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Interpretation of RSR′ in pulmonic stenosis
Clinical
communications
Interpretation
of RSR’ in pulmonic
R. Curtis Ellison, Washington, D.C. Olli S. Miettinen,
stenosis
M.D.* M.D., Ph.D.
Boston, Mass.
For The Joint Defects**
Study on the Natural
History
of Congenital
It has been suggested that in pulmonic stenosis (PSI a ventricular complex with an RSR’ pattern in Lead V, tends to indicate less severe disease than does a “pure R-wave.“1-5 The present study was undertaken (1) to test this proposition in a large series, and (2) to determine how the magnitude of the R’ voltage relates to that of “pure R” at comparable levels of PS severity. Patients and methods
The data were derived laborative follow-up study heart defects. A total of tients with isolated valvular
Received
for publication
September
Reprint requests to: O.S. Miettinen, gy, Harvard School of Public Health, Mass. 02115. ‘Present Address: Pediatric pital, 3600 Reservoir Rd,
from a national colof three congenital 603 nonoperated paPS, demonstrated at
24, 1973. M.D., Department 665 Huntington
Cardiology, Georgetown N.W., Washington, DC.
of EpidemioloAvenue, Boston, University 29907.
Hos-
**The Joint Study on the Natural History of Congenital Heart Defects is sponsored by grant HL 10986 and other grants from the National Heart and Lung Institute and is a collaborative study involving the following institutions and investigators: The University of Colorado Medical Center and School of Medicine, Denver, Colorado (S.G. Blount, L.L. Kelminson, J. Nora, R. Spanglerl; Columbia-Presbyterian Medical Center - Babies Hospital, College of Physicians and Surgeons of Columbia University, New York, New York (S. Blumenthal, W.M. Gersony, H. Gelband, C.J. Hayes, M.J. Jesse, E. Krongradl; Mayo Clinic and Mayo Medical School, Rochester, Minnesota (J.W. DuShane, W.H. Weidman); Buffalo Children’s Hospital, State University of New York at Buffalo, Buffalo, New York (E.C. Lambert, H.R. Wagner, A.R. Hohnl; The Children’s Hospital Medical Center, Harvard Medical School, Boston, Massachusetts. (A.S. Nadas, R.C. Ellison, A. Goldblatt, J.F. Keane, W.H. Plauth); and Johns Hopkins Medical School and Hospital, Baltimore, Maryland (RD. Rowe, R.M. Freedom, J.O. Humphries, C.A. Neill, E.W. Nugent, J. Padmanabhan, P.J. Varghese). The coordinating center for the study is the Harvard School of Public Health, Boston, Massachusetts (OS. Miettinen); S.C. Mitchell and E.M.K. Dar-by provide liaison with the National Heart and Lung Institute.
July, 1974, Vol. 88, No. 1, pp. 7-10
Heart
cardiac catheterization, were admitted to that study. The admission data of 539 of these patients were analyzed. The primary reason for exclusion was incompleteness of data. Also, in order to prevent difficulty in interpretation due to bundle branch block, any patient was excluded if the QRS duration exceeded the following limits: for infants in their first year of life, 80 msec.; in the 1 to 7 year category, 90 msec.; and in patients 8 years of age or older, 100 msec. Measurements of right ventricular systolic pressure (RVSP) and gradient across the pulmonic valve (PVG) were made at routine cardiac catheterization, with the patient in a resting state and under light sedation (a mixture of demerol, 25 mg. per milliliter; phenergan, 6.25 mg. per milliliter; and chlorpromazine, 6.25 mg. per milliliter in a dosage of 1 ml. per 20 pounds of body weight, up to a maximum dose of 2.0 ml.). Measurements of the R, S, and R’ voltages of Lead V, had been made from the standard electrocardiogram at the participating clinics. The ventricular complex was classified as an RSR’ pattern if, in the positive deflection, there was a notch which returned to, or reached below, the isoelectric line, and if the second positive component exceeded the first CR’ > RX There were 108 patients with such an RSR’ pattern fR’ Group), leaving 431 patients with an R pattern (R Group). (The latter group included 17 patients who had a second positive deflection which was smaller than the first. These second deflections averaged only 2.6 mm., and a multivariate analysis indicated that they were uninformative in estimating RVSP or PVG.) The R’ and R groups had similar distributions of age and QRS duration. The median ages were American
Heart Journal
7
Ellison
and
Miettinen
. 250
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Fig. 1. A, The right ventricular systolic pressure (RVSP) related to the voltage of the R-wave in Lead VI in 108 patients with pulmonic stenosis and an RSR’ pattern. The regression equation is RVSP (mm. Hg) = 54.2 + (1.45) R’, where R’ is deflection in millimeters (1 mm. = 0.1 mV.). B, The right ventricular systolic pressure related to the voltage of the R-wave in Lead VI in 414 patients with pulmonic stenosis and a “pure R” \?rave in Lead Vr between 1 and 36 mm. The regression equation is RVSP (mm. Hg) = 47.4 + (2.92) R, where R is deflection in millimeters (1 mm. = 0.1 mV.1.
9.4 and 8.4 years, respectively, with ranges from 0.0 to 52 years and from 0.1 to 50 years, respectively. For QRS duration the mean values were 76 msec. for the R’ Group and 73 msec. for the R Group. The severity implications of the presence of an RSR’ pattern were evaluated by comparing the R’ and R groups with respect to the distributions of RVSP and PVG. To evaluate what magnitude of R’ compares to a particular value of R in terms of similar severity, RVSP and PVG were related to the voltage of R’ in the R’ Group and to that of R in the R Group. The respective regression parameters were compared.
Results The values of RVSP and PVG in the R’ Group were generally lower than in the R Group, as shown in Table I.
8
The relationship of RVSP to voltage is shown separately for the R’ and R groups in Fig. 1. For the R’ Group, the regression equation is RVSP (mm. Hg) = 54.2 + (1.45) R’ and for the entire R Group, it is RVSP (mm. Hg) = 50.3 + (2.66) R, where the voltages are entered in terms of millimeters deflection (1 mm. = 0.1 mV.). In Fig. 1, A, all 108 patients with an RSR’ pattern are shown. Fig. 1, B shows the 414 patients of the R Group who had values of R between 1 and 36 mm., which corresponded to the range of voltages found in the R’ Group; for these 414 patients, RVSP (mm. Hg) = 47.4 + (2.92) R. The above equations indicate a significantly greater increase in RVSP for a given increase in voltage for a pure RIwave than for an RI-wave (for the slope difference, two-sided p=O.OOl). From the regression equations it is possible to determine an equivalent R magnitude for a given R’ voltage:
July, 1974, Vol. 88, No. 1
Interpretation
“Equivalent R” = (0.5) R’ + 2 mm. Thus, when utilizing the voltages in Lead V, in attempting to estimate severity in pulmonic stenosis, an observed R’ voltage is estimated to have the same meaning as an R voltage whose magnitude is one-half the R’ deflection plus 2 mm. For example, an R’ magnitude of 20 mm. would be the equivalent of a pure R magnitude of (0.5) 20 mm. + 2 mm. = 12 mm. When using PVG in place of RVSP, the equivalence relationship between R’ and R was identical to that determined with RVSP. Discussion
One goal of the Natural History Study of congenital heart defects has been to attempt to estimate severity from the clinical picture, electrocardiogram, and chest x-ray. At the onset of this endeavor in PS, it was found that 20 per cent of the patients showed an RSR’ pattern in Lead V, with a dominant RI-wave. Since the voltage of the dominant positive deflection in Lead V, is one of the factors utilized in the assessment of severity (the final result of which will be presented in a subsequent publication), this study was designed primarily to determine how the magnitude of an R’-wave should be interpreted, in comparison with an R-wave, in the estimation of severity in PS. Although an RSR’ pattern in Lead V, is more frequently associated with the presence of an atrial-septal defect or other type of volume overload of the right ventricle, it is not uncommonly found in patients with PS. Most investigators report that such cases usually show only mild or moderate degrees of obstruction; the pattern is rarely seen in patients with severe disease.1-5 The mechanism producing this pattern in patients with PS is unknown. Studies by Blount, Munyan, and Hoffman1 of atrial-septal defect indicated that the terminal forces producing an R’ in Lead V, resulted from hypertrophy of the outflow tract of the right ventricle. Boineau, Spach, and Ayers6 produced a similar electrocardiographic pattern by creating atrial-septal defects in dogs. They found the pattern to be related to dilatation of the right ventricle and hypertrophy of the high free wall of the right ventricle and of the crista supraventricularis; no evidence for abnormalities in the conducting system were found. Fowler4 found a pattern of terminal conduction delay by vectorcardiogram
American
Heart Journal
of RSR’ in pulmonic
stenosis
I. Comparison of RVSP and PVG in R Group and R Group Table
R’ Group
R Group
cn = 1081
In = 431)
R VSP: Range Mean Median
31-205
(mm. 73 71
Hg)
28-260
(mm. 89 79
Hg)
PVG: Range Mean Median RVSP = right ventricular PVG = pulmonic-valve
14-190 55 51 systolic gradient.
15-240 70 59
pressure.
in a high percentage of patients with mild PS; he suggested mild dilatation of the right ventricle, similar to that occurring in atrial-septal defect, as a possible mechanism for the vectorcardiographic finding. The present study supports the contention that in PS the presence of an RSR’ pattern in Lead V, suggests less severe disease than the presence of a QR, R, or RS pattern. However, the severity difference between patients with a dominant R’ and those with an R-wave appears to be rather small, and the severity varies widely in both groups. The study also suggests that for a given voltage of a dominant R’-wave the severity tends to be lesser than for a pure R-wave of equal magnitude. Thus, for any given R’ there is a smaller “equivalent R” corresponding to the same degree of severity. Use of the attenuated value for R should improve the correlation between the electrocardiogram and the hemodynamic state in patients with pulmonic stenosis. Summary
An RSR’ pattern in Lead V, (with R’ the dominant positive deflection) was found in 108 of 539 patients (20 per cent) with valvular pulmonic stenosis admitted to a national co-operative study of congenital heart defects. On the average, patients with an RSR’ pattern showed lower right ventricular-to-pulmonary artery pressure gradients (mean = 55 mm. Hg) than patients with a QR, R, or RS pattern (mean = 70 mm. Hg). Moreover, an R’-wave of a given voltage was associated with generally lower right ventricular systolic pressures and gradients than an R-wave of equal amplitude. Quantitatively, these data
9
Ellison
and
Miettinen
suggest that in patients with an RSR’ complex in Lead V,, the R’ voltage has the same severity implication as a “pure R” of magnitude (0.5) R’ + 2 mm. REFERENCES 1.
2.
10
Blount, S. G., Jr., Munyan, E. A., Jr., and Hoffman, M. S.: Hypertrophy of the right ventricular outflow tract. A concept of the electrocardiographic findings in atrial-septal defect, Am. J. Med. 22~784, 1957. Bassingthwaighte, J. B., Parkin, T. W., DuShane, J. W.,
3.
4. 5. 6.
Wood, E. H., and Burchell, H. B.: The electrocardiographic and hemodynamic findings in pulmonary stenosis with intact ventricular septum, Circulation 28:983, 1963. Burch, G. E., and DePasquale, N. P.: Electrocardiography in the diagnosis of congenital heart disease, Philadelphia, 1967, Lea and Febiger, p. 320. Fowler, R. S.: Terminal QRS conduction delay in pulmonary stenosis in children, Am. J. Cardiol. 21:669, 1968. Nadas, A. S., and Fyler, D. C.: Pediatric cardiology, Philadelnhia. 1972. W. B. Saunders Co.. D. 543. Boineau,*J. P., Spach, M. S., and Ayers,‘d. R.: Genesis of the electrocardiogram in atrial-septal defect, AM. HEART J. 68:637, 1964.
July, 1974, Vol. 88, No. 1
communications
Interpretation
of RSR’ in pulmonic
R. Curtis Ellison, Washington, D.C. Olli S. Miettinen,
stenosis
M.D.* M.D., Ph.D.
Boston, Mass.
For The Joint Defects**
Study on the Natural
History
of Congenital
It has been suggested that in pulmonic stenosis (PSI a ventricular complex with an RSR’ pattern in Lead V, tends to indicate less severe disease than does a “pure R-wave.“1-5 The present study was undertaken (1) to test this proposition in a large series, and (2) to determine how the magnitude of the R’ voltage relates to that of “pure R” at comparable levels of PS severity. Patients and methods
The data were derived laborative follow-up study heart defects. A total of tients with isolated valvular
Received
for publication
September
Reprint requests to: O.S. Miettinen, gy, Harvard School of Public Health, Mass. 02115. ‘Present Address: Pediatric pital, 3600 Reservoir Rd,
from a national colof three congenital 603 nonoperated paPS, demonstrated at
24, 1973. M.D., Department 665 Huntington
Cardiology, Georgetown N.W., Washington, DC.
of EpidemioloAvenue, Boston, University 29907.
Hos-
**The Joint Study on the Natural History of Congenital Heart Defects is sponsored by grant HL 10986 and other grants from the National Heart and Lung Institute and is a collaborative study involving the following institutions and investigators: The University of Colorado Medical Center and School of Medicine, Denver, Colorado (S.G. Blount, L.L. Kelminson, J. Nora, R. Spanglerl; Columbia-Presbyterian Medical Center - Babies Hospital, College of Physicians and Surgeons of Columbia University, New York, New York (S. Blumenthal, W.M. Gersony, H. Gelband, C.J. Hayes, M.J. Jesse, E. Krongradl; Mayo Clinic and Mayo Medical School, Rochester, Minnesota (J.W. DuShane, W.H. Weidman); Buffalo Children’s Hospital, State University of New York at Buffalo, Buffalo, New York (E.C. Lambert, H.R. Wagner, A.R. Hohnl; The Children’s Hospital Medical Center, Harvard Medical School, Boston, Massachusetts. (A.S. Nadas, R.C. Ellison, A. Goldblatt, J.F. Keane, W.H. Plauth); and Johns Hopkins Medical School and Hospital, Baltimore, Maryland (RD. Rowe, R.M. Freedom, J.O. Humphries, C.A. Neill, E.W. Nugent, J. Padmanabhan, P.J. Varghese). The coordinating center for the study is the Harvard School of Public Health, Boston, Massachusetts (OS. Miettinen); S.C. Mitchell and E.M.K. Dar-by provide liaison with the National Heart and Lung Institute.
July, 1974, Vol. 88, No. 1, pp. 7-10
Heart
cardiac catheterization, were admitted to that study. The admission data of 539 of these patients were analyzed. The primary reason for exclusion was incompleteness of data. Also, in order to prevent difficulty in interpretation due to bundle branch block, any patient was excluded if the QRS duration exceeded the following limits: for infants in their first year of life, 80 msec.; in the 1 to 7 year category, 90 msec.; and in patients 8 years of age or older, 100 msec. Measurements of right ventricular systolic pressure (RVSP) and gradient across the pulmonic valve (PVG) were made at routine cardiac catheterization, with the patient in a resting state and under light sedation (a mixture of demerol, 25 mg. per milliliter; phenergan, 6.25 mg. per milliliter; and chlorpromazine, 6.25 mg. per milliliter in a dosage of 1 ml. per 20 pounds of body weight, up to a maximum dose of 2.0 ml.). Measurements of the R, S, and R’ voltages of Lead V, had been made from the standard electrocardiogram at the participating clinics. The ventricular complex was classified as an RSR’ pattern if, in the positive deflection, there was a notch which returned to, or reached below, the isoelectric line, and if the second positive component exceeded the first CR’ > RX There were 108 patients with such an RSR’ pattern fR’ Group), leaving 431 patients with an R pattern (R Group). (The latter group included 17 patients who had a second positive deflection which was smaller than the first. These second deflections averaged only 2.6 mm., and a multivariate analysis indicated that they were uninformative in estimating RVSP or PVG.) The R’ and R groups had similar distributions of age and QRS duration. The median ages were American
Heart Journal
7
Ellison
and
Miettinen
. 250
25C
l
le
.
l l
l 2oc
l l
:
l
e
e
l
l e l
l
l l
l
4
l ee
le oee
i5a
//
. a
E I 9 h
l
l
l m l
$ 0 le l
l l
. l
l l
l
l
l
CA
30
10
R’ Voltage
40
i$,
10
20
R Voltage
30
40
inV1
Fig. 1. A, The right ventricular systolic pressure (RVSP) related to the voltage of the R-wave in Lead VI in 108 patients with pulmonic stenosis and an RSR’ pattern. The regression equation is RVSP (mm. Hg) = 54.2 + (1.45) R’, where R’ is deflection in millimeters (1 mm. = 0.1 mV.). B, The right ventricular systolic pressure related to the voltage of the R-wave in Lead VI in 414 patients with pulmonic stenosis and a “pure R” \?rave in Lead Vr between 1 and 36 mm. The regression equation is RVSP (mm. Hg) = 47.4 + (2.92) R, where R is deflection in millimeters (1 mm. = 0.1 mV.1.
9.4 and 8.4 years, respectively, with ranges from 0.0 to 52 years and from 0.1 to 50 years, respectively. For QRS duration the mean values were 76 msec. for the R’ Group and 73 msec. for the R Group. The severity implications of the presence of an RSR’ pattern were evaluated by comparing the R’ and R groups with respect to the distributions of RVSP and PVG. To evaluate what magnitude of R’ compares to a particular value of R in terms of similar severity, RVSP and PVG were related to the voltage of R’ in the R’ Group and to that of R in the R Group. The respective regression parameters were compared.
Results The values of RVSP and PVG in the R’ Group were generally lower than in the R Group, as shown in Table I.
8
The relationship of RVSP to voltage is shown separately for the R’ and R groups in Fig. 1. For the R’ Group, the regression equation is RVSP (mm. Hg) = 54.2 + (1.45) R’ and for the entire R Group, it is RVSP (mm. Hg) = 50.3 + (2.66) R, where the voltages are entered in terms of millimeters deflection (1 mm. = 0.1 mV.). In Fig. 1, A, all 108 patients with an RSR’ pattern are shown. Fig. 1, B shows the 414 patients of the R Group who had values of R between 1 and 36 mm., which corresponded to the range of voltages found in the R’ Group; for these 414 patients, RVSP (mm. Hg) = 47.4 + (2.92) R. The above equations indicate a significantly greater increase in RVSP for a given increase in voltage for a pure RIwave than for an RI-wave (for the slope difference, two-sided p=O.OOl). From the regression equations it is possible to determine an equivalent R magnitude for a given R’ voltage:
July, 1974, Vol. 88, No. 1
Interpretation
“Equivalent R” = (0.5) R’ + 2 mm. Thus, when utilizing the voltages in Lead V, in attempting to estimate severity in pulmonic stenosis, an observed R’ voltage is estimated to have the same meaning as an R voltage whose magnitude is one-half the R’ deflection plus 2 mm. For example, an R’ magnitude of 20 mm. would be the equivalent of a pure R magnitude of (0.5) 20 mm. + 2 mm. = 12 mm. When using PVG in place of RVSP, the equivalence relationship between R’ and R was identical to that determined with RVSP. Discussion
One goal of the Natural History Study of congenital heart defects has been to attempt to estimate severity from the clinical picture, electrocardiogram, and chest x-ray. At the onset of this endeavor in PS, it was found that 20 per cent of the patients showed an RSR’ pattern in Lead V, with a dominant RI-wave. Since the voltage of the dominant positive deflection in Lead V, is one of the factors utilized in the assessment of severity (the final result of which will be presented in a subsequent publication), this study was designed primarily to determine how the magnitude of an R’-wave should be interpreted, in comparison with an R-wave, in the estimation of severity in PS. Although an RSR’ pattern in Lead V, is more frequently associated with the presence of an atrial-septal defect or other type of volume overload of the right ventricle, it is not uncommonly found in patients with PS. Most investigators report that such cases usually show only mild or moderate degrees of obstruction; the pattern is rarely seen in patients with severe disease.1-5 The mechanism producing this pattern in patients with PS is unknown. Studies by Blount, Munyan, and Hoffman1 of atrial-septal defect indicated that the terminal forces producing an R’ in Lead V, resulted from hypertrophy of the outflow tract of the right ventricle. Boineau, Spach, and Ayers6 produced a similar electrocardiographic pattern by creating atrial-septal defects in dogs. They found the pattern to be related to dilatation of the right ventricle and hypertrophy of the high free wall of the right ventricle and of the crista supraventricularis; no evidence for abnormalities in the conducting system were found. Fowler4 found a pattern of terminal conduction delay by vectorcardiogram
American
Heart Journal
of RSR’ in pulmonic
stenosis
I. Comparison of RVSP and PVG in R Group and R Group Table
R’ Group
R Group
cn = 1081
In = 431)
R VSP: Range Mean Median
31-205
(mm. 73 71
Hg)
28-260
(mm. 89 79
Hg)
PVG: Range Mean Median RVSP = right ventricular PVG = pulmonic-valve
14-190 55 51 systolic gradient.
15-240 70 59
pressure.
in a high percentage of patients with mild PS; he suggested mild dilatation of the right ventricle, similar to that occurring in atrial-septal defect, as a possible mechanism for the vectorcardiographic finding. The present study supports the contention that in PS the presence of an RSR’ pattern in Lead V, suggests less severe disease than the presence of a QR, R, or RS pattern. However, the severity difference between patients with a dominant R’ and those with an R-wave appears to be rather small, and the severity varies widely in both groups. The study also suggests that for a given voltage of a dominant R’-wave the severity tends to be lesser than for a pure R-wave of equal magnitude. Thus, for any given R’ there is a smaller “equivalent R” corresponding to the same degree of severity. Use of the attenuated value for R should improve the correlation between the electrocardiogram and the hemodynamic state in patients with pulmonic stenosis. Summary
An RSR’ pattern in Lead V, (with R’ the dominant positive deflection) was found in 108 of 539 patients (20 per cent) with valvular pulmonic stenosis admitted to a national co-operative study of congenital heart defects. On the average, patients with an RSR’ pattern showed lower right ventricular-to-pulmonary artery pressure gradients (mean = 55 mm. Hg) than patients with a QR, R, or RS pattern (mean = 70 mm. Hg). Moreover, an R’-wave of a given voltage was associated with generally lower right ventricular systolic pressures and gradients than an R-wave of equal amplitude. Quantitatively, these data
9
Ellison
and
Miettinen
suggest that in patients with an RSR’ complex in Lead V,, the R’ voltage has the same severity implication as a “pure R” of magnitude (0.5) R’ + 2 mm. REFERENCES 1.
2.
10
Blount, S. G., Jr., Munyan, E. A., Jr., and Hoffman, M. S.: Hypertrophy of the right ventricular outflow tract. A concept of the electrocardiographic findings in atrial-septal defect, Am. J. Med. 22~784, 1957. Bassingthwaighte, J. B., Parkin, T. W., DuShane, J. W.,
3.
4. 5. 6.
Wood, E. H., and Burchell, H. B.: The electrocardiographic and hemodynamic findings in pulmonary stenosis with intact ventricular septum, Circulation 28:983, 1963. Burch, G. E., and DePasquale, N. P.: Electrocardiography in the diagnosis of congenital heart disease, Philadelphia, 1967, Lea and Febiger, p. 320. Fowler, R. S.: Terminal QRS conduction delay in pulmonary stenosis in children, Am. J. Cardiol. 21:669, 1968. Nadas, A. S., and Fyler, D. C.: Pediatric cardiology, Philadelnhia. 1972. W. B. Saunders Co.. D. 543. Boineau,*J. P., Spach, M. S., and Ayers,‘d. R.: Genesis of the electrocardiogram in atrial-septal defect, AM. HEART J. 68:637, 1964.
July, 1974, Vol. 88, No. 1