Left Ventricular Mass Regression after A V R

DR. Kumaravel

Myoarchitecture of the ventricle

The adult ventricular mass is made up of a three dimensional network of myocardial cells

The network is highly structured and arranged in three different layers in which the myocardial cells have a preferred orientation

L V has sub epicardial, middle, deep layerThe superficial and deep layers are anchored

at the ventricular orifices to Fibrous skeleton of the heart

CONT..

This suggests that myocardial contraction plays an actual role in cardiac valve function

The middle layer is unique to the L V shows a circumferential pattern . No planes of fibrous septation are present between three layer

Pathophysiology in A S

PRESS OVERLOAD

INCREASED SYSTOLIC STRESS

WALL THICKENING Concentric LVH

A S

A S causes gradual obstruction to the LVOT, LV output is maintained by the development of LVH.

Myocardial hypertrophy in patient with AS is characterized by increased gene expression of collagen I and collagen II and fibronection that is associated with Rennin angiotension system.

In late stage of sever AS the LV decompensate with resulting dilated cardiomyopathy

Leads low cardiac output and PHT.

Pressure overload increase the systolic wall stress provides the stimulus to increase wall thickness and normalizes peak systolic stress this progress to concentric hypertrophy where the ratio of cavity to wall thickness is markedly less than normal.

Myocardial hypertrophy in AS is caused by new myofibrils added in parallel to myocytes, no new myocytes are added but existing myocytes become thicker , not longer with normal myocytes

A R

VOLUME OVERLOAD

INC diastolic stress

Inc L V volume

Eccentric lv hypertrophy.

Volume overload increase in diastolic stress provides a stimulus for elongation of myofibrils to increase LV volume because of increase LV volume by Laplace law systolic stress increase to induce wall thickening , which reduces stress and produces eccentric hypertrophy. The ratio of ventricular radius to wall thickness remains normal.

L V mass index of 200g/m”—good systolic function and only hypertrophy of myocardial cells.

L V mass of 200—300g/m”—mild degenerative changes were present.

L V mass of >300g/m” multiple degenerative changes in ultra structure and LV systolic function was greatly depressed.

Degenerative changes.

Mitochondrial changes, Disruption of sarcomeric units ,Nonoriented growth of fiber components,Disappearance of organelles,Increase in nonmuscular tissue in association

with myocardial hypertrophy.Leads to loss of ionotrophic strength and

irreversibility.

Post A V R L V structure

The degree of improvement in L V structure function depends type and extent of secondary cardiomyopathy at operation, coexisting diseases, permananent intraoperative L V damage ,energy loss and regurgitation across the valve replacement devices

A SWhen L V end diastolic pressure is low at

operation L V wall thickness and mass regression substantially to 200g/m to 133g/m( kennedy study)

The regression continue for more then one year

When L V end diastolic pressure has become importantly elevated before AVR either because of afterload mismatch or reduced contractility L V MASS reduced after operation.

Krayenbuchl and coll showed that the preoperatively enlarged muscle fiber diameter shortens with in 1-2 yrs after aortic valve replacment as part of process but with some increase in intertial fibrosis , later the fibrosis tented to decrease

But the myocardium did not return to normal

Aortic allograft and stentless valves replacement leads to greater resolution of L V hypertrophy.

Turbulence may be an important factor in reversing ventricular remodeling after implantation of a prosthetic valve as well as relief or reduction of pressure gradient across the LV outflow tract .

Mechanical valves oriented to place the major flow orifice to take advantage of eccentric flow pattern in the aorta have optimal performance in that orientation.

A RRegression of muscle fiber diameter after

AVR also occur after operation for A R.Decrease in interstitial fibrosis content is

greater after valve replacement for AR.Abolishing LV volume overload must be

performed within 6 months of its inception to permit toward normal in exp studies.

L V sys &dia function is mildly or moderately depressed at rest or stress testing usually associated with moderate cardiomegaly L V mass regression occur.

Sever preoperative reduction of resting or stressed LV Sys function often indicates irreversible deterioration

LV reverse remodeling imparted by aortic valve replacement for severe aortic stenosis; is it durable? A cardiovascular MRI study sponsored by the American Heart Association

Robert WW Biederman1*, James A Magovern3, Saundra B Grant1, Ronald B Williams1, June A Yamrozik1, Diane A Vido1, Vikas K Rathi1, Geetha Rayarao1, Ketheswaram Caruppannan1,2 and Mark Doyle1

* Corresponding author: Robert WW BiedermanAuthor Affiliations 1 Center for Cardiovascular Magnetic Resonance Imaging,

The Gerald McGinnis Cardiovascular Institute, Department of Medicine, Division of Cardiology, Allegheny General Hospital, Drexel University College of Medicine, Pittsburgh, Pennsylvania, USA

2 Division of Internal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA

3 Department of Surgery, Division of Cardiothoracic Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA

Journal of Cardiothoracic Surgery 2011, 6:53 doi:10.1186/1749-8090-6-53

Abstract Background

In patients with severe aortic stenosis (AS), long-term data tracking surgically induced effects of afterload reduction on reverse LV remodeling are not available. Echocardiographic data is available short term, but in limited fashion beyond one year. Cardiovascular MRI (CMR) offers the ability to serially track changes in LV metrics with small numbers due to its inherent high spatial resolution and low variability.

Hypothesis We hypothesize that changes in LV structure and function following

aortic valve replacement (AVR) are detectable by CMR and once triggered by AVR, continue for an extended period.

Methods Tweny-four patients of which ten (67 ± 12 years, 6 female) with

severe, but compensated AS underwent CMR pre-AVR, 6 months, 1 year and up to 4 years post-AVR. 3D LV mass index, volumetrics, LV geometry, and EF were measured.

AbstractResults

All patients survived AVR and underwent CMR 4 serial CMR's. LVMI markedly decreased by 6 months (157 ± 42 to 134 ± 32 g/m2, p < 0.005) and continued trending downwards through 4 years (127 ± 32 g/m2). Similarly, EF increased pre to post-AVR (55 ± 22 to 65 ± 11%,(p < 0.05)) and continued trending upwards, remaining stable through years 1-4 (66 ± 11 vs. 65 ± 9%). LVEDVI, initially high pre-AVR, decreased post-AVR (83 ± 30 to 68 ± 11 ml/m2, p < 0.05) trending even lower by year 4 (66 ± 10 ml/m2). LV stroke volume increased rapidly from pre to post-AVR (40 ± 11 to 44 ± 7 ml, p < 0.05) continuing to increase non-significantly through 4 years (49 ± 14 ml) with these LV metrics paralleling improvements in NYHA. However, LVmass/volume, a 3D measure of LV geometry, remained unchanged over 4 years.

AbstractConclusion

After initial beneficial effects imparted by AVR in severe AS patients, there are, as expected, marked improvements in LV reverse remodeling. Via CMR, surgically induced benefits to LV structure and function are durable and, unexpectedly express continued, albeit markedly incomplete improvement through 4 years post-AVR concordant with sustained improved clinical status. This supports down-regulation of both mRNA and MMP activity acutely with robust suppression long term.

Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation

Hildo J. Lamb, PhD*,*,1, Hugo P. Beyerbacht, MD, Albert de Roos, MD*, Arnoud van der Laarse, PhD, Hubert W. Vliegen, MD, Ferre Leujes, MD, Jeroen J. Bax, MD and Ernst E. van der Wall, MD * Radiology, Leiden, The NetherlandsCardiology, Leiden University Medical Center, Leiden, The Netherlands

Manuscript received March 6, 2002; revised manuscript received August 16, 2002, accepted September 6, 2002.

AbstractOBJECTIVES:

The aim of this study was to evaluate the effect of aortic valve

replacement (AVR) on left ventricular (LV) function and LV remodeling, comparing patients with aortic valve stenosis to patients with aortic regurgitation.

BACKGROUND: Aortic valve disease is associated with eccentric or concentric

LV hypertrophy and changes in LV function. The relationship

between LV geometry and LV function and the effect of LV remodeling after AVR on diastolic filling, in patients with aortic valve stenosis compared with aortic regurgitation, are largely unknown.

METHODS: Nineteen patients with aortic valve disease (12 aortic valve

stenosis, 7 aortic regurgitation) were studied using magnetic

resonance imaging to assess LV geometry and LV function before and 9 ± 3 months after AVR. Ten age-matched healthy males served as control subjects.

AbstractRESULTS: Before AVR, the ratio between left

ventricular mass index (LVMI) and left ventricular end-diastolic volume index (LVEDVI) was only increased in patients with aortic valve stenosis (1.37 ± 0.16 g/ml) compared with control subjects (0.93 ± 0.08 g/ml, p < 0.05). After AVR, LVMI/LVEDVI decreased significantly in aortic valve stenosis (to 1.15 ± 0.14 g/ml, p < 0.0001), but increased significantly in aortic regurgitation

(1.02 ± 0.20 g/ml to 1.44 ± 0.27 g/ml, p <

0.0001). Before AVR, diastolic filling was impaired in both aortic valve stenosis and aortic regurgitation. Early after AVR, diastolic filling improved in patients with aortic valve stenosis, whereas patients with aortic regurgitation showed a deterioration in diastolic filling

AbstractCONCLUSIONS: Early after AVR,

patients with aortic valve stenosis show a decrease in both LVMI and LVMI/LVEDVI and an improvement in

diastolic filling, whereas in patients with aortic regurgitation, LVMI decreases less rapidly than LVEDVI, causing concentric remodeling of the LV, most likely explaining the observed deterioration of diastolic filling in these patients.

Left Ventricular Mass Regression One Year After Transcatheter Aortic Valve Implantation

Apostolos Tzikas, MD, Marcel L. Geleijnse, MD, PhD, Nicolas M. Van Mieghem, MD, Carl J. Schultz, MD, PhD, Rutger-Jan Nuis, MS, Bas M. van Dalen, MD, PhD, Giovanna Sarno, MD, PhD, Ron T. van Domburg, PhD, Patrick W. Serruys, MD, PhD, Peter P.T. de Jaegere, MD, PhD* Department of Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands

Accepted for publication September 17, 2010.

AbstractBackground: Left ventricular (LV) hypertrophy is

associated with LV diastolic dysfunction and constitutes a risk factor for cardiac morbidity and mortality. The objective of this study was to investigate the degree of LV mass regression and the changes of LV diastolic function one year after transcatheter aortic valve implantation (TAVI).

Methods: Echocardiography was performed at baseline, before discharge, and at one-year follow-up in 63 consecutive patients with severe aortic stenosis who underwent TAVI with the Medtronic CoreValve System (Medtronic Inc, Minneapolis, MN). The LV mass was calculated using the Devereux formula and indexed to body surface area.

AbstractResults: One-year all-cause mortality was 29%. The

LV mass index decreased from 126 ± 42 g/m2 at baseline to 110 ± 30 g/m2 at one-year follow-up (p < 0.001). Left ventricular ejection fraction and LV diastolic function did not change significantly. Mean transaortic gradient decreased from 47 ± 19 mm Hg at baseline to 9 ± 5 mm Hg at discharge and 9 ± 4 mm Hg at one year (p < 0.001), and was accompanied by significant clinical improvement. More than mild paravalvular aortic regurgitation

was found in 24% and 15% of patients at discharge and one-year follow-up, respectively.

Conclusions: A significant regression in LV mass was found one year after TAVI. However, regression was incomplete and was not accompanied by an improvement in LV diastolic function

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