With the patient on the left side and using the bell, there is a mid-diastolic murmur. If you suspect the diagnosis but cannot hear anything abnormal, ask the patient to perform sit ups and then listen again. In severe MS, the murmur begins soon after aortic closure and is long. In patients still in sinus rhythm there is presystolic accentuation of the murmur.
If the mitral valve is still mobile there is an opening snap. This sounds like a tiny hammer blow but more usually like a more than usually discrete start to the murmur. A palpable opening snap causes the ‘tapping’ apex.
Wide splitting of the second sound is caused by delay of pulmonary closure. A malar flush as a result of chronic pulmonary hypertension is no longer common. Pulmonary hypertension may also cause a right ventricular impulse, and the basal pansystolic murmur and systolic waves of tricuspid regurgitation. A basal immediate diastolic murmur, louder on inspiration (Graham Steele murmur), may occur as a result of pulmonary regurgitation, but may be confused with the similar murmur from aortic regurgitation.
The pulse is often irregular as a result of atrial fibrillation. The jugular venous pressure may be high and, if there is tricuspid regurgitation, there will be prominent venous systolic waves shown as large amplitude waves timed with the central pulse. The apex beat may be displaced if there is right ventricular dilatation, but there should be a still region between the right and LV impulses. In MS uncomplicated by right ventricular dilatation, the apex beat is not displaced.
Ankle-swelling and ascites may develop as a result of right ventricular failure
Murmurs associated with concomitant rheumatic disease of the other heart valves may also be heard, and evidence of atrial arrhythmias should be looked for.
MS develops years after acute rheumatic fever, and has a good prognosis in the asymptomatic phase. Exertional breathlessness is the most common symptom. Severe MS is suggested by a long mid-diastolic apical murmur starting soon after the second sound, with a widely-split second sound. An opening snap after the second heart sound, denotes a mobile valve .
Acute mitral regurgitation (MR) can be a life-threatening event, while chronic MR presents in a more indolent fashion. Intervention for MR may be desirable before symptom onset, and so careful follow up and monitoring are at the centre of patient care. It is acutely responsive to haemodynamic changes, and these must be taken into careful consideration when assessing the severity of MR, as signs of severity may alter according to the prevailing loading conditions.
Chronic mitral regurgitation
The mortality in severe mitral regurgitation of all aetiologies with and without symptoms is around 5% per year.68 However, the natural history usually depends on the aetiology and distinguishing between secondary and primary MR has important implications for treatment:
Secondary mitral regurgitation
This largely reflects the underlying LV dysfunction. However, the presence of moderate or severe regurgitation (regurgitant orifice area ≥20 mm2) independently worsens the prognosis.69,70 This type of MR is more likely to progress due to the associated left ventricular remodelling. Treatment decisions are often difficult due to the underlying ventricular disease.