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 Mary’s 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

......

Posterior wall

Theoretical midwall fibre

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

.

.

.

.

LVIDd LVIDs

a

a

a’

a’

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

Patient characteristics and echo results of hypertensives with LVH and control

subjectsHypertensives with

LVHControl subjects

Age (years) 46+/-2.4* 40+/-1.7SBP (mmHg) 170+/-3.7* 124+/-2.3DBP (mmHg) 100+/-1.6* 77+/-7.6ECG voltage 39+/-3.3* 27+/-1.3IVS diastole (cm) 1.4+/-0.04* 1.1+/-0.02LVID diastole (cm) 4.7+/-0.08 4.8+/-0.08PWT diastole (cm) 1.3+/-0.05* 1.0+/-0.02LVID systole (cm) 3.1+/-0.11 3.0+/-0.07PWT systole (cm) 1.6+/-0.05* 1.2+/-0.02LVMI (g/m2) 140+/-3.6* 92+/-3.1RWT 0.55+/-0.02* 0.41+/-0.01CESS (kdyne/cm2) 166.4+/-9.6 150.6+/-6.7

*p<0.01 versus controls

Endocardial systolic function in patients with LVH and controls

0102030

40506070

LVH 62.5 34.5Control 66.4 37

EF (%) FS (%)

Cardiac output and midwall LV systolic function in patients with LVH and controls

0

5

10

15

20

25

LVH 4.32 17.9Control 4.55 21.6

CO (l/min) Midwall FS (%)

*

*p < 0.01 versus control group

Treatment study: hypertensives with LVH (males=28, females=4)

Baseline BP control 6 months postBP control

Age (years) 50+/-2.0 - -SBP (mmHg) 174+/-4.1 138+/-1.8* 143+/-2.8*DBP (mmHg) 103+/-1.9 84+/-1.2* 86+/-1.4*Heart rate (b/min) 66+/-2.0 66+/-2.1 65+/-1.9ECG voltage 39+/-2.4 - 36+/-2.4IVS diast (cm) 1.48+/-0.03 1.41+/-0.03 1.35+/-0.03*LVID diast(cm) 4.71+/-0.10 4.61+/-0.07 4.64+/-0.08PWT diast (cm) 1.30+/-0.03 1.28+/-0.02 1.26+/-0.02LVID syst (cm) 2.98+/-0.12 2.88+/-0.08 2.82+/-0.07PWT syst (cm) 1.62+/-0.04 1.54+/-0.05 1.51+/-0.04LVMI (g/m2) 145+/-3.8 133+/-3.5 124+/-3.4*RWT 0.56+/-0.02 0.56+/-0.02 0.55+/-0.02CESS (kdyne/cm2) 152.0+/-9.7 131.0+/-8.1 130.4+/-7.3

*p<0.01 versus controls

Changes in endocardial systolic function with treatment and LVH regression

0

20

40

60

80

Baseline 65.6 37BP control 67 386/12 BP control 69.3 39.5

EF (%) FS (%)

Changes in cardiac output and midwall LV systolic function with treatment and LVH

regression

0

5

10

15

20

25

Baseline 4.48 18.7BP control 4.37 206/12 BP control 4.34 21.9

CO (l/min) Midwall FS (%)

*

*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