VOL 60, No 5, NOVEMBER 1979 3. Mathur PP: Cardiovascular effects of a new antiarrhythmic agent, disopyramide phosphate. Am Heart J 84: 764, 1972 4. Befeler B, Willis PW: The hemodynamic effects of Norpace (parts I and II). Angiology 26: 99, 1975 5. Danilo P, Rosen MR: Cardiac effects of disopyramide. Am Heart J 92: 532, 1976 6. Vismara LA, Vera Z, Miller RR, Mason DT: Efficacy of di- sopyramide phosphate in the treatment of refractory ventricular tachycardia. Am J Cardiol 39: 1027, 1977 7. Deano DA, Wu D, Mautner RK, Sherman RH, Ehsami AE, Rosen KM: The antiarrhythmic efficacy of intravenous therapy with disopyramide phosphate. Chest 71: 597, 1977 8. Horwitz LD, Bishop VS, Stone HL, Stegall HF: Continuous measurement of internal left ventricular diameter. J Appl Physiol 24: 738, 1968 9. Horwitz LD, Bishop VS: Left ventricular pressure dimension relationships in the conscious dog. Cardiovasc Res 6: 163, 1972 10. Barnes GE, Bishop VS, Horwitz LD, Kasper RL: The max- imum derivatives of left ventricular pressure and transverse in- ternal diameter as indices of the inotropic state of the left ven- tricle in conscious dogs. J Physiol 235: 571, 1973 11. Horwitz LD: Effects of intravenous anesthetic agents on left ventricular function in dogs. Am J Physiol 232: H44, 1977 12. Leshin SJ, Mullins CB, Templeton GH, Mitchell JH: Dimen- sional analysis of ventricular function: effects of anesthetics and thoracotomy. Am J Physiol 222: 540, 1972 13. Hinderling PH. Garrett ER: Pharmacokinetics of the an- tiarrhythmic disopyramide in healthy humans. J Phar- macokinet Biopharm 4: 199, 1976 14. Schmid PG, Nelson LD, Mark AL, Herstad DD, Abboud FM: Inhibition of adrenergic vasoconstriction by quinidine. J Phar- macol Exp Ther 188: 124, 1974 Interventricular Septal Thickness and Left Ventricular Hypertrophy An Echocardiographic Study SANTOSH KANSAL, M.D., DAVID ROITMAN, M.D., AND L. THOMAS SHEFFIELD, M.D. SUMMARY Septal and left ventricular posterior wall (LVPW) thicknesses and their ratios were studied at the left ventricular outflow tract and left ventricular cavity in 66 patients with echocardiographically diagnosed left ventricular concentric hypertrophy, 20 with idiopathic hypertrophic subaortic stenosis (IHSS), and 34 nor- mal subjects. Concentric hypertrophy was due to hypertension in 41 subjects and to valvular disease in 15 sub- jects. Septal thickness in normal subjects was related to body surface area (p < 0.02). In 12% of normal sub- jects, 39% of patients with concentric hypertrophy and 95% with IHSS, the septal/LVPW ratio was 2 1.3. Thirty-two percent of patients with hypertension, 78% with aortic stenosis, and 60% with aortic insufficiency had septal/LVPW ratios 1.3 at left ventricular midcavity level. In conclusion, a septal/LVPW thickness ratio of 1.3 is common in patients with concentric left ven- tricular hypertrophy and may also occur in normal subjects. A ratio 1.5 may be more specific for genetically determined asymmetric septal hypertrophy. SINCE THE INTRODUCTION of the term asymmetric septal hypertrophy (ASH) in 1973,1 con- troversy has arisen regarding its clinical and echo- cardiographic significance. The diagnosis of ASH is based on echocardiographic analysis that shows dis- proportionate septal thickness and a ratio of septal-to- left ventricular free wall of 1.3 or more.2 This specific ratio has led to study of the septum and its relationi to the left ventricular free wall in many congenital and acquired cardiac diseases, and has revealed that many diseases, such as pulmonary hypertension,3 pulmonary stenosis,4 congenital malformation of the mitral valve,' 6 coarctation of the From the Allison Laboratory of Exercise Electrophysiology, Department of Medicine, University of Alabama School of Medicine, Birminighan, Alabama. Address for correspondence: L. Thomas Sheffield, M.D., Univer- sity Station, Department of Medicine, Birmingham, Alabama 35294. Received August 16, 1978; revision accepted April 17, 1979. Circulation 60, No. 5, 1979. aorta, and aortic valvular disease5 7manifest dis- proportionate septal thickness. In this study we assessed the interventricular septal and left ventricular free wall thicknesses and their ratio in patients with concentric hypertrophy. We also compared patients who had idiopathic hypertrophic subaortic stenosis (IHSS) with normal subjects. Subjects and Methods One hundred twenty patients were studied, in- cluding 66 patients with concentric left ventricular hypertrophy, 20 patients with IHSS, and 34 normal subjects. In the first group, the diagnosis of concentric hyper- trophy was based on echocardiographic measurement of left ventricular posterior wall and interventricular septum thickness of . 11 mm in the absence of a small left ventricular outflow tract or abnormal systolic anterior motion of the mitral valve. This hypertrophy was due to various primary conditions (table 1). In several patients more than one disease was present, 1 058 C IRCULATION by guest on June 6, 2018 http://circ.ahajournals.org/ Downloaded from
Transcript
VOL 60, No 5, NOVEMBER 1979
3. Mathur PP: Cardiovascular effects of a new antiarrhythmicagent, disopyramide phosphate. Am Heart J 84: 764, 1972
4. Befeler B, Willis PW: The hemodynamic effects of Norpace(parts I and II). Angiology 26: 99, 1975
6. Vismara LA, Vera Z, Miller RR, Mason DT: Efficacy of di-sopyramide phosphate in the treatment of refractory ventriculartachycardia. Am J Cardiol 39: 1027, 1977
7. Deano DA, Wu D, Mautner RK, Sherman RH, Ehsami AE,Rosen KM: The antiarrhythmic efficacy of intravenous therapywith disopyramide phosphate. Chest 71: 597, 1977
8. Horwitz LD, Bishop VS, Stone HL, Stegall HF: Continuousmeasurement of internal left ventricular diameter. J ApplPhysiol 24: 738, 1968
9. Horwitz LD, Bishop VS: Left ventricular pressure dimension
relationships in the conscious dog. Cardiovasc Res 6: 163, 197210. Barnes GE, Bishop VS, Horwitz LD, Kasper RL: The max-
imum derivatives of left ventricular pressure and transverse in-ternal diameter as indices of the inotropic state of the left ven-tricle in conscious dogs. J Physiol 235: 571, 1973
11. Horwitz LD: Effects of intravenous anesthetic agents on leftventricular function in dogs. Am J Physiol 232: H44, 1977
12. Leshin SJ, Mullins CB, Templeton GH, Mitchell JH: Dimen-sional analysis of ventricular function: effects of anesthetics andthoracotomy. Am J Physiol 222: 540, 1972
13. Hinderling PH. Garrett ER: Pharmacokinetics of the an-tiarrhythmic disopyramide in healthy humans. J Phar-macokinet Biopharm 4: 199, 1976
14. Schmid PG, Nelson LD, Mark AL, Herstad DD, Abboud FM:Inhibition of adrenergic vasoconstriction by quinidine. J Phar-macol Exp Ther 188: 124, 1974
Interventricular Septal Thicknessand Left Ventricular Hypertrophy
An Echocardiographic Study
SANTOSH KANSAL, M.D., DAVID ROITMAN, M.D., AND L. THOMAS SHEFFIELD, M.D.
SUMMARY Septal and left ventricular posterior wall (LVPW) thicknesses and their ratios were studied atthe left ventricular outflow tract and left ventricular cavity in 66 patients with echocardiographically diagnosedleft ventricular concentric hypertrophy, 20 with idiopathic hypertrophic subaortic stenosis (IHSS), and 34 nor-mal subjects. Concentric hypertrophy was due to hypertension in 41 subjects and to valvular disease in 15 sub-jects. Septal thickness in normal subjects was related to body surface area (p < 0.02). In 12% of normal sub-jects, 39% of patients with concentric hypertrophy and 95% with IHSS, the septal/LVPW ratio was 2 1.3.Thirty-two percent of patients with hypertension, 78% with aortic stenosis, and 60% with aortic insufficiencyhad septal/LVPW ratios 1.3 at left ventricular midcavity level.
In conclusion, a septal/LVPW thickness ratio of 1.3 is common in patients with concentric left ven-tricular hypertrophy and may also occur in normal subjects. A ratio 1.5 may be more specific for geneticallydetermined asymmetric septal hypertrophy.
SINCE THE INTRODUCTION of the termasymmetric septal hypertrophy (ASH) in 1973,1 con-troversy has arisen regarding its clinical and echo-cardiographic significance. The diagnosis of ASH isbased on echocardiographic analysis that shows dis-proportionate septal thickness and a ratio of septal-to-left ventricular free wall of 1.3 or more.2
This specific ratio has led to study of the septum andits relationi to the left ventricular free wall in manycongenital and acquired cardiac diseases, and hasrevealed that many diseases, such as pulmonaryhypertension,3 pulmonary stenosis,4 congenitalmalformation of the mitral valve,' 6 coarctation of the
From the Allison Laboratory of Exercise Electrophysiology,Department of Medicine, University of Alabama School ofMedicine, Birminighan, Alabama.
Address for correspondence: L. Thomas Sheffield, M.D., Univer-sity Station, Department of Medicine, Birmingham, Alabama35294.
Received August 16, 1978; revision accepted April 17, 1979.Circulation 60, No. 5, 1979.
aorta, and aortic valvular disease5 7manifest dis-proportionate septal thickness.
In this study we assessed the interventricular septaland left ventricular free wall thicknesses and theirratio in patients with concentric hypertrophy. We alsocompared patients who had idiopathic hypertrophicsubaortic stenosis (IHSS) with normal subjects.
Subjects and Methods
One hundred twenty patients were studied, in-cluding 66 patients with concentric left ventricularhypertrophy, 20 patients with IHSS, and 34 normalsubjects.
In the first group, the diagnosis of concentric hyper-trophy was based on echocardiographic measurementof left ventricular posterior wall and interventricularseptum thickness of . 11 mm in the absence of a smallleft ventricular outflow tract or abnormal systolicanterior motion of the mitral valve. This hypertrophywas due to various primary conditions (table 1). Inseveral patients more than one disease was present,
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SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
Patients with Con-
Number ofPrimary disease patients
Chronic renal failure with hypertension 41 (62%)Aortic stenosis 10 (16%)Aortic Insufficiency 5 (8%)Aortic stenosis and insufficiency 2 (3%)Aortic and mitral valve disease 3 (4%)Essential hypertension with and without
congestive heart failure 5 (7%)Total 66 (100%)
but only the principal disease was used for classifica-tion in this study. In this group, 37 (55%) were malesand 30 (45%) were females; ages ranged from 16-70years (mean 50 years).
In the second group, all 20 patients had beenclinically suspected of IHSS and all had echocar-diographic evidence of septal hypertrophy, abnormalanterior systolic excursion of the anterior mitral cusp,with or without any provocation, and small left ven-tricular outflow tract. None of these patients had aor-tic valvular disease, hypertension or chronic renal dis-ease. In II patients, the diagnosis was confirmed bycatheterization, and another four had relatives withtypical IHSS. There were 10 males and 10 females,and the age range was 19-63 years (mean 34 years).The third group included 34 normal subjects who
were hospital employees and medical staff with nor-mal medical histories, symptom reviews, and cardio-vascular examinations. The four subjects with a
A
septal-to-free wall ratio > 1.3 had no abnormalsystolic excursion of the mitral valve even afterprovocation with amyl nitrite. This group consisted of22 males (65%) and 12 females (35%); age range was20-54 years (mean 30 years).
Echocardiograms were recorded on a strip chartusing a 2.22-MHz transducer of 0.5-cm diameter and7.5-10 cm focal length. Echocardiograms were per-formed via the third or fourth left intercostal spacealong the left sternal border with the patient in thesupine position. The 30° left lateral position was usedfor patients with inadequate records in the supine posi-tion. To evaluate the level of maximum septalthickness, we measured septal and left ventricularposterior wall thicknesses at the left ventricular out-flow tract and at the middle of the left ventricularcavity.The level of left ventricular outflow tract was
defined as the level of the anterior mitral leaflet whereboth the interventricular septum and left ventricularposterior wall were simultaneously recorded whilescanning from aortic root toward the mitral valve (fig.1). The left ventricular midcavity level was taken justbelow the mitral valve where only discontinuousreflections from the edges of the leaflets were evident,with the transducer directed posteriorly to pick up themaximum septal and posterior wall excursions.
Interventricular septal thickness was measured, asshown in figure 1, from the most distinct echoes in-cluding right and left endocardial surfaces at end-diastole, which was determined by the peak of the Rwave of the simultaneously-recorded ECG. Right sep-tal wall echoes were demarcated by proper damping.Echoes reflected from the tricuspid annulus were notincluded in the measurements. The left ventricular
B
RI VS
_ _ __ _ ~~~~~~~~~~~~~~~~Rv
stAr4Yt . 4xA:Mz\AUL 4
LV CAYITY
FIGURE 1. Echocardiogram ofa normal subject at left ventricular midcavity (A) and left ventricular out-
flow tract (B) showing left ventricular posterior wall and interventricular septum measurements. AML -
anterior mitral leaflet; Ao = aorta; ENDO = endocardium; L VIS = left side ofinterventricular septum; LV
= left ventricle; L VOT left ventricular outflow tract; PERI pericardium; R VIS = right side of inter-
ventricular septum; R V = right ventricle; R VC = right ventricular cavity.
posterior wall was measured at end-diastole from theendocardium, which was clearly demarcated fromposterior chordae tendineae on the basis of theirsmaller posterior excursion compared with that of theleft ventricular posterior wall. The measurement wascontinued to the strong reflection where epicardiummeets pericardium or, if pericardial effusion was pres-ent, to the epicardial-fluid interface reflection. Pairs ofseptal and left ventricular posterior wall mea-surements were made during the same cardiac cycle,and the average of at least three cycles was taken.Each patient's records were measured simultaneouslyby two investigators.Body surface area was estimated by height and
weight.8 The diagnosis of concentric hypertrophy was
based on a left ventricular free wall and septalthickness > 11 mm.9
Results
Concentric Hypertrophy
Records adequate for analysis were obtained from40 patients at the left ventricular outflow tract, and in66 at the level of the left ventricular midcavity. Theratio of the interventricular septum to the left ven-tricular posterior wall (IVS/LVPW) at the left ven-
tricular outflow tract and the left ventricular mid-cavity were identical (1.3 ± 0.2 [mean ± SD]).Measurements from three clinical subgroups follow.
Chronic Renal Failure with Hypertension
In 28 patients measured at left ventricular outflowtract and 41 at left ventricular midcavity the meanIVS/LVPW ratio was the same at both levels (1.270.2 [table 2]).
A ortic Stenosis
Five patients were measured at left ventricular out-flow tract level and nine at left ventricular midcavity.
Mean IVS/LVPW thickness ratios were 1.5 ± 0.2 and1.4 ± 0.2, respectively.
Aortic Insufficiency
Four patients were measured at left ventricular out-flow tract level and five at left ventricular midcavity.IVS/LVPW thickness ratios were 1.2 ± 0.2 and 1.30. 1, respectively.
IHSS
Six patients were measured at left ventricularoutflow tract level and 20 at left ventricular midcavity.The mean IVS./LVPW ratios were the same at bothlevels, 1.9 ± 0.3. In one patient, IVS/LVPW at leftventricular midcavity was 1. 18. This patient hadtypical clinical and echocardiographic features ofIHSS and had concentric left ventricular hypertrophysecondary to IHSS.
Normal Subjects
Records at the left ventricular outflow tract levelfrom 24 subjects were satisfactory for measurement,yielding a mean IVS/LVPW ratio of 1.24, while in 34subjects at left ventricular midcavity level the ratiowas 1.16 ± 0.2 (table 2, figs. 2 and 3).The number of patients in each group who had a
septal-to-left ventricular free wall ratio 1.3 (figs. 4and 5) at left ventricular midcavity level was deter-mined. Table 3 shows that 12% of normal subjects,39% of patients with concentric left ventricular hyper-trophy, and 95% of patients with IHSS had a ratio of> 1.3. According to this criterion, 78% of patientswith aortic stenosis, 60% with aortic insufficiency and32% with chronic renal failure also had ASH.
Interventricular septum and left ventricularposterior wall thicknesses were considered in relationto body surface area. This correlation was studied bylinear regression equation. Patients with edema, which
TABLE 2. Ventricular Wall Measurements and Ratios
Measurements at left ventricular outflow tract (mm) Measurements at left ventricular midcavity (mm)IVS/LVPW IVS/LVPW
No. of ratio No. of ratiopatients (range and patients (range and
Diagnosis studied IVS LVPW mean SD studied IVS LVPW mean SD)Concentric R 8.6-22 R 10-18 R 0.7-1.8 R 12-26 R 11-29 R 0.97-1.86hypertrophy 40 MV 16.8 = 3.1 M 13 = 2.2 M 1.3 - 0.24 66 M 18 = 2.7 M 14.3 f 2.2 M 1.3 =i 0.22
Chronic renalfailure with R 8.6-22 R 10-18 R 0.7-1.8 R 12-26 R 11-18 R 0.97-1.75hypertension 28 M 16.7 3.0 M 13.4 2.3 M 1.27 23 41 M 18 - 2.7 M 14.3 2.4 M 1.27 - 0.22Aortic R 12-21 R 10-15 R 1.2-1.8 R 15-25 R 12-19 R 1-1.9stenosis 5 M 18 = 3.6 M 12 = 1.9 M 1.5 == 0.26 9 M 19.7 - 3.0 M 14 - 2.2 M 1.4 i 0.23Aortic R 12-18 R 12-15 R 1-1.4 R 15-20 R 12-15 R 1-1.5insufficiency 4 M 15.6 f2.9 M 12.8 1.4 M 1.2 =f0.2 5 M 18 t= 2.0 M 14 1.0 M 1.3 0.18
R 18-24 R 10-12 R 1.5-2.2 R 14.6-28 R 8-15 R 1.2-2.6IHSS 6 M 21 = 2.3 M 11 - 1 M 1.9 - 0.29 20 M 21 = 4.2 M 11.0 1.6 MI.9 - 0.39
Normal R 6-11 R 5-8.6 R 0.8-1.6 R 6.6-16 R 6-10 R 0.9-1.57subjects 24 M 8.6 i 1.6 M 7 1.3 M 1.24 i 0.23 34 M 9.6 - 2.0 MI 8.3 1.0 M 1.16 0.2
Abbreviations: R = range; M = mean; IVS = interventricular septum; LVPW = left ventricular posterior wall; IHSS =idiopathic hypertrophic subaortic stenosis.
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SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
=
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CONCENTRIC I.H.S.S. NORMALHYPERTROPHY N = 6 N = 24
N = 40FIGURE 2. Interventricular septum-to-left ventricular pos-terior wall thickness ratio at the level ofleft ventricular out-
flow tract (LVOT) in patients with concentric hypertrophyor idiopathic hypertrophic subaortic stenosis (IHSS) andnormal subjects.
would affect body weight, were not included in the cor-
relation of measurements with body surface area.
In normal subjects interventricular septum and leftventricular posterior wall thicknesses measured at theleft ventricular outflow tract (fig. 6) were more
strongly related to body surface area (p < 0.02) thanwere the same measurements made at left ventricularmidcavity (p < 0.05) (fig. 7). There was no significantrelation of body surface area to the IVS/LVPW ratio(p < 0.22).
In patients with IHSS, left ventricular posteriorwall thickness at left ventricular midcavity was
significantly related to body surface (p < 0.01), butother measurements were not (p > 0.15).
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N = 66FIGURE 3. Interventricular septum-to-left ventricular pos-terior wall thickness ratio (IVS/LVPW) at left ventricularmidcavity level (L VC) in patients with concentric hyper-trophy or idiopathic hypertrophic subaortic stenosis (IHSS)and normal subjects.
Discussion
According to the previous reports,2 12 normalseptal-to-left ventricular posterior wall ratio is 1: 1,
while recently higher ratios have been reported byMaron and Bahler.6 13 The maximum septal/pos-terior wall ratio at midcavity in one of our normalsubjects was between 1.5 and 1.6, an unusually highvalue. Maron' has reported the maximum ratio of 1.4.This minor difference may be due to use of differentfiducial points for end-diastole. In the present studythe maximum septal thickness in one normal subjectwas 14 mm; Bahler13 has reported 16 mm.
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FIGURE 4. Interventricular septum-to-left ventricular pos-terior wall thickness ratio (IVS/LVPW) at left ventricularoutflow tract (L VOT) in patients with chronic renal failure(CRF), aortic stenosis (AS) and aortic insufficiency (AI).
N = 41 N = 9 N = 5FIGURE 5. Interventricular septum-to-left ventricular pos-terior wall thickness ratio (IVS/LVPW) at left ventricularmidcavity level (L VC) in patients with chronic renal failure(CRF), aortic stenosis (AS) and aortic insufficiency (AI).
Septal/Left Ven-
Number andpercentage of Number and
subjects having percentage ofIVS/LVPW subjects having> 1.3 at left IVS/LVPW
ventricular out- > 1.3 at midDiagnosis flow tract left ventricle
In normal subjects the evidence of disproportionateseptal hypertrophy was more frequent (24%), and theratio was higher (mean ratio 1.24) at the left ven-tricular outflow tract level than at left ventricular mid-cavity. This variation was due to the relatively thinnerleft ventricular posterior wall at left ventricular out-flow tract. The interventricular septum and left ven-tricular posterior wall are relatively thicker at the levelof left ventricular cavity. Disproportionate septalthickness has been reported in young athletes14 andweight lifters.'5 According to Bulkley,16 the septum isdisproportionately thick in the embryo and frequentlyin neonates as well.
There have been few echocardiographic reports onconcentric left ventricular hypertrophy. In this study,39% of patients had disproportionate septal hyper-trophy by a conventional criterion. Abbasi7 reported aseptal-to-free wall ratio of 1.2 ± 0.1 in such patients;according to Criley,17 40.6% of patients with malig-
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TABLE 3. Distribution of Subjects withtricular Posterior Wall Ratio > 1.3
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SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
I IVSA LVPW|
I'I I
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ILI FIGURE 6. Relation of interventricular
septum (IVS) and left ventricular posteriorwall (L VPW) thickness at left ventricularoutflow tract (L VOT) to body surface area(BSA) (m2) in normal subjects. Dense linessignify more than one subject with samebody surface area.
0 1.4 1.5 1.6 1.7 1.8 1.9 2.0 2.1
B.S.A. (M2)N = 24
nant hypertension have disproportionate septal hyper-trophy.
In this study 32% of patients with chronic renalfailure with hypertension had ASH, while Abbasi'8and Schott'9 reported 39% and 5% of patients, respec-
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tively. These authors used a ratio of 1.5 as criterion forASH.Maron reported ASH in 10% of aortic stenosis
patients.6 The ratio was normal (1.03 ± 0.06) in 11patients with fixed left ventricular outflow obstruction
IIFIGURE 7. Relation of interventricular sep-tum (IVS) and left ventricular posterior wall(LVPW) thickness at left ventricular mid-cavity level (L VC) to body surface area (BSA)(m2) in normal subjects. Dense lines signifymore than one subject with same body surfacearea.
1.4 1.5 1.6 1.7 1.8 1.9 2.0 2.1B.S.A. (m2)
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reported by Henry.2 The present report shows a higherincidence of ASH in aortic valvular disease owing topatient selection; all the patients in the present studyhad increased left ventricular wall thickness. Theyrepresent a more severely diseased group than wouldresult from the consecutive selection of patients withaortic valvular disease regardless of the presence ofleft ventricular hypertrophy.ASH has been reported in diverse diseases such as
pulmonary stenosis or hypertension,4' 6 congenitalmitral valve deformities, coarctation of the aorta,supravalvular ring of left atrium and ventricular septaldefect,3 6 mitral valve prolapse,20 acromegaly,2' in-ferior myocardial infarction,22 and hyperthyroid-ism.23 It also appears in normal subjects and weightlifters.14 Considering this, there is doubt that ASHdetermined on the basis of an IVS/LVPW ratioof > 1.3 has definite association with geneticallydetermined hypertrophic cardiomyopathy. Even dis-organized cardiac muscle cells are also not specific forthis entity.16 It seems preferable that an IVS/LVPWratio of > 1.3 not be used to designate ASH due to itsoccurrence in normal subjects and in patients withconcentric left ventricular hypertrophy. Abbasi hasreported evidence that a ratio of 1.5 has increasedspecificity for inherited ASH,1' 24, 25 and Maron6 andShah26 have agreed with this position. A ratio of > 1.5can differentiate normal subjects from patients withIHSS, but this figure cannot satisfactorily differen-tiate patients with IHSS from patients with concentrichypertrophy, inasmuch as 18% of the latter group hadratios > 1.5. Absolute septal thickness of < 15 mmdistinguishes normal subjects from IHSS but will notdifferentiate between IHSS and left ventricular hyper-trophy because 50% of patients in latter group hadseptal thickness > 15 mm.The cause of ASH is not understood. In normal
healthy subjects it may be a persistence of the neonatalpattern. According to Bahler,13 more physically activethan sedentary people have thick interventricular sep-ta. Of the four persons in the present study who haveIVS/LVPW > 1.3, none is athletic.ASH may be an early marker of concentric left ven-
tricular hypertrophy due to its occasional presence inaortic valvular disease and hypertensive patients in theabsence of abnormally increased left ventricularposterior wall thickness, and one presumes that withthe progression of the disease, concentric hypertrophywill develop. This view is consistent with that ofBahler.'3ASH may also be an early marker of generalized
cardiomyopathy due to various systemic diseases inwhich myopathy is a feature, such as thyrotoxicosis,Pompe's disease and Friedreich's ataxia.
Since normal cardiac size varies in proportion tobody size, it was not surprising to find inter-ventricular septal and left ventricular posterior wallthicknesses significantly related to body surface area.The wide fluctuation in weight of patients on chronicdialysis degraded this relationship. Abnormal in-creases in left ventricular wall thickness due to hyper-trophy also reduce the relation of these measure-
ments to body surface area. However, since in IHSSthe posterior left ventricular wall is not primarilyaffected by hypertrophy as is the septum, it is expectedthat the relationship of this measurement to body sur-face area is preserved in this group of patients.Any study involving measurements made by M-
mode echocardiography must take account of the pit-falls and limitations of this method. Wall thicknessesare accurate only when the measuring beam is perpen-dicular to the structure measured, and internal dimen-sions vary according to the orientation of the measur-ing beam. Interface reflections can be insufficientlyclear to yield less than 2 mm of imprecision. Differentelectrocardiographic landmarks for end-diastole indifferent studies may account for minor differences inseptal and left ventricular posterior wall thicknessesand their ratio.
It was not generally appreciated at the inception ofthis study that most accurate echocardiographicmeasurements of thicknesses must be taken from firstmajor impulse of the proximal interface to the firstmajor impulse of the distal interface ("leading edge toleading edge').27 When optimum damping is used, asit was in this study, the imprecision contributed byaftervibrations from intracardiac interfaces is small.The measurement procedure used in this study issimilar to that used in previous studies of septalthickness, and thus is directly comparable with them.
In conclusion, a septal/free wall thickness ratio of> 1.3 is too common in concentric left ventricularhypertrophy and even in normal subjects to be a usefulcriterion of ASH. A ratio of > 1.5 at midcavity levelwill differentiate normal subjects from IHSS, but thisecho will frequently fail to distinguish concentric leftventricular hypertrophy from IHSS. An absolute sep-tal thickness of 15 mm will differentiate normal sub-jects from IHSS, but will not differentiate betweenIHSS and concentric left ventricular hypertrophy.
AcknowledgmentThe authors gratefully acknowledge Gladys Poe and Maria Clark
for recording the echocardiograms; Faye Sprinkel for assistance incompiling clinical data; Katharine Kirk, Ph.D. for assisting innumerical analysis; and Myrnie Driskill, Juanita Brasher and BettyDoyle for assisting in the preparation of this manuscript.
Referencesl. Henry WL, Clark CE, Epstein SE: Asymmetric septal hyper-
trophy (ASH): The unifying link in the IHSS disease spectrum.Circulation 47: 827, 1973
2. Henry WL, Chester CE, Epstein SE: Asymmetric septal hyper-trophy. Echocardiographic identification of the patho-gnomonic anatomic abnormality of IHSS. Circulation 47: 225,1973
3. Maron BJ, Edwards JE, Ferrans VJ, Clark CE, Lebowitz EA,Henry WL, Epstein SE: Congenital heart malformationsassociated with disproportionate ventricular septal thickening.Circulation 52: 926, 1975
4. Goodman DJ, Harrison DC, Popp RL: Echocardiographicfeatures of primary pulmonary hypertension. Am J Cardiol 33:438, 1974
5. Maron B, Clark C, Henry W, Fukuda T, Edwards J, MathewsE, Redwood D, Epstein S: Is the disproportionately thickenedventricular septum always genetically transmitted ASH? (abstr)Circulation 54 (suppl II): 11-80, 1976
6. Maron BJ, Clark CE, Henry WL, Fukuda T, Edwards JE,
1064 ClIRCULATION
by guest on June 6, 2018http://circ.ahajournals.org/
13. Bahler AS, Teichholz LE, Gorlin R, Herman MV: Correlationsof electrocardiography and echocardiography in determinationof left ventricular wall thickness: study of apparently normalsubjects. Am J Cardiol 39: 189, 1977
14. Teare D: Asymmetrical hypertrophy of the heart in youngadults. Br Heart J 20: 1, 1958
15. Menapace FJ, Hammer WJ, Kessler KK, Ritzer T, Bove AA,Warner HH, Spann JF: Echocardiographic measurements ofleft ventricular wall thickness in weight lifters: a problem withthe definition of ASH. Am J Cardiol 39: 276, 1977
16. Bulkley BH, Weisfeldt ML, Hutchins GM: Asymmetric septalhypertrophy and myocardial fiber disarray. Features of normal,developing, and malformed hearts. Circulation 56: 292, 1977
20. Chandraratna PAN, Tolentino AO, Mutucumarana W, GomezAL: Echocardiographic observations on the associationbetween mitral valve prolapse and asymmetric septal hyper-trophy. Circulation 55: 622, 1977
21. Bodem R, Albig M, Barwich D, Sonnenblick EH: The heart inacromegaly: echocardiographic findings. Circulation 54 (supplII): 11-79, 1976
22. Henning H, O'Rourke RA, Crawford MH, Righetti A,Karliner J: Inferior myocardial infarction as a cause ofasymmetric septal hypertrophy. Am J Cardiol 41: 817, 1978
23. Symons C, Richardson PJ, Feizi 0: Hypertrophic car-diomyopathy and hyperthyroidism: a report of three cases.Thorax 29: 713, 1974
24. Abbasi AS: Echocardiography in the differential diagnosis ofthe large heart. Am J Med 60: 677, 1976
25. Criley JM, Lennon PA, Abbasi AS, Blaufuss AH: Hyper-trophic cardiomyopathy. In Clinical CardiovascularPhysiology, edited by Levine H. New York, Grune and Strat-ton, 1976, pp 771-827
26. Shah M, Sylvester LJ: Echocardiography in the diagnosis ofhypertrophic obstructive cardiomyopathy. Am J Med 62: 830,1977
27. Sahn DJ, DeMaria A, Kisslo J, Weyman A: Recommendationsregarding quantitation in M-mode echocardiography: results ofa survey of echocardiographic measurements. Circulation 58:1072, 1978
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