LETTERS
is present. In this sense, echocardiography is a useful tool in screening systolic ejection murmurs for possible cardiac catheterization. From Table I, I note that 13 of 14 patients with apparent mid-systolic aortic cusp separation of 15 mm or less and with cardiac catheterization had a significant gradient across the aortic valve or significantly reduced aortic valve area. The one discrepancy was Patient 1 in whom apparent mid-systolic aortic cusp separation was reported at a maximum of 13 mm. In Figure 1 from Case 1, I measure an 18 mm cusp separation in the complex labeled number 3. I am also disturbed by two other facets of the study. First, the authors do not report the interobserver and intraobserver reproducibility of the measurement of aortic separation. Clearly, this measurement is subjective to a certain extent. For example, in Figures 3 and 4, I would have measured aortic cusp separations as significantly less than the authors’ arrows indicate. Second, every patient in this series except the first had significant aortic stenosis. Thus, there is no control group of patients with a normal aortic valve or a diseased aortic valve without stenosis with which to test the hypothesis that aortic cusp separation does detect aortic stenosis. I remain convinced that if one is careful to measure cusp separation only in situations where cusp echoes are clearly identified (for example not Figure 5 and probably not Figure 2) and if one does not expect exact correlation between cusp separation and aortic valve orifice, the echocardiographic examination of aortic cusp separation does provide useful clinical information. Particularly, cusp separation of less than 15 mm appears to have a relatively high level of sensitivity and specificity for hemodynamic aortic stenosis. However, like any other laboratory examination, these findings must be correlated with other clinical and laboratory data available on the patient. Karl E. Hammermeister, MD Cardiovascular Disease Section Veterans Administration Hospital Department of Medicine University of Washington Seattle, Washington Reference 1. Chang S. Ctwmnts S, Chart9 J: A&c stenosis: echocardiographic and surgical description of aortic stenosis. Am J Cardiol 39:499-504.
cusp separation 1977
REPLY
It is interesting that Hammermeister would disregard the echocardiogram of every patient with suspected aortic stenosis if the cusp separation was not “clearly defined.” Picture book clarity is not the goal. As he indicates, the echocardiogram was a useful screening method to identify abnormal aortic valve motion in patients who had clinical symptoms of syncope, heart failure, systolic ejection murmur or chest pain. We did not appreciate the clinical seuerity of the aortic stenosis from the echocardiogram. Cases 3,4,7,9,10,13 and 14 did not have evidence of left ventricular hypertrophy in the echocardiogram, angiogram or electrocardiogram or at surgery. Yet they all had an abnormal aortic valve echocardiogram and a gradient exceeding 45 mm Hg. This agrees with Hammermeister’s premise that reduced cusp separation indicates severity of obstruction. However, Cases 3,18,i16,120 and 22 exhibited apparent systolic cusp separation of 15 mm or greater; these patients also exhibited hemodynamically significant aortic stenosis. The point is that in each patient there was so much variation in cusp separation, secondary to transducer position,
respiratory changes, systolic displacement of the aortic root and manipulation of instrumentation, one could not definitely say which cusp separation in the tracing was truly representative of the severity of the obstruction. Variations in interobserver and intraobserver measurements were meaningless. The arrows in the illustrations, with the exception of those in Figure 2, demonstrate leaflet tissue motion selected as representative of the variety of cusp motion. The illustrations were not meant to be precise areas from which the measurements in Table I were derived. We believed that inclusion of echocardiograms and discussion of normal aortic cusp separation and congenital bicuspid aortic stenosis would have been redundant. Ample study of normal and congenital bicuspid aortic valve motion can be found in published studies.‘-*e We continue to support the conclusions presented in our article. The echocardiogram was useful to detect underlying aortic disease, but clinical severity of the obstruction was based on the patient’s history, physical examination and cardiac catheterization. Sonia Chang Department of Medicine Echocardiographic Laboratory Medical College of Ohio at Toledo Toledo, Ohio Stephen Clement% MD Division of Cardiology Emory University Clinic Atlanta, Georgia John Chang Echocardiographic Laboratory Riverside Hospital Toledo, Ohio References 1. Fetge&aum H: Echocardiography. second edition. Philadelphia, Lea 6 Feblger. 1976. p 141-146 2. champ L M-Mode Ecfvxxdiogaphic Techniques and Pattern Recognition. Philadelphia, Lea 6. Febiger. 1976, p 53-54: 60-61 3 Meyer R: Pediatric Echocardiography. Philadelphia. Lea 8 Febiger, 1977. p 70-76. 167-193 4 Wllllamr R, Tucker C: Echocardiographic Diagnosis of Congenital Heart Disease. Boston, Link Brown, 1977, p 17-20. 171-176 5 Frtedorakf V Jr: Textbook of Echocardiography. Philadelphia, WB Saunders. 1977, p 63-66.90-95 6. F&or J, Schtant R: Eckcardiography: A Teaching Atlas. New York. Grune 8 Sbanon. 1976. p 22-25. 161 7 Gol~g S, Man H, S&t D: Pediatric and Adolescent Echocardiography. Chicago, Year Bock hkiical Publishers. 1975. p 45-47, 90-96 J, et al: Echocardiographic recognition of the congenital a. Nanda N, Qramfak R, Maw&j bicusc4d aortic valve. Circutatlon 49:670-675. 1974 R. Shah P: Echocardiography of the normal and diseased aortic valve. Ra9. Ora& diology 96:1-6. 1970 10. F&f 0. Swnma C. Vacoub M: Echocardiwraohv of the acitic valve: studies of normal aoftic Gal&. aorkstenosis. aortic regurg%aiion and mixed aortic disease. Br Heart J 36:341-351, 1974
LEFT VENTRICULAR
COMPLIANCE
Gaasch et al.’ report that an index of end-diastolic distensibility (dV/dP), defined as the inverse slope of a tangent to the pressure-volume curve at end-diastole, may be calculated as: dV/dP,df = l/k’P and that end-diastolic volume compliance, likewise may be calculated as (dV/dP),d normalized for end-diastolic volume:
Merch 1978
(dV/VdP),+
= l/K’P - l/V
7hs Amwkan &nrmal of CARMOLOGY
Vofume 41
617
LETTERS
where P = end-diastolic pressure, V = end-diastolic volume and k’ = the slope of In P-V relation obtained by the double coordinate method. They add that another method of evaluating left ventricular diastolic volume compliance utilizes a single coordinate of end-diastolic pressure and volume and a constant pressure intercept (b) of 0.43 mm Hg. This method assumes that the end-diastolic pressure-volume relation can be represented as: In P = kV + In 0.43. This equation
can be rearranged
and rewritten
as:
K = (In P - In 0.43)/V. Because the values for the slope of the In P-V relation are similar by the single and double coordinate methods, they conclude that estimates of end-diastolic compliance would likewise be little changed if the simplified (single pressurevolume coordinate) method of obtaining (dV/VdP),d were used in place of the multiplied coordinate approach. Therefore, because left ventricular (dV/VdP),d may be calculated as: (dV/VdP),d
= l/kP . l/v,
zation rested in the difference between the distensibility of the left ventricle as a chamber and the distensibility of a unit volume of myocardium. If one considers an adult’s heart and a child’s heart, both with normal myocardium, dV/dP is lower in the child’s heart than in the adult’s heart, in part by virtue of the smaller operating volume of the child’s heart. The distinction between chamber and muscle distensibility is of critical importance in any discussion of the diastolic properties of the left ventricle. The limitations of these early studies are well known,3,4 and the observation made by Fantini and Michelucci has been discussed by Cove11 and ROSS.~To a great extent, the basis of these limitations originates in the calculation of left ventricular compliance from a single end-diastolic coordinate of pressure and volume and an assumed fixed (zero volume) pressure intercept. These oversimplifications were necessary before we were able to measure accurately diastolic pressure and volume throughout diastole; however, with the availability of angiographic catheters with distally mounted micromanometers, we now analyze our clinical data in terms of chamber compliance (pressure-volume data) and myocardial stiffness (muscle stress-strain data).4s6s7 Our current nomenclature and methodology are outlined in a recent article in this Journal.4 William H. Gaasch, MD Cardiac Noninvasive Laboratory New England Medical Center Hospital Boston, Massachusetts
we point out that assuming K = (In P - In 0.43)/V, it derives that (dV/VdP),d
and simplifying
=
1
1
References
(In P - In 0.43) . p ’ v ’ V
eta1:
for V,
(dV/VdP),d
=
1 (In P - In 0.43) - P
Thus P becomes the only determinant of (dV/VdP),d and V is not considered. In fact, in the paper of Gaasch et al., all the patients with the same left ventricular end-diastolic pressure have identical values of (dV/VdP) (for example, when left ventricular end-diastolic pressure = 11 mm Hg, (dV/VdP) = 2.8-10-2/mm Hg for Patients 1, 3 and 8 in spite of different values of end-diastolic volume). Because left ventricular end-diastolic pressure not only is an expression of left ventricular end-diastolic compliance but also is an index of left ventricular insufficiency, we think that this mathematical joke has no clinical meaning. Fabio Fantini, MD Antonio Michelucci, MD University of Florence Florence, Italy Reference 1. Gaasch WH, Gukmaaa MA, Wslsaer E, et al: Diastolic compliance in man. Am J Cardiol36:193-201. 1975
of the left ventricle
REPLY
In an analysis of length-performance relations in diseased ventricles of varying dimensions and compliance, we utilized left ventricular end-diastolic distensibility (dV/dP), normalized for end-diastolic volume (dV/VdP), as an index of muscle parallel elasticity. ls2 The rationale for this normali-
618
March 1978
The Amerkan
Journal of CARDIOLCGY
1. baa& WH, BatSa WE, CJbafar AA, at afz Ml venbicular stress and compliance In man, with special reference to nofmalizad ventricular function curves. Circulation 45~746-762. 1972 2. Gaasch WH, Galnones MA, Walsser E, Diastolic compliance of the left ventricle in man. Am J Card101 X:193-201. 1975 3. Mlnky I: Assessment of passive elastic stiffness of cardiac muscle: mathematical concepts. physiologic and clinical considerations. directions of futwe research. Prog Cardiovasc Dis 28~277-308, 1976 4. Gaaach WH, Levlna HJ, Guleoaaa MA, at 111: Left ventricular compliance: mechanisms and clinical implications. Am J Cardiol 38:645-653. 1976 5. Covall JW, Ffaas J Jr: Nature and significance of alterations in myocardial compliance. Am J Cardiol 32:449-455. 1973 6. Gaaach WH, Cola JS, Galaones MA, et al: Dynamic determinants of left ventricular diastolic pressure-volume relations in man. Circulation 51:317-323. 1975 7. Gaasch WH, Slag GHL, Cofa JS, et d: Postextrasystolic compliice of the left ventricle. Circulation 56540-544. 1977
ELECTROCARDlOGRAPHfC LEFT ATRIAL ENLARGEMENT VERSUS INTERATRIAL CONDUCTION /DEFECT
Josephson et al.’ suggest that the term left atrial enlargement should be replaced by interatrial conduction defect. We used this term in 1976.2 Employing high gain vectorcardiography, X-ray films and echocardiography, we concluded that “one cannot assess with certitude the separate contribution made by conduction delay and hypertrophy or dilatation to the enlargement of PsE loop.” In many patients “the posteroanterior ratio of the P loop in the horizontal plane was increased in spite of a normal size left atrium.” It is well known that the large posteriorly oriented P loop corresponds to the wide and deep negative terminal deflection of P waves recorded in lead VI of the conventional electrocardiogram. Josephson et al. confirmed our findings when they concluded that the “electrocardiographic pattern termed left atria1 enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.” Follow-up studies using electrocardiography,3 vectorcardi-
Volume 41
is present. In this sense, echocardiography is a useful tool in screening systolic ejection murmurs for possible cardiac catheterization. From Table I, I note that 13 of 14 patients with apparent mid-systolic aortic cusp separation of 15 mm or less and with cardiac catheterization had a significant gradient across the aortic valve or significantly reduced aortic valve area. The one discrepancy was Patient 1 in whom apparent mid-systolic aortic cusp separation was reported at a maximum of 13 mm. In Figure 1 from Case 1, I measure an 18 mm cusp separation in the complex labeled number 3. I am also disturbed by two other facets of the study. First, the authors do not report the interobserver and intraobserver reproducibility of the measurement of aortic separation. Clearly, this measurement is subjective to a certain extent. For example, in Figures 3 and 4, I would have measured aortic cusp separations as significantly less than the authors’ arrows indicate. Second, every patient in this series except the first had significant aortic stenosis. Thus, there is no control group of patients with a normal aortic valve or a diseased aortic valve without stenosis with which to test the hypothesis that aortic cusp separation does detect aortic stenosis. I remain convinced that if one is careful to measure cusp separation only in situations where cusp echoes are clearly identified (for example not Figure 5 and probably not Figure 2) and if one does not expect exact correlation between cusp separation and aortic valve orifice, the echocardiographic examination of aortic cusp separation does provide useful clinical information. Particularly, cusp separation of less than 15 mm appears to have a relatively high level of sensitivity and specificity for hemodynamic aortic stenosis. However, like any other laboratory examination, these findings must be correlated with other clinical and laboratory data available on the patient. Karl E. Hammermeister, MD Cardiovascular Disease Section Veterans Administration Hospital Department of Medicine University of Washington Seattle, Washington Reference 1. Chang S. Ctwmnts S, Chart9 J: A&c stenosis: echocardiographic and surgical description of aortic stenosis. Am J Cardiol 39:499-504.
cusp separation 1977
REPLY
It is interesting that Hammermeister would disregard the echocardiogram of every patient with suspected aortic stenosis if the cusp separation was not “clearly defined.” Picture book clarity is not the goal. As he indicates, the echocardiogram was a useful screening method to identify abnormal aortic valve motion in patients who had clinical symptoms of syncope, heart failure, systolic ejection murmur or chest pain. We did not appreciate the clinical seuerity of the aortic stenosis from the echocardiogram. Cases 3,4,7,9,10,13 and 14 did not have evidence of left ventricular hypertrophy in the echocardiogram, angiogram or electrocardiogram or at surgery. Yet they all had an abnormal aortic valve echocardiogram and a gradient exceeding 45 mm Hg. This agrees with Hammermeister’s premise that reduced cusp separation indicates severity of obstruction. However, Cases 3,18,i16,120 and 22 exhibited apparent systolic cusp separation of 15 mm or greater; these patients also exhibited hemodynamically significant aortic stenosis. The point is that in each patient there was so much variation in cusp separation, secondary to transducer position,
respiratory changes, systolic displacement of the aortic root and manipulation of instrumentation, one could not definitely say which cusp separation in the tracing was truly representative of the severity of the obstruction. Variations in interobserver and intraobserver measurements were meaningless. The arrows in the illustrations, with the exception of those in Figure 2, demonstrate leaflet tissue motion selected as representative of the variety of cusp motion. The illustrations were not meant to be precise areas from which the measurements in Table I were derived. We believed that inclusion of echocardiograms and discussion of normal aortic cusp separation and congenital bicuspid aortic stenosis would have been redundant. Ample study of normal and congenital bicuspid aortic valve motion can be found in published studies.‘-*e We continue to support the conclusions presented in our article. The echocardiogram was useful to detect underlying aortic disease, but clinical severity of the obstruction was based on the patient’s history, physical examination and cardiac catheterization. Sonia Chang Department of Medicine Echocardiographic Laboratory Medical College of Ohio at Toledo Toledo, Ohio Stephen Clement% MD Division of Cardiology Emory University Clinic Atlanta, Georgia John Chang Echocardiographic Laboratory Riverside Hospital Toledo, Ohio References 1. Fetge&aum H: Echocardiography. second edition. Philadelphia, Lea 6 Feblger. 1976. p 141-146 2. champ L M-Mode Ecfvxxdiogaphic Techniques and Pattern Recognition. Philadelphia, Lea 6. Febiger. 1976, p 53-54: 60-61 3 Meyer R: Pediatric Echocardiography. Philadelphia. Lea 8 Febiger, 1977. p 70-76. 167-193 4 Wllllamr R, Tucker C: Echocardiographic Diagnosis of Congenital Heart Disease. Boston, Link Brown, 1977, p 17-20. 171-176 5 Frtedorakf V Jr: Textbook of Echocardiography. Philadelphia, WB Saunders. 1977, p 63-66.90-95 6. F&or J, Schtant R: Eckcardiography: A Teaching Atlas. New York. Grune 8 Sbanon. 1976. p 22-25. 161 7 Gol~g S, Man H, S&t D: Pediatric and Adolescent Echocardiography. Chicago, Year Bock hkiical Publishers. 1975. p 45-47, 90-96 J, et al: Echocardiographic recognition of the congenital a. Nanda N, Qramfak R, Maw&j bicusc4d aortic valve. Circutatlon 49:670-675. 1974 R. Shah P: Echocardiography of the normal and diseased aortic valve. Ra9. Ora& diology 96:1-6. 1970 10. F&f 0. Swnma C. Vacoub M: Echocardiwraohv of the acitic valve: studies of normal aoftic Gal&. aorkstenosis. aortic regurg%aiion and mixed aortic disease. Br Heart J 36:341-351, 1974
LEFT VENTRICULAR
COMPLIANCE
Gaasch et al.’ report that an index of end-diastolic distensibility (dV/dP), defined as the inverse slope of a tangent to the pressure-volume curve at end-diastole, may be calculated as: dV/dP,df = l/k’P and that end-diastolic volume compliance, likewise may be calculated as (dV/dP),d normalized for end-diastolic volume:
Merch 1978
(dV/VdP),+
= l/K’P - l/V
7hs Amwkan &nrmal of CARMOLOGY
Vofume 41
617
LETTERS
where P = end-diastolic pressure, V = end-diastolic volume and k’ = the slope of In P-V relation obtained by the double coordinate method. They add that another method of evaluating left ventricular diastolic volume compliance utilizes a single coordinate of end-diastolic pressure and volume and a constant pressure intercept (b) of 0.43 mm Hg. This method assumes that the end-diastolic pressure-volume relation can be represented as: In P = kV + In 0.43. This equation
can be rearranged
and rewritten
as:
K = (In P - In 0.43)/V. Because the values for the slope of the In P-V relation are similar by the single and double coordinate methods, they conclude that estimates of end-diastolic compliance would likewise be little changed if the simplified (single pressurevolume coordinate) method of obtaining (dV/VdP),d were used in place of the multiplied coordinate approach. Therefore, because left ventricular (dV/VdP),d may be calculated as: (dV/VdP),d
= l/kP . l/v,
zation rested in the difference between the distensibility of the left ventricle as a chamber and the distensibility of a unit volume of myocardium. If one considers an adult’s heart and a child’s heart, both with normal myocardium, dV/dP is lower in the child’s heart than in the adult’s heart, in part by virtue of the smaller operating volume of the child’s heart. The distinction between chamber and muscle distensibility is of critical importance in any discussion of the diastolic properties of the left ventricle. The limitations of these early studies are well known,3,4 and the observation made by Fantini and Michelucci has been discussed by Cove11 and ROSS.~To a great extent, the basis of these limitations originates in the calculation of left ventricular compliance from a single end-diastolic coordinate of pressure and volume and an assumed fixed (zero volume) pressure intercept. These oversimplifications were necessary before we were able to measure accurately diastolic pressure and volume throughout diastole; however, with the availability of angiographic catheters with distally mounted micromanometers, we now analyze our clinical data in terms of chamber compliance (pressure-volume data) and myocardial stiffness (muscle stress-strain data).4s6s7 Our current nomenclature and methodology are outlined in a recent article in this Journal.4 William H. Gaasch, MD Cardiac Noninvasive Laboratory New England Medical Center Hospital Boston, Massachusetts
we point out that assuming K = (In P - In 0.43)/V, it derives that (dV/VdP),d
and simplifying
=
1
1
References
(In P - In 0.43) . p ’ v ’ V
eta1:
for V,
(dV/VdP),d
=
1 (In P - In 0.43) - P
Thus P becomes the only determinant of (dV/VdP),d and V is not considered. In fact, in the paper of Gaasch et al., all the patients with the same left ventricular end-diastolic pressure have identical values of (dV/VdP) (for example, when left ventricular end-diastolic pressure = 11 mm Hg, (dV/VdP) = 2.8-10-2/mm Hg for Patients 1, 3 and 8 in spite of different values of end-diastolic volume). Because left ventricular end-diastolic pressure not only is an expression of left ventricular end-diastolic compliance but also is an index of left ventricular insufficiency, we think that this mathematical joke has no clinical meaning. Fabio Fantini, MD Antonio Michelucci, MD University of Florence Florence, Italy Reference 1. Gaasch WH, Gukmaaa MA, Wslsaer E, et al: Diastolic compliance in man. Am J Cardiol36:193-201. 1975
of the left ventricle
REPLY
In an analysis of length-performance relations in diseased ventricles of varying dimensions and compliance, we utilized left ventricular end-diastolic distensibility (dV/dP), normalized for end-diastolic volume (dV/VdP), as an index of muscle parallel elasticity. ls2 The rationale for this normali-
618
March 1978
The Amerkan
Journal of CARDIOLCGY
1. baa& WH, BatSa WE, CJbafar AA, at afz Ml venbicular stress and compliance In man, with special reference to nofmalizad ventricular function curves. Circulation 45~746-762. 1972 2. Gaasch WH, Galnones MA, Walsser E, Diastolic compliance of the left ventricle in man. Am J Card101 X:193-201. 1975 3. Mlnky I: Assessment of passive elastic stiffness of cardiac muscle: mathematical concepts. physiologic and clinical considerations. directions of futwe research. Prog Cardiovasc Dis 28~277-308, 1976 4. Gaaach WH, Levlna HJ, Guleoaaa MA, at 111: Left ventricular compliance: mechanisms and clinical implications. Am J Cardiol 38:645-653. 1976 5. Covall JW, Ffaas J Jr: Nature and significance of alterations in myocardial compliance. Am J Cardiol 32:449-455. 1973 6. Gaaach WH, Cola JS, Galaones MA, et al: Dynamic determinants of left ventricular diastolic pressure-volume relations in man. Circulation 51:317-323. 1975 7. Gaasch WH, Slag GHL, Cofa JS, et d: Postextrasystolic compliice of the left ventricle. Circulation 56540-544. 1977
ELECTROCARDlOGRAPHfC LEFT ATRIAL ENLARGEMENT VERSUS INTERATRIAL CONDUCTION /DEFECT
Josephson et al.’ suggest that the term left atrial enlargement should be replaced by interatrial conduction defect. We used this term in 1976.2 Employing high gain vectorcardiography, X-ray films and echocardiography, we concluded that “one cannot assess with certitude the separate contribution made by conduction delay and hypertrophy or dilatation to the enlargement of PsE loop.” In many patients “the posteroanterior ratio of the P loop in the horizontal plane was increased in spite of a normal size left atrium.” It is well known that the large posteriorly oriented P loop corresponds to the wide and deep negative terminal deflection of P waves recorded in lead VI of the conventional electrocardiogram. Josephson et al. confirmed our findings when they concluded that the “electrocardiographic pattern termed left atria1 enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.” Follow-up studies using electrocardiography,3 vectorcardi-
Volume 41
