A 30-year-old man with a 3 day history of increasing breathlessness and frank haemoptysis was suspected of having pulmonary embolism and anticoagulated with heparin. Haemoptysis worsened so anticoagulation was reversed and he was transferred to our institution.Pulmonary and bronchial angiography revealed a small right pulmonary artery and a prominent right intercostobronchial trunk which was embolised. However, haemoptysis recurred and a contrast enhanced ECG-gated CT scan confirmed a hypoplastic right pulmonary artery and showed thrombosed right pulmonary veins that had no communication to the left atrium, a 'bulky' right hilum and thickened bronchial walls with smooth mucosal indentations into the airway lumen (figures 1 and 2). Bronchoscopy confirmed carinal and right bronchial varices. A ventilation perfusion (V/Q) scan showed normal ventilation but very little perfusion of the right lung.The patient underwent a standard dissectional stapled right pneumonectomy. Intraoperatively, the right main bronchus and distal trachea were encircled by bronchial veins which were the only means by which the lung could drain as the native pulmonary veins had no discernable flow. In addition there were a number of venous collaterals to the chest wall. Postoperatively the patient had no further haemoptysis and repeat bronchoscopy showed resolution of the varices.Histopathology showed thrombosed pulmonary veins with signs of recanalisation and a dilated bronchial venous plexus involving the hilar bronchial submucosa. There was an acquired moderate degree of chronic inflammation involving the pulmonary artery wall causing stenosis.
DISCUSSIONTracheal varices from pulmonary venous occlusive disease may cause massive haemoptysis.1 Cases with similar findings to ours have been reported but with a different aetiology; idiopathic hilar fibrosis causing pulmonary vein occlusion.
2In our patient there was no hilar fibrosis and the aetiology of the pulmonary venous thrombosis remains unclear. The prominent collateral circulation within the walls of the airways were tracheal varices caused by pulmonary venous thrombosis.
Learning point▸ Massive haemoptysis can occur secondary to non-embolic pathologies and this should be considered in young patients with no risk factors for pulmonary embolism in whom early systemic anticoagulation may be life threatening.
BackgroundThe evidence on the impact of patient-prosthesis Mismatch (PPM) on survival thus far has been conflicting. The aim of this study was to 1) study the effect of PPM on survival after isolated aortic and mitral valve replacement and 2) Assess the interaction between left ventricular function and PPM on survival.MethodsThe study cohort was patients who underwent isolated Aortic valve replacement (AVR) and Mitral valve replacement (MVR) over a 10-year period from 2008 to 2018. PPM was defined using the projected indexed effective orifice area (EOAi). The cohort was divided into different groups based on the degree of PPM. The severity of PPM was classified using threshold values of EOAi used in the literature. The Kaplan- Meier method was used to compare survival by degree of PPM. Multivariate Cox proportional hazards models were used to generate adjusted hazard ratios (HR) with 95% confidence intervals. An interactive term for ejection fraction (EF) was added to test whether EF modifies the effect of the PPM grade on survival. In addition, sub-group analysis based on left ventricular function was performed.ResultsIn the AVR cohort, there were a total of 1953 patients. The distribution of patients in the different PPM categories was as follows: no PPM 59.7%; moderate PPM 36.8%; severe PPM 3.5%. There was no significant difference in survival between the different groups. At 10 years, the adjusted HR between patients with severe PPM versus no PPM was 1.1(CI 0.5–2.4, p > 0.05) and the HR between those with moderate PPM versus no PPM was 0.97 (CI 0.74–1.23, p > 0.05). In the MVR cohort, there were a total of 298 patients. The distribution of PPM is as follows: no PPM 59.4%; and with PPM 40.6%. Again, there was no significant difference in survival between the groups. At 5 years, the adjusted HR between patients with PPM versus no PPM was 1.45 (CI 0.67–3.14, p > 0.05). In both groups, there was no significant interaction between left ventricular function (LVF) and degree of PPM on survival.ConclusionsIn our study cohort, the degree of PPM was not an independent predictor of survival after AVR or MVR. There was also no significant interaction between LV function and degree of PPM on survival.
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