In April 2009, a 32-year-old female patient was referred to our hospital with acute chest pain. She was diabetic, nicotine dependent and had a family history of coronary heart disease. The electrocardiogram showed a previously documented complete left bundle branch block. Cardiac troponin T was elevated (1.18 ng/ml, CK and CK-MB normal, LDH 333 U/l), C-reactive protein serum concentration was 157 mg/l (normal \ 5), white blood count was normal. Coronary angiography showed a thrombotic occlusion of the mid-LAD as culprit lesion (Fig. 1a, left panel). Additionally, a smooth lesion in the small PDA of the right coronary artery could be detected (Fig. 1a, right panel). The patient’s past medical history was complex. Aortic valve replacement with a biological prosthesis had been performed in 2006 due to infective endocarditis. Interestingly, 6 months before the acute coronary syndrome, i.e. in November 2008, the patient had been admitted to an external department with diffuse, non-symmetric arthralgia and a recurrent purpuric rash over her distal lower extremities. Hemorrhagic leukocytoclastic vasculitis had been diagnosed by skin biopsy (Fig. 1b). Laboratory tests conducted at that time had revealed a profound reduction in renal clearance (creatinine 2.4 mg/dl, cystatin C 3.3 mg/l, GFR 16-20 ml/min). Urinanalysis had shown proteinuria (0.84 g/24 h) and glomerular hematuria with detection of acanthocytes. These findings suggest that renal impairment had been caused by a glomerulonephritis. Monotherapy with prednisolone had been performed followed by chemotherapy with cyclophosphamid due to recurrence of symptoms after dose reduction of prednisolone. At the current admission to our department with an acute coronary syndrome, revascularization was performed by direct implantation of a bare metal stent in the midLAD. Because of the small vessel diameter there was no indication for a PCI of the PDA. However, the unusual lesion pattern in two distinct coronary vessels in a young patient with no further evidence of coronary heart disease was highly suspicious for coronary embolism, particularly in the light of the patient’s history of valve replacement 2 years earlier. During admission, the patient was recurrently subfebrile (\38 C), serum concentration of C-reactive protein remained elevated. Transesophageal echocardiography was performed twice. No typical endocarditic vegetations could be detected. However, thickening of the cusps of the bioprosthesis only two years after implantation as well as a mild aortic regurgitation were noticed. Immunosuppressant therapy was stopped. Serial blood cultures drawn at consecutive days yielded Granulicatella adiacens which proved to be highly sensitive to penicillin (MIC 0.004 mg/l). In one additional sample a b-lactamase positive, penicillin-resistant Staphylococcus aureus was obtained which was tested to be sensitive to oxacillin (MIC 0.25 mg/l). These positive microbiological results and the assumed embolic coronary event made the diagnosis of prosthetic valve endocarditis very likely and J. Poss M. Bohm H. Kilter (&) Universitatsklinikum des Saarlandes, Klinik fur Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Kirrberger Strase, 66421 Homburg/Saar, Germany e-mail: heiko.kilter@uks.eu
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Jun 1, 2011
Walter Hofmann + 4
