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Severe Aortic Stenosis Without Left Ventricular Hypertrophy: Prevalence, Predictors, and Short

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Severe Aortic Stenosis Without Left Ventricular Hypertrophy: Prevalence, Predictors, and Short 250 Heart 1996;76:250-255 Severe aortic stenosis without left ventricular hypertrophy: prevalence, predictors, and short- term follow up after aortic valve replacement Heart: first published as 10.1136/hrt.76.3.250 on 1 September 1996. Downloaded from Christian Seiler, RolfJenni Abstract Left ventricular hypertrophy is crucial to the Objectives-The purpose of the present adaptation of the systemic circulation to pres- study in patients with severe aortic steno- sure or volume overload.' In severe aortic sis was to assess the prevalence of absent stenosis the detection of extreme left ventricu- left ventricular hypertrophy (LVH) (deter- lar hypertrophy indicates a poor prognosis.2 mined according to mass criteria), to On the other hand, there are reports that some identify predictors of absent LVH, and to patients show no or only a slight hypertrophic assess short-term left ventricular adapta- response to the severe long-term increase in tion and prognosis after aortic valve afterload.3-5 Both excessive and minimal or no replacement. hypertrophic responses to severe aortic steno- Methods-Left ventricular mass (LVM) sis have been shown to be related to increased was determined by echocardiography in perioperative and postoperative mortality after 109 men and 101 women with severe aortic valve replacement.6-8 When hypertrophy aortic stenosis (mean pressure gradient is excessive, systolic dysfunction increases < 50 mm Hg). LVH was defined as mortality.6 It has been suggested that LVM > 109 g/m2 in women and LVM increased left ventricular hypertrophy associ- > 134 glm2 in men. ated with increased vascular resistance in the Results-One hundred and eighty nine coronary microvasculature may contribute to patients showed LVH (group 1) (90%; subendocardial ischaemia and lead to ventricu- mean (SD) age 65 (14) years), and 21 lar dysfunction.9 The mechanism relating min- showed no LVH (group 2) (10%, age 57 imal or no hypertrophy in severe aortic (21) years P = 0-02 for difference in age). stenosis to increased postoperative mortality Twelve (6%) of those without LVH had has not been elucidated.78 Moreover, the fre- increased relative wall thickness (that is, quency of and factors associated with an > 0 45 with LV concentric remodelling) absence of the hypertrophic response to severe and nine (4%) showed no macroscopically aortic stenosis are not known. An association http://heart.bmj.com/ detectable hypertrophic adaptation. The of female gender with small, hypercontractile following variables were associated with left ventricles showing increased relative wall the absence of LVH: low body surface thickness has been suggested.4 area, low body mass index, and increased Thus the purpose of the present, retrospec- cardiac index. 76/210 patients were fol- tive study in patients with severe aortic stenosis lowed up a mean ofsix months after aortic was (a) to determine the prevalence of absent valve replacement. The frequency of ade- left ventricular hypertrophy according to mass quate ventricular adaptation to the criteria, (b) to identify factors associated with on September 27, 2021 by guest. Protected copyright. decreased afterload after aortic valve the lack of left ventricular hypertrophy, and (c) replacement was higher in patients with to assess ventricular adaptation to the LVH than in those without. Mortality six decreased afterload and the outcome six months after aortic valve repacement was months after aortic valve replacement in lower, but not significantly, in patients patients with and without left ventricular with LVH (7-6%) than in those without hypertrophy. LVH (12.5%, P = 0.10). Conclusions-A tenth of patients with University Hospital, severe aortic stenosis did not develop Patients and methods Department of LVH according to mass criteria; 4% of the STUDY POPULATION Internal Medicine, patients did not have any macroscopic From 1989 to 1992 all echocardiographic Cardiology, Bern, Switzerland signs of myocardial adaptation to the studies performed at the University Hospital C Seiler pressure overload despite longstanding of Zurich (about 16 000) were reviewed to University Hospital, disease. Small body size was indepen- identify patients fulfilling the following crite- Department of dently associated with lack of LVH ria: (1) severe aortic stenosis with a mean Internal Medicine, to mass criteria. Six months pressure gradient across the aortic valve of Cardiology, Zurich, according Switzerland after aortic valve replacement, ventricu- > 50 mm Hg, (2) no more than mild aortic R Jenrni lar adaptation was more often adequate in regurgitation, (3) no clinical signs of coronary Correspondence to: patients with LVH than in those without. artery disease, and (4) no more than mild Dr C Seiler, University the aortic Hospital, Department of mitral regurgitation. In 194 patients Internal Medicine, (Heart 1996;76:250-255) valve area was calculated using the continuity Cardiology, Freiburgstrasse, Switzerland. equation; it was 0-67 (0 22) cm2. Eight CH-3010 Bern, were Accepted for publication Keywords: valvular heart disease; aortic stenosis; patients fulfilling these criteria excluded 13 March 1996 hypertrophy; gender because of poor quality M mode echocardio- Severe aortic stenosis without left ventricular hypertrophy: prevalence, predictors, and short-term follow up after aortic valve replacement 251 Eccentric LVH Concentric LVH cardiogram (ECG) on VHS video tape and were analysed off-line using a track ball sys- tem. To minimise the effect of respiratory vari- S ations on the assessment of dimensions and velocity spectra, the data reported are the 0.LQl Heart: first published as 10.1136/hrt.76.3.250 on 1 September 1996. Downloaded from (I) EDD' ESD EDD ESD mean of at least three beats. Doppler echocar- 0m 0 diographic data were evaluated by two inde- cm pendent observers who performed all PW lV measurements after the end of the study. -J Serial, cross sectionally guided M mode 109/134 recordings were made by standard techniques x 0) INormal LV geometry I Concentric LV remodellinc with the subject in a supine left oblique posi- c I tion.10 '- cn -L 0 E 00. S ECHOCARDIOGRAPHIC MEASUREMENTS ,0 I Left ventricular (LV) measurements were EDD' ESD I EDD iJ ED obtained at end systole and at end diastole. End diastolic measurements were made PW______ PW according to the American Society of 0.45 Echocardiography (ASE) convention (that is, the leading edge method"). The LV measure- Relative LV wall thickness ments included interventricular septal thick- ness at end diastole (S), the posterior wall thickness at end diastole (PW), and the LV *- Concordant change in LV mass and relative wall internal dimension at end systole (ESD) and thickness after AVR at end diastole (EDD) (fig 1). From the dias- indicating adequate adaptation of tolic measurements, left ventricular mass LV geometry in response to decreased wall stress (LVM) was calculated from the ASE-conven- tion measurements according to the equation Figure 1 LVmass and relative wall thickness. Schematic M mode echocardiograms of differentforms ofLVgeometry are shownfor the combined values ofLVmass index (MI) of Troy et al'2: LVM (g) = 1-04{(EDD + S + (y axis; calculated on the basis ofechocardiographic measurements by the ellipsoidformula PW)3- (EDD)3}. This estimate of LVM has of Troy et al'2) and relative LV waUl thickness (Th) (x axis; Th = 2PW + EDD"8). The been shown to correlate strongly with LVM broken lines indicate the limit between normal and increased LVMI and Th, respectively.'318 Arrows indicate the direction ofadequate adaptation ofLVgeometry in derived from the Penn conventions (that is, response to the decreased afterload after aortic valve replacement. BSA, body surface area the trailing edge method'3). Accordingly, in Mi2; EDD, end diastolic diameter; ESD, end systolic diameter; LVH, left ventricular LVM-Penn values (subsequently referred to as hypertrophy; PW, posterior wall; S, septal wall. LVM) were calculated with the following regression equations: graphic images. Two hundred and ten patientss LVM-Penn (males) = 0-93 (LVM-ASE) http://heart.bmj.com/ (109 men and 101 women) were finally -17-92 g; LVM-Penn (females) = included in the study. Information on clinical 0-88 (LVM-ASE) - 9 g status of these patients was obtained by reviewing their charts. LVM-Penn measurements have been shown to correlate strongly with necropsy and DOPPLER ECHOCARDIOGRAPHIC RECORDING angiographic data on LVM. 14-7 Left ventricu- Doppler echocardiographic recordings were lar mass index (LVMI) was calculated by performed using a real time phased array sectorr dividing LVM by body surface area (BSA, on September 27, 2021 by guest. Protected copyright. scanner (Sonos 500, Hewlett Packard, mi2). Andover, Massachusetts, USA) with inte- Criteria for left ventricular hypertrophy grated colour Doppler facilities and a trans- (LVH) according to LVMI were LVMI > 134 ducer containing a 2-5 MHz crystal set forr g/m2 for men and LVMI > 109 g/m2 for imaging and continuous wave (CW) Doppler. women, representing the sex-specific 97th per- The recordings were stored together with ai centile of a widely used reference standard in a trace from the peripheral lead of the electro- general population sample'3 (fig 1). The entire study population was divided into two groups according to their LVMI: patients with LVH (group 1) and patients without LVH (group Table 1 Demographic data 2). We analysed the prevalence of absent LVH LVH No LVH P determined by mass criteria and the demo- Number 189 21 graphic, clinical, echocardiographic, and Age (yr) 65 (14) 57 (21) 0-02 haemodynamic factors associated with it. Female/male (% female) 96/93 (51) 6/15 (29) NS Body surface area (BSA, m2) 1-88 (0-28) 1-72 (0-23) 0 007 In patients without LVH we determined the Body mass index (BMI, kg/M2) 25 (3) 24 (3) 0 047 prevalence of an increase in relative LV wall Obese (BMI > 30 kg/M2) 17/185 (9%) 0/25 0-12 > Heartrate 76 (16) 78 (11) NS thickness (2PW .
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