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Asymmetric Septal Hypertrophy in Patients with Aortic Stenosis: an Adaptive Mechanism Or a Coexistence of Hypertrophic Cardiomyopathy?

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Asymmetric Septal Hypertrophy in Patients with Aortic Stenosis: an Adaptive Mechanism Or a Coexistence of Hypertrophic Cardiomyopathy? View metadata, citation and similar papers at core.ac.uk brought to you by CORE J AM cou,providedCARDIOl by Elsevier - Publisher783 Connector 1983.1(3)783-9 Asymmetric Septal Hypertrophy in Patients With Aortic Stenosis: An Adaptive Mechanism or a Coexistence of Hypertrophic Cardiomyopathy? OTTO M. HESS, MD, JAKOB SCHNEIDER, MD, MARCO TURINA, MD, JOHN D. CARROLL, MD, FACC, MARTIN ROTHLIN, MD, HANS P. KRAYENBUEHL, MD Zurich, Switzerland Myocardial histologic features andventricular left dy• 1 and 2 (26.5 versus 29.1IJ.; NS), but muscle fiber di• namics were assessed in 24 patients with severe aorticameter of the septum in group 1 was significantlysmaller stenosis, 12 with (group 1) and 12 without (group(24.4 2) IJ.; P < 0.01) than that ofanterolateral the wall in associated asymmetric septalhypertrophy.In 10patients group 2. No morphologic abnormalities typical for hy• from group 1,echocardiographyshowed a septal/pos• pertrophic cardiomyopathy (fiberdisarray)were seen in teriorwall ratio of 1.5; in the other 2, asymmetric septalsamples from the patients in either group. By 18 months hypertrophywas diagnosed by direct inspection at thepostoperatively, septal wall thickness had decreased sig• time of surgery. Septal myectomy in all 12 patientsnificantly in from 2.0 to 1.5 em< (p0.01) and posterior group 1 was completed at the time of aortic valvewall re• thickness from 1.4 to 1.2 cm< (p0.05) in group 1. In group 2, septal wall thickness decreased from 1.5 placement. Septal histologicfeatures were assessedfrom to 1.3 em (NS) and posterior wall thickness from 1.4 to surgical specimens in 10 patients in groupTransseptal 1. 1.2 em (NS) 8 months postoperatively. endomyocardial biopsy specimens ofanterolateral the Asymmetric septalhypertrophyin patients with aor• wall taken during preoperative cardiac catheterization tic stenosis is an adaptive mechanism to the long-stand• were evaluated by light microscopy in 10 patients froming pressure overload, and hence there is no evidence of group 1 and all patients of group 2. coexistenceof idiopathichypertrophiccardiomyopathy Leftventricularend-diastolic and peak systolic pres•and aortic valve disease. Although the degree of valve sure, peak pressure gradient, calculated valve areaobstruction and was similar in both groups,ventricular left angiographic muscle mass did not differ significantlyejection in performance wassignificantlylower in the group groups 1 and 2; ejection fraction (68 versus%; prob• 58 without asymmetric hypertrophy, probably because these ability [p]< 0.01) waslargerand end-diastolic volumepatients had a more advanced stage of myocardial dis• (109 versus 144 ml/m"; difference not significant[NS]) ease. After successful valve replacement, there is a sig• was smaller in group 1 than in group 2. Muscle fibernificant regression of septalhypertrophyin patients with diameter of theanterolateralwall was similar in groups aortic stenosis and asymmetric septalhypertrophy. Asymmetricseptalhypertrophyhas been found to be theit can alsooccur in patientswith severe aortic stenosis characteristicabnormalityin patientswithhypertrophiccar• (4-8),and it has beensuggestedthat in these patients it is diomyopathy(1-3). It is definedechocardiographicallyby due to acoexistenceof secondaryhypertrophyand hyper• adisproportionalthicknessof theinterventricularseptum as trophiccardiomyopathy.This hypothesiswas based on the comparedwith the leftventricularposteriorwall.However, preoperativeechocardiographicfinding ofasymmetricseptal hypertrophyin patientswith severe aortic stenosis(4,5). In somepatients(5),histologicexaminationof theexcised From the Department of Internal Medicme, Medical Policlinic, Car•septal tissuedemonstratedmorphologicabnormalitiestyp• diology, Institute of Pathology and Surgical Chruc A, University Hospital,ical of hypertrophiccardiomyopathy.In anotherstudy, Zurich, Switzerland. This study was supported by the Swiss NationalThompsonandco-workers(6) found noregressionof myo• Science Foundation, Zurich, Switzerland. Manuscript received July 28, 1982; revised manuscript received October 19, 1982, accepted Octobercardialhypertrophyaftersuccessfulvalvereplacement,and 25, 1982. intraventricularpressuregradientsin four of six patients Address for reprints: Otto M. Hess, MD, Department of Internal Med•suggestedcoexistenceof hypertrophiccardiomyopathyand icine, Medical Policlinic, Division of Cardiology, University Hospital, Raermstrasse 100, 8091 Zurich, SWitzerland. aortic valvedisease. © 1983 by the Amencan College of Cardiology 0735-1097/83/030783-7$0300 784 J AM COLL CARDIOL HESS ET AL 1983;1(3)783-9 The purposeof the presentstudy was toexaminethe whom a good qualityechocardiogramwas not obtained, asym• histologic features of themyocardiumand leftventricular metric septal hypertrophy was diagnosed or excluded by left ven• hemodynamicsin 24 patientswith severe aortic stenosis,tricularcineangiographyor by visual and digital inspection of the 12 with and 12 without asymmetric septal hypertrophy,left inventricularoutflow tract during aortic valve replacement, or order todeterminewhetherthelatterconditionis an adaptive by both. M-mode andtwo-dimensionalechocardiographywere repeated mechanism to the long-standing pressure overload or whether 17.6 monthspostoperativelyin group I and 8.1 months postop• it representsa combinationofbothsecondaryhypertrophy eratively in groupQuantitative 2. evaluation of the M-mode echo• andhypertrophiccardiomyopathy. cardiogramsincluded the same variables as during the preoperative examination.However, in two patients from group I and in one patient from group 2, a good qualityechocardiogramwas not Methods obtained. Studypatients.Twenty-fourpatients (7 women and 17 men) Cardiaccatheterization.Informed consent was obtained from with an average age of 51 years (range 25 to 69) were studied.all patients. Premedication consisted of 10chlordiazepoxide mg of Twelve patients (group 1) had severe aortic stenosis with asym•or of 5 mg of diazepam given orally I hour before the procedure. metric septalhypertrophy(mean systolic ventricular-aortic pres•Left ventricular pressure was measured in 24 patients by a Millar sure gradient 74 mm Hg, mean aortic valve areaem", 0.69mean 7F-micromanometerthat had been advanced into the left ventricle aorticregurgitantfraction0.17),and 12 patients (group 2) hadthrough a transseptally introduced 11.5Brockenbrough F guiding severe aortic stenosis butasymmetric no septal hypertrophy (mean catheter (9). The patients then received intravenous heparin in a systolic pressure gradient 67 mm Hg, mean aortic valve areadose 0.74 of 10,000 units. Themicromanometerwas calibrated by ern",mean aorticregurgitantfraction0.18).The 24 patients with superimposing the micromanometer tracing withconventional the severe aortic stenosis were selected from a cohort of 161 patientspressure tracing (9,11). with aortic stenosis with or without aortic regurgitation who under•Monoplane left ventricular cineangiography in the right ante• went cardiaccatheterizationduring the same time interval betweenrior oblique position was performed at midinspiration at a filming October 1977 and January 1982 as did our 24 patients. All patientsrate of 50frames/soQuantitative evaluationend-diastolic of and had M-modeechocardiography,and asymmetric septal hypertro•end-systolic frames for the calculationventricular of left volumes phy was found in only 14 patients. Thus, the incidence of asym•and ejection fraction was carried out according to our standard metric septalhypertrophyin our cohort of 161 patients with aortictechnique(II). Left ventricular muscle mass wascalculatedac• stenosis was9.0%.Two of the 14 patients with asymmetric septalcording to the technique of Rackley et al. (12). hypertrophy were,however,not included in the present study. Left ventricularendomyocardialbiopsy.At the end of the Coronary arteriography was carried out in all 24 patients. catheterization procedure,endomyocardial two biopsies were per• There was a 50% stenosis of the left circumflex coronary arteryformed in 10 of the 12 patients from group I and m all patients in only one patient from group 1; a 50% stenosis of the left anteriorfrom group 2, using a King's College bioptome (9) introduced descending coronary artery was detected in one patient from group into the left ventricle throughBrockenbrough the guiding catheter. 2. Minimal to mild mitralregurgitationwas present in three patients The biopsy specimens were taken fromanterolateral the wall of from group 1(regurgitantfraction ranging from 0.050.14). to All the left ventricle, and other than transient prematureventricular patients had sinus rhythm atpreoperative the evaluation. complexes during most biopsies,complications no occurred in any Echocardiography.M-mode echocardiograms(Organon of the 22 patients. Immediately after the biopsyperformed, was Teknika) were recorded shortly beforepreoperativecardiac cath• the material was fixedglutaraldehyde in and embedded in Epon eterization in theanteroposteriorposition or in the right anterior for quantitative morphometry(9,13,14).The muscle fiber diameter decubitus position according to our standard technique (9). Left and the extent of interstitial fibrosis were determined from semi• ventricularinternaldiameter,shortening of the internal diameter, septal wall thickness andposteriorwall thickness (Fig. I) as well thin sections (1J.L). From several sections of each biopsy specimen, as heart rate weredeterminedin all patients. Two-dimensionalthe muscle fiber diameter wasdeterminedusing a mechanical•
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