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Prominent R wave and shallow S wave in Lead V1 as a result of lateral myocardial infarction
PROMINENT R WAVE AND SHALLOW S WAVE IN LEAD RESULT OF LATERAL MYOCARDIAL INFARCTION I,. LEVY, II, M.D.,
H. J. JACOBS, M.D., H. P. CHASTANT, H. B. STRAUSS M.D.
NEW ORLEANS,
Vi AS A
M.D., AND
LA.
a recent study of electrocardiographic patterns in myocardial D URING infarction’ we observed a group of cases in which significant QRS changes were noted in the precordial Lead Vi. These consisted of an increase in amplitude of the R wave and decrease in amplitude of the S wave due to the absence of normal electromotive forces in the opposing left ventricular walls. It is the purpose of this communication to present twelve cases demonstrating such a pattern and to discuss its genesis. The sequence of normal ventricular activation has been depicted by Gardberg and Ashman. Four stages of ventricular activation may be utilized to describe the sequence of electrical activity which results in the QRS configuration usually obtained in Lead VI in adults. In the first stage, a small initial R wave results from septal activation .which causespositivity at the precordial electrode. This is probably due to a greater initial area of activation on the left side of the septum. In the second stage, depolarization of the septum progresses, and the wave front extends to involve the adjacent left and right ventricular walls and to break through the epicardial area of the apical region of the right ventricle, resulting in beginning ne,gativity at the precordial site. In the third stage, right ventricular activation has proceeded almost to completion, and maximal negativity results as the wave of excitation is spreading through the free and basilar walls of the left ventricle, the apical region of the left ventricle having become depolarized. The fourth stage results in decreased negativity due to shrinking of the shell of activation which is extending through the high lateral and basal walls of the left ventricle. The effects of activation in the pulmonary conus area have been neglected in the above discussion. A clear three-dimensional picture of electrical activation may be secured by referring to the paper by Gardberg and Ashman. The QRS changes produced by infarction as observed in our cases affect mainly stages two and three. The QRS configuration in Lead Vi is a resultant of electrical activity in opposing right and left ventricular walls, the septum not significantly affecting the potential in these stages. The process of infarction results in a disappearance of the deep S wave which normally appears and its replacement by a large R wave. This is due to absence of normal opposing electromotive forces in the left ventricle. The right and left ventricular areas From the Heart Station of Charity Hospital of Louisiana at New Orleans and the Department of Tnterual Medicine of Louisiana State University School of Medicine. Received for publication March 11, 1950. 447
a high nent
Fig. 1.-A. Case 1. There is a recent posterior rnyocardial infawtion R wave in VI followed by a small S wave in VI. B, Case 2. There is a recent anterolateral myorardial infarction with R wave in VI followed by a very small S wave in Vj.
C. Case in VI followed
3.
There is a posterolateral by a small S wave in VI.
mywardial
infarclion
with
wit,11
promirl~~rll
01 and
Q:,:, and
V:LI.:,.~ awl
VG and
a high
Qz,:~ and a pmmiIL wave
whose electromotive forces play a predominant role in the production of the JZRS configuration in Lead Vr will depend on the degree of rotation of the heart on its anteroposterior, longitudinal, and transverse axes.2 LTnless previous tracings have been made, once infarction has occurred the degree of rotation about the three axes is difficult to estimate from the electrocardiogram. The electrocardiograms of Figs. 1 to 4 were recorded from presented clinical pictures characteristic of myocardial infarction. limb leads and Leads VI through V ti were recorded in all cases.
patients who The standard A prominent
LEVY
ET
AL.:
LEAD
V, IN
Fig. 2.--O, Case 4. There is a healed Rv have in VI, E. Case 5. There is a recent posterolateral *en t R wave in VI. 3’. Case 6. There is it posterior myocardial
LATERAL
posterior
MYOCARDIAL
myocardial
myocardial infarction
infarction
infarction with
&?,a and
449
INFARCTION
with
with
QZ,S and
Q1,z.a and
a prominent
a prom
VS,~ and R wave
inont.
a pl -omiin VI.
R wave in VI occurred as a result of m\rocardial infarction localized elec trocar .diographically in the posterior wall in three cases (1, 4, 6), in the post erowall in one case (2). lat era1 wall in eight cases (3, 5, 7-12), and in the anterolateral In Cases 8 and 12 there was also a prominent R wave in Lead VR; this was due to the absence of opposing electrical effects in the posterolateral infarcted vvall.
.\CIERICz\N
HI:.\KT
JOURN.\
wave
in \ ,:;, VI’
and ,“a”(’
in 7
Although the variation in cardiac rotation accounts for the fact that the tential from slightly different ventricular areas exerts a prominent effec ‘t at PO’ xordial position 1, the area of the left ve,ntricle which yields the major par tion w electromotive forces consists of the lateral wall. In clock\; viseOf the opposing wall uill yield the major opposing force: i; in rot ated hearts the anterolateral
LEVY
ET
AI..
:
IX4D
VI
IN
LXTERAI,
MYOCARDIAI.
INFARCTION
451
Fig. 4.-J, Case 10. There is a posterolateral myorardial infarction with &?.a and V&,6 and promiR wave in VI. K, Case 11. There is a posterolateral myocardial infarction with Qr,s and VG and a high R wave in VI. L, Case 12. There is a post,erolateral myocardial infarction with Qx,a and VS. VP and a prominent R wave in VI, VR. VaR, VaR. V3R is taken at the fifth intercostal space in the right midclavicular line and VIR is taken at the fifth intercostal space in the anterior axillary line. nent
counterclockwise-rotated hearts the posterolateral wall will contribute the predominating opposing forces. Strictly posterior or posteroseptal infarction usually does not result in a high VI since electromotive forces produced in this area are directed mainly perpendicular to the frontal plane.
Just as one finds high ‘I‘ waveti frccluc~~~~I!, recortlctl fro111 ixccxxdial positiorrs 1, 2, and 3 when posterior ischemia with inverted T 2‘3 is present and depression of KS-T segments in the precordial leads seen opposite posterior injury, one ma>’ therefore expect at times to find QRS changes when leads are taken at chest areas where the predominant electromotive forces are directly opposed to those of the infarcted region. SUMMAKY
Twelve cases are presented with electrocardiograms showing a prominent R wave and decrease in amplitude of the S wave in Lead \:I due to myocardial infarction disturbing the normal opposing electromotive forces which cause it deep S wave in Lead VI. We wish to thank Dr. Richard of this subject and the consequent
Ashman completion
for his suggestions of this paper.
which
prompted
the
investigation
KEFI
Levy,
L, II, and Hyman, A.: Uifficultie,s in the Electrocardiographic Myocardial Infarction, AM. HEART J. 39243, 1950. Gardberg, M., and Ashman, R.: QRS Complex of Electrocardiogram, 72:210. 1943.
Interpretation &Arch.
Int.
of Med.
H. J. JACOBS, M.D., H. P. CHASTANT, H. B. STRAUSS M.D.
NEW ORLEANS,
Vi AS A
M.D., AND
LA.
a recent study of electrocardiographic patterns in myocardial D URING infarction’ we observed a group of cases in which significant QRS changes were noted in the precordial Lead Vi. These consisted of an increase in amplitude of the R wave and decrease in amplitude of the S wave due to the absence of normal electromotive forces in the opposing left ventricular walls. It is the purpose of this communication to present twelve cases demonstrating such a pattern and to discuss its genesis. The sequence of normal ventricular activation has been depicted by Gardberg and Ashman. Four stages of ventricular activation may be utilized to describe the sequence of electrical activity which results in the QRS configuration usually obtained in Lead VI in adults. In the first stage, a small initial R wave results from septal activation .which causespositivity at the precordial electrode. This is probably due to a greater initial area of activation on the left side of the septum. In the second stage, depolarization of the septum progresses, and the wave front extends to involve the adjacent left and right ventricular walls and to break through the epicardial area of the apical region of the right ventricle, resulting in beginning ne,gativity at the precordial site. In the third stage, right ventricular activation has proceeded almost to completion, and maximal negativity results as the wave of excitation is spreading through the free and basilar walls of the left ventricle, the apical region of the left ventricle having become depolarized. The fourth stage results in decreased negativity due to shrinking of the shell of activation which is extending through the high lateral and basal walls of the left ventricle. The effects of activation in the pulmonary conus area have been neglected in the above discussion. A clear three-dimensional picture of electrical activation may be secured by referring to the paper by Gardberg and Ashman. The QRS changes produced by infarction as observed in our cases affect mainly stages two and three. The QRS configuration in Lead Vi is a resultant of electrical activity in opposing right and left ventricular walls, the septum not significantly affecting the potential in these stages. The process of infarction results in a disappearance of the deep S wave which normally appears and its replacement by a large R wave. This is due to absence of normal opposing electromotive forces in the left ventricle. The right and left ventricular areas From the Heart Station of Charity Hospital of Louisiana at New Orleans and the Department of Tnterual Medicine of Louisiana State University School of Medicine. Received for publication March 11, 1950. 447
a high nent
Fig. 1.-A. Case 1. There is a recent posterior rnyocardial infawtion R wave in VI followed by a small S wave in VI. B, Case 2. There is a recent anterolateral myorardial infarction with R wave in VI followed by a very small S wave in Vj.
C. Case in VI followed
3.
There is a posterolateral by a small S wave in VI.
mywardial
infarclion
with
wit,11
promirl~~rll
01 and
Q:,:, and
V:LI.:,.~ awl
VG and
a high
Qz,:~ and a pmmiIL wave
whose electromotive forces play a predominant role in the production of the JZRS configuration in Lead Vr will depend on the degree of rotation of the heart on its anteroposterior, longitudinal, and transverse axes.2 LTnless previous tracings have been made, once infarction has occurred the degree of rotation about the three axes is difficult to estimate from the electrocardiogram. The electrocardiograms of Figs. 1 to 4 were recorded from presented clinical pictures characteristic of myocardial infarction. limb leads and Leads VI through V ti were recorded in all cases.
patients who The standard A prominent
LEVY
ET
AL.:
LEAD
V, IN
Fig. 2.--O, Case 4. There is a healed Rv have in VI, E. Case 5. There is a recent posterolateral *en t R wave in VI. 3’. Case 6. There is it posterior myocardial
LATERAL
posterior
MYOCARDIAL
myocardial
myocardial infarction
infarction
infarction with
&?,a and
449
INFARCTION
with
with
QZ,S and
Q1,z.a and
a prominent
a prom
VS,~ and R wave
inont.
a pl -omiin VI.
R wave in VI occurred as a result of m\rocardial infarction localized elec trocar .diographically in the posterior wall in three cases (1, 4, 6), in the post erowall in one case (2). lat era1 wall in eight cases (3, 5, 7-12), and in the anterolateral In Cases 8 and 12 there was also a prominent R wave in Lead VR; this was due to the absence of opposing electrical effects in the posterolateral infarcted vvall.
.\CIERICz\N
HI:.\KT
JOURN.\
wave
in \ ,:;, VI’
and ,“a”(’
in 7
Although the variation in cardiac rotation accounts for the fact that the tential from slightly different ventricular areas exerts a prominent effec ‘t at PO’ xordial position 1, the area of the left ve,ntricle which yields the major par tion w electromotive forces consists of the lateral wall. In clock\; viseOf the opposing wall uill yield the major opposing force: i; in rot ated hearts the anterolateral
LEVY
ET
AI..
:
IX4D
VI
IN
LXTERAI,
MYOCARDIAI.
INFARCTION
451
Fig. 4.-J, Case 10. There is a posterolateral myorardial infarction with &?.a and V&,6 and promiR wave in VI. K, Case 11. There is a posterolateral myocardial infarction with Qr,s and VG and a high R wave in VI. L, Case 12. There is a post,erolateral myocardial infarction with Qx,a and VS. VP and a prominent R wave in VI, VR. VaR, VaR. V3R is taken at the fifth intercostal space in the right midclavicular line and VIR is taken at the fifth intercostal space in the anterior axillary line. nent
counterclockwise-rotated hearts the posterolateral wall will contribute the predominating opposing forces. Strictly posterior or posteroseptal infarction usually does not result in a high VI since electromotive forces produced in this area are directed mainly perpendicular to the frontal plane.
Just as one finds high ‘I‘ waveti frccluc~~~~I!, recortlctl fro111 ixccxxdial positiorrs 1, 2, and 3 when posterior ischemia with inverted T 2‘3 is present and depression of KS-T segments in the precordial leads seen opposite posterior injury, one ma>’ therefore expect at times to find QRS changes when leads are taken at chest areas where the predominant electromotive forces are directly opposed to those of the infarcted region. SUMMAKY
Twelve cases are presented with electrocardiograms showing a prominent R wave and decrease in amplitude of the S wave in Lead \:I due to myocardial infarction disturbing the normal opposing electromotive forces which cause it deep S wave in Lead VI. We wish to thank Dr. Richard of this subject and the consequent
Ashman completion
for his suggestions of this paper.
which
prompted
the
investigation
KEFI
Levy,
L, II, and Hyman, A.: Uifficultie,s in the Electrocardiographic Myocardial Infarction, AM. HEART J. 39243, 1950. Gardberg, M., and Ashman, R.: QRS Complex of Electrocardiogram, 72:210. 1943.
Interpretation &Arch.
Int.
of Med.