Early rapidly developing constrictive pericarditis after aortic valve surgery

A 58-year-old male patient underwent aortic valve replacement surgery (On-X mechanical prosthesis, ring size 23 mm) due to severe aortic valve stenosis with preserved LV function and normal coronary arteries. The postoperative period was complicated by third-degree AV block and sustained ventricular tachycardias and a DDD-ICD implantation was implanted. After 3 months of surgery, the patient presented with symptoms of progressive fatigue, dyspnoea on exertion and generalised peripheral oedema. No chest pain was reported. The patient had gained 30 kg in weight in 3 months. Physical examination revealed a raised jugular venous pressure with prominent vein pulsations, normal cardiac soundswith normal artificial valve clicks and no murmurs. Auscultation of the lungs was normal. The patient had a palpable liver of 4 cm, noticeable ascites, and extensive pitting oedema from ankle to hip. Laboratory results revealed elevated liver enzymes and moderately raised NT-proBNP (328 pmol/l) without other abnormalities. Electrocardiogram revealed a sinus rhythm with ventricular pacing. Chest X-ray demonstrated an enlarged heart but no pulmonary congestion. The echocardiogram was limited by severely impaired image quality. Left ventricular function was normal, right heart function was mildly impaired and LV diastolic function was normal with E/A ratio 2.7 (E 0.82; A 0.30; deceleration time 153 ms), with normal E/E’ ratio 7.4 (E’=11.1) (Fig. 1a–c). The mechanical aortic valve was sufficient. Respiratory variation of transmitral flow velocity signal appeared >25 % but not conclusive because of limited interpretability due to low echo quality. During echocardiography, an echodense layer or mass was seen at the LV apex outside the myocardium, which could be pericardial fluid (blood or thrombus), thickened pericardium or epicardial fat. A chest CT proved the layer to be a thickened pericardium (6 mm) (Fig. 1d, e). Although unlikely so soon after surgery, the signs of previously absent right-sided heart failure and the thick pericardium suggested the diagnosis of constrictive pericarditis without any signs of calcification yet. Other causes such as inflammatory (normal CRP) or autoimmune disorders (M-protein negative) were ruled out. Differential diagnostics now included constrictive pericarditis and restrictive cardiomyopathy. The normal E’ of 11.1 makes restrictive cardiomyopathy unlikely (in which the myocardium itself is diseased). To confirm the diagnosis of constrictive pericarditis (which would have severe consequences for the patient as a re-thoracotomy would be necessary), we performed a right heart catheterisation. The right heart catheterisation revealed a diastolic dip plateau phase (Fig. 2a) and right atrial Y wave further confirming our diagnosis of constrictive pericarditis (Fig. 2b). We did not perform simultaneous left-sided pressure measurements with the mechanoprothesis in situ. At that stage, we discussed reoperation with the cardiothoracic surgeon and decided to perform pericardiectomy. Surgery revealed a thickened pericardium and an extensive fibrous net/rind of the thickened pericardium was found and removed (Fig. 1f). Histological examination of the removed material confirmed the diagnosis with signs of chronic fibrotic inflammation. After pericardiectomy, the patient recovered slowly with a regimen J. J. Brugts (*) :A. Constantinescu :K. Caliskan : O. C. Manintveld Department of Cardiology (Heart Failure, Transplantation & Mechanical Circulatory Support Unit), Erasmus MC, Thoraxcenter, ‘s Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands e-mail: [email protected]