1. Left Ventricular Mass Regression after A V R DR. Kumaravel

2. 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 layer The superficial and deep layers are anchored at the ventricular orifices to Fibrous skeleton of the heart

3. 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

4. Pathophysiology in A S PRESS OVERLOAD INCREASED SYSTOLIC STRESS WALL THICKENING Concentric LVH

5. 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.

6. 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

7. A R VOLUME OVERLOAD INC diastolic stress Inc L V volume Eccentric lv hypertrophy.

8. 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.

9. 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.

10. 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.

11. 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, permananentintraoperative L V damage ,energy loss and regurgitation across the valve replacement devices

12. A S When 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

13. 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.

14. A R Regression 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.

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

16. 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 Biederman Author 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

17. 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.

18. Abstract Results 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.

19. Abstract Conclusion 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.

20. 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 derLaarse, PhD, Hubert W. Vliegen, MD, FerreLeujes, 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.

21. Abstract OBJECTIVES: The aim of this study was to evaluate the effect of aortic valvereplacement (AVR) on left ventricular (LV) function and LV remodeling,comparing patients with aortic valve stenosis to patients withaortic regurgitation. BACKGROUND: Aortic valve disease is associated with eccentric or concentricLV hypertrophy and changes in LV function. The relationshipbetween LV geometry and LV function and the effect of LV remodelingafter AVR on diastolic filling, in patients with aortic valvestenosis compared with aortic regurgitation, are largely unknown. METHODS: Nineteen patients with aortic valve disease (12 aortic valvestenosis, 7 aortic regurgitation) were studied using magneticresonance imaging to assess LV geometry and LV function beforeand 9 ± 3 months after AVR. Ten age-matched healthy malesserved as control subjects.

22. Abstract RESULTS: Before AVR, the ratio between left ventricular mass index (LVMI)and left ventricular end-diastolic volume index (LVEDVI) wasonly 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 significantlyin 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 bothaortic valve stenosis and aortic regurgitation. Early afterAVR, diastolic filling improved in patients with aortic valvestenosis, whereas patients with aortic regurgitation showeda deterioration in diastolic filling

23. Abstract CONCLUSIONS: Early after AVR, patients with aortic valve stenosis show adecrease in both LVMI and LVMI/LVEDVI and an improvement indiastolic filling, whereas in patients with aortic regurgitation,LVMI decreases less rapidly than LVEDVI, causing concentricremodeling of the LV, most likely explaining the observed deteriorationof diastolic filling in these patients.

24. Left Ventricular Mass Regression One Year After Transcatheter Aortic Valve Implantation ApostolosTzikas, 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.

25. Abstract Background: Left ventricular (LV) hypertrophy is associated with LV diastolicdysfunction and constitutes a risk factor for cardiac morbidityand mortality. The objective of this study was to investigatethe degree of LV mass regression and the changes of LV diastolicfunction 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 severeaortic stenosis who underwent TAVI with the Medtronic CoreValveSystem (Medtronic Inc, Minneapolis, MN). The LV mass was calculatedusing the Devereux formula and indexed to body surface area.

26. Abstract Results: One-year all-cause mortality was 29%. The LV mass index decreasedfrom 126 ± 42 g/m2 at baseline to 110 ± 30 g/m2 at one-year follow-up (p < 0.001). Left ventricular ejectionfraction and LV diastolic function did not change significantly.Mean transaortic gradient decreased from 47 ± 19 mm Hgat baseline to 9 ± 5 mm Hg at discharge and 9 ±4 mm Hg at one year (p < 0.001), and was accompanied by significantclinical improvement. More than mild paravalvular aortic regurgitationwas found in 24% and 15% of patients at discharge and one-yearfollow-up, respectively. Conclusions: A significant regression in LV mass was found one year afterTAVI. However, regression was incomplete and was not accompaniedby an improvement in LV diastolic function

27. Thank u