose tissue to atria1 weight in some cases, and the unavoidable inclusion of a few hearts with mild undetectable ventricular hypertrophy. The broad range of normal weight observed indicates that in a given case this method is probably more suitable for the detection of substantial degrees of hypertrophy than for the rigid definition of normality. Atria weighing 29 grams or more were considered to be hypertrophied. In addition, when one atrium exceeded the other by 7 grams or more, it was considered to be hypertrophied, as previously reported,2 regardless of its absolute weight. The pathologic classification for ventricular
small heart
large heart
+ septum.
hypertrophy has been previously described (Table I) .2,3 All ECG’s were interpreted without knowledge of the pathologic findings. The criterion of left atria1 involvement described by Morris and colleagues’ was used, namely, the terminal negative portion of the P wave in Lead Vr is 1 mm. or more in depth with a duration of 0.04 second or more. A hand lens was used to aid in this determination. All ECG’s with normal sinus rhythm taken within three months of death were evaluated for left atria1 involvement. Results
At postmortem examination there were 127 hearts with detectable atria1 hypertrophy; 38 had left atria1 hypertrophy only, 48 hearts had right atria1 hypertrophy only, and 41 hearts had biatrial hypertrophy.
324
Romhilt
et al.
Table II. Correlation
of left atrid
involvement clnd driul
involvement
Left atria1 Postmortem
j&ding
Left atria1 hypertrophy only Right atrial hypertrophy ody Biatrial hypertrophy Total left atria1 hypertrophy Total right atria1 hypertrophy No atrial hypertrophy
I
Total
38 48 41 79 89 143
There were 143 hearts without detectable hypertrophy of either atrium. Of the 79 hearts with left atria1 hypertrophy, 35 (44.3 per cent) had left atrial involvement on the ECC;, and 31 (34.8 per cent) of the 89 hearts with right atria1 hypertrophy had left atria1 involvement on the ECG (Table II). Of the 143 hearts without atria1 hypertrophy, 32 (22.4 per cent) had left atria1 involvement on the EC(;; however, 23 of the 32 had ventricular hypertrophy. Despite the high incidence of left atria1 involvement in hearts without left atrial hypertrophy, there was a significant correlation between left atria1 involvement on the ECG and left atria1 hypertrophy (p < 0.01, chi square test) but not between left atria1 involvement on the ECG and right atria1 hypertrophy. Left atria1 involvement was also correlated with ventricular hypertrophy. One hundred and seventeen of the 270 hearts had left ventricular hypertrophy, 49 had right ventricular hypertrophy, and 104 were without ventricular hypertrophy. Fifty-two (44.4 per cent) of the 117 hearts with left ventricular hypertrophy had left atria1 involvement on the ECG, while 17 (34.7 per cent) of the 49 hearts with right ventricular hypertrophy had left atria1 involvement on the ECG (Table III). There was a significant correlation between left ventricular hypertrophy and left atria1 involvement on the ECG (p < 0.001, chi square test), but not between right ventricular hypertrophy and left atria1 involvement. The correlation of atria1 and ventricular hypertrophy (Table II I) shows that left atria1 involvement was more often present if left ventricular hypertrophy and left atria1 hypertrophy coexisted, than if
hypertrophy
----
1
No left atria1
inzlolcement ------
--_
No.
GI /(I
No.
18 14 17 35 31 32
47.4 29.2 41.5 44.3 34.8 22.4
20 34 24 44 58 111
/
c,’ 10
52.6 70.8 58.5 55.7 65.2 77.6
left ventricular hypertrophy and normal atria1 weight were present. There were 9 hearts (11.5 per cent) with left atria1 involvement on the ECG that did not have hypertrophy of either atria or ventricle at post mortem. This group of 9 patients had the following clinical findings: one had an acute myocardial infarction; 2 had fluid overload and pulmonary edema at the time of the ECG with left atria1 involvement; 3 had carcinoma of the lung, one of whom had pneumonia and congestive heart failure and the other two had old myocardial infarcts; and 3 had no apparent clinical cardiopulmonary findings. Thus, left atria1 involvement occurred in 3 (3.8 per cent) hearts that did not have any apparent cardiopulmonary abnormality. Electrocardiographic evidence of left atria1 involvement frequently was noted to be transient. It was present on all ECG’s in the three months prior to death in only 37 (45.7 per cent) of the 81 patients with left atrial involvement. If patients with only one ECG in the three months prior to death are excluded, only 16 (26.7 per cent) of 60 patients with multiple ECG’s had left atria1 involvement on all ECG’s in the three months prior to death. There was no difference in the incidence of postmortem left atria1 hypertrophy in the patients with transient left atria1 involvement compared to those with left atria1 involvement on all ECG’s. Discussion
Morris and colleagues’ initially described left atria1 involvement in patients with mitral and aortic valvular disease but recognized that it. could occur in any form of left-sided heart disease. The presence of
Volume Number
53 3
Left atria1 involvement
Table III. -
Correlation
of left atria1
Postmortem jinding
involvement and ventricular
Total
Left ventricular hypertrophy Left atria1 hypertrophy Biatrial hypertrophy Right atria1 hypertrophy Normal atria1 weight Right ventricular hypertrophy Right atria1 hypertrophy Biatrial hypertrophy Left atria1 hypertrophy Normal atria1 weight Without ventricular hypertrophy Normal atria1 weight Right atria1 hypertrophy Left atrial hypertrophy Biatrial hypertrophy
117
/
52 26 32 9 50
49
left atria1 involvement on the ECG has subsequently been described in patients with hypertensive cardiovascular disease.4 Morris and co-workers’ deliberately chose the term “left atria1 involvement” to describe the negative terminal force of the P wave in Vr, rather than left atria1 enlargement or left atria1 hypertrophy. Kasser and Kennedy5 reported a significant correlation between left atria1 involvement and changes in angiographically determined left atria1 volume and, to a lesser extent, increases in left atria1 pressure. Saunders and co-workers6 described a tendency for P wave abnormalities including left atria1 involvement to occur more frequently with larger left atria as observed at the time of open-heart surgery. We have demonstrated a significant correlation between the electrocardiographic finding of left atria1 involvement and postmortem evidence of left atria1 hypertrophy. This is in contrast to the findings of Mazzoleni and associates?who found a poor correlation between postmortem left atria1 hypertrophy and the duration of the P wave in the limb leads and the shift of the P axis to the left on the ECG. However, we did not find the terminal negative P wave vector to be a sensitive criterion for detecting left atria1 hypertrophy, since only 44.3
No.
44.4 57.7 43.8 44.4 38.0
65
34.7 36.0 33.3 66.7 26.7
32
9 2 2 4
11.5 11.5 7.1 11.1 33.3
92
9 1 1 1
12 78 14 9 3
%
No left atria1 involvement
1.5 14 4 19 17
25 6 3 15 104
hypertrophy
Left atria1 involvement ___-No.
325
/
%
11 18 5 31
55.6 42.3 56.2 55.6 62.0
16 4 1 11
65.3 64.0 66.7 33.3 73.3
69 13 8 2
88.5 88.5 92.9 88.9 66.7
per cent of the cases with left atria1 hypertrophy were recognized. Kasser and Kennedy5 found the accuracy of left atria1 involvement in predicting normal or increased left atria1 volume or pressure to be 66 per cent. In our study electrocardiographic evidence of left atria1 involvement would have correctly predicted normal or hypertrophied left atria in 66.7 per cent of the cases. The presence of left atria1 involvement in hearts with right atria1 hypertrophy only (29.2 per cent) is probably related to the lack of specificity in separating the P wave into left atria1 and right atria1 forces. This has been noted by Brody and colleagues* in normal subjects and by Chou and Helm9 in patients with P pulmonale. When our patients had left atria1 involvement on the ECG and right atria1 hypertrophy at post mortem, the presence of right atria1 hypertrophy was usually apparent on the ECG by the tall peaked P waves in Leads II, III, and aVr, and by a tall initial component of the P wave in Lead Vr, but this was not always true (Fig. 1). For this reason the interpretation of left atria1 involvement should be made cautiously in the presence of the findings of right atria1 enlargement on the ECG.
326
Romhilt
Am. Heart 3. March, 1972
et al.
Fig. 1. ECG tracing from a 67-year-old man with pulmonary emphysema, chronic bronchitis, and car pulmonale who died of pneumonia and respiratory insufficiency. There was no evidence of pulmonary edema or fluid overload at the time of the ECG. The QRS complexes are consistent with pulmonary emphysema and car pulmonale; in addition, left atria1 involvement is present. At postmortem, right atria1 and right ventricular hypertrophy were marked while the left atrium, left ventricle, and coronary arteries were normal.
The correlation between left atria1 involvement on the ECG and left ventricular hypertrophy at post mortem plus the lack of correlation with right ventricular hypertrophy supports the concept that left atria1 involvement reflects left-sided heart disease. Again the sensitivity of left atria1 involvement for the detection of left ventricular hypertrophy is not high (44.4 per cent). Despite the lack of correlation between left atria1 involvement on the ECG and right ventricular hypertrophy at post mortem, 34.7 per cent of hearts with anatomic right ventricular hypertrophy had the electrocardiographic finding of left atria1 involvement. The incidence of left atria1 involvement in hearts with right ventricular hypertrophy in some instances is probably related to the right atria1 hypertrophy that frequently accompanies right ventricular hypertrophy (Table III) and to the lack of specificity of separating the P wave into the left atria1 and right atria1 forces, as discussed above. The finding of only a 3.8 per cent incidence of left atria1 involvement in hearts without anatomic evidence of ventricular or atria1 hypertrophy or any clinical or postmortem findings of cardiopulmonary disease indicates that electrocardiographic evidence of left atria1 involvement is a specific criterion for heart disease. It was unexpected to find that electrocardiographic evidence of left atria1 involvement was transient in 54.3 per cent of these patients. We have demonstrated
that in patients with acute pulmonary edema, left atria1 involvement is commonly present during the acute episode and disappears upon resolution of the pulmonary edema.‘O Thus, it appears that the production of left atria1 involvement is the culmination of many variables including leftsided heart disease, left atria1 hypertrophy, left ventricular hypertrophy, sustained or temporary increases in left atria1 volume or pressure, and possibly intra-atria1 conduction delays. Summary
Left atria1 involvement, defined as the terminal negativity of the P wave in Lead Vr of 1 mm. or more in depth and a duration of 0.04 second or more, was evaluated in 270 autopsied caseswith the use of a chamber dissection technique for the determination of atria1 and ventricular hypertrophy. Left atria1 involvement was present in the following: 35 (44.3 per cent) of 79 hearts with left atria1 hypertrophy, 31 (34.8 per cent) of 89 hearts with right atria1 hypertrophy, 32 (22.4 per cent) of 143 hearts without atria1 hypertrophy, 52 (44.4 per cent) of 117 hearts with left ventricular hypertrophy, 17 (34.7 per cent) of 49 hearts with right ventricular hypertrophy, 9 (11.5 per cent) of 78 hearts without anatomic evidence of atria1 or ventricular hypertrophy, and 3 (3.8 per cent) of 78 hearts without anatomic evidence of atria1 or ventricular hypertrophy or any clinical or postmortem findings of cardiopulmonary
Volume Number
a3 3
disease. Left atria1 involvement has a significant correlation with left atria1 hypertrophy (p < 0.01) and left ventricular hypertrophy (p < 0.001). Left atria1 involvement was frequently noted to be transient. The presence of left atria1 involvement on the ECG appears to be the result of many factors including left-sided heart disease, left atria1 hypertrophy, left ventricular hypertrophy, increases in left atria1 volume or pressure, and possibly intra-atria1 conduction delays.
Left atria1 involvement
4.
5.
6.
7. REFERENCES Morris, J. J., Estes, E. H., Whalen, R. E., Thompson, H. K., and McIntosh, H. D.: Pwave analysis in valvular heart disease, Circulation 29:242, 1964. Bove, K. E., Rowlands, D. T., and Scott, R. C.: Observations on the assessment of cardiac hypertrophy utilizing a chamber partition techniaue. Circulation 33:.558, 1966. Rdmhilt, D. W., Bove, K. E., Norris, R. J., Conyers, E., Conradi, S., Rowlands, D. T., and Scott, R. C.: A critical appraisal of the electro-
8.
9. 10.
327
cardiographic criteria for the diagnosis of left ventricular hypertrophy, Circulation 40:185, 1969. Tarazi, R. C., Miller, A., Frohlich, E. D., and Dustan, H. P.: Electrocardiographic changes reflecting left atria1 abnormality in hypertension, Circulation 34:818, 1966. Kasser, I., and Kennedy, J. W.: The relationship of increased left atria1 volume and pressure to abnormal P waves on the electrocardiogram, Circulation 39:339, 1969. Saunders, J. L., Calatayud, J. B., Schulz, K. J., Maranhao. V.. Gooch. A. S.. and Goldberg. H.: Evaluation of’ECG criteria’ for P wave a&ormalities, AM. HEARTJ. 74:757, 1967. Mazzoleni, A., Wolff, R., Wolff, L., and Reiner, L.: Correlation between component cardiac weights and electrocardiographic patterns in 185 cases, Circulation 30:808, 1964. Brody, D. A., Cox, J. W., McEachran, A. B., Giles. H. H.. and Ruesta. V. 1.: Soatial oarameters and shape factors of the”norma1 a&al vectorcardiogram and its scalar components, Circulation 39:229, 1969. Chou, T. C., and Helm, R. A.: The pseudo P pulmonale, Circulation 32:96, 1965. Romhilt, D. W., and Scott, R. C.: Left atria1 involvement in acute pulmonary edema, AM.
HEARTJ. 83:328, 1972.
si~dicance
of left atrial
invdvement
Donald W. Romhilt, M.D. Kevin E. Bove, M.D. Sandra Conradi, M.D. Ralph C. Scott, M.D. Cincinnati, Ohio
I
n 1964 Morris and colleagues’ reported that in many forms of left-sided heart disease a terminal negative deflection of the P wave in Lead Vr of 1 mm. or more in depth with a duration of 0.04 second or more was observed in the electrocardiogram (ECG). This electrocardiographic finding was termed “left atria1 involvement.” Although anatomic studies were not available, they noted that electrocardiographic evidence of left atria1 involvement sometimes occurred in patients with left-sided heart disease with normal mean left atria1 pressure and normal left atria1 size by radiologic examination. Despite the obvious limitations this type of P wave abnormality has commonly been equated with left atria1 enlargement or hypertrophy. In the following study Morris’s electrocardiographic sign of left atria1 involvement was correlated with anatomic evidence of atria1 and ventricular hypertrophy in 270 autopsied cases employing a chamber dissection technique for the determination of atria1 and ventricular hypertrophy.2
Methods Cases were selected for the chamber dissection technique at random from autopsies performed at the University of Cincinnati Medical Center from 1962 to 1968, provided at least one technically satisfactory 12 lead ECG taken within three months of death was available. Those cases with ECG’s displaying atria1 fibrillation or atria1 flutter on all available ECG’s within the three months prior to death were excluded. Cases with ECG’s having both atria1 fibrillation or flutter and sinus rhythm within three months of death were included. In these cases, only those ECG’s with normal sinus rhythm were evaluated for terminal negativity of the P wave in Lead Vr. The criteria used for the pathologic determination of atria1 and ventricular hypertrophy have been reported by Bove, Rowlands, and Scott.2 After removal of epicardial fat, each atrium, the ventricular septum, and each ventricle were isolated for the identification of hypertrophy. In hearts with normal ventricular weight, the
From the Division of Cardiology, Departments of Internal Medicine and Pathology, University of Cincinnati Medical Center, Cincinnati. Ohio 45229. Supported by United States Public Health Service Grants HE-08578, HE-6307, HE-5445 and HE-5776, and also in part by the Heart Association of Southwestern Ohio, Inc. Received for publication May 28, 1971. Reprint requests to: Donald W. Romhilt, M.D., Dept. of Internal Medicine, College of Medicine, University of Cincinnati, Cincinnati. Ohio 45229.
322
American
Heart
Journal
March, 1972
Vol. 83, No. 3, bp. 322-327
Volume Number
83 3
Left atria1 involvement
323
Table I* 1. Normal LV + S < 175 grams (< 200 grams if individual > 70 inches tall) RV < 65 grams (< 75 grams if individual > 70 inches tall) (LV + S)/RV = 2.1 to 3.6 2. Right ventricular hypertrophy A. Small heart LV + S = normal range RV = normal range (LV + S)/RV < 2.1 B. Large heart LV + S = normal range RV > 75 grams (LV+ S)/RV < 2.1 C. Combined ventricular hypertrophy with right ventricular predominance LV + S > 220 grams RV > 75 grams (LV + S)/RV < 2.1 3. Left ventricular hypertrophy A. Isolated left ventricular hypertrophy; small heart LV + S = normal range RV = normal range (LV + S),‘RV > 3.6 B. Isolated left ventricular hypertrophy; large heart LV + S > 200 grams RV < 75 grams (LV + S)/RV > 3.6 C. Combined ventricular hypertrophy with left ventricular predominance; LV + S = 175 to 220 grams (individuals < 70 inches tall) RV > 60 grams (individuals < 70 inches tall) (LV + S)/RV = normal D. Combined ventricular hypertrophy with left ventricular predominance; LV + S > 220 grams RV > 75 grams (LV + S)/RV = normal or high *Abbreviations:
LV.
left ventricle;
RV, right
ventricle;
LV + S. left ventricle
upper limit of observed weight for each atrium was 28 grams.2 The breadth of the range of normal values (11 to 28 grams) was attributed to variation in atria1 weight with body size, the considerable contribution of nondissectable atria1 adipose tissue to atria1 weight in some cases, and the unavoidable inclusion of a few hearts with mild undetectable ventricular hypertrophy. The broad range of normal weight observed indicates that in a given case this method is probably more suitable for the detection of substantial degrees of hypertrophy than for the rigid definition of normality. Atria weighing 29 grams or more were considered to be hypertrophied. In addition, when one atrium exceeded the other by 7 grams or more, it was considered to be hypertrophied, as previously reported,2 regardless of its absolute weight. The pathologic classification for ventricular
small heart
large heart
+ septum.
hypertrophy has been previously described (Table I) .2,3 All ECG’s were interpreted without knowledge of the pathologic findings. The criterion of left atria1 involvement described by Morris and colleagues’ was used, namely, the terminal negative portion of the P wave in Lead Vr is 1 mm. or more in depth with a duration of 0.04 second or more. A hand lens was used to aid in this determination. All ECG’s with normal sinus rhythm taken within three months of death were evaluated for left atria1 involvement. Results
At postmortem examination there were 127 hearts with detectable atria1 hypertrophy; 38 had left atria1 hypertrophy only, 48 hearts had right atria1 hypertrophy only, and 41 hearts had biatrial hypertrophy.
324
Romhilt
et al.
Table II. Correlation
of left atrid
involvement clnd driul
involvement
Left atria1 Postmortem
j&ding
Left atria1 hypertrophy only Right atrial hypertrophy ody Biatrial hypertrophy Total left atria1 hypertrophy Total right atria1 hypertrophy No atrial hypertrophy
I
Total
38 48 41 79 89 143
There were 143 hearts without detectable hypertrophy of either atrium. Of the 79 hearts with left atria1 hypertrophy, 35 (44.3 per cent) had left atrial involvement on the ECC;, and 31 (34.8 per cent) of the 89 hearts with right atria1 hypertrophy had left atria1 involvement on the ECG (Table II). Of the 143 hearts without atria1 hypertrophy, 32 (22.4 per cent) had left atria1 involvement on the EC(;; however, 23 of the 32 had ventricular hypertrophy. Despite the high incidence of left atria1 involvement in hearts without left atrial hypertrophy, there was a significant correlation between left atria1 involvement on the ECG and left atria1 hypertrophy (p < 0.01, chi square test) but not between left atria1 involvement on the ECG and right atria1 hypertrophy. Left atria1 involvement was also correlated with ventricular hypertrophy. One hundred and seventeen of the 270 hearts had left ventricular hypertrophy, 49 had right ventricular hypertrophy, and 104 were without ventricular hypertrophy. Fifty-two (44.4 per cent) of the 117 hearts with left ventricular hypertrophy had left atria1 involvement on the ECG, while 17 (34.7 per cent) of the 49 hearts with right ventricular hypertrophy had left atria1 involvement on the ECG (Table III). There was a significant correlation between left ventricular hypertrophy and left atria1 involvement on the ECG (p < 0.001, chi square test), but not between right ventricular hypertrophy and left atria1 involvement. The correlation of atria1 and ventricular hypertrophy (Table II I) shows that left atria1 involvement was more often present if left ventricular hypertrophy and left atria1 hypertrophy coexisted, than if
hypertrophy
----
1
No left atria1
inzlolcement ------
--_
No.
GI /(I
No.
18 14 17 35 31 32
47.4 29.2 41.5 44.3 34.8 22.4
20 34 24 44 58 111
/
c,’ 10
52.6 70.8 58.5 55.7 65.2 77.6
left ventricular hypertrophy and normal atria1 weight were present. There were 9 hearts (11.5 per cent) with left atria1 involvement on the ECG that did not have hypertrophy of either atria or ventricle at post mortem. This group of 9 patients had the following clinical findings: one had an acute myocardial infarction; 2 had fluid overload and pulmonary edema at the time of the ECG with left atria1 involvement; 3 had carcinoma of the lung, one of whom had pneumonia and congestive heart failure and the other two had old myocardial infarcts; and 3 had no apparent clinical cardiopulmonary findings. Thus, left atria1 involvement occurred in 3 (3.8 per cent) hearts that did not have any apparent cardiopulmonary abnormality. Electrocardiographic evidence of left atria1 involvement frequently was noted to be transient. It was present on all ECG’s in the three months prior to death in only 37 (45.7 per cent) of the 81 patients with left atrial involvement. If patients with only one ECG in the three months prior to death are excluded, only 16 (26.7 per cent) of 60 patients with multiple ECG’s had left atria1 involvement on all ECG’s in the three months prior to death. There was no difference in the incidence of postmortem left atria1 hypertrophy in the patients with transient left atria1 involvement compared to those with left atria1 involvement on all ECG’s. Discussion
Morris and colleagues’ initially described left atria1 involvement in patients with mitral and aortic valvular disease but recognized that it. could occur in any form of left-sided heart disease. The presence of
Volume Number
53 3
Left atria1 involvement
Table III. -
Correlation
of left atria1
Postmortem jinding
involvement and ventricular
Total
Left ventricular hypertrophy Left atria1 hypertrophy Biatrial hypertrophy Right atria1 hypertrophy Normal atria1 weight Right ventricular hypertrophy Right atria1 hypertrophy Biatrial hypertrophy Left atria1 hypertrophy Normal atria1 weight Without ventricular hypertrophy Normal atria1 weight Right atria1 hypertrophy Left atrial hypertrophy Biatrial hypertrophy
117
/
52 26 32 9 50
49
left atria1 involvement on the ECG has subsequently been described in patients with hypertensive cardiovascular disease.4 Morris and co-workers’ deliberately chose the term “left atria1 involvement” to describe the negative terminal force of the P wave in Vr, rather than left atria1 enlargement or left atria1 hypertrophy. Kasser and Kennedy5 reported a significant correlation between left atria1 involvement and changes in angiographically determined left atria1 volume and, to a lesser extent, increases in left atria1 pressure. Saunders and co-workers6 described a tendency for P wave abnormalities including left atria1 involvement to occur more frequently with larger left atria as observed at the time of open-heart surgery. We have demonstrated a significant correlation between the electrocardiographic finding of left atria1 involvement and postmortem evidence of left atria1 hypertrophy. This is in contrast to the findings of Mazzoleni and associates?who found a poor correlation between postmortem left atria1 hypertrophy and the duration of the P wave in the limb leads and the shift of the P axis to the left on the ECG. However, we did not find the terminal negative P wave vector to be a sensitive criterion for detecting left atria1 hypertrophy, since only 44.3
No.
44.4 57.7 43.8 44.4 38.0
65
34.7 36.0 33.3 66.7 26.7
32
9 2 2 4
11.5 11.5 7.1 11.1 33.3
92
9 1 1 1
12 78 14 9 3
%
No left atria1 involvement
1.5 14 4 19 17
25 6 3 15 104
hypertrophy
Left atria1 involvement ___-No.
325
/
%
11 18 5 31
55.6 42.3 56.2 55.6 62.0
16 4 1 11
65.3 64.0 66.7 33.3 73.3
69 13 8 2
88.5 88.5 92.9 88.9 66.7
per cent of the cases with left atria1 hypertrophy were recognized. Kasser and Kennedy5 found the accuracy of left atria1 involvement in predicting normal or increased left atria1 volume or pressure to be 66 per cent. In our study electrocardiographic evidence of left atria1 involvement would have correctly predicted normal or hypertrophied left atria in 66.7 per cent of the cases. The presence of left atria1 involvement in hearts with right atria1 hypertrophy only (29.2 per cent) is probably related to the lack of specificity in separating the P wave into left atria1 and right atria1 forces. This has been noted by Brody and colleagues* in normal subjects and by Chou and Helm9 in patients with P pulmonale. When our patients had left atria1 involvement on the ECG and right atria1 hypertrophy at post mortem, the presence of right atria1 hypertrophy was usually apparent on the ECG by the tall peaked P waves in Leads II, III, and aVr, and by a tall initial component of the P wave in Lead Vr, but this was not always true (Fig. 1). For this reason the interpretation of left atria1 involvement should be made cautiously in the presence of the findings of right atria1 enlargement on the ECG.
326
Romhilt
Am. Heart 3. March, 1972
et al.
Fig. 1. ECG tracing from a 67-year-old man with pulmonary emphysema, chronic bronchitis, and car pulmonale who died of pneumonia and respiratory insufficiency. There was no evidence of pulmonary edema or fluid overload at the time of the ECG. The QRS complexes are consistent with pulmonary emphysema and car pulmonale; in addition, left atria1 involvement is present. At postmortem, right atria1 and right ventricular hypertrophy were marked while the left atrium, left ventricle, and coronary arteries were normal.
The correlation between left atria1 involvement on the ECG and left ventricular hypertrophy at post mortem plus the lack of correlation with right ventricular hypertrophy supports the concept that left atria1 involvement reflects left-sided heart disease. Again the sensitivity of left atria1 involvement for the detection of left ventricular hypertrophy is not high (44.4 per cent). Despite the lack of correlation between left atria1 involvement on the ECG and right ventricular hypertrophy at post mortem, 34.7 per cent of hearts with anatomic right ventricular hypertrophy had the electrocardiographic finding of left atria1 involvement. The incidence of left atria1 involvement in hearts with right ventricular hypertrophy in some instances is probably related to the right atria1 hypertrophy that frequently accompanies right ventricular hypertrophy (Table III) and to the lack of specificity of separating the P wave into the left atria1 and right atria1 forces, as discussed above. The finding of only a 3.8 per cent incidence of left atria1 involvement in hearts without anatomic evidence of ventricular or atria1 hypertrophy or any clinical or postmortem findings of cardiopulmonary disease indicates that electrocardiographic evidence of left atria1 involvement is a specific criterion for heart disease. It was unexpected to find that electrocardiographic evidence of left atria1 involvement was transient in 54.3 per cent of these patients. We have demonstrated
that in patients with acute pulmonary edema, left atria1 involvement is commonly present during the acute episode and disappears upon resolution of the pulmonary edema.‘O Thus, it appears that the production of left atria1 involvement is the culmination of many variables including leftsided heart disease, left atria1 hypertrophy, left ventricular hypertrophy, sustained or temporary increases in left atria1 volume or pressure, and possibly intra-atria1 conduction delays. Summary
Left atria1 involvement, defined as the terminal negativity of the P wave in Lead Vr of 1 mm. or more in depth and a duration of 0.04 second or more, was evaluated in 270 autopsied caseswith the use of a chamber dissection technique for the determination of atria1 and ventricular hypertrophy. Left atria1 involvement was present in the following: 35 (44.3 per cent) of 79 hearts with left atria1 hypertrophy, 31 (34.8 per cent) of 89 hearts with right atria1 hypertrophy, 32 (22.4 per cent) of 143 hearts without atria1 hypertrophy, 52 (44.4 per cent) of 117 hearts with left ventricular hypertrophy, 17 (34.7 per cent) of 49 hearts with right ventricular hypertrophy, 9 (11.5 per cent) of 78 hearts without anatomic evidence of atria1 or ventricular hypertrophy, and 3 (3.8 per cent) of 78 hearts without anatomic evidence of atria1 or ventricular hypertrophy or any clinical or postmortem findings of cardiopulmonary
Volume Number
a3 3
disease. Left atria1 involvement has a significant correlation with left atria1 hypertrophy (p < 0.01) and left ventricular hypertrophy (p < 0.001). Left atria1 involvement was frequently noted to be transient. The presence of left atria1 involvement on the ECG appears to be the result of many factors including left-sided heart disease, left atria1 hypertrophy, left ventricular hypertrophy, increases in left atria1 volume or pressure, and possibly intra-atria1 conduction delays.
Left atria1 involvement
4.
5.
6.
7. REFERENCES Morris, J. J., Estes, E. H., Whalen, R. E., Thompson, H. K., and McIntosh, H. D.: Pwave analysis in valvular heart disease, Circulation 29:242, 1964. Bove, K. E., Rowlands, D. T., and Scott, R. C.: Observations on the assessment of cardiac hypertrophy utilizing a chamber partition techniaue. Circulation 33:.558, 1966. Rdmhilt, D. W., Bove, K. E., Norris, R. J., Conyers, E., Conradi, S., Rowlands, D. T., and Scott, R. C.: A critical appraisal of the electro-
8.
9. 10.
327
cardiographic criteria for the diagnosis of left ventricular hypertrophy, Circulation 40:185, 1969. Tarazi, R. C., Miller, A., Frohlich, E. D., and Dustan, H. P.: Electrocardiographic changes reflecting left atria1 abnormality in hypertension, Circulation 34:818, 1966. Kasser, I., and Kennedy, J. W.: The relationship of increased left atria1 volume and pressure to abnormal P waves on the electrocardiogram, Circulation 39:339, 1969. Saunders, J. L., Calatayud, J. B., Schulz, K. J., Maranhao. V.. Gooch. A. S.. and Goldberg. H.: Evaluation of’ECG criteria’ for P wave a&ormalities, AM. HEARTJ. 74:757, 1967. Mazzoleni, A., Wolff, R., Wolff, L., and Reiner, L.: Correlation between component cardiac weights and electrocardiographic patterns in 185 cases, Circulation 30:808, 1964. Brody, D. A., Cox, J. W., McEachran, A. B., Giles. H. H.. and Ruesta. V. 1.: Soatial oarameters and shape factors of the”norma1 a&al vectorcardiogram and its scalar components, Circulation 39:229, 1969. Chou, T. C., and Helm, R. A.: The pseudo P pulmonale, Circulation 32:96, 1965. Romhilt, D. W., and Scott, R. C.: Left atria1 involvement in acute pulmonary edema, AM.
HEARTJ. 83:328, 1972.