Endocardial systolic function in patients with LVH and controls

Endocardial systolic function in patients with LVH and controls

Midwall left ventricular systolic function in cardiac hypertrophy J Mayet, B Wasan, B Ariff, N Chapman, M Shahi, NR Poulter, PS Sever, RA Foale, SAMcG Thom Peart-Rose Clinic and Department of Cardiology St Marys Hospital, Imperial College, London Is LV systolic function preserved in LVH? Discrepancy between experimental and human studies Former suggest myocardial function depressed Latter indicate it is preserved Experimental and human studies not strictly compatible Experimental studies measure myocardial or myofibril function Human studies have assessed whole heart function by utilising endocardial measurements

Midwall LV shortening It is often assumed that the inner and outer parts of the LV wall thicken equally in systole Myocardial shortening in subendocardial is greater than subepicardial layers Therefore a theoretical mid-point in the LV wall shows relative migration toward the epicardium throughout contraction Epicardial migration of theoretical midwall fibre during systole ... ... Theoretical midwall fibre Posterior wall

Midwall LV shortening Anatomic reasons why assessing shortening at the midwall may be preferable At the midwall circumferentially orientated fibres predominate while at the epicardium and endocardium fibres are longitudinally orientated When circumferential wall stress is considered to assess stress-shortening relations then correct anatomic plane is being addressed What is the relationship between endocardial and midwall shortening in normal subjects and those with LVH? 38 previously untreated hypertensives with LVH compared with normotensive controls (healthy volunteers) No patient had significant co-morbidity Each underwent full two-dimensional

echocardiographic examination How does regression of LVH effect midwall shortening? 32 hypertensive subjects with LVH 24 previously untreated 8 uncontrolled on existing medication Echocardiography at baseline Treated with ramipril with addition of felodipine and bendrofluazide if required Echocardiography after BP control Echocardiography after a further 6 months of BP control Calculations from echocardiographic data

RWT = 2xPWTd / LVIDd FS = 100 x (LVIDd - LVIDs) / LVIDd End-diast volume = 7 x (LVIDd)3 / (2.4+LVIDd) End-syst volume = 7 x (LVIDs)3 / (2.4+LVIDs) CO = HR x SV = HR x (EDV- EDV) EF = 100 x (EDV - ESV) / EDV cESS = SBPx1/2LVIDs2x{1+[(1/2LVIDs+PWTs)2/(1/2LVIDs+1/2PWTs)2]} / [(1/2LVIDs+PWTs)2-1/2LVIDs2] Calculations from echocardiographic data

In order to calculate fractional shortening at the midwall, the position of a theoretical midwall fibre in systole needs to be known This can be calculated by using a cylindrical model of the LV with the assumption that volume remains constant through the cardiac cycle (1/2LVID+1/2PWT)2 - (1/2LVID)2 End-diastolic volume = ___________________________________________ (1/2LVID+PWT)2 - (1/2LVID)2 (1/2LVIDs+a)2 -(1/2LVIDs)2 End-systolic volume = __________________________________________

(1/2LVID+PWT)2 - (1/2LVID)2 Where a is the distance from the posterior wall endocardium of the theoretical midwall fibre at end-systole Because end-diastolic volume = end-systolic volume a can be calculated From this: Midwall FS (%) = 100 x [(LVID+PWT)-(LVIDs+2a)] / (LVID+PWT) Calculation of midwall fractional shortening .

a . a LVIDd LVIDs Midwall fractional shortening % = [(LVIDd + 2a) - (LVIDs + 2a)] / (LVIDd + 2a) a . . a

Patient characteristics and echo results of hypertensives with LVH and control subjects Age (years) SBP (mmHg) DBP (mmHg) ECG voltage IVS diastole (cm) LVID diastole (cm) PWT diastole (cm) LVID systole (cm) PWT systole (cm) LVMI (g/m2) RWT 2 CESS (kdyne/cm ) Hypertensives with LVH

46+/-2.4* 170+/-3.7* 100+/-1.6* 39+/-3.3* 1.4+/-0.04* 4.7+/-0.08 1.3+/-0.05* 3.1+/-0.11 1.6+/-0.05* 140+/-3.6* 0.55+/-0.02* 166.4+/-9.6 Control subjects 40+/-1.7 124+/-2.3 77+/-7.6 27+/-1.3 1.1+/-0.02

4.8+/-0.08 1.0+/-0.02 3.0+/-0.07 1.2+/-0.02 92+/-3.1 0.41+/-0.01 150.6+/-6.7 *p<0.01 versus controls Endocardial systolic function in patients with LVH and controls 70 60 50 40 30 20 10

0 LVH Control EF (%) FS (%) 62.5 66.4 34.5 37 Cardiac output and midwall LV systolic function in patients with LVH and controls 25 *

20 15 10 5 0 LVH Control CO (l/min) Midwall FS (%) 4.32 4.55 17.9 21.6 *p < 0.01 versus control group

Treatment study: hypertensives with LVH (males=28, females=4) Age (years) SBP (mmHg) DBP (mmHg) Heart rate (b/min) ECG voltage IVS diast (cm) LVID diast(cm) PWT diast (cm) LVID syst (cm) PWT syst (cm) LVMI (g/m2) RWT CESS (kdyne/cm2) Baseline

BP control 50+/-2.0 174+/-4.1 103+/-1.9 66+/-2.0 39+/-2.4 1.48+/-0.03 4.71+/-0.10 1.30+/-0.03 2.98+/-0.12 1.62+/-0.04 145+/-3.8 0.56+/-0.02 152.0+/-9.7 138+/-1.8* 84+/-1.2* 66+/-2.1

1.41+/-0.03 4.61+/-0.07 1.28+/-0.02 2.88+/-0.08 1.54+/-0.05 133+/-3.5 0.56+/-0.02 131.0+/-8.1 6 months post BP control 143+/-2.8* 86+/-1.4* 65+/-1.9 36+/-2.4 1.35+/-0.03* 4.64+/-0.08 1.26+/-0.02 2.82+/-0.07

1.51+/-0.04 124+/-3.4* 0.55+/-0.02 130.4+/-7.3 *p<0.01 versus controls Changes in endocardial systolic function with treatment and LVH regression 80 60 40 20 0 Baseline BP control 6/12 BP control

EF (%) FS (%) 65.6 67 69.3 37 38 39.5 Changes in cardiac output and midwall LV systolic function with treatment and LVH regression 25 *

20 15 10 5 0 Baseline BP control 6/12 BP control CO (l/min) Midwall FS (%) 4.48 4.37 4.34 18.7 20

21.9 *p < 0.01 versus baseline What is the relationship between endocardial and midwall shortening in normal subjects and those with LVH? LVH group had a higher BP and a higher LVMI Endocardial measures of LV systolic function were similar between the 2 groups Midwall systolic function was significantly depressed in the LVH group How does regression of LVH effect midwall shortening? Good BP control was achieved There was significant regression of LVH Endocardial fractional shortening was not significantly changed

Midwall shortening improved with LVH regression Discussion In spite of similar endocardial systolic function, midwall systolic function is significantly depressed in subjects with LVH secondary to hypertension Midwall shortening is improved with regression of LVH using an ACE inhibitor and calcium antagonist based treatment regime A reduced midwall shortening has been found to be associated with a lower exercise performance Depressed midwall shortening has been shown to be an independent predictor of an adverse outcome in hypertensive subjects, particularly in those subjects with additional LVH

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