AORTIC STENOSIS ECHO CARDIOLOGY/MEDICINE.PPTX

AS ECHO CARDIOLOGY.PPTX

1. assessment of AS SEVERITY AND WHEN TO INTERVENE ? Presenter - Dr.R.SPANDANA , 2 nd year postgraduate

2. Epidemiology 1-2 % aged 65 or older 12 % aged 75 or older 3.4% aged older than 75 had severe AS. Rate of progression from aortic sclerosis to stenosis – 1.8% to 1.9% per year. Braunwald 12 th edition pg 1399

3. Valvular AS – 3 principal causes: A congenital bicuspid valve with superimposed calcification, calcification of a normal trileaflet valve, and rheumatic disease. AS – severe atherosclerosis of the aorta and aortic valve (rare – homozygous type II hyperlipoproteinemia, severe hypercholesterolemia)

4. Fixed obstruction to left ventricular (LV) outflow Above the valve (supravalvular stenosis) Below the valve (discrete subvalvular stenosis) Dynamic subaortic obstruction - caused by hypertrophic cardiomyopathy

5. U nicuspid , bicuspid, tricuspid, & quadricuspid . Unicuspid valves usually are severely narrowed at birth and produce symptoms in infancy.

6. Normal aortic valve Congenital bicuspid aortic stenosis. A false raphe is present at 6 o’clock.

7. Rheumatic aortic stenosis. The commissures are fused with a fixed central orifice. Calcific aortic stenosis

8. Generally, repeat imaging is performed every 6 to 12 months for severe AS, every 1 to 2 years for moderate AS, and every 3 to 5 years for mild AS, ESC 2021 GUIDELINES ON VALVULAR HEART DISEASE

9. Severity depends upon measurement of mean pressure gradient (the most robust parameter), peak transvalvular velocity (Vmax), and valve area. Discordant cases should take account of additional parameters: functional status, stroke volume, Doppler velocity index,156 degree of valve calcification, LV function, the presence or absence of LV hypertrophy, flow conditions, and the adequacy of BP control. ECHO EVALUATION

10. Natriuretic peptides –predict free survival and outcome in normal and low-flow severe aortic stenosis Exercise testing may unmask symptoms and is recommended for risk stratification of asymptomatic patients with severe aortic stenosis. Exercise echocardiography provides additional prognostic information by assessing the increase in mean pressure gradient and change in LV function.

11. D iagnostic workup CCT is the preferred imaging tool to assess: ( i ) aortic valve anatomy, (ii) annular size and shape, (iii) extent and distribution of valve and vascular calcification, (iv) risk of coronary ostial obstruction, (v) aortic root dimensions, (vi) optimal fluoroscopic projections for valve deployment, and (vii) feasibility of vascular access (femoral, subclavian, axillary, carotid, transcaval or transapical).

12. Myocardial fibrosis is a major driver of LV decompensation in aortic stenosis (regardless of the presence or absence of CAD), which can be detected and quantified using CMR. Amyloidosis is also frequently associated with aortic stenosis in elderly patients (incidence 9 - 15%). When cardiac amyloidosis is clinically suspected, based on symptoms (neuropathy and hematologic data), diphosphonate scintigraphy and/or CMR should be considered

13. Clinical, anatomical and procedural factors that influence the choice of treatment modality for an individual

14. The prognosis of patients with normal-flow, low-gradient aortic stenosis and preserved ejection fraction is similar to that of moderate aortic stenosis—regular clinical and echocardiographic surveillance is recommended

15. Special patient populations CAD and aortic stenosis frequently coexist. Both simultaneous SAVR and CABG, and SAVR late after CABG, carry a higher procedural risk than isolated SAVR. Patients aged <70 years with mean gradient progression >5 mmHg/year benefit from SAVR at the time of CABG once baseline peak gradient exceeds 30 mmHg. ESC 2021 VALVULAR HEART DISEASE GUIDELINES

16. PCI and TAVI - C ombined or staged SURTAVI trial , there was no significant difference in the primary endpoint (all-cause mortality or stroke at 2-year follow-up) in intermediate-risk patients with severe aortic stenosis and noncomplex CAD (SYNTAX score <22) undergoing either TAVI and PCI or SAVR and CABG [16.0% (95% CI, 11.122.9) vs. 14% (95% CI, 9.221.1); P = 0.62]. D iffuse CAD

17. ESC LVEF <55% (IIA)

18. DECISION MAKING?

19. CASE #1 : ASYMPTOMATIC PATIENT WITH SEVERE AS (STAGE C 1) 75 YEAR old women with calcific AS Asymptomatic (confirmed by ETT) BNP :190pg/ml LVEF:60% Grading of AS severity on ECHO: Severely calcified valve Peak jet velocity :5.1m/s (1 year ago:4.8m/s) Peak/mean gradient : 104/64 mmHg AVA:0.65 cm ² Indexed AVA:0.35cm²/m²

20. Clinical dilemma in true asymptomatic severe AS ( C1 stage) Early << Prophylactic >> AVR? Or Watchful waiting?

21. CASE 2# 82 year woman, HTN – ACEI No CAD NYHA III, HF hospitalization LVEF – 65% Global longitudinal strain : 13% Grade 2 diastolic dysfunction Echo: AVA :0.64 cm2, iAVA:0.36cm2/m2 Doppler velocity index :0.19 Peak/mean gradient : 44/26mmHg SVI: 29 ml/m2

22. Paradoxical low flow, low gradient Class I indication of AVR (2021 – ACC-AHA)

23. CASE 3: AC01.0005011140 74 YEAR OLD, DM ANEMIA EF-60% Asymptomatic Exercise testing: normal Next year came with symptoms Echo: AVA : 0.9cm2, Peak/mean gradient : 107/67mmHg

24. Case 4 AC01.0003681487 Name: ABC Age: 84 years, female Asymptomatic severely calcified AS ACS-NSTEMI NSVT, Paroxysmal AF HFpEF NTproBNP : 9620 pg /ml ECHO: E/e: 22.5 PG: 123 mmHG , MG : 73 mmHG AVA : 0.5 cm2