Valvular heart disease Flashcards
What is aortic stenosis?
What is the most common cause?
What are other causes of AS?
Obstruction of blood flow across the aortic valve from left ventricle due to pathological narrowing.
Commonest cause: acquired senile calcification 80% of patients (age-related degeneration)
Other causes:
- Congenital causes (bicuspid aortic valve, Williams syndrome)
- Rheumatic heart disease
What is the pathophysiology of AS?
- Calcification of the normal trileaflet valves is the most common cause of AS in adults (80% cases)
- The valvular endocardium is damaged as a result of abnormal blood flow across the valve
- Endocardial injury stimulates inflammatory process (similar to atherosclerosis) and leads to deposition of calcium on the valve
- Calcification occurs slowly and is subclinical until the disease is fairly advanced
- A pressure gradient develops between the left ventricle and the aorta (increased afterload)
- Long standing pressure overload leads to the development of left ventricular hypertrophy (LVH) - this allows the ventricle to maintain a normal wall stress (afterload) despite the pressure overload produced by stenosis
- As the stenosis worsens, the adaptive mechanism fails and left ventricular wall stress increases - systolic function declines as wall stress increases and eventually, the heart fails.
- Unicuspid and bicuspid valves experience shear and mechanical stresses from birth and therefore, the pathological processes and stenosis occur earlier than in trileaflet valves
Rheumatic Heart Disease
- In rheumatic disease, an autoimmune inflammatory reaction is triggered by prior Streptococcus infection that targets the valvular endothelium, leading to inflammation and eventually calcification.
What are the risk factors for AS?
- Age
- Congenital bicuspid valve
- Rheumatic fever
- Chronic kidney disease
Common presentation of AS?
Suspect AS in any elderly patient presenting with decreased exercise tolerance, SOB on exertion, exertional angina, syncope, dizziness & heart failure.
Classic triad of symptoms:
- Angina
- Syncope
- Heart failure
What are the signs of AS?
- Slow rising pulse with narrow pulse pressure (diminished & delayed carotid upstroke - parvus et tardus)
- Heaving, non-displaced apex beat
- Ejection systolic murmur (crescendo-decrescendo murmur heard in the base, left sternal border, radiating to the carotid.)
- Quiet A2 heart sound - in severe AS, A2 may be inaudible.
- Palpable thrill as the murmur peaks later in systole.
What is the key investigation used for diagnosis of AS? What information does this investigation give?
Transthoracic doppler echocardiography
- Left ventricular size and function
- Pressure gradient across the aortic valve
What ECG changes can we expect to see in AS?
ECG will be abnormal in 90% of patients
Common findings:
- LVH due to pressure overload
- May show absent Q waves, AV block, hemi block or bundle branch block.
Prognosis of AS?
If symptomatic, prognosis is poor without treatment
Angina + AS = 50% survival for 5 years
Syncope + AS = 50% survival for 3 years
HF + AS = mean survival without treatment = 2yrs
Risk of sudden death in asymptomatic or minimally symptomatic patients = rare - 2%
Management of AS
Prompt valve replacement is indicated in those symptomatic and asymptomatic patients with severe AS or deteriorating ECGs or poor ejection fraction.
TAVI may be attempted in those not fit for surgery.
What is mitral regurgitation?
What are the causes?
Backflow through the mitral valve during systole.
Acute MR: IE, ischaemic papillary muscle dysfunction, rupture, acute rheumatic fever, acute dilation of LV due to myocarditis or ischaemia.
Chronics MR: Same as above but also myxomatous degeneration of the mitral leaflets (too much tissue in mitral valve) or chordae tendineae, mitral valve prolapse and mitral annular enlargement.
Pathophysiology of mitral regurgitation
- Back flow of blood from the left ventricle to the left atrium during systole because the mitral valve is not competent
- Mild MR is seen in 80% of normal individuals (no valve is entirely perfect)
- Chronic MR can be mild or moderate and can be asymptomatic for years however, with progression of disease, eccentric cardiac hypertrophy occurs which leads to elongation of the myocardial fibres and increased left ventricular end-diastolic volume.
- This is a compensatory mechanism which increases total stroke volume to maintain adequate cardiac output (120% volume needed to achieve 100% CO)
- This increases the workload for the LV and LA and they will enlarge to accomodate this change.
- Prolonged volume overload leads to LV hypertrophy, enlargement (compensatory) and dysfunction & eventually progressive heart failure
Risk factors for Mitral regurgitation
- Mitral valve prolapse
- History of rheumatic heart disease
- Infective endocarditis
- History of cardiac trauma
- History of MI
- History of congenital heart disease
- History of ischaemic heart disease
- Left ventricular systolic dysfunction
- Hypertrophic cardiomyopathy
- Anorectic or dopaminergic drugs
Signs & symptoms of mitral regurgitation
Symptoms:
- exertional dyspnoea**
- orthopnoea
- paroxysmal nocturnal dyspnoea
- lower extremity oedema
- fatigue
- palpitations
- symptoms of causative factor (eg. fever)
Signs:
- AF
- Auscultation: PANSYSTOLIC murmur at apex and radiating to axila (high pitched continuous murmur)
- Soft S1
- Split S2
- Loud P2 (pulmonary htn)
- Displaced hyperdynamic apex beat (left and down suggesting larger heart)
Investigations for mitral regurgitation
ECG: AF, LA enlargement, LV hypertrophy
CXR: LA & LV enlargement, central pulmonary artery enlargement, mitral valve calcification, pulmonary oedema
Transthoracic echocardiogram is definitive testing - Estimation of LV and LA size and function
Can tell us about the cause of MR
Can tell us about the severity of MR
Management of mitral regurgitation
Acute MR medical emergency and immediate surgery is indicated! - Severe acute MR associated with hypotension is an indication for intra-aortic balloon counterpulsation
Medication:
- Vasodilators ACEi or hydralazine
Rate control for AF
- B-blockers, CCB’s, Digoxin
Anticoagulation for AF or atrial flutter, hx of embolism, prosthetic valve, additional mitral stenosis.
Diuretics in fluid overload and if breathless
- Regular echo in moderate and severe MR
- Infectious endocarditis prophylaxis is important
