CHECK OUT MORE RESOURCES ON HEART ANATOMY/PHYSIOLOGY AND AORTIC STENOSIS HERE:
https://www.cvphysiology.com/Heart%20Disease/HD009b
https://www.kenhub.com/en/library/anatomy/heart-valves
http://pressbooks-dev.oer.hawaii.edu/anatomyandphysiology/chapter/heart-anatomy/
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/physical-examination-in-aortic-valve-disease-do-we-still-need-it-in-the-modern
https://www.aana.com/docs/default-source/aana-journal-web-documents-1/p309-315.pdf?sfvrsn=4b115ab1_6
https://emedicine.medscape.com/article/150638-overview#showall
https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.113.300156
AORTIC STENOSIS
What is it?
most common valvular disorder in western aging population (29% of pts older than 65)
aortic valve narrowing causing left ventricular outflow obstruction
Etiology
Calcific stenosis is the most common cause in North America and Europe
Rheumatic Valve Disease is the most common cause in developing world
Congenital bicuspid aortic valve will have earlier onset calcified aortic stenosis
Other Causes (less Common)= alkaptonuria, SLE, radidation, type II lipoproteinemia, Fabry disease, HOCM
Pathophysiology: How does it develop?
Three layers to valves: fibrosa, spongiosa, ventricularis or atrialis; the outer sheath consists of endothelial cells and interstitial cells
Aortic valve endothelial disruption-->inflammatory cell infiltrations --> increased inflammatory molecules are released and promote fibroblast activation, oxidative stress, and oxidative modification of lipids to form foam cell plaques--> valve matrix remodeling and fibrosis--> calcification with inflammatory conversion of myofibroblasts and fibrosis cause leaflet immobility --> stenosis
Rheumatic disease? inflammatory process fuels the immune infiltration and subsequent gross changes described above
Pathophysiology What are the cardiovascular complications?
DO YOU KNOW ABOUT FRANK-STARLING?? REVIEW IT HERE FOR A BETTER GRIP ON AORTIC STENOSIS WITH THIS YOU TUBE VIDEO (SOURCE OF ABOVE IMAGE): https://www.youtube.com/watch?v=NmUYrwuLzaM
Stenosis of the valve leads to obstruction of left ventricle outflow increased LV systolic pressure
Obstruction of LV outflow means there is more volume in ventricle--> increased end diastolic pressure (blood can’t get out as easy) and decreased aortic pressure
Now LV muscle must work harder to push the blood out…. increased afterload and increased LV volume left ventricular hypertrophy to maintain SV
This is a Preload dependent state: blood is left at the end of systole and contributes to increased end diastolic volume… Frank starling tells us this will increase preload and in turn increase force of contraction so the LV muscle can push the blood out of the stenotic valve and maintain SV
Over time LV hypertrophy will lead to decompensation… myocardial oxygen need increases and myocardial perfusion time decreases with increased increased lv mass and increased lv ejection time… at some point, oxygen supply cannot keep up with the need, and this is when the patient will decompensate
decompensation: afterload cannot be overcome by LV contraction despite hypertrophy, so there is reduced ejection fraction and cardiac output (CO= HR x SV)
over time, diastolic dysfunction will occur as greater filling pressures are needed to distend the stiff, thick LV atrial hypertrophy and dysfunction
AS leads to heart failure when heart cannot maintain adequate CO and EF fails
Presentation: What do your AS pts look like and why
develop over time, symptoms present in pts >70 with normal three leaflet valves
exertional dyspnea= because there is impaired CO and worsening as pulmonary venous htn develops
angina= due to oxygen mismatch
syncope= due to cerebral perfusion decrease as CO fails
Pulsus parvus et tardus= slow rising, late peaking, low amplitude carotid impulse (increase LV ejection time, decrease CO)
Heart Murmur= MID SYSTOLIC EJECTION MURMUR OVER THE RIGHT SECOND INTERCOSTAL SPACE (radiation into carotids)
paradoxical splitting of S2 heart sound as increased transaortic pressure gradient causes late closing of the aortic valve
Wide pulse pressure… De musset’s sign (head bob with systolic pulse) Quincke pulse (systolic ulsation on light compression of nail bed)
Evaluation of Valvular Pathology
Echocardiography is the main method of diagnosis
ECG may show signs of LVH (lateral ST depression and T wave inversion, LV strain pattern)
Stress testing may reveal AS in asymptomatic patients, or help with determining severity of pts with known AS
Treatment of AS
Medical therapy does not affect aortic disease enough to be warranted for use with known AS
AS is definitive treatment is aortic valve replacement, but who gets it?
Percutaneous aortic balloon valvuloplasty= palliative treatment in severe AS who are not candidates for surgical replacement
Who Gets AVR? its based on the symptoms and/or reduced ventricular systolic function
- symptomatic patients with severe AS with high transaortic gradient
- symptomatic patients with severe AS and LVEF <50%
- Asymptomatic patients with severe AS with LVEF <50% (sign of LV systolic dysfunction) (these patients may have symptoms with exercise testing
Repeat imaging timeline…
mild? 3-5 years
moderate? 1-2 years
severe? 6-12 months
SOURCES:
Carabello BA. Introduction to Aortic Stenosis. Circulation Research. 2013;113:179-185. Available from: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.113.300156
Pujari SH, Agasthi P. Aortic Stenosis. [Updated 2021 Dec 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557628/
Siliste RN, Siliste Calin. Physical Examination of aortic valve disease: do we still need it in the modern era?. Journal of Cardiology Practice. 2020;18(12). Available from: escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/physical-examination-in-aortic-valve-disease-dowe-still-need-it-in-the-modern
Sverdlov AL, Ngo DT, Chapman MJ, Ali OA, Chirkov YY, Horowitz JD. Pathogenesis of aortic stenosis: not just a matter of wear and tear. Am J Cardiovasc Dis. 2011;1(2):185-199. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253493/
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