which feels pretty similar to aortic insufficiency, right, on first glance, but maybe i’m wrong, and maybe there are different considerations. only one way to find out. let’s go for it.
regurgitate aortic stenosis, as the term suggests, as is self-explanatory, is the abnormal narrowing of the aortic valve...... the narrowing, the narrowing. but what about SCLEROSIS? not stenosis but sclerosis? sclerosis is calcification and thickening of the valve WITHOUT narrowing. so stenosis always means narrowing.
aortic stenosis is the most common valve disease in the US and europe. it affects about 4% of patients older than 75, and fewer patients over 65. mostly for old people. it’s the second most common cause of cardiac surgery. we can classify it as mild, moderate, or severe depending on the valve area, the velocity across the valve, and the pressure gradient across the valve.
risk factors include congenital bicuspid valve, of course, because it’s supposed to have three cusps, and that allows for a bigger area of hole for blood to flow through, and when there’s only two cusps it’s harder for the thing to open all the way. makes sense, makes sense. and then there’s the degeneration which is what causes AS in old age, just regular degeneration, and then hypercholesterolemia also does it, as well as rheumatic heart disease, and radiation therapy.
patients may be asymptomatic or have chest pain, shortness of breath on exertion, passing out, signs of heart failure and GI bleeding due to angiodysplasia (it’s where your blood vessels are just forming out of control in a bad way just in a way that’s not expected). findings on physical exam depend on severity of stenosis, but all patients have a systolic ejection murmur at the second interostal space which radiates to the carotid arteries.
how do we diagnose it? echocardiography.
how do we treat it? valve replacement or valvulotomy. medical treatment doesn’t really work, becuase this is a mechanical problem requiring a mechanical solution.
what about prognosis? if you’re asymptomatic you’ll probably be fine, but when you develop symptoms and don’t get a valve replacement, that’s when your prognosis starts to look a little worse.
now that the summary is over we’ll give some more details about some of those points. for example you really do start to see more calcific AS when you get old. like when you’re 85 or older you have a 4% chance of having a calcified aortic valve. that still doesn’t seem super high to me, but i guess it’s a consideration.
if you have many risk factors, the valve area will narrow gradually, which then increases the pressure and velocity gradient across the valve.
again, it’s the most common valvular disease in the US and europe, and the second most common cause of cardiac surgery. that’s kind of interesting....... second most common cause of heart surgery! damn..... damn!
half the patients with aortic stenosis will also have significant coronary artery disease. that’s a lot of people.
so there’s the calcific aortic stenosis that only seems to happen in old age, but then there’s the congenital bicuspid valve which is another common cause of aortic stenosis. this presents at age 30-40, and the prevalence is about 14 cases for every 1000 people.
it’s also possible to get aortic stenosis due to drugs, but they don’t elaborate.
in developing countries you’re most likely to get aortic stenosis from rheumatic heart disease. there’s also radiation as a cause.
a good way to remember the risk factors for calcific aortic stenosis is by just remembering that it’s the same as the ones for atherosclerosis. age >60, smoking, hypertension, and hypercholesterolemia. those will cause AS and atherosclerosis.
let’s talk about pathogenesis. the normal aortic valve has three thin leaflets. we begin to have problems when we get lipid accumulation, inflammation, and calcification. these things all lead to obstruction of the valve itself, which leads to, you know, the same old things that cause the LV to work too hard. if it’s harder to push things through the valve then the LV has to get stronger and stronger eventually get pretty big and causing all kinds of hypertrophic problems. we don’t want our heart to get too big.
aging also causes collagen in the leaflets to be destroyed. calcium then builds up, making the valve thicker and reducing the leaflet motility, causing stenosis.
like i said, bicuspid valves don't open as widely as normal valves. this causes turbulent flow, which leads to increased scarring, thickness, and stenosis of the valve. the effects start to become apparent around 30-40 years of age.
rheumatic fever damages the aortic valve, producing fibrosis and fusion fo the leaflets. they start to stick together which causes stenosis. if your flaps are stuck together the area of the hole gets smaller and it gets harder to pump blood across it.
so what do we do if we suspect a patient of having aortic stenosis? we gotta recall that many patients are asymptomatic even if they have severe LV outflow obstruction. but if they do have symptoms, they’ll include chest pain, exertional dyspnea (shortness of breath with exercise), syncope (passing out), signs of heart failure (fatigue, weakness), and GI bleeding due to angiodysplasia. we also want to do a nice physical exam on them. we’ll look for jugular venous distension (JVD) because of all that pressure building up in the heart. also look for a weak, delayed carotid pulse (parvus et tardus). also may hear crackles on lung exam, lower extremity edema, paradoxical splitting of S2 in advanced disease, S4 present... these are all sort of in the weeds kinds of details that may not make sense to any of us, not really. like the whole s1 s2 s3 thing like i’m not really going to ever fully learn that methinks. but i’ll write it here for posterity.
when considering this diagnosis, we’ll also consider regular old angina, CHF or pulmonary edema, regular old syncope, or some other cause of systolic murmur (mitral or tricuspid insufficiency or hypertrophic cardiomyopathy).
to establish the diagnosis, we can consider getting labs, specifically BNP, which is useful for asymptomatic patients with severe stenosis in predicting symptom onset and need for surgery. it can also help predict mortality in patients with severe disease. BNP is a biomarker of congestive heart failure and is synthesized in the heart. it physiologically decreases blood pressure via vasodilation, reduction of cardiac preload, and suppression of sympathetic tone.
it’s so fucking cold in here, bro, and people keep coming inside and letting the cold air in like can we stopppppp holy shit dude it’s freeeeezing in here i feel like i’m going to get fuckin aortic stenosis just by my little frail little leaflets, errrr, freezing up. my heart is surely working harder now, isn’t it..... it’s cold.
but yeah, about BNP, it gets released when the wall stretches out. so like when you have that enlarging LV due to aortic stenosis, you’re going to stretch out those walls and BNP is going to go ahead and get released. interesting, right? BNP increases with age which makes sense because your heart is going to keep working harder as you get older. women happen to have higher BNP than men. no need to poeticize that one. women’s hearts working harder, something.... men being terrible.....
drugs that we use to treat heart failure affect BNP levels. for example, diuretics and vasodilators decrease the filling pressure in the atria and ventricles which then decrease BNP levels. ACE inhibitors and ARBs and spironolactone also decrease BNP.
we can use BNP to screen! when we screen it every year, we decrease incidence of LV dysfunction and heart failure, and we can prevent emergency hospitalizations or major CV events. i imagine this is because if you find someone with high BNP you can intervene faster and prevent things from getting emergent... you have a better sense of what’s happening in the heart that way.
if a patient has low or normal BNP, we can confidently rule out CHF as a diagnosis. BNP is actually most useful for excluding heart failure in ER patients presenting with acute dyspnea. so if someone comes in and has new shortness of breath, get a BNP, and it’s normal, you can rest assured their heart is okay. at least it’s not in failure. simply put, BNP complements clinical judgment and other testing. it’s not an end-all-be-all, but when you can conceptualize it, it can be a helpful little marker of how hard the heart is working, how stretched out the walls are getting.
again, echocardiography is the key diagnostic tool for aortic stenosis. it can also help us find severity and LV function. it might show us LV hypertrophy, thickened and immobile aortic valve, and dilated aortic root. it’s a helpful imaging test. cardiac catheterization can be used when noninvasive tests can’t establish the diagnosis. ECG may show LV hypertrophy, left atrial enlargement, ST-T changes, AV block, hemiblock, or bundle branch block.
chest xray is usually not helpful, but it might show calcification of aortic cusps, left atrial enlargement, pulmonary congestion, poststenotic dilatation of aorta.
hey, exercise stress testing can only be used for asymptomatic patients. don’t do it in patients with severe stenosis and symptoms!! you might kill them or something!!!
if you have limiting symptoms like dyspnea, you have a 50% chance of surviving for another year without symptoms. in other words, you in danger, girl. your time is limited. but if you are able to do a stress test and it’s benign, you have a very low risk of death.
so then how do we manage it? this is a chronic condition so the management is chronic. we avoid strenuous activity in moderate/severe AS. that sucks. but don’t make your heart work too hard because it actually cant’ and you may actually fall over and die. rip. treatment is not always recommended in asymptomatic patients, but you should still do echo every 3-5 years in mild AS cases, or every 1-2 years if it’s moderate, or every year if it’s severe.
how to decide when to do a valve replacement all depends on when symptoms start. every month, 2% of symptomatic AS patients DIE. so the symptoms really do change our management. we’re not too concerned unless they’re having shortness of breath or chest pain or whatever else.
aortic valve replacement is indicated for patients with severe stenosis and symptoms, LVEF < 50%, patients s/p CABG or other vascular surgery, abnormal stress test, high risk of rapid progression, extremely severe stenosis, or severe ventricular hypertrophy without hypertension.
medical treatment generally doesn’t change much and doesn’t improve survival. again, mechanical problems require mechanical solutions.
finally, to speak more about the prognosis, aortic stenosis has the worst prognosis of all the valvular lesions, and it has increased morbidity and mortality in the elderly. asymptomatic patients do just fine and have a mortality rate less than 1% per year. they got this. once again, survival is much harder when symptoms appear, and wthout valve replacement, one in four of these people die every year. 70% of symptomatic patients without valve replacement die within 3 years. valve replacement MAY improve survival... the may is doing a lot of heavy lifting there, damn. and finally, in patients with Heyde’s syndrome (aortic steoniss with colonic angiodysplasia), valve replacement decreased rebleeding by 81% in patients with GI hemorrhage. i guess that’s relevant but honestly i have never seen the word Heyde in my life.
anyway, i’m still cold, but that’s it for aortic stenosis. that’s all she wrote. let’s move on.
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