Valvular Disease / Heart Disease (Fri 27th)

Question 1

Describe the main causes/ aetiology of valvular heart disease

Answer 1

Valve disease causes:

1. Stenosis- the failure of a valve to open completely thereby impairing forward flow of blood
2. Insufficiency in contrast results from failure of a valve to close completely allowing a reversed flow of blood

Question 2

Describe the causes/ aetiology/ histology and clinical features of valvular heart disease: Rheumatic Heart Disease

Answer 2

Causes:

• Rheumatic fever develops 2 weeks after Strep A sore throat.
• Has a cross-reaction of anti strep Ab with connective tissue components, affects joints, skin and heart.
• Chronic valve damage can result, mainly mitral and aortic, leads to heart malfunction and susceptibility to infective endocarditis.
• Can be acute or chronic (this is characterised by organisation of the acute inflammation with fibrosis – fish mouth valve).
• 99% of cases of mitral stenosis are caused by rheumatic carditis

Clinical Features:

• Sydenham’s chorea: neurological disorder with -
• involuntary purposeless rapid movements
• Carditis
• Erythema marginatum of the skin
• Migratory polyarthritis of large joints

Histology:

• Rheumatic fever is most likely a hypersensitivity reaction induced by Group A streptococci
• It is thought that M proteins of certain strains of Streptococci cross react with glycoproteins of the heart
• The onset of symptoms 2-3 weeks after infection and the absence of Streptococci from the lesions supports the concept that rheumatic fever is immunologically mediated

Question 3

Describe the clinical consequences of valvular heart disease

Answer 3

May be asymptomatic
  Murmur
  Heart failure
  Atrial Fibrilation (mitral stenosis)
  Syncope/ Drop attacks (aortic stenosis)
  Endocarditis risk

Question 4

Purpose of valves?

Answer 4

To direct flow, prevent back-flow.

Question 5

Describe Calcific Aortic Stenosis

Answer 5

Description:
Nodular calcific masses on aortic side of cusps
No commisural fusion
Free edges of cusps are not involved
Stellate-shape systolic orifice

Main causes:
Thought to develop like an atheroma
Aortic valve stenosis (hardening) develops into Calcific Aortic Stenosis

Treatment:
Classic aortic valve replacement
Stented AVR

Risk factors:
Male
Metabolic Syndrome
Renal Failure
Hyperlipidemia
Age
Obesity, smoking, stress, hypertension (high BP)

Question 6

Describe Valve Ring Dilation and Leaflet Degeneration (ageing)

Answer 6

• Degenerative mitral valve disease is a common disorder affecting around 2% of the population
• Leads to leaflet prolapse (leaflets do not close properly) resulting in mitral valve regurgitation
• Can be due to thin leaflets in fibroelastic degeneration in 60+ has no genetic component.
• Or can be due to Barlow’s Degeneration, thick leaflets in people under 60 years. Some genetic component.

Treatment
- Recommended treatment = Mitral valve reconstruction, as opposed to valve replacement with a bioprosthetic or mechanical valve. Valve repair is associated with improved event free survival according to some authors .

Question 7

Describe Endocarditis

Answer 7

Endocarditis is an infection of the endocardium, which is the inner lining of your heart chambers and heart valves. Endocarditis generally occurs when bacteria, fungi or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to damaged areas in your heart.

Pathology of Infective Endocarditis:

• Seeding of the blood with microbes
• Obvious portal of entrance (i.e. known infection, surgery procedure, intravenous drug users….)
• Occult source (i.e. gut, oral cavity..)
• Streptococci and staphylococci account for 80% of cases of infective endocarditis (Gram + cocci)

Epidemiology of Infective Endocarditis:

• Annual incidence of 3 – 9 cases / 100,000 persons in industrialised countries
• Male : female ratio > 2 : 1
• Highest rates associated with prosthetic valves, intra-cardiac devices, unrepaired cyanotic congenital heart diseases, or a history of infective endocarditis
• 50% of cases have no known history of heart disease

Risk Factors of Infective Endocarditis

• Age related degenerative valvular lesions (damage)
• Haemodialysis
• Co-existing diabetes, HIV infection, intravenous drug use
• > 1/3 of US cases are health care-associated
• When infective endocarditis is suspected, echocardiography should be performed as soon as possible.

Clinical Features:

• Fever, chills, fatigue, lassitude, loss of weight
• Glomerulonephritis (immune mediated)
• Murmurs
• Features due to microemboli (Subungual haemorrhage, Janeway lesions, Osler nodes, Roth spots)
• Septic embolism to peripheral organs ( Cerebral complications and MI).

Duke Criteria for the Diagnosis of Infective Endocarditis:

• Pathological Criteria: micro- organism identifiedin culture or examination of vegetation (abnormal growth).
• Clinical criteria: positive blood culture

Question 8

Describe Heart Failure

Answer 8

• Condition in which the heart is unable to provide sufficient pump action to maintain blood flow to meet the needs of the body.
• The heart works as a unit with both ventricles contracting in unison.
• Heart failure usually involves both the right and left sides, giving symptoms and signs related to both - congestive cardiac failure.
• Sometimes left or right heart failure predominates, e.g. RHF in chronic obstructive airways disease, and LVF in myocardial infarction.

- Causes of HF: Ischaemic heart disease
Hypertension
Lung disease COPD (cor pulmonale)
Valvular heart disease
Congenital heart disease
Cardiomyopathy (several types)

Diagnosing HF:
History
Examination
Chest X-RAY
ECG 
Echocardiography
BNP ( B type natriuretic peptide: hormone released into plasma by stressed myocytes in CF). 

Effects of Left HF:
General: pulmonary congestion, breathlessness
Chronic LHF: dyspnoea on exertion, poor renal perfusion, Renin-Angiotensin system activation (Poor renal perfusion is sensed by the juxtaglomerular apparatus, which secretes renin.
Renin converts angiotensinogen in the blood to angiotensin1. This in turn is converted by ACE (angiotensin converting enzyme) to angiotensin2, which increases blood pressure directly by vasoconstriction and by increasing adrenal secretion of aldosterone.
ACE inhibitors are used to treat heart failure as well as hypertension. Diuretic drugs are another mainstay of treatment) and peripheral oedema
Acute Left HF: Pulmonary oedema and frothy blood stained sputum

Right = peripheral oedema, hepatic congestion, raised Jugular Venous Pressure,

Congestive = right and left