Understanding Aortic Stenosis: A Complete Guide for Patients

Medically Reviewed & Edited

Board-Certified Invasive Cardiologist
Encinitas and La Jolla, CA

Developed with digital research and writing assistance, then medically reviewed and edited by Dr. Rasch to ensure clinical accuracy and adherence to current evidence-based guidelines.

Last reviewed and updated on June 27, 2026

When I tell a patient that their aortic valve is getting tight, the first question is almost always the same: “Is this serious?” The honest answer is that aortic stenosis can be serious, and it’s also one of the most fixable problems I treat. The challenge isn’t whether we can solve it. We can. The challenge is timing, because this condition stays quiet for years and then changes quickly. My job, and a big part of yours, is to recognize that turning point and act on it before your heart pays a price.

Aortic stenosis means your aortic valve has become stiff and narrowed, so it no longer opens the way it should. That valve is the one-way door between your heart’s main pumping chamber, the left ventricle, and your body’s largest artery, the aorta. Every time your heart beats, that door is supposed to swing wide open and let blood flow out freely. In aortic stenosis, the door only opens partway, and your heart has to generate much higher pressure to force the same amount of blood through a smaller opening.

This is the most common valve problem we see in adults. It affects roughly 1 to 2 percent of people over 65, and closer to 1 in 8 people over 75. Here in San Diego, I diagnose it often, frequently as a surprise finding when a patient comes in for something else and I hear a murmur. I want to walk you through what’s actually happening inside your chest, how we measure it, what the symptoms mean, and how we decide when it’s time to act.

What Happens to the Valve

Your aortic valve normally has three thin, flexible flaps, called leaflets, that open and close more than 100,000 times a day. In the most common form of aortic stenosis, calcium gradually builds up on those leaflets over many years, the way mineral deposits build up on an old faucet. The leaflets thicken, stiffen, and stop opening fully. This usually becomes a problem in a person’s 70s or 80s.

For a long time we thought of this as simple wear and tear, like a part that just gets old. We now understand it’s a more active process than that. It starts with tiny injuries to the valve surface, followed by cholesterol particles working their way in, inflammation, and then calcium laying down in earnest. It shares a lot of biology with the same plaque that builds up in arteries and causes coronary artery disease. That connection helps explain why the risk factors overlap so closely with the ones I talk about for heart attacks and strokes.

There’s a second common path to aortic stenosis, and it shows up much earlier in life. Some people are born with a valve that has only two leaflets instead of three. We call this a bicuspid aortic valve, and it’s one of the most common conditions people are born with. A two-flap valve handles the daily mechanical stress less gracefully than a three-flap valve, so it tends to calcify and narrow a few decades sooner. A bicuspid patient might face valve narrowing in their 50s or 60s rather than their 80s. Bicuspid valves account for a large share of the aortic valve procedures we perform.

A third cause, rheumatic heart disease, follows untreated strep throat infections and scars the valve over time. It’s now uncommon in the United States, but it remains a major cause of valve disease in parts of the world with less access to antibiotics.

Who Tends to Develop It

Age is the strongest driver. The longer that valve has been opening and closing, the more chance calcium has had to accumulate. Men develop calcific aortic stenosis somewhat more often than women.

Many of the other risk factors are the same ones tied to artery disease, which makes sense given the shared biology. High blood pressure puts extra strain on the valve and the heart muscle, so getting your numbers under control matters. You can read more about that in my guide to high blood pressure. High cholesterol plays a role too, and I pay close attention to LDL cholesterol in these patients. One inherited factor I check for is lipoprotein(a), a particle you’re born with a set level of. Elevated lipoprotein(a) is linked to faster valve calcification, and it’s something I want to know about even though we can’t change the valve disease with medication. Diabetes, smoking, and kidney disease round out the list.

There’s also an early, milder finding called aortic sclerosis, which means the valve is thickened but not yet narrowed enough to obstruct flow. About a quarter of adults over 65 have it. Most people with aortic sclerosis never go on to develop significant stenosis, but a small percentage do each year, which is why it’s worth noting and keeping an eye on.

The Symptoms, and Why They Show Up Late

Here is the part of aortic stenosis that catches people off guard. For years, often a decade or more, you can have a narrowing valve and feel completely fine. Your heart is remarkably good at compensating. The muscle of the left ventricle thickens to generate the extra pressure it needs, and you go about your life with no clue anything is wrong.

That’s exactly why this condition is sneaky. The symptoms tend to arrive only once the narrowing is severe and your heart has run out of ways to keep up. When symptoms do come, they fall into three classic patterns, and I want you to know them.

The first is shortness of breath, usually with exertion at first. You might notice you’re winded walking up a hill or a flight of stairs that never used to bother you. My guide to cardiac shortness of breath goes deeper on this. The second is chest pain or pressure with activity, sometimes felt as tightness or squeezing. The third, and the one that worries me most, is lightheadedness or fainting, especially during exertion. If you’ve passed out or come close to it, that’s not something to wait on. My guide to lightheadedness and fainting explains why.

These symptoms happen because a severely narrowed valve caps how much blood your heart can deliver. At rest you’re fine, but the moment your body asks for more, during a brisk walk, climbing stairs, carrying groceries, your heart simply can’t push enough blood through that tight opening to meet the demand.

The arrival of symptoms is the single most meaningful moment in this disease. It marks the point where the math changes. Without a new valve, people with symptomatic severe aortic stenosis face a steep drop in survival, with mortality reaching as high as 50 percent within a year or two of symptoms starting. I don’t share that number to frighten you. I share it because the same studies show that replacing the valve at that point restores survival close to normal. The danger is in waiting, not in the condition itself once we treat it.

How We Find It and Measure It

Often the first clue is a sound. When I listen to your heart and hear a particular kind of murmur, a harsh sound over the upper right chest that travels up toward the neck, that’s a signal to look closer. A few features on exam tell me the narrowing may be advanced: a murmur that peaks late, a pulse in the neck that rises slowly, and a softening of the normal “lub-dub” closing sound of the valve.

The test that confirms and grades aortic stenosis is the echocardiogram, an ultrasound of the heart. It’s painless, uses no radiation, and gives me a moving picture of your valve. I can watch the leaflets move, see how stiff they’ve become, and most importantly, measure three numbers that tell me how severe the narrowing is.

The first is the speed of blood as it jets through the narrowed opening, called the peak velocity. A tighter valve forces blood through faster, like putting your thumb over a garden hose. The second is the mean gradient, the average pressure difference between the pumping chamber and the aorta. A bigger pressure gap means a tighter valve. The third is the valve area, the actual size of the opening the blood has to squeeze through.

We sort severity into stages. Severe aortic stenosis is generally defined by a peak velocity of 4 meters per second or higher, a mean gradient of 40 mm Hg or more, or a valve area of about 1.0 square centimeter or less. When the velocity climbs to 5 meters per second or beyond, we call it very severe. Milder stages sit below those thresholds, and I’ll often describe your valve as mild, moderate, or severe so you have a clear sense of where you stand.

Sometimes the picture is less straightforward. A few patients have a valve that looks severely narrowed by area, but the pressure numbers are lower than expected because the heart isn’t pumping forcefully. We call these low-flow, low-gradient cases, and they take extra work to sort out. I may order a special echocardiogram done with a medication that gently revs up the heart, or a cardiac MRI or CT scan, to confirm how severe things really are. The point is that not every case is read off a single number, and getting the staging right is what lets us make the right call on timing.

How Often We Check You

If your valve is narrowed but not yet severe, the plan is watchful monitoring, and the interval depends on how tight things are. For mild aortic stenosis, an echocardiogram every 3 to 5 years is usually enough. For moderate stenosis, I move to every 1 to 2 years. Once you reach severe stenosis, even without symptoms, I want to see you every 6 to 12 months.

These visits aren’t just box-checking. Aortic stenosis tends to progress at a fairly steady pace once it gets going, and tracking your numbers over time tells me how fast your valve is changing. A valve that’s narrowing quickly gets my attention sooner. Just as much, these visits are when I ask careful questions about how you’re actually feeling, because the appearance of symptoms can change the plan overnight.

When It’s Time to Replace the Valve

This is the heart of the matter, so let me be clear about how I think through it. The strongest reason to replace an aortic valve is severe stenosis plus symptoms. If your valve is severely narrowed and you’ve developed breathlessness, chest pain, or fainting, replacing the valve is recommended, and I rarely advise waiting. The benefit is large and the risk of delay is real.

There are also situations where I recommend a new valve even when you feel fine. The clearest is when severe stenosis has begun to weaken the pump. If your echocardiogram shows your ejection fraction, the percentage of blood your heart squeezes out with each beat, has dropped below 50 percent, that’s a sign the valve is taking a toll, and I’ll recommend acting before symptoms arrive. Another straightforward case is when you’re already having heart surgery for another reason, such as bypass surgery. If we’re operating anyway and your valve is severely narrowed, it makes sense to address it in the same setting.

Beyond those, there’s a group of asymptomatic patients where I lean toward earlier action even with normal pump function. That includes very severe narrowing, a valve that’s narrowing unusually fast year over year, a blood marker of heart strain called BNP that’s markedly elevated, or an exercise test where you develop symptoms or your blood pressure fails to rise normally. In these situations I weigh the upside of acting early against your individual surgical risk, and we decide together.

One number from the research stays with me. In a large US study, fewer than half of patients who had a clear reason to get a valve replacement actually received one. Aortic stenosis is undertreated, often because symptoms get chalked up to aging or being out of shape. I’d rather see you and tell you that you don’t need anything yet than have you wait at home through symptoms that we could fix.

TAVR or Surgery: Choosing the Right Valve Procedure

When it’s time, there are two well-established ways to give you a new valve, and choosing between them is one of the more satisfying conversations I have, because both options are genuinely good.

The first is transcatheter aortic valve replacement, known as TAVR or TAVI. We thread a new valve up through an artery, usually in the groin, and deploy it inside your old valve without opening the chest or stopping the heart. Most patients are lightly sedated, stay in the hospital a day or two, and are back to normal activity within a week or two. TAVR has transformed this field, and for most patients over a certain age it’s now the first choice.

The second is surgical aortic valve replacement, or SAVR, the traditional open-heart operation. The surgeon removes the diseased valve and sews in a new one. It’s a bigger procedure with a longer recovery, but it’s a mature, reliable operation with decades of track record, and for certain patients it remains the better choice.

Age and life expectancy guide much of the decision. For patients under 65, or anyone with a long life expectancy ahead of them, surgery is generally recommended, mainly because surgical tissue valves have the longest proven durability, often more than 20 years. For patients between 65 and 80, either approach is reasonable, and we make the call together based on your anatomy, your other health conditions, and your preferences. For patients over 80, or those with shorter life expectancy, TAVR through the groin is usually preferred. And for anyone at high or prohibitive surgical risk at any age, TAVR is the answer as long as we expect a meaningful, good-quality recovery.

It helps to know the honest trade-offs. TAVR offers a lower risk of dying in the first month, a shorter hospital stay, less bleeding, and a lower chance of atrial fibrillation afterward. Surgery, on the other hand, has a lower rate of leak around the valve, a lower chance of needing a permanent pacemaker afterward (roughly 6 percent with surgery versus about 15 percent with TAVR), and a longer durability record. Neither is simply better. They’re different tools, and matching the tool to the patient is the whole art of it. My full TAVR guide walks through the procedure and recovery in detail if you want to go deeper.

Why There’s No Pill for This

Patients often ask whether a medication can melt the calcium away or at least slow it down. I wish I could say yes. As of now, no medication has been shown to slow the progression of aortic stenosis. That includes statins, which was a real disappointment to the field. Because the valve disease shares so much biology with artery plaque, we expected cholesterol-lowering statins to help. Several well-run trials tested exactly that, and they didn’t slow the valve narrowing.

That doesn’t mean medication is pointless. I still treat your blood pressure, your cholesterol, and your other risk factors carefully, because doing so protects your arteries, your heart muscle, and your overall health, and it makes you a stronger candidate if you do need a procedure down the road. Statins remain worthwhile for those reasons, as I cover in my piece on the broader benefits of statins. What I won’t do is pretend a pill is treating the valve itself. The valve is a mechanical problem, and the definitive fix is mechanical.

Living Well With Aortic Stenosis

If you’ve been diagnosed, the most useful things you can do are simple. Keep your monitoring appointments, because the entire strategy depends on catching the turning point. Tell me promptly if anything changes, especially new breathlessness, chest discomfort, or any lightheadedness or fainting. Don’t talk yourself out of mentioning a symptom because you think it’s just age. That’s the exact instinct that leads people to wait too long.

Stay active within the limits we discuss. For mild to moderate stenosis, most people can exercise normally, and staying fit helps your heart and the rest of you. For severe stenosis, I’ll give you specific guidance, and I’ll usually steer you away from very intense, all-out exertion until your valve is fixed. Eat in a way that supports your heart and arteries, manage your blood pressure and cholesterol, and keep up with the rest of your care, including regular dental visits, since valve disease makes good dental hygiene worth the attention.

I also want to take the fear down a notch where I honestly can. A diagnosis of aortic stenosis is not a diagnosis of decline. It’s a heads-up that somewhere down the road, maybe years from now, you’ll likely need a valve, and that we have excellent ways to give you one. Patients who stay engaged with monitoring and act at the right moment do remarkably well. Many tell me afterward that they hadn’t realized how limited they’d become until the new valve gave them their energy back.

If you’d like a clear, personalized read on where your valve stands and what the plan should be, our office is glad to help. To get in touch, visit our practice website. For TAVR, surgery, or a structural-heart opinion when the time comes, we work closely with the team at San Diego Cardiovascular Associates.

Common Questions Patients Ask Me

Can aortic stenosis be reversed without surgery?

No. There’s no medication or lifestyle change that reverses or even reliably slows the valve narrowing. The calcium doesn’t dissolve. When the valve becomes severely narrowed and starts causing problems, the only durable fix is a new valve, placed either by catheter (TAVR) or by surgery. The good news is that those procedures work very well.

How fast does aortic stenosis get worse?

It varies, but once narrowing is established it tends to progress steadily rather than in sudden jumps. That’s why I track your numbers over time. Some valves narrow slowly over many years, while others, including some bicuspid valves and valves in people with high lipoprotein(a), move faster. Your monitoring interval is set by how severe and how fast-moving your particular valve is.

Is it safe to exercise with aortic stenosis?

With mild to moderate stenosis, yes, regular exercise is encouraged and good for you. With severe stenosis, I give individualized guidance and usually advise against maximal, all-out exertion until the valve is treated, because a severely narrowed valve limits how much blood your heart can deliver when demand spikes. Always check with your cardiologist about what’s appropriate for your stage.

What’s the difference between aortic stenosis and aortic regurgitation?

They’re opposite problems with the same valve. Stenosis means the valve won’t open wide enough, so blood can’t get out easily. Aortic regurgitation means the valve won’t close tightly, so blood leaks backward into the heart. Some people have a bit of both. The symptoms and the timing of treatment differ, which is why getting the diagnosis precise matters.

Will I need a pacemaker after a valve procedure?

Some patients do, because the valve sits close to the heart’s electrical wiring. The chance is higher with TAVR (around 15 percent) than with surgery (around 6 percent). It’s one of the trade-offs we weigh when choosing between the two approaches, and it’s something I’ll discuss with you specifically based on your anatomy and rhythm.

I feel completely fine. Why would I ever need treatment?

Most of the time, feeling fine means we keep monitoring and do nothing. But there are a few situations where I’d recommend a new valve even without symptoms: if your heart’s pumping strength has dropped, if the narrowing is very severe or progressing fast, or if you’re already having heart surgery for another reason. In those cases, acting before symptoms start protects your heart muscle.

References

Otto, Catherine M., David E. Newby, and Graham S. Hillis. “Calcific Aortic Stenosis: A Review.” JAMA 332, no. 23 (2024): 2014-2026.

Otto, Catherine M., Rick A. Nishimura, Robert O. Bonow, Blase A. Carabello, John P. Erwin, Federico Gentile, Hani Jneid, et al. “2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.” Journal of the American College of Cardiology 77, no. 4 (2021): e25-e197.

Lindman, Brian R., Marie-Annick Clavel, Patrick Mathieu, Bernard Iung, Patrizio Lancellotti, Catherine M. Otto, and Philippe Pibarot. “Calcific Aortic Stenosis.” Nature Reviews Disease Primers 2 (2016): 16006.

Carabello, Blase A. “Aortic Stenosis.” New England Journal of Medicine 346, no. 9 (2002): 677-682.

Goody, Philip R., Mohammed Rabiul Hosen, David Christmann, Sebastian Zietzer, Felix Jansen, Georg Nickenig, and Sven Thomas Niepmann. “Aortic Valve Stenosis: From Basic Mechanisms to Novel Therapeutic Targets.” Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 4 (2020): 885-900.

Dutta, Punashi, Joy F. James, Hail Kazik, and Joy Lincoln. “Genetic and Developmental Contributors to Aortic Stenosis.” Circulation Research 128, no. 9 (2021): 1330-1343.

Thiago, Luciana, Selma R. Tsuji, Jovana Nyong, Maria Eduarda Puga, Aécio Flávio Teixeira de Góis, Álvaro N. Atallah, Stela Verzinhasse Peres, and Rachel Riera. “Statins for Aortic Valve Stenosis.” Cochrane Database of Systematic Reviews 9 (2016): CD009571.

Carabello, Blase A., and Fred A. Crawford. “Valvular Heart Disease.” New England Journal of Medicine 337, no. 1 (1997): 32-41.

Writing Committee Members, Catherine M. Otto, Rick A. Nishimura, Robert O. Bonow, Blase A. Carabello, John P. Erwin, Federico Gentile, et al. “2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary.” Journal of the American College of Cardiology 77, no. 4 (2021): 450-500.

Published on damianrasch.com. The above information was composed by Dr. Damian Rasch, drawing on individual insight and bolstered by digital research and writing assistance. The information is for educational purposes only and does not constitute medical advice.