Home D Cardiovascular Conditions Degenerative aortic stenosis: Overview, Causes, Symptoms, Diagnosis, Treatment, and Management

Degenerative aortic stenosis: Overview, Causes, Symptoms, Diagnosis, Treatment, and Management

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Degenerative aortic stenosis is a common valve problem of aging in which the aortic valve gradually becomes stiff and narrow. Aortic stenosis (a narrowed heart valve) often progresses quietly for years, so many people feel “fine” until the valve reaches a tipping point. When that happens, everyday activities—walking uphill, carrying groceries, climbing stairs—can suddenly feel harder, and fainting or chest pressure may appear without warning. The condition matters because the heart must push against a tight opening, which can lead to heart muscle thickening, heart failure, and dangerous rhythm problems.

This article explains how degenerative aortic stenosis develops, who is most at risk, which symptoms deserve prompt attention, how clinicians confirm and grade severity, and what modern treatment and long-term management typically look like.

Table of Contents

What degenerative aortic stenosis does

The aortic valve sits between the heart’s main pumping chamber (the left ventricle) and the aorta, the body’s largest artery. Each heartbeat, the valve opens to let oxygen-rich blood leave the heart, then closes to prevent backflow. In degenerative aortic stenosis, the valve’s leaflets gradually thicken, stiffen, and develop calcium deposits. Over time, the opening becomes smaller—like a door that cannot fully swing open.

That narrowing changes the physics of blood flow. The heart must generate higher pressure to push blood through a tighter opening. Early on, the body compensates by thickening the heart muscle (left ventricular hypertrophy). This can maintain forward flow for a while, but it comes at a cost: thick muscle can become stiff, so the heart fills less efficiently between beats. People may start to feel short of breath on exertion even before the pumping strength looks “weak” on tests.

As stenosis progresses, the heart may no longer keep up with demand. The pressure overload can lead to:

  • Reduced exercise capacity because the heart cannot increase output quickly
  • High filling pressures that cause breathlessness and fluid congestion
  • Microvascular angina (chest pressure) even without major coronary blockages
  • Electrical instability, including atrial fibrillation or conduction problems in some patients
  • Heart failure, sometimes with preserved pumping strength at first, then later with reduced strength

Degenerative aortic stenosis is often described by stages rather than a single moment of onset. Many patients spend years in a “compensated” phase, followed by a more fragile phase where symptoms emerge. Once typical symptoms appear—especially exertional chest pressure, fainting, or breathlessness—the risk of hospitalization and death rises if the valve is not treated.

One of the most important practical points is that the valve itself usually does not “get better” with lifestyle measures or medication. Medications can support the heart and treat related conditions (like high blood pressure or fluid overload), but they do not reliably reverse a calcified, narrowed valve. For most people with severe symptomatic disease, valve replacement—surgical or transcatheter—is the treatment that changes prognosis.

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Why the valve narrows over time

Degenerative aortic stenosis is not simply “wear and tear.” Modern research shows it behaves more like an active biological process that shares features with atherosclerosis (plaque disease) and bone formation. The valve’s surface can become injured or dysfunctional over time, allowing lipids and inflammatory cells to enter the tissue. This inflammation triggers remodeling: fibrosis (scar-like thickening) and then calcification (mineral deposition) that makes the leaflets rigid.

Several overlapping mechanisms drive this progression:

  • Endothelial dysfunction: the valve’s lining becomes less protective, allowing inflammation and lipid entry
  • Inflammation: immune cells and signaling molecules promote tissue remodeling
  • Fibrosis: collagen builds up, thickening the leaflets and reducing flexibility
  • Osteogenic signaling: cells in the valve adopt “bone-like” behavior, promoting calcification
  • Mechanical stress: turbulent flow and high pressure across the valve amplify injury, especially when the valve is already mildly abnormal

Degenerative disease most commonly affects a normal three-leaflet valve in older adults. However, some people have a bicuspid aortic valve (two leaflets instead of three). Bicuspid anatomy creates abnormal flow patterns and higher mechanical stress, so stenosis often develops earlier—sometimes decades earlier—than in people with tricuspid valves. Even when the topic is “degenerative” disease, bicuspid valve is important because it changes timelines, screening recommendations, and sometimes the choice of procedure.

Progression speed varies. Some people remain stable for years; others progress steadily. Clinicians often watch for signs that suggest faster risk:

  • Rapid increases in valve gradients on echocardiography over serial exams
  • Heavy valve calcification on imaging
  • New symptoms or declining exercise capacity
  • Signs of heart strain (thickening, reduced strain measures, rising pressures)

It is natural to ask whether statins, calcium supplements, or other medications can slow the valve. Large clinical trials have not shown a consistent benefit of statins in stopping established calcific aortic stenosis progression, even though statins remain essential for preventing heart attacks and strokes in appropriate patients. Similarly, most people should not assume that simply reducing dietary calcium will help. Valve calcification is driven by complex signaling and inflammation, not just calcium intake.

The “why” matters because it shapes prevention strategy. You cannot undo decades of valve remodeling with a short-term fix, but you can reduce additional cardiovascular stressors (blood pressure, diabetes, smoking) and catch progression earlier through appropriate surveillance.

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Risk factors and who needs screening

Degenerative aortic stenosis becomes more common with age, but age alone does not tell the full story. Risk rises when factors that promote inflammation, calcification, or abnormal valve stress stack together over time. Some risk factors are modifiable; others are not.

Major non-modifiable risk factors include:

  • Older age, especially after 65
  • Male sex, though women are also commonly affected and may present differently
  • Bicuspid aortic valve (often present from birth)
  • Family history of aortic valve disease or early valve replacement
  • Chronic kidney disease, especially advanced disease, which accelerates calcification

Modifiable or partially modifiable risk factors often overlap with cardiovascular risk:

  • High blood pressure
  • High LDL cholesterol and metabolic syndrome
  • Diabetes or insulin resistance
  • Smoking history
  • Obesity and low physical activity
  • Chronic inflammatory states

It helps to separate “risk of developing stenosis” from “risk of complications once stenosis exists.” For example, high blood pressure does not cause a calcified valve by itself, but it increases the workload on the left ventricle, so symptoms may appear earlier and heart failure risk may rise once stenosis becomes significant.

Who should be screened?
There is no universal population screening program for aortic stenosis. Instead, clinicians use targeted evaluation:

  • Anyone with a new heart murmur should be assessed, especially if the murmur is loud or late-peaking.
  • People with symptoms suggestive of valve disease (exertional breathlessness, chest pressure, fainting, unexplained fatigue) should be evaluated promptly.
  • People with bicuspid aortic valve need structured follow-up because stenosis and aortic enlargement can develop over time.
  • Older adults with multiple risk factors may benefit from careful auscultation and a low threshold for echocardiography if symptoms are present or functional capacity is declining.

In real practice, the most common missed opportunity is not “lack of screening,” but misattribution: assuming shortness of breath is just deconditioning, assuming dizziness is “normal aging,” or attributing reduced activity to arthritis without considering that the person stopped walking because they feel winded. A simple question often clarifies: “What did you stop doing in the last year, and why?”

If you already have known mild or moderate aortic stenosis, the key is not constant testing—it is scheduled surveillance with a clear plan. Regular echocardiography at intervals matched to severity helps detect the moment when the risk-benefit balance shifts toward valve replacement, ideally before an emergency admission forces decisions.

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Symptoms, stages, and complications

Degenerative aortic stenosis can be deceptively quiet. Many people compensate by slowing down without noticing it: taking elevators instead of stairs, choosing flatter routes, pausing more often. Symptoms often emerge when the valve becomes severely narrowed or when the heart can no longer compensate for the pressure load.

Classic symptoms (especially concerning when triggered by exertion) include:

  • Breathlessness: new shortness of breath when walking, climbing stairs, or doing routine chores
  • Chest pressure or tightness: sometimes called angina, even in people without major coronary blockages
  • Dizziness or fainting: lightheadedness or passing out during activity or immediately after exertion
  • Fatigue and reduced stamina: “I run out of energy sooner than I used to”

Other symptoms that may appear as the disease advances include:

  • Swelling in legs or abdomen from fluid retention
  • Waking at night short of breath or needing extra pillows
  • Palpitations, especially if atrial fibrillation develops
  • Declining appetite or unintentional weight loss in advanced heart failure

Why symptoms can appear suddenly
The heart’s ability to compensate can mask severity until a threshold is crossed. Once the valve is very tight, small additional stressors—anemia, infection, dehydration, new atrial fibrillation, or uncontrolled blood pressure—can tip someone into heart failure symptoms quickly.

Complications clinicians watch for include:

  • Heart failure: initially often with preserved pumping strength, later possibly reduced strength
  • Arrhythmias: atrial fibrillation can worsen breathlessness and raise stroke risk; ventricular arrhythmias are less common but can occur in advanced disease
  • Sudden cardiac death: risk increases after symptoms develop and with advanced cardiac damage
  • Bleeding issues in some patients: severe aortic stenosis can be associated with acquired clotting-factor problems and gastrointestinal bleeding patterns in certain cases
  • Procedural risk: untreated severe stenosis increases risk of complications during non-cardiac surgery, especially major operations

Asymptomatic does not always mean low risk. Some people who claim no symptoms will show clear limitation on a supervised exercise test. Others avoid activity so effectively that symptoms stay hidden. That is why clinicians sometimes use objective assessments—exercise testing, biomarkers, imaging evidence of heart strain—to decide whether “watchful waiting” remains safe.

When to seek urgent care
Seek emergency evaluation if you have aortic stenosis (known or suspected) and develop:

  • Fainting or near-fainting
  • Chest pressure with breathlessness, sweating, or nausea
  • Sudden severe shortness of breath
  • Rapid palpitations with weakness, dizziness, or chest discomfort

The most helpful stance is timely honesty about function. If you notice a steady drop in what you can do over weeks to months, bring it up early. In aortic stenosis, delayed reporting can delay the one intervention—valve replacement—that most strongly improves survival and quality of life when symptoms begin.

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How it’s diagnosed and graded

Diagnosis of degenerative aortic stenosis centers on echocardiography, supported by clinical assessment and, when needed, additional imaging. The goal is not only to confirm stenosis, but to determine severity, understand why symptoms are happening, and decide when valve replacement is appropriate.

1) Clinical evaluation
Clinicians start with symptom history and a physical exam. A classic murmur can suggest stenosis, but murmur intensity does not reliably equal severity, especially in older adults or people with low flow states. The exam helps prioritize testing, not replace it.

2) Transthoracic echocardiography (TTE)
TTE is the primary test because it measures both anatomy and hemodynamics. Key measurements include:

  • Peak velocity across the valve (how fast blood jets through the narrowed opening)
  • Mean pressure gradient (average pressure difference across the valve)
  • Aortic valve area (calculated estimate of opening size)
  • Left ventricular size, thickness, and pumping strength
  • Other valve disease (mitral regurgitation, tricuspid regurgitation) that can change symptoms and decisions

Severity is typically described as mild, moderate, or severe. Clinicians interpret numbers in context because measurement errors (especially left ventricular outflow tract diameter) can meaningfully change calculated valve area.

3) The “discordant” stenosis problem
A common real-world challenge is discordant grading: the valve area appears severe, but gradients and velocity look only moderate, or vice versa. This happens in low-flow states and requires careful work-up rather than assumptions. Clinicians may evaluate:

  • Stroke volume index and flow status
  • Blood pressure at the time of testing (high blood pressure can alter gradients)
  • Left ventricular function and strain
  • Whether the Doppler beam alignment was optimal

In specific cases, additional testing may include:

  • Dobutamine stress echocardiography to clarify severity in low-flow, low-gradient stenosis with reduced pumping strength
  • CT aortic valve calcium scoring to support severity assessment when echocardiography remains uncertain
  • Transesophageal echocardiography (TEE) if images are limited or procedural planning needs detail

4) Staging beyond the valve
Modern care increasingly evaluates “cardiac damage” from stenosis—changes in the heart muscle, left atrium, pulmonary pressures, and right heart function. Two patients with the same valve numbers can have very different risk based on how much the heart has remodeled. This broader staging can influence timing: the goal is to intervene before irreversible damage accumulates.

5) Monitoring intervals
Follow-up echocardiography is scheduled based on severity and change rate. The point is consistency: using comparable measurements over time and reassessing symptoms at each step. A well-run follow-up plan prevents both over-testing and dangerous delays.

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Treatment and long-term management

Treatment strategy depends on severity, symptoms, heart function, and overall health. For mild or moderate stenosis, management focuses on monitoring and reducing cardiovascular strain. For severe stenosis—especially when symptoms are present—valve replacement is the intervention that changes outcomes.

1) Medications: what they can and cannot do
No medication reliably “opens” a calcified valve. However, medications can improve safety and comfort by treating related conditions:

  • Blood pressure control reduces strain on the left ventricle
  • Diuretics can relieve fluid overload in heart failure (used carefully to avoid low blood pressure)
  • Rate or rhythm control can stabilize atrial fibrillation
  • Statins, diabetes medications, and smoking cessation reduce overall cardiovascular risk even if they do not stop valve calcification

Because severe stenosis makes the heart sensitive to sudden drops in blood pressure, clinicians personalize dosing and avoid overly aggressive vasodilation in some patients. The right plan balances symptom relief with hemodynamic stability.

2) When valve replacement is recommended
Valve replacement is generally considered when:

  • Severe stenosis causes symptoms (breathlessness, chest pressure, syncope)
  • Severe stenosis leads to reduced pumping strength
  • Selected asymptomatic patients show high-risk features (for example, very severe hemodynamics, rapid progression, or objective evidence of limited exercise capacity)

3) Surgical vs transcatheter replacement
There are two main approaches:

  • SAVR (surgical aortic valve replacement): open or minimally invasive surgery with a prosthetic valve. It is often preferred in younger patients, those needing additional cardiac surgery (like bypass), or when anatomy is not suitable for transcatheter valves.
  • TAVR/TAVI (transcatheter aortic valve replacement/implantation): a valve is delivered through an artery (often the femoral artery) without opening the chest. It is widely used in older adults and in many intermediate or lower surgical-risk patients, depending on anatomy, age, and expected lifespan.

The best choice is made by a multidisciplinary Heart Team. Practical factors include age, frailty, life expectancy, valve anatomy, vascular access, need for future coronary access, and the likelihood of needing another valve procedure later. “Lifetime planning” matters more now because more patients undergo TAVR at younger ages, and clinicians must consider durability and future options.

4) What to expect after replacement
Most people notice meaningful improvement in breathlessness and exercise tolerance over weeks to months, especially when symptoms were driven by the valve. Recovery differs by approach:

  • TAVR often has faster initial recovery, with earlier return to daily activities
  • SAVR has a longer recovery period but may be optimal for certain anatomies and younger patients

After either procedure, follow-up includes echocardiography to confirm valve function, medication review (including antiplatelet or anticoagulant decisions), and rehabilitation or guided reconditioning when appropriate.

5) Long-term management and prevention
Even after valve replacement, cardiovascular care continues:

  • Treat high blood pressure, diabetes, and cholesterol to protect heart muscle and vessels
  • Stay current on dental care and infection prevention strategies to reduce endocarditis risk
  • Report new symptoms early: breathlessness, swelling, palpitations, fever, or declining stamina
  • Attend scheduled follow-up imaging to monitor valve performance

When to seek care sooner
Contact your clinician promptly for new chest pressure, fainting, sudden breathlessness, rapid palpitations, or signs of heart failure (rapid weight gain, swelling, needing more pillows to breathe). Degenerative aortic stenosis is manageable, but outcomes depend on timely recognition of the moment when monitoring should shift to definitive treatment.

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References

Disclaimer

This article is for educational purposes and does not provide medical advice, diagnosis, or treatment. Degenerative aortic stenosis can lead to serious complications, including heart failure, dangerous symptoms with exertion, and increased risk during illness or surgery. Decisions about testing frequency, exercise limits, medications, and valve replacement (surgical or transcatheter) should be made with a qualified clinician, ideally a cardiologist experienced in valve disease. Seek urgent medical attention for fainting, chest pressure with shortness of breath, sudden severe breathlessness, or rapid palpitations with dizziness.

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