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Table I. Significant Q wavesin 22 patients with myocardi-
al infarction
4. Body position
ECG leads
Head-up only
Supine only
I
II III aVR aVF V, V2 V, V4 VS V6
1
5.
3 2
6.
1
9
2 1 1
4 7 6 3 2 4 1
1
1 1
Both
positions. While it may be possible for the head-up position to obscurethe diagnosisof myocardial infarction, no suchexampleswere observed in this study. Rather, the ECG extent of the infarction was altered by positional changes(Fig. 2). Significant Q waves were recorded in seven patients with dilated cardiomyopathy or hypertension who had not suffered previous infarctions. Q waves were recorded in the upright and supine position in five patients, two of whom also had Q waves recorded in additional leadsonly in the upright position. Two patients had significant Q waves in the supine position that were not present in the upright position. It has long been recognized that standing can produce potentially important QRS changesas compared to the QRS of the supineECG, probably due to the alteration in the position of the heart in relation to the recording electrodeson the body surface.2-8 The importance of lesser amounts of change in body position has received little attention. ,This study demonstratesthat a relatively small changein body position, from the supine to the 60-degree head-up position, can produce significant alterations in the ECG. The head-up position generally decreasesvoltagein the lateral precordial leadsand can produce frontal plane axis &ii of up to 55 degrees.As expected, this can influence the occurrenceof pathologic Q wavesand impair the diagnostic accuracy of the ECG for left ventricular hypertrophy. The best way to eliminate this potential source of diagnostic error is to obtain the ECG in the supine position whenever possible.When this can not be done,the patient’s position should be noted on the tracing and comparisonwith supine ECGs should be made with caution. REFERENCES
1. Marriott H. Practical electrocardiography. Baltimore, Md: The WiUians & Wilkins Co, 198251. 2. Feldman T, Borow KM, Neumann A, Lang RM, Childers RW. Relation of electrocardiographic R-wave amplitude to chauges in left ventricular chamber size and posiiton in normaI subjects. Am J Cardiol 1985$5:1168. 3. Watanabe K, Bhargava V, Froelicher VF. The relationship
7. 8.
January 1999 Heart Journal
between -exercise-induced R-wave amplitude changes and QRS vector loops. J Electrocardiol 1981;14:129. Shapiro W, Benson AS, Pipberger HV. Differences between supine and sitting Frank-lead electrocardiograms. J Electrocardiol 1976;9:303. Riekkinen H, Rautaharju P. Body position, electrode level, and respiration effects on the Frank lead electrocardiogram. Circulation 1976;57:40. Dougherty JD. Change in the frontal QRS axis with changes in the anatomic positions of the heart. J Electrocardiol 1970; 3:299. Sigler LH. Electrocardiographic changes occurring with alterations of posture from recumbent to standing positions. AM HEART J 1938;15:146. Gramble P, McManus H, Jensen D, Froelicher V. A comparison of the standard la-lead electrocardiogram to exercise electrode placements. Chest 1984;85:616.
Interatrial septal thWeMg preventing percutaneous mitral valve bailoon valvulopleety Khalid H. Sheikh, MD, Charles J. Davidson, MD, Thomas N. Skelton, MD, JamesW. Nesmith, BA, Katherine Kisslo, RDMS, and Thomas M. Bashore, MD. Durham,
N.C.
Since the initial report of percutaneous mitral balloon valvuloplasty to treat rheumatic mitral stenosisby Inoue et al.,’ several groups2-4 have reported successfulresults, From the Department of Medicine, Division of Cardiology, Duke University Medical Center. Reprint requesta: Thomas M. Bashore, MD, Box 3012, Duke Medical Center, Durham, NC 27710.
I. Echocardiographic, hemodynamic, and clinical parameters in control and patient populations .Table
Interatrial septal thickness (cm) Case No.
P-S
Normal Subjects 1 0.86 2 0.23 3 0.47 4 0.50 5 0.43 6 0.51 7 0.77 8 0.73 9 0.24 10 0.35 Mean * SD
A-I 0.66 0.24 0.42 0.36 0.38 0.35 0.69 0.76 0.35 0.41
AVG 0.76 0.24 0.45 0.43 0.41 0.44 0.73 0.75 0.30 0.38 0.49 f 0.19
LA size (cm) 3.75 4.75 3.52 2.23 3.70 3.10 3.50 2.70 4.38 3.75 3.54 z!z0.74
Rhythm
h4R
NSR NSR NSR NSR NSR
0 0 0 0 0
NSR
0
NSR NSR NSR NSR
0 0 0 0
P-S, posterosuperior position interatrial septal tbickneas; A-I, anteroinferior position interatrial septal thickness; AVG, averaged values; LA, left atrium; MR, mitral regurgitation; NSR, normal sinus rhythm.
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II. Echocardiographic, hemodynamic, and clinical parameters in mitral stenosispatients Znteratrial septal thickness (cm)
Case no.
P-S
Unsuccessful transseptal 1 1.94 2 1.38 Successful tranweptal 0.17 1 0.61 2 3 0.55 4 0.46 5 0.59 6 0.85 0.56 7 8 0.44 9 0.53 10 0.43 Mean f S.D.
A-I
AVG
LA size (cm)
1.85 1.31
1.89 1.35
3.81 5.10
0.66 0.59 0.55 0.37 0.78 1.00 0.51 0.51 0.56 0.55
0.72 0.60 0.55 0.42 0.69 0.93 0.54 0.48 0.55 0.49 0.60 * 0.15
8.64 8.06 4.05 5.80 4.19 5.26 4.49 4.66 5.20 3.61 5.40 + 1.69
MVA, mitral valve area; MV grad, mean mitral fibrillation; LVEDP, left ventricular end-diastolic
Rhythm
MR
NSR NSR
0 0
AF AF NSR AF NSR NSR NSR
0 0 0 l+ 0 l+ 0 0 0 2+
NSR NSR NSR
Duration of CL zzz-IV CHF (mo)
MV grad (mm Hg)
150 6
1.6 0.8
12.0 22.0
45 378 120 1 12 312 24 22 60 216 119 + 136
1.8 1.6 1.0 0.8 1.0 1.3 1.1 1.2 1.0 1.4 1.2 +- 0.3
10.8 6.4 25.0 16.4 12.9 11.6 17.8 13.1 19.0 8.0 14.1 f 5.6
valve gradient; LAP, mean left atrial pramore; pressure; other abbreviations ae in Table I.
with both hemodynamic and symptomatic improvement. As the procedure involves transseptal puncture of the interatrial septum and the advancement of balloon dilation catheters a.crossthe septum, the interatrial septum createsa site of resistanceto advancement of the valvular dilation catheters.6*BWe have noted inability to advance the balloon dilation catheters acrossthe interatrial septum in 2 of an initial 13 percutaneousmitral valvuloplasties attempted. In both instancesa thickened interatrial septum was noted on two-dimensional echocardiography, which prompted a retrospective examination of interatrial septal thickening in thesepatients as a possiblereasonfor technical failure. All patients had been referred to Duke University Medical Center for percutaneous balloon mitral valvuloplasty to relieve rheumatic mitral stenosis. Procedures were performed between January 21, 1987, and January 12,1988. Percutaneousvalvuloplasty wasperformed with the technique describedby McKay et al.9All patients were brought to the catheterization laboratory and had venous accesssecured through the right femoral vein. A 7F Critikon catheter (Critikon, Inc., Tampa, Fla.) was advanced to the pulmonary artery and pulmonary capillary wedgeposition. A 7F micromanometer pigtail catheter (Millar Instruments, Houston, Texas) wasadvanced to the left ventricle. An 8.5 F Brockenbrough catheter (USC1 Division of C.R. Bard, Billerica, Mass.) was then positioned in the foramen ovale and, with a hollow end-hole needle, wasadvanced into the left atrium. Hemodynamic measurementswere obtained through the Brockenbrough catheter, and cardiac output wasdetermined by oximetry and expired gas collection. Mitral valve area was calculated by meansof the Gorlin equation. An 8F transseptal catheter introducer (USCI) was then placed in the left
MVA (cm’)
CHF,
congestive
heart
LAP (mm Hd 16 30 26 8 22 24 20 23 21 20 28 22 21.4 + 5.4 failure;
LVEDP (mm W 4 20 16 4 8 8 5 10 5 11 8 12 8.7 * 3.7
CL, class; AF, atriai
atrium through which a 7F Critikon balloon flotation catheter was advanced to the left atrium and then to the left ventricle. In 9 of I3 patients this catheter was advanced to the descendingaorta aswell. A single 260 cm 0.38 J wire was then placed through the balloon flotation catheter, the catheter wasremoved, and a double-barreled sheath (Mansfield Scientific Inc., Mansfield, Mass.) was used to place a secondwire acrossthe valve. The interatrial septum was then dilated with an 8 mm, 3 cm long balloon catheter (Mansfield Scientific Inc.), followed by the passageof two larger balloon catheters (15 or 20 mm) that were positioned across the mitral valve. In two patients, though transseptsl needlepuncture wassuccessful, the 20 mm balloon catheter could not be advanced into the left atrium through the interatrial septum, despite numerousattempts. Both of these patients subsequently underwent open mitral commissurotomy. In all patients, two-dimensional echocardiogramsand Doppler examinations (including color-flow mapping) were reviewed for assessmentof interatrial septal thicknessand left atrial chamber size and valvular regurgitation. All data were measuredby an observer blinded to the catheterization results. Subcostal four-chamber views obtained with either a 2.5 MHz or a 3.5 MHz transducer were available in 12 of 13 mitral stenosispatients. Care wastaken to adjust gain settings for optimal visualization without introduction of artifact. Thickness wasmeasured on the two-dimensional image from brightest echo to brightest echo on either side of the interatrial septum. Measurementswere madeat the widest points both above and below the fossa ovalis. Left atrial dimension was measured from the parasternal long-axis view at end systole. A transesophagealechocardiogramthat used a 5 MHz transducer was obtained in one patient undergoing
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Flg. 1. Interatrial septal thickness in a normal subject (A) and in a patient with mitral stenosisin whom transseptal balloon catheter passagewas successful (B). Subcostal four-chamber views demonstrate normal interatrial septal width between left atrium (LA) and right atrium (RA).
open mitral commissurotomy at the time of surgery. A normal adult control group for analysis of interatrial septal thickness was identified by analysis of echocardiographic data from 10 consecutive adult patients between the agesof 35 and 65 who had technically adequate and entirely normal two-dimensional and Doppler echocardiography. Statistical comparisonsbetween patient groups were made by two-tailed Student’s t test. Wilcoxon’s rank sum test for unpaired samples was used to compare significanceof interatrial septal thickness differences. Echocardiographic, clinical, and hemodynamic parameters in the three populations are shownin Tables I and II. Although interatrial septal thickness was slightly
increasedin mitral stenosispatients asa group in comparison with the normal subjects, these differences were not statistically significant. Analysis of the duration of rheumatic valvular disease, presence of atria1 fibrillation, degree of mitral insufficiency, mitral valve area, mean mitral gradient, mean left atrial pressure,or left ventricular end-diastolic pressurefailed to reveal any correlation with interatrial septal thickness. Subcostal four-chamber views from a normal subject and from a patient with mitral stenosis in whom transseptal balloon catheter passagewas successfulare shown in Fig. 1. Similarly, a subcostal four-chamber view and the transesophageal view obtained at the time of open commissurotomyfrom
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Fig. 2. Interatrial septal thickness in a patient in whom transseptal balloon catheter passagewas unsuccessful.Subcostalfour-chamber view (A) and a transesophagealview (B) demonstratethe interatrial septum (ices)with measuredwidth denoted by arrows. In the subcostal view, the right atrium (RA) is closestto .the transducer. In the transesophagealview, the left atrium (LA) is closestto the transducer. Prominent interatrial septal thickening is noted in comparisonto the patients in Fig. 1.
one of the mitral stenosispatients in whom transseptal balloon catheter passagewas unsuccessfulare shown in Fig. 2. The marked interatrial septal thickening is contrasted with both the normal subject and the patient with mitral stenosis in whom transseptal balloon catheter passagewas successful.Comparison of interatrial septal thickness between the two mitral stenosis patients in whom transseptal balloon catheter passagewasunsuccessful with both normal subjects and with mitral stenosis patients in whom valvuloplasty could be performed showed significant differences (Fig. 3). In both patients
undergoing open commissurotomy, atrial hypertrophy without evidence of laminar clot was noted at surgery. Theseresults indicate that somepatients with rheumatic mitral stenosishave increased atrial septal thickness, when compared to normal individuals. A technical limitation to adequateexamination of the interatrial septum by two-dimensional echocardiography has been that most standard echocardiographic views place the interatrial septum in the far field of the ultrasound beam, where lateral resolution is limited. Most authorities’ therefore suggest a subcostal four-chamber examination of this
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2 I 0L 0
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I
I
m
Normol Subjects
(TJ
Mitral Stenosissuccessful tronsseptal
m
Mitral Stenosisunsuccessful tronsseptol
I
I
0.1 0:2 0:3 0:4 0:5 0:6 0:7 018 0.9 1.0 1.1 1.2 1.3 14 INTERATRIAL SEPTAL THICKNESS (cm 1
I
1
I
1.5
1.6
1.7
1.8
January 1989 Heart Journal
1.9
Fig. 3. Interatrial septal thickness in each subject from all three populations is displayed. Significant differences existed between the interatrial septal thickness measurementsobserved in unsuccessful transseDtalDatients and in those obtained from both normal subjectsand successfultransseptal patients 0, < 0.05). -
structure to minimize this limiation. All of our analyzed studies were performed from this view. Even with this method, however, the r&.olution with which interatrial septi. thickness can be measured is limited. This may have contributed to our. inability to show a significant difference between inter&trial septal thickness between normal subjectsand most patienta with mitral stenosis. Increasedinteratrial’ieptel width hasbeen reported8 in a variety of disorders, including lipomatous hypertrophy of the atrial septum, amyioidosis, secundumatria1 septal defect (ASD), left at&l thrombi, left atrial tumors, and septal cysts. The cause of increased interatrial septal thickness in this group o$patients is likely due to hypertrophy of the left atrial wall. The presenceof most of the above-mentioned causeswas excluded at the time of surgery or by clinical evaluation. Although atrial chamber enlargement is well recognized in mitral stenosis,atria1 wall hypertrophy is gene&y not evaluated by routine clinical studies. Pathologic $tudiesgslo of the atria1 wall in patients with rheumatic ,mitral stenosishave noted gross, as well 88 cellular atrial hjrpertrophy and fibrosis. This may be present to varying degreesin patients with mitral stenosis.An accurate cli&cal description of this phenomenon has, however, been limited by the unavailability of techniques that discriminate accurately normal atria1 thickness from abnormal thickness. We were not able to demon&rate that the development of hypertrophy correlated with either severity or duration of mitral stenosis,as BBBeseed by a variety of clinical and hemodynamic variables. Our resulta demonstrate that marked atria1 septal thickening does appear to occur in some patients with rheumatic mitral stenosis,and that this condition can be of clinical significance in patients undergoing attempted percutaneous mitral balloon valvuloplasty. Given the technical difficulties in performing transseptal mitral valvuloplasty in patients with a thickened interatrial septum, patients with marked atria1 septal thickening
should either be considered candidates for a retrograde valvuloplasty approach12or should be treated surgically.
REFERENCES
K, OwakiT, NakamuraT, Kitamura F, Miyamoto N. Clinicalapplicationof transvenousmitral commissurotomy by a newballooncatheter.J ThoracCardiovascSurg 1984; 87:394-402. 2. McKay CR, KawanishiDT, RahimtoolaSH. Catheterballoon &uloplasty of the mitral valve in adults using a double-balloon techniaue.JAMA 1987:257:1753-61. 3. McKay RG,Lock JE, gafianRD, ComePC, Diver DJ, Bairn DS, Berman AD, Warren SE, Mandell VE, Royal HD, GrossmanW. Balloondilation of mitral stenosisin adult patients:postmortemandpercutaneous mitral valvuloplasty studies.J Am Co11 Cardiol1987;%723-31. 4. ComePC, Riley MF, Diver DJ, Morgan JP, Safian RD, McKay RG.Noninvasiveassessment of mitralstenosis before and after percutaneous balloonmitral valvuloplasty.Am J Cardiol1988;61:817-25. 5. PandianNG, IsnerJM, HougenTJ, DesnoyewMR, McInerney K, Salem DN. Percutaneous balloonvalvuloplasty of 1. Inoue
6.
7.
8.
9. 10.
11.
mitral stenosis aided by cardiac ultrasound. Am J Cardiol 1987;59:380-1. Acar J, Vahanian A, Michel PL, Trabelsi S, Slama M, Dermine P, Ben-Ismail M, Cormier B. Percutaneous mitral commissurotomy. A report of 90 cases. J Am Co11 Cardiol 1988;ll:ZZOA. Armstrong WF. Congenital heart disease. In: Feigenbaum HF, editor. Echocardiography. 4th ed. Philadelphia: Lea & Febiger, 1986:402. Silverman PM, Guadalajara JF, Kiss10 JA, Godwin JD, Korobkin M. Lipomatous hypertrophy of the atrial septum: diagnosis by combined two-dimensional echocardiography and computerized tomography. Am J Cardiol t984:54:11567. Thiedemann KV, Ferrans VJ. Left atrial ultrastructure in mitral valvular disease. Am J Pathal 1977;89:575-604. Unverferth DV, Fertel RH, Unverferth BJ, Leier CV. Atria1 fibrillation in mitral stenosis: histologic,hemodynamicand metabolic factors. Int J Cardiol 1984:5:143-52. Babic W, Pajcic P, Djurisic F, V&ine M, Grujicic SM. Percutanous transarterial balloon valvuloplaaty for mitral valve stenosis. Am J Cardiol 1986;57:1101-9.