A male in his 70s with a 33 mm Carbomedics mechanical mitral valve, presented with increasing breathlessness, despite being treated with antibiotics for a community acquired pneumonia. He was afebrile and tachypnoeic at rest, requiring 60% humidified oxygen. Inflammatory markers were modestly elevated with a CRP of 34 mg/L and NT-proBNP 9,031 pg/ml. Chest x-ray (CXR) demonstrated a right perihilar airspace density projected in the basal portion of the right upper lobe and a new, small right sided pleural effusion. Overall CXR findings were felt more likely to represent consolidation than heart failure. Despite treatment with IV antibiotics, he deteriorated and repeat CXR showed bilateral pulmonary infiltrates consistent with features of pulmonary oedema. Trans-thoracic echocardiogram (TTE) revealed dehiscence of the mechanical mitral valve extending along the anterior and antero-lateral aspect of the valve annulus. This gave rise to a severe, anteriorly directed, paravalvular regurgitation. Transoesophageal echocardiogram (TOE) confirmed TTE findings of mechanical mitral valve dehiscence with no clear vegetation or evidence of infective endocarditis. He improved with high flow oxygen and IV diuretics. Repeat CXR showed resolution of peri-hilar airspace shadowing suggestive of heart failure. He was declined for re-do mitral valve intervention due to frailty and high surgical risk. There a few reported cases describing the uncommon clinical entity of unilateral pulmonary oedema, representing only 2% of cardiogenic pulmonary oedema presentations.1,2 Unilateral pulmonary oedema has a 7 -fold higher mortality than bilateral pulmonary oedema, usually due to delayed or missed diagnosis.2 Dilatation and plethora of the right upper pulmonary vein results in airspace opacification within the right upper lobe, resulting in CXR appearances which are often mistaken for consolidation.3 Unilateral pulmonary oedema is usually caused by severe, eccentric mitral regurgitation (MR) resulting in increased hydrostatic pressures in the right upper lobe.4 The eccentric jets adjacent to the LA atrial wall are easier to reach the posterior pulmonary veins but ultimately, the angle between the regurgitant jet and the pulmonary vein determines the degree of regurgitation into each vein.4 Out of the four pulmonary veins, the right upper superior pulmonary vein is better aligned to posterior regurgitant flow leading to a unilateral pulmonary oedema.4 Elevated natriuretic peptide levels may help to differentiate unilateral cardiogenic pulmonary oedema from other causes.5 TTE, when used in combination with TOE, provides greater specificity and sensitivity for a diagnosis of mechanical valve failure. 2D- and 3D-TOE provides more comprehensive assessment of mitral valve leaflets, mechanical valve function and the mechanism and severity of MR, particularly in eccentric and/or multiple jets. TOE additionally provides better visualisation of the upper pulmonary veins and detection of systolic flow reversal indicative of severe MR. In conclusion, acute, prosthetic valve failure should be suspected in cases failing to respond to antibiotic therapy and progressive CXR changes suggest of acute, decompensated heart failure. Mechanical valve dehiscence is associated with high morbidity and mortality. Surgical intervention with mitral valve repair or replacement should ideally take place before progressing into acute decompensated heart failure since this worsens postoperative outcomes.6
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Tomlinson et al. (2024) studied this question.
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