Maximal aortic valve pressure gradients by Doppler echocardiography

Maximal aortic valve pressure gradients by Doppler echocardiography

Erratum Review of the article “Six- and TwelveMonth Follow-up of the Phase I Thrombolvsis in Mvocardial Infarction (TIMI) T&l” publiihed in the August...

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Erratum Review of the article “Six- and TwelveMonth Follow-up of the Phase I Thrombolvsis in Mvocardial Infarction (TIMI) T&l” publiihed in the August 1; 1988; issue (pages 179 to 185) indicates that mortality for 1 group of patients was reported incorrectly in Table IV. The correct figures for the patients with reperfusion without early reocclusion (n = 108) at 6 months was 3.7 and at 12 months was 5.6. The latter numbers were correct in the text but not in the abstract. The abstract should also be modified as follows: “For patients with sustained patency (reperfusion without reocclusion by hospital discharge), there was an extremely low, although insignificant, decrease in mortality at 6 and 12 months (3.7% and 5.6%) compared with patients without early reperfusion who survived to hospital discharge (5.9% and 8.4%)” Genell

L. Knatterud,

PIID

Baltimore, Maryland 3 October 1988

Maximal Aortic Valve Gradients by Doppler Echocardiography

Pressure

Penn and Dumesnili described a new noninvasive technique to measure maximal aortic valve pressure gradients in valvular aortic stenosis. They used a manual technique of extrapolating maximal accelerating and decelerating velocities from pulsed-wave Doppler tracings of the left ventricular outflow tract to estimate maximal continuous wave Doppler aortic valve velocities. They report an excellent correlation with continuous wave Doppler and catheterization data. We are concerned with the validity of this new technique. In this extrapolation technique, slight variations in the placement of the extrapolation lines may result in markedly different derived maximal velocities, The investigators do report low intraobserver and interobserver variability, but do not report if the observers were blinded to either continuous wave Doppler or cardiac catheterization results, a prerequisite that is absolutely necessary for proper validation of their technique. In addition, the scientific basis for a relation of their extrapolation data and the degree of aortic stenosis is not explained by them, nor is it immediately apparent to the reader. In our echocardiographic laboratory, we have not readily observed a distinct left * Letters (from the United States) concerning a particular article in the Journal must be receivedwithin 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 double-spaced typewritten pages. Two copies must be submitted.

ventricular outflow Doppler profile correlating with the degree of aortic stenosis. We have previously studied 100 patients with aortic stenosis by echocardiography and cardiac catheterization and found a good correlation between noninvasively and invasively derived aortic valve area (r = 0.83) mean valve gradient (r = 0.86), and peak valve gradient (r = 0.83)2. Tracings-from 10 patients in this group with well-defined pulsed wave Doppler spectra were selected to attempt to validate the technique of Penn and Dumesnil. The left ventricular outflow tract velocity profiles were reviewed independently by 2 experienced echocardiographers. Each was blinded to the corresponding continuous wave Doppler and cardiac catheterization data. A mean of 3 beats/patient was extrapolated as described by Penn and Dumesnil. The resultant derived maximal velocity was compared with the continuous wave result. Although there was a low intraobserver variability (median variance 0.04 m/s each observer) and a reasonable interobserver correlation of the derived pulsed wave maximal aortic velocities (r = 0.72), we found a very poor correlation of the derived data with peak continuous wave Doppler velocities (r = 0.40, observer 1; r = 0.35, observer 2). There was a mean difference between the derived data and peak continuous wave velocities of -1.0 f 0.9 m/s for observer 1 and -0.6 f 0.9 m/s for observer 2. Thus, we were unable to validate this new technique when 2 experienced echocardiographers are blinded to the corresponding continuous wave Doppler and cardiac catheterization data. In view of our findings, we feel this technique has minimal clinical utility for either confirming or defining aortic valve pressure gradients noninvasively. Stuart Charts

T. ttigano Jae K. Oh P. Tatkrcio

Rochester, Minnesota 29 March 1988 1. Penn IM, Dumesnil JG. A new and simple method to measure maximal aortic valve pressure gradients by Doppler echocardiography. Am J Cardiol

1988,61:382-385.

2. Oh JK, Taliercio CP, Holmes DR, Reeder GS, Bailey KR, Seward JB, Tajik AJ. Prediction of the severityof aortic stenosisby Doppler aortic valve area determination: prospective Doppler-cath correlation in 100 patients. JACC

tic valve peak gradient and the catheterization peak gradient correlate moderately well at r = 0.83, it must be pointed out that this is not as precise as previously published data from their laboratory’ nor our published data (r = 0.93). They then retrospectively applied our technique with low intraobserver variability (median variance 0.04 m/s and “reasonable” intraobserver correlation of the pulse wavederived maximal gradient (r = 0.72). This is adequate and confirms that our method can be simply and reliably performed with minimal error. Their next step, we believe, is erroneous. They procede to compare their pulse wave-derived data with their continuous wave values. This comparison of 2 different Doppler techniques fails to use the cardiac catheterization data to determine which in fact was the correct reading. As such, it is a validation of neither technique. It certainly does not have the substance of an evaluation, let al’one a rebuttal of our method. If we were to assume that the continuous wave correlation with peak valve gradient was excellent. i.e.. r >0.9, then how could we explain the underestimation of pulse wave extrapolated jets? Skjaerpe,2 Pasipoularides3 and their co-workers have experimentally and clinically described the increase in velocities as the jet moves through the left ventricular outflow tract into the stenotic aortic valve. In our study, we prospectively looked for the maximal well-defined pulse wave tracing and this was usually located high in the outflow tract, at the valvular or immediate subvalvular level. In the retrospective analysis of Higano, Oh and Taliercio, the lower pulse wave-extrapolated values may well relate to the fact that the pulse wave signal used for the continuitv eauation and which they presumably used ‘to do their ext rapolation is located lower in the outflow tract (see Figure 3 of reference 2). Thus, although we appreciate the seriousness with which Higano, Oh and Taliercio have taken our anproach, we would hope that a prospectiveattempt to record the maximal velocity would be as fruitful in their hands as it has been in other laboratories that have used our technique. Jean

THE AMERICAN

JOURNAL

MB MD

Calgary Sainte-Foy, Canada 28 April 1988

1988;11:1227-1234.

REPLr: We should clarify that the observers were blinded to continuous wave Doppler and cardiac catheterization results. The pulse wave extrapolation and analysis were performed well after echocardiography and catheterization of all the patients in this study, in a random blinded fashion. More important, Higano, Oh and Taliercio make reference to a study in press that we must presume examines the Doppler assessment of aortic stenosis. Although their “noninvasively” derived aor-

Ian M. Penn, G. Dumesd,

1. Currie PJ, Seward JB, Reeder GS, Vlietstra RE, Bresnaha DR, Bresnahan JF, Smith HC, Hagler DJ, Tajik AJ. Continuous-wave Dopp ler echocardiographic assessmentof severityof calcific aortic stenosis:a simultaneous Dopplercatheter correlative study in 100 adult parients. Circulation

1985;71:1162-1169.

2. Skjaerpe T, Hegrenaes L, Hatle L. Noninvasive estimation of valve area in patients with aortic stenosisby Doppler ultrasound and two dimensional echocardiography. Circulution 1985;72:811-818.

3. Pas&o&rides A, Murgo JP, Bird JJ, Craig WE. Fluid dynamics of aortic stenosis:mechanisms for the presence of subvalvular,pressure gradients. Am J Physioi 1981;246:H542-H 550.

OF CARDIOLOGY

NOVEMBER

15.

1988

1151