Cardiac Condition
Heart Valve Disease
A group of conditions in which one or more of the heart's four valves fails to work correctly — either narrowing to restrict forward flow, or leaking to allow blood to flow back. Both create strain on the heart that, if unaddressed, leads to permanent damage.
Overview
What Is Heart Valve Disease?
The heart has four valves — aortic, mitral, tricuspid, and pulmonary — each acting as a one-way gate that keeps blood moving in a single direction. Valve disease occurs when a valve becomes too narrow to open fully, too damaged to close properly, or both simultaneously.
The heart's valves open and close approximately 100,000 times every day. Over a lifetime, this mechanical demand takes its toll — particularly on the valves on the left side of the heart, which operate under much higher pressures. Valve disease may develop gradually over decades, or — in the case of infection or rupture — suddenly over hours.
There are two fundamental mechanisms by which a valve can malfunction. Understanding which mechanism is present — and to what degree — is the foundation of all management decisions.
S
Mechanism One
Stenosis — the valve that cannot open
The valve leaflets thicken, stiffen, or fuse together, restricting the opening and forcing the heart to pump against increased resistance. The chamber upstream must work progressively harder, its walls thickening in response. Over time, the muscle becomes exhausted and begins to fail. Forward flow is obstructed.
Aortic Stenosis
Mitral Stenosis
Pulmonary Stenosis
R
Mechanism Two
Regurgitation — the valve that cannot close
The valve leaflets fail to meet properly when closed, allowing blood to leak backwards with each heartbeat. The chamber must accommodate the normal forward volume plus the regurgitant volume returning from the previous beat. Chambers dilate progressively under this volume overload. Over time, the muscle stretches beyond recovery. Backward leakage accumulates.
Mitral Regurgitation
Aortic Regurgitation
Tricuspid Regurgitation
Valve disease may be congenital — present from birth, as in a bicuspid aortic valve — or acquired, developing through age-related calcification, rheumatic fever, infection (endocarditis), or as a secondary consequence of another heart condition such as heart failure or cardiomyopathy. The distinction shapes both treatment and follow-up planning.
Aortic Stenosis
The Most Common Valve Disease
Aortic stenosis — narrowing of the aortic valve — is the most prevalent valve disease in the developed world. It is predominantly a disease of age: calcific plaque progressively deposits on the valve leaflets over decades, gradually restricting opening until the heart can no longer compensate.
Calcific (degenerative) aortic stenosis is the most common form, affecting around 3–5% of people over 75. The same risk factors that drive coronary artery disease — smoking, hypertension, raised cholesterol — promote calcification of the valve, though the process is not simply atherosclerosis and statins have not been shown in trials to slow its progression.
Bicuspid aortic valve (BAV) is the most common congenital heart defect, present in 1–2% of the population. Instead of three leaflets, the aortic valve has only two, which are subject to abnormal turbulent flow and accelerated calcification. Patients with BAV typically develop significant stenosis 10–20 years earlier than those with a normal tricuspid valve, presenting in their 50s and 60s rather than their 70s and 80s. BAV is also associated with aortic root dilatation, which requires separate monitoring.
Rheumatic aortic stenosis, caused by immune-mediated leaflet fusion following streptococcal throat infection, is now rare in the UK but remains a significant burden in developing countries. It typically affects the mitral valve simultaneously.
The Silent Progression
Aortic stenosis is characteristically silent for years or even decades. The left ventricle adapts to the pressure overload by thickening its walls — a process called concentric hypertrophy — maintaining adequate cardiac output despite the narrowed valve. Patients may have severe stenosis on echocardiography yet feel entirely well.
This compensated phase cannot last indefinitely. As the stenosis worsens and the hypertrophied muscle stiffens, the heart's capacity to meet demand is eventually exceeded. At the point of symptom onset — whether angina, syncope, or breathlessness — the prognosis without intervention changes sharply.
Echocardiography measures the gradient across the aortic valve and calculates the effective valve area — the two key markers of severity
Unlike coronary artery disease, where risk factor modification can slow or halt progression, there is currently no medical therapy proven to slow the calcification of the aortic valve. Once severe symptomatic stenosis is reached, valve replacement is the only effective treatment.
The Classic Symptom Triad — Mean Survival Without Intervention
~5
YearsAngina
Chest tightness on exertion — caused by the hypertrophied muscle outstripping its blood supply under demand. Mean survival after onset: approximately five years without valve replacement.
~3
YearsSyncope
Blackout — typically on exertion, when peripheral vessels dilate but cardiac output cannot increase to compensate. Mean survival after onset: approximately three years without valve replacement.
~2
YearsHeart Failure
Breathlessness — the left ventricle has decompensated and can no longer maintain adequate output. The most ominous of the three. Mean survival after onset: approximately two years without valve replacement.
These figures — derived from the landmark natural history studies of Horstkotte and Loogen — remain foundational in understanding why symptomatic severe aortic stenosis demands urgent intervention.
Echocardiographic Severity Classification
Stage I
Mild
Valve Area > 1.5 cm²
Mean Gradient < 25 mmHg
Follow-up echo: every 3–5 years. No restriction on activity.
Stage II
Moderate
Valve Area 1.0–1.5 cm²
Mean Gradient 25–40 mmHg
Follow-up echo: every 1–2 years. Monitor for symptom onset.
Stage III
Severe
Valve Area < 1.0 cm²
Mean Gradient > 40 mmHg
Follow-up echo: every 6–12 months. Exercise testing if asymptomatic. Intervention planning when symptomatic.
Stage IV
Very Severe
Valve Area < 0.6 cm²
Mean Gradient > 60 mmHg
Early intervention may be considered even without symptoms — the risk of sudden events overtakes the risk of the procedure.
Intervention
Replacing the Aortic Valve — TAVI & Surgery
Once aortic stenosis becomes symptomatic, valve replacement is the only treatment that improves survival. Two approaches are available — catheter-based TAVI and open surgical replacement — each with specific advantages. The choice is made by a multidisciplinary Heart Team.
Transcatheter
TAVI
Transcatheter Aortic Valve Implantation
- A compressed replacement valve is delivered via a catheter — usually through the femoral artery in the groin — and expanded within the diseased native valve without removing it
- No open-heart surgery, no sternotomy. Performed under conscious sedation or general anaesthetic in a catheter laboratory
- Typical hospital stay 2–3 days; full recovery within 2–4 weeks
- Now the standard choice for patients at intermediate, high, or prohibitive surgical risk
- Large randomised trials (PARTNER 3, Evolut Low Risk) have established TAVI as non-inferior to surgery in low-risk patients — transforming its use across all age groups
- Risk of permanent pacemaker in approximately 10–20% of cases due to conduction disturbance at the time of valve deployment
- The replacement valve sits inside the native calcified valve — a process called valve-in-valve if a second procedure is ever needed
Surgical
SAVR
Surgical Aortic Valve Replacement
- The chest is opened via a median sternotomy, the patient placed on cardiopulmonary bypass, the diseased valve excised, and a prosthetic valve sewn into position
- Allows simultaneous coronary artery bypass grafting (CABG), aortic root repair, and other cardiac procedures during the same operation
- Typical hospital stay 7–10 days; full recovery 6–12 weeks
- Preferred in younger, lower-risk patients — particularly those under 65 — where valve durability over 20+ years is a priority
- A mechanical valve lasts indefinitely but requires lifelong anticoagulation with warfarin. A biological (tissue) valve requires no anticoagulation but typically needs replacement after 12–20 years
- Lower pacemaker rate than TAVI
- Allows choice of mechanical valve — not available via TAVI — for patients who are willing to take anticoagulation and want a durable solution
The Heart Team Decision
No cardiologist or surgeon makes this decision alone. The Heart Team — comprising interventional cardiologists, cardiac surgeons, imaging specialists, anaesthetists, and often a geriatrician — reviews each patient's anatomy, surgical risk scores, CT imaging, and personal preferences before recommending the optimal approach.
Factors favouring TAVI include advanced age, frailty, prior chest surgery, and anatomical features that make sternotomy hazardous. Factors favouring surgery include young age, a concurrent indication for bypass surgery, a bicuspid valve with anatomy less suited to TAVI, and the patient's preference for a mechanical valve to avoid future re-intervention.
In many centres, coronary angiography — or CT coronary angiography — is performed as part of the pre-procedural workup, to identify any coronary artery disease that may need treatment at the same time. Dr Nijjer provides this assessment, ensuring the coronary anatomy is fully evaluated before the Heart Team finalises the plan.
Asymptomatic Severe Aortic Stenosis
Managing the patient with severe stenosis who has no symptoms is one of the more nuanced areas of cardiology. Current guidelines favour regular monitoring with exercise stress testing to unmask symptoms that patients may be unknowingly avoiding — many subconsciously reduce their activity to prevent breathlessness or dizziness.
Intervention is recommended in asymptomatic patients who develop exercise-induced symptoms during testing, whose ejection fraction is declining below 50%, who have very severe stenosis with a peak gradient above 60 mmHg, or whose BNP is rising progressively on serial measurements. Dr Nijjer follows each of these parameters at every review appointment.
The landmark AVATAR and RECOVERY trials have recently provided trial evidence supporting early intervention over continued watchful waiting in selected asymptomatic patients with very severe stenosis — a shift in practice that is gradually being incorporated into updated guidelines.
Mitral Regurgitation
The Leaking Valve — Primary & Secondary
Mitral regurgitation — the most common valve disease in the UK — occurs when the mitral valve fails to close fully during systole, allowing blood to leak back from the left ventricle into the left atrium. The single most important distinction in MR is whether the valve itself is diseased, or whether it is leaking as a consequence of another heart condition.
Type One
Primary (Organic) MR — The valve itself is diseased
The mitral valve leaflets, chordae tendineae, or papillary muscles are structurally abnormal, causing them to prolapse, rupture, or fail to coapt. The most common cause in the developed world is mitral valve prolapse (MVP) — myxomatous degeneration of the valve leaflets, which become floppy and billowing, prolapsing back into the atrium during systole.
Primary MR is usually amenable to surgical repair — the preferred option in experienced centres, where repair rates exceed 95% for degenerative disease. Repair preserves the native valve structure, avoids the need for anticoagulation, and results in better long-term left ventricular function than replacement.
Mitral Valve Prolapse
Chordal Rupture
Rheumatic Fever
Endocarditis
Congenital
Type Two
Secondary (Functional) MR — The valve is normal; the heart has changed around it
The mitral valve leaflets are structurally intact, but the valve leaks because the heart itself has enlarged or distorted — pulling the papillary muscles apart, dilating the valve annulus, or tethering the leaflets so they can no longer meet. This is the characteristic mitral regurgitation of dilated cardiomyopathy and ischaemic heart disease.
Secondary MR is fundamentally different in management. Treating the valve directly has less benefit — the priority is treating the underlying cause (heart failure therapy, coronary revascularisation). In selected patients, MitraClip — a catheter-based repair — has been shown to reduce hospitalisation and improve quality of life (COAPT trial).
Dilated Cardiomyopathy
Ischaemic Heart Disease
Heart Failure
HCM with SAM
Transoesophageal echocardiography (TOE) provides the detailed valve anatomy needed to plan repair
The hallmark of mitral valve prolapse is a mid-systolic click and late systolic murmur on auscultation — a characteristic sound that experienced cardiologists recognise immediately. Most people with MVP never develop significant regurgitation; a minority progress to require intervention.
The Timing Dilemma
Severe primary MR presents a particular challenge. Unlike aortic stenosis — where symptoms reliably signal the point of decompensation — the left ventricle in chronic MR adapts remarkably well, maintaining normal ejection fraction for many years while silently dilating. Symptoms may not develop until irreversible ventricular damage has already occurred.
Waiting for symptoms before intervening risks missing the optimal window. Operating too early exposes the patient to unnecessary surgical risk. The art lies in identifying the precise moment when the benefit of surgery outweighs its risk.
Current guidelines recommend referral for surgery — even in the asymptomatic patient — when any of the following thresholds are crossed:
Left ventricular end-systolic diameter > 40 mm • Ejection fraction falling below 60% • New-onset atrial fibrillation • Systolic pulmonary artery pressure > 50 mmHg at rest
These thresholds reflect the point at which the ventricle is beginning to fail under the volume burden — before symptoms develop. Dr Nijjer monitors each of these parameters at every echocardiographic review, using the trend over time as much as any single measurement.
Repair or Replacement?
Preferred wherever possible
Mitral Valve Repair
- Native valve preserved — no prosthetic material
- No long-term anticoagulation required
- Better preservation of left ventricular function
- Lower operative mortality than replacement
- Techniques: chordal replacement, leaflet resection, ring annuloplasty, Alfieri edge-to-edge stitch
- Repair rates >95% for posterior leaflet prolapse in expert centres
When repair is not feasible
Mitral Valve Replacement
- Biological (tissue) prosthesis — no anticoagulation; re-operation after 12–20 years
- Mechanical prosthesis — lifelong warfarin; theoretically indefinite durability
- Used when anatomy is too complex or calcified for reliable repair
- Chordal preservation technique maintains ventricular geometry where possible
For patients at prohibitive surgical risk, MitraClip — a transcatheter edge-to-edge repair device delivered via a catheter across the atrial septum — clips the two mitral leaflets together, reducing regurgitation without open surgery. In secondary MR, the COAPT trial demonstrated that MitraClip significantly reduced heart failure hospitalisations and improved quality of life in carefully selected patients.
Other Valve Conditions
Aortic Regurgitation, Mitral Stenosis
& Tricuspid Regurgitation
While aortic stenosis and mitral regurgitation account for the majority of valve disease encountered in clinical practice, three further conditions — aortic regurgitation, mitral stenosis, and tricuspid regurgitation — each require specialist assessment and monitoring.
AR
Aortic Regurgitation
The aortic valve leaks blood back into the left ventricle during diastole — the opposite mechanism to aortic stenosis. The left ventricle dilates progressively under this volume overload, often tolerating severe regurgitation for many years without symptoms. Causes include a bicuspid aortic valve, aortic root dilatation (including Marfan syndrome), rheumatic disease, and endocarditis. The timing of surgery follows similar principles to MR — monitoring ventricular dimensions and function closely, intervening before irreversible dilatation occurs. Vasodilators (ACE inhibitors or nifedipine) may be used to reduce the regurgitant volume and delay progression in the asymptomatic phase.
MS
Mitral Stenosis
The mitral valve leaflets thicken and fuse at the commissures — almost exclusively from previous rheumatic fever — narrowing the valve opening and raising left atrial pressure. The elevated pressure in the left atrium causes breathlessness, promotes atrial fibrillation, and raises pulmonary artery pressure. Atrial fibrillation in the context of mitral stenosis carries a particularly high embolic risk, requiring anticoagulation. Where the valve anatomy is suitable, percutaneous mitral commissurotomy — balloon dilatation of the fused valve across a catheter — can relieve obstruction without surgery. When not suitable, surgical repair or replacement is required.
TR
Tricuspid Regurgitation
The tricuspid valve — on the right side of the heart — most commonly leaks as a secondary consequence of left-sided heart disease: elevated left-heart pressures cause right heart enlargement, pulling the tricuspid annulus apart and preventing leaflet coaptation. Primary tricuspid disease (from endocarditis, carcinoid, or congenital causes) is less common. Significant TR was historically undertreated — considered an inevitable accompaniment to left heart disease. This view is changing: isolated tricuspid valve surgery and new transcatheter tricuspid interventions (TRILUMINATE, CLASP systems) are demonstrating meaningful improvements in quality of life in selected patients, even those not undergoing concurrent left-sided surgery.
Investigation
How Valve Disease Is Assessed
Diagnosing valve disease is only the beginning. The cardiologist's ongoing role is to stage its severity precisely, trend its progression over time, and determine the optimal moment — neither too early nor too late — for intervention.
Each review integrates echo measurements, symptoms, exercise capacity, and biomarkers into a decision on whether to continue monitoring or refer for intervention
- Echocardiogram The cornerstone of valve assessment. Measures valve area, peak and mean gradients, regurgitant volume and fraction, left ventricular dimensions and ejection fraction, left atrial size, and pulmonary artery pressure. Repeated serially to track progression. Transthoracic echo (TTE) is first-line; transoesophageal echo (TOE) provides superior resolution of valve anatomy before repair planning or when TTE windows are poor.
- ECG Identifies left ventricular hypertrophy (pressure overload in AS), left atrial enlargement (MS, MR), atrial fibrillation, and conduction abnormalities. A useful longitudinal marker — new AF in a known MR patient triggers an earlier intervention threshold.
- Exercise Stress Test Indispensable in the management of asymptomatic severe valve disease. Unmasks exertional symptoms the patient may not volunteer, and reveals abnormal haemodynamic responses — blunted blood pressure rise, exercise-induced pulmonary hypertension — that influence intervention timing even in the "asymptomatic" patient.
- BNP / NT-proBNP Rising natriuretic peptide levels in a patient who denies symptoms may reflect subclinical haemodynamic deterioration. Serial BNP is increasingly incorporated into surveillance of severe asymptomatic AS and MR — a rising trend is a prompt to reassess closely and consider earlier referral.
- Cardiac CT Essential in the pre-TAVI workup: CT of the aorta and iliofemoral vessels defines the anatomy for catheter access, measures the aortic annulus for valve sizing, and identifies calcification patterns that influence device selection and deployment. CT can also assess leaflet morphology — distinguishing bicuspid from tricuspid valves — and evaluate the coronary ostia prior to intervention planning.
- CT Coronary Angiography In selected patients — particularly younger, lower-risk individuals being considered for TAVI — CTCA can replace invasive coronary angiography as part of the pre-procedural coronary assessment. Dr Nijjer interprets CTCA in this context, identifying any significant coronary disease that would need treatment at the time of or before the valve procedure.
- Invasive Coronary Angiography Standard practice before surgical aortic valve replacement and before TAVI in patients with intermediate-to-high coronary disease probability. Performed via the radial artery as a day-case or short-stay procedure. Dr Nijjer performs this assessment as part of the pre-operative workup, using pressure-wire (iFR) measurement where a coronary narrowing of uncertain significance is found — determining precisely whether it needs treating before or during the valve procedure.
- Cardiac MRI The most accurate method for quantifying regurgitant volumes in MR and AR — superior to echocardiography when echo measurements are discordant or technically limited. In AS, late gadolinium enhancement on MRI identifies myocardial fibrosis, which is a powerful predictor of adverse outcomes after valve replacement and influences the urgency of intervention.
Coronary Assessment Before Valve Intervention Coronary artery disease coexists in a significant proportion of patients with valve disease — particularly those with aortic stenosis, who share the same risk factors. Dr Nijjer provides specialist coronary assessment — invasive angiography, pressure-wire evaluation, and CT coronary angiography — ensuring the coronary anatomy is fully characterised before any valve procedure is undertaken.
After Intervention
Living With a Prosthetic Valve
The choice between a mechanical and a biological prosthetic valve is one of the most personal decisions in cardiac surgery — balancing the lifelong commitment of anticoagulation against the certainty of a re-operation in the future.
This decision is made jointly between the patient, cardiologist, and surgeon, taking into account age, lifestyle, occupation, other health conditions, the patient's values and preferences, and the valve position (the mitral position places greater mechanical stress on a prosthesis than the aortic). There is no universally correct answer — the right valve is the one that best matches the individual.
Option One
Mechanical Valve
Durability
Theoretically indefinite — no structural degradation expected over a lifetime
Anticoagulation
Warfarin for life — mandatory. INR monitoring required (target 2.5–3.5)
Re-operation
Not anticipated from valve failure, but possible for other reasons
Best suited to
Younger patients (under 60–65) who are willing to take warfarin and can maintain regular INR monitoring
Audible click
The valve produces a clicking sound — patients notice it; some find it reassuring, others find it intrusive
Option Two
Biological (Tissue) Valve
Durability
Typically 12–20 years before structural deterioration — younger patients degrade valves faster
Anticoagulation
Aspirin only (3 months of warfarin post-implant; then none unless AF is present)
Re-operation
Likely required — either redo surgery or valve-in-valve TAVI at the time of degeneration
Best suited to
Older patients (over 65–70), or those who cannot safely take anticoagulation, or who wish to avoid it for lifestyle reasons
Future options
A degenerated surgical bioprosthesis can often be treated with valve-in-valve TAVI, avoiding redo open-heart surgery
Annual echocardiography is standard for all prosthetic valve patients — detecting early structural change before it becomes symptomatic
All patients with a prosthetic valve require lifelong cardiology follow-up. Annual echocardiography detects early structural deterioration, valve thrombosis, or paravalvular leak — changes that, if identified promptly, can be managed with far greater safety than if discovered at an advanced stage.
Infective endocarditis — infection on a prosthetic valve — is rare but serious. Patients with prosthetic valves should carry a valve card, inform all treating clinicians, and maintain meticulous dental hygiene. Any unexplained fever in a patient with a valve prosthesis requires blood cultures before antibiotics are started.
DOACs and Prosthetic Valves
Direct oral anticoagulants (DOACs — apixaban, rivaroxaban, edoxaban) are not suitable for patients with mechanical heart valves — warfarin remains mandatory. DOACs can, however, be used in patients with a bioprosthesis who develop atrial fibrillation. Dr Nijjer reviews all anticoagulation decisions in the context of each patient's full clinical picture.
Further Information
Patient Resources
The British Heart Foundation provides patient information on all forms of valve disease, including guides on what to expect before and after valve surgery or TAVI. The Heart Valve Voice charity advocates for earlier detection and better access to valve interventions, and provides resources for patients navigating a new diagnosis.
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Concerned About a Heart Valve Condition?
Whether you have a murmur, a recent echocardiogram finding, or symptoms you want properly evaluated, Dr Nijjer provides expert valve assessment — diagnosis, ongoing surveillance, and coordination of intervention when the time is right.