Clinical review: Valvular heart disease

The four most common disorders of valvular heart disease - aortic stenosis and regurgitation, and mitral stenosis and regurgitation - and strategies for their management.

Coloured MRI scans through the chest of a patient with mitral regurgitation (Photo: Zephyr/Science Photo Library)
Coloured MRI scans through the chest of a patient with mitral regurgitation (Photo: Zephyr/Science Photo Library)

Section 1: Epidemiology and aetiology

Despite significant advances in the diagnosis and management of valvular heart disease (VHD), it continues to impose a significant morbidity and mortality burden. This is mainly due to an increase in the ageing population and associated degenerative valvular lesions, as well as other comorbidities such as ischaemic heart disease (IHD) and heart failure.

VHD is more prevalent in the elderly (13% among those over 75 years, compared with only 0.7% among those aged 18-44 years).1 Prevalence among those aged over 65 in the UK has been estimated at about 1m.2

The 2001 European VHD Survey showed that aortic stenosis (AS) is the most prevalent (43%), followed by mitral regurgitation (MR) at 32%, aortic regurgitation (AR) 13%, and mitral stenosis (MS) 12%.3 The prevalence of significant AS among the elderly is 1-3%, with AR less than 1%, and MR 2%.

Primary disorders of the other valves are rare among the elderly.4 This review focuses on the four most common disorders.

The epidemiology of VHD shows a male predominance of AS and MR, and a female predominance of MS and rheumatic heart disease.3,4

Aetiology and classification
The aetiologies of common individual valvular lesions are illustrated in Table 1.

Table 1: Aetiologies of individual valvular lesions
Valvular lesion Causes


Degenerative, bicuspid (congenital), rheumatic


Degenerative, bicuspid (congenital), rheumatic AR, infective endocarditis, aortic root disease (aortic dissection, vasculitis, connective tissue disorders such as Marfan's syndrome)


Mainly rheumatic, rare causes include malignant carcinoid, rheumatoid arthritis, systemic lupus erythematosus (SLE), Fabry disease


Mitral valve prolapse, rheumatic fever, infective endocarditis, IHD, Marfan's syndrome, SLE

Section 2: Making the diagnosis

The clinical features vary depending on the valvular lesion (Table 2).

Table 2: Signs and symptoms of individual VHD
Valvular Symptoms (in moderate) Signs (in moderate to severe VHD)
AS Angina, exertional syncope or dyspnoea

Latent period of 10-20 years before symptoms onset
Small and slow-rising pulse

Laterally displaced apical impulse

Aortic component of S2 reduced (degenerative form) and disappears in severe AS

Fourth heart sound (S4)

Ejection systolic murmur radiating to both carotids
AR Exertional dyspnoea, paroxysmal nocturnal dyspnoea and orthopnoea Collapsing pulse (water-hammer type), wide pulse pressure

Head-nodding with each heartbeat (de Musset sign)

‘Pistol-shot’ (systolic and diastolic) sounds over femoral artery

Capillary pulsations

Apical impulse displaced laterally and inferiorly

Early diastolic decrescendo murmur
MS Dyspnoea, cough, haemoptysis, chest pain, systemic embolism Mitral facies – pink patches on the face

AF, jugular venous pressure – prominent ‘a wave’ if sinus rhythm

Tapping apical impulse and diastolic thrill

Opening snap and low-pitched rumbling mid-diastolic murmur
MR Dyspnoea Brisk hyperdynamic pulse

Hyperdynamic cardiac impulse deviated laterally

Pansystolic murmur

Systolic click is due to mitral valve prolaps

Guidelines released in 20145 have incorporated the staging on progression of VHD, based on symptomatic status and ventricular function (Table 3).

Table 3: Stages of progression of VHD




A At risk Patients with risk factors for developing VHD
B Progressive Progressive VHD (mild to moderate and asymptomatic)
C Asymptomatic severe C1 - ventricle compensated

C2 - ventricle decompensated
D Symptomatic severe Symptoms due to VHD

Adapted from Nishimura et al, J Am Coll Cardiol 2014: 63 (22); e57-e185

It is crucial to correlate symptoms and clinical signs with results from investigations, as modern tests may uncover incidental and benign valvular lesions which may not have clinical relevance. Routine blood tests such as FBC may show anaemia due to lower gastrointestinal blood loss in AS, or due to infective endocarditis.

Raised inflammatory markers with fever and new murmur may indicate endocarditis. Chest X-ray may reveal cardiomegaly or pulmonary congestion.

ECG is crucial. AF can complicate most valvular lesions and worsens symptoms in AS and MS. Significant AS usually shows features of left ventricular hypertrophy on ECG. Transthoracic echocardiography is crucial to establish the diagnosis and grade severity of the lesion.

Transoesophageal echocardiography and MRI are useful if echocardiographic images are suboptimal.

Section 3: Managing the condition

Management strategies for individual valvular lesions are detailed in Table 4.The indications for surgery depend on the valve and are beyond the scope of this review.

Detailed evaluation of VHD should include assessment in heart valve centres of excellence by a multidisciplinary team (heart valve teams), consisting of cardiologists, cardiothoracic surgeons, and intensivists to assess symptoms, severity of valve disorder, and correlation between the two, as well as patient expectations, life expectancy, and the risk-benefit ratio of treatment.

Recent guidelines5 provide guidance on indications for transcutaneous aortic valve replacement and mitral valve repair in patients deemed unsuitable for open heart surgery.

Current guidelines recommend endocarditis prophylaxis only for high-risk patients (such as patients with prosthetic valve, previous endocarditis, or congenital heart disease) undergoing high-risk procedures.

Table 4: Management of valvular lesions

Valvular lesion

Medical management

Surgical treatments


Medical therapy does not improve outcome

Treatment of heart failure with diuretics, vasodilators

Modification of atherosclerotic risk factors

Aortic valve replacement (AVR) recommended in patients with severe symptomatic AS, patients with severe AS undergoing coronary artery bypass graft (CABG), surgery on ascending aorta or other valve or in asymptomatic patients with severe AS and left ventricular ejection fraction (LVEF) ≤50% or abnormal exercise test

Autograft of pulmonary valve and artery (Ross procedure) in young

Balloon valvuloplasty – as bridge to surgery or if patients require urgent major non-cardiac surgery

Percutaneous transcatheter aortic valve implant in patients unsuitable for conventional AVR


ACE inhibitors in patients with chronic severe AR and hypertension if surgery contraindicated

Beta-blockers delay aortic root dilation in Marfan’s syndrome

Valve sparing aortic replacement in young patients (if combined aortic root dilation and AR)

Pulmonary autograft to replace aortic valve in young patients

Aortic valve replacement – used widely


Diuretics, nitrates, beta-blockers to improve symptoms

Anticoagulation if AF, embolism or left atrial thrombus

Percutaneous/open mitral commissurotomy if suitable

Mitral valve replacement


Acute MR – vasodilators (nitroprusside, nitrate), diuretics, intra-aortic balloon pump

Chronic MR – role of medical therapy if HF

Mitral valve repair when feasible

Mitral valve replacement

Section 4: Prognosis

Severe AS patients have a five-year survival risk of 15-50%.3 Predictors of poor prognosis include older age, associated atherosclerosis, echocardiographic features such as calcification, and impaired LV function.

Acute severe AR has a poor prognosis in the absence of intervention. Onset of symptoms in chronic severe AR also indicates 10-20% annual mortality without surgery.3 Among patients with normal LV function and without symptoms, LV end systolic diameter >5cm predicts a high risk of symptoms, heart failure or death.3

In MS, onset of symptoms predicts poor prognosis without intervention. Pregnancy and AF worsen symptoms. Acute MR (usually due to chordal rupture) has a high mortality if not operated on. Factors predicting poor prognosis in chronic MR include increasing age and pulmonary hypertension.

Section 5: Case study

An 82-year-old man presented with a six-month history of reducing exercise tolerance due to shortness of breath, chest tightness and exertional syncope.

His background history included type 2 diabetes mellitus with nephropathy and neuropathy, COPD, and hypertension.

Clinical examination revealed BP 150/72 mmHg, heart rate 64 bpm regular, grade 3 ejection systolic murmur radiating to the carotids, and bilateral wheeze on chest auscultation.

ECG showed sinus rhythm with LV hypertrophy. Echocardiography showed a calcified aortic valve with a mean gradient of 66 mmHg, severe left ventricular hypertrophy, and LVEF of 40%. He was referred to the cardiologist and reviewed in the valve clinic by a multidisciplinary team. He was referred for pulmonary function tests, which showed FEV1/FVC ratio of 35%.

In view of his comorbidities, he was deemed unsuitable for conventional valve replacement and was placed on a waiting list for a percutaneous transcatheter aortic valve implant.

While awaiting the procedure, the patient developed acute pulmonary oedema requiring hospitalisation, IV diuretics, inotropic support, and non-invasive ventilation. Following stabilisation, he had a transvalvular balloon valvuloplasty as an interim measure, reducing the transaortic mean gradient to 36 mmHg.

Nine months after his initial presentation, he underwent a percutaneous transcatheter aortic valve implant via the trans-femoral route, complicated by a self-resolving femoral haematoma and a TIA.

He was discharged 25 days later. His follow-up one year post-procedure has shown persistent improvements in exercise tolerance, quality of life score, and complete resolution of chest pain and syncope.

This case illustrates the role of percutaneous transcatheter aortic valve implant in management of patients with AS and severe comorbidities precluding conventional valve replacement. However, percutaneous transcatheter aortic valve implant is a new technique that is not yet widely available and most patients will therefore have to wait before the procedure, during which time decompensation may require stabilisation.

Section 6: Evidence base

Clinical trials

  • Glower D, Ailawadi G, Argenziano M et al. EVEREST II randomized clinical trial: predictors of mitral valve replacement in de novo surgery or after the MitraClip procedure. J Thorac Cardiovasc Surg 2012; 143(4 Suppl): S60-3.
  • Leon MB, Smith CR, Mack M et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med 2010; 363: 1597-607.



Dr Rajiv Sankaranarayanan is cardiology specialist registrar in electrophysiology, University Hospitals South Manchester and honorary research fellow, University of Manchester

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This is an updated version of an article that was first published in April 2013.


  1. Nkomo VT, Gardin JM, Skelton TN et al. Burden of valvular heart diseases: a population-based study. Lancet 2006; 368: 1005-11.
  3. Vahanian A, Alfieri O, Andreotti F et al. Guidelines on the management of valvular heart disease (version 2012). Eur Heart J 2012; 33: 2451-96.
  4. Malhotra A. The changing burden of valvular heart disease. BCS Editorial. 2012.
  5. American College of Cardiology/American Heart Association. Nishimura RA, Otto CM, Bonow RO et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014 Jun 10; 129(23): e521-643

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