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Cardiovascular · Clinical trials

Aortic Stenosis Clinical Trials

Approved therapies, the pivotal-trial endpoints they were judged on, the magnitude of benefit — and the drugs that failed their endpoints, and why.

Indication overview

About aortic stenosis — and why its trials are hard

Aortic stenosis (AS) is narrowing of the aortic valve that obstructs left-ventricular outflow, most commonly from age-related calcific degeneration of a trileaflet valve or earlier degeneration of a congenital bicuspid valve. As the valve area falls, the left ventricle hypertrophies to sustain output; once severe AS becomes symptomatic, producing exertional dyspnea, angina, or syncope, prognosis without valve replacement is poor, with survival often measured in a few years. Importantly, there is NO disease-modifying drug for aortic stenosis. Multiple randomized statin trials aimed at slowing calcific progression failed, including SEAS (simvastatin plus ezetimibe), SALTIRE (atorvastatin), and ASTRONOMER (rosuvastatin), none of which slowed hemodynamic progression or reduced valve events. Medical therapy is therefore limited to managing comorbidities and heart failure symptoms; vasodilators and diuretics must be used cautiously in severe AS. Definitive treatment is mechanical relief of obstruction through valve replacement: surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR/TAVI). Landmark trials (PARTNER, Evolut) extended TAVR from inoperable to high-, intermediate-, and low-surgical-risk patients, making it the dominant approach for many.

Indication
Aortic Stenosis
ICD-10-CM
I35.0 — Nonrheumatic aortic (valve) stenosis

Approved therapies & pivotal evidence

What's been approved — and by how much it moved the endpoint

Drug (brand)ApprovedSettingPivotal trialPrimary endpointMagnitude of benefit
None (no disease-modifying pharmacotherapy exists) (N/A)N/ADefinitive treatment is procedural: TAVR/TAVI or surgical aortic valve replacement (SAVR)PARTNER series and Evolut Low Risk (device trials, NEJM 2010-2019)Composite of death, stroke, and rehospitalization (device outcome, not a drug endpoint)TAVR proven non-inferior or superior to SAVR across inoperable, high-, intermediate-, and low-risk populations; no drug slows AS progression, so no pharmacologic magnitude applies

Where trials have failed

Drugs that missed their endpoint — and what contributed

The most instructive lessons in aortic stenosis development come from programmes that failed the endpoint that mattered.

Drug / trialEndpoint outcomeWhat contributed
Simvastatin plus ezetimibe — SEAS (NEJM 2008)Intensive lipid lowering did NOT reduce the primary composite of aortic-valve and ischemic cardiovascular events and did not slow aortic-stenosis progressionCalcific AS progression is not lipid-dependent once established; a modest reduction in ischemic events did not affect valve outcomes, and a cancer safety signal was noted
Atorvastatin — SALTIRE (NEJM 2005)Atorvastatin did NOT slow the progression of calcific aortic stenosis (no difference in aortic-jet velocity or valve calcium score)Statin-driven LDL reduction failed to alter established valvular calcification, undermining the lipid hypothesis for AS
Rosuvastatin — ASTRONOMER (Circulation 2010)Rosuvastatin did NOT reduce the rate of progression of aortic-jet velocity in mild-to-moderate ASEven earlier-stage, high-intensity statin intervention failed to slow hemodynamic progression, closing the door on statins as disease-modifying therapy for AS

Choosing the right endpoint

Primary endpoints that matter in aortic stenosis trials

  • Aortic-jet velocity / valve area progression — Echo/Doppler measures of hemodynamic severity; primary progression endpoint in the failed statin trials (SALTIRE, ASTRONOMER)
  • All-cause death — Hard outcome anchoring TAVR vs SAVR device trials and any therapy in symptomatic severe AS
  • Disabling stroke — Key procedural safety/efficacy endpoint in TAVR trials, often within a composite with death and rehospitalization
  • Rehospitalization for valve/heart failure — Component of the composite endpoint in the PARTNER and Evolut TAVR programs
  • Aortic-valve and ischemic CV events (composite) — Primary combined endpoint in SEAS, which the drug failed to reduce

How iNGENū runs aortic stenosis trials

Physician-led design, built for FDA submission

Endpoint & biomarker strategy

Board-certified specialists design endpoints and patient selection aligned to current FDA guidance for this indication.

FDA-ready data

Built to ICH-GCP and 21 CFR 312.120, with direct FDA submission — data accepted by the FDA, EMA and MHRA.

Faster, lower-cost delivery

~4-week ethics via the TGA CTN scheme, up to 43.5% R&D rebate, and 80–90% below US CRO cost.

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Frequently asked questions

Aortic Stenosis clinical trials — FAQs

Is there any medication that treats aortic stenosis?
No. There is no disease-modifying drug for aortic stenosis. Statin trials (SEAS, SALTIRE, ASTRONOMER) failed to slow progression. Medications only manage symptoms and comorbidities; definitive treatment for severe symptomatic AS is valve replacement by TAVR/TAVI or surgery (SAVR).
Why did statins fail in aortic stenosis?
Although calcific AS shares risk factors with atherosclerosis, once valve calcification is established its progression is not driven by LDL cholesterol. Randomized statin trials showed no slowing of aortic-jet velocity or valve-area decline, so lipid lowering does not modify the disease course of AS.
What is the difference between TAVR and SAVR?
SAVR is open-heart surgical replacement of the aortic valve; TAVR/TAVI implants a valve via catheter, usually through the femoral artery, without open surgery. Landmark trials extended TAVR from inoperable to low-surgical-risk patients, and it is now the preferred approach for many, especially older patients.

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