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New murmurs in patients with prosthetic heart valves
  1. N A Cromie1,
  2. S J Walsh1,
  3. A A M Ahmed2,
  4. G Campalani2
  1. 1Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland
  2. 2Department of Cardiac Surgery, Royal Victoria Hospital, Belfast, Northern Ireland
  1. Correspondence to:
 Dr Nicholas A Cromie, Royal Victoria Hospital, Belfast BT12 6BA, UK; 
 cardiac.research{at}royalhospitals.n-i.nhs.uk

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Case 1

A 58 year old woman with previous replacement of a bicuspid aortic valve (size 23 St Jude Medical prosthesis) in 1994 for aortic stenosis, presented with a three week history of increasing shortness of breath. During this time she had stopped her diuretic as she had suffered an acute exacerbation of gout. On initial assessment, an ejection systolic murmur and early diastolic murmur were noted. The patient was found to be in moderate left heart failure (Killip class II). Echocardiography demonstrated a peak systolic velocity of 4.7 m/sec across the aortic valve (peak gradient of 85 mm Hg). There was moderate aortic regurgitation and it appeared that the prosthesis was malfunctioning. There was no evidence of endocarditis and the patient’s international normalised ratio was therapeutic at 2.1. Radiographic valve screening was performed and the appearances are demonstrated in fig 1.

Figure 1

Valve screening. (A) Left anterior oblique view in diastole; (B) left anterior oblique view in systole; (C) left lateral view in diastole; (D) left lateral view in systole.

CASE 2

A 19 year old woman had undergone tricuspid valve replacement for staphylococcal endocarditis (there was no evidence of intravenous drug abuse) in October 1998. A size 29 St Jude Medical prosthesis was implanted. During routine follow up in February 2001, a transthoracic echocardiogram was performed. It showed that the tricuspid valve prosthesis was “functioning satisfactorily”. By March 2001 the patient started to develop signs of tricuspid regurgitation. A pansystolic murmur was noted at the lower left sternal edge and this was associated with giant CV waves. There was no overt right heart failure. A transoesophageal echocardiogram was performed. This demonstrated that the tricuspid valve was malfunctioning and mild to moderate tricuspid regurgitation was noted. The patient’s C-reactive protein was normal (<7 mg/l), as were the white blood cell count and erythrocyte sedimentation rate. The patient was apyrexial and had no clinical evidence of infective endocarditis. The international normalised ratio was 2.5. The valve was eventually excised and the appearances of the valve are shown in fig 2.

Figure 2

Prosthetic valve pathology. (A) Tricuspid valve prosthesis inflow; (B) tricuspid valve prosthesis outflow.

QUESTIONS

  1. What is the differential diagnosis to explain the presentation of these patients.

  2. What pathological mechanisms are possible causes of prosthetic valve obstruction and what has happened in case 2?

  3. What is the most helpful investigation to differentiate these pathological mechanisms?

  4. What are the therapeutic options for patients with prosthetic valve obstruction?

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