Suspected inflammatory cardiomyopathy. Prevalence of Borrelia burgdorferi in endomyocardial biopsies with positive serological evidence.

BACKGROUND: Cardiac involvement in Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, has been reported to occur in 0.3-4 % of infected patients in Europe. Cardiac manifestations may include conduction disturbances, and also myocarditis, pericarditis, and left ventricular dysfunction. We investigated the prevalence of B. burgdorferi DNA in endomyocardial biopsies from patients with suspected inflammatory heart disease and positive serology for B. burgdorferi. METHODS AND RESULTS: In 64 patients, endomyocardial biopsies were taken after exclusion of coronary heart disease by coronary angiography, and investigated with polymerase chain reaction (PCR) for the presence of B. burgdorferi and cardiotropic viruses. B. burgdorferi DNA was not detected in any of the endomyocardial biopsies. Viruses, particularly parvovirus B19, were detected as infectious agents in 19 (30 %) patients. CONCLUSION: The results of our study demonstrate that PCR analysis of endomyocardial biopsies from patients with suspected inflammatory heart disease, including individuals with dilated cardiomyopathy (DCM) and positive serology for B. burgdorferi, did not reveal the B. burgdorferi genome in any biopsy sample.

Varicose veins: a critical review of the definition and the therapeutical options.

This review intends to give an overview of the present therapeutic options for varicose vein disease. The definition of varicose vein disease and its recurrence are made and discussed with new aspects including duplexsonography assessment. All therapeutic approaches have developed and refined their treatment modalities, the open surgical as well as the endovenous techniques. In particular the “new” endovenous techniques are described with regard to safety and outcome, the published literature in this respect is summarized. The studies comparing the different techniques are listed, the prospective long term studies comparing the new techniques with the so called gold standard (open surgery) shall decide on the fate of the different techniques.

[Tumor markers in the assessment of malignant and benign pericardial effusion]. / Tumormarker im Perikarderguss bei malignen und nichtmalignen Perikardergüssen.

BACKGROUND: The differential diagnosis of pericardial effusion is often challenging because different etiologies can be discussed. Of particular therapeutic and prognostic importance is the definitive differentiation of malignant pericardial effusion from benign effusions. The definitive diagnosis of malignant pericardial effusion is established by a positive cytological examination of the pericardial fluid. However, pericardial fluid cytology, although specific has variable sensitivity. Tumor markers are often investigated after pericardiocentesis but their utility as an aid for the diagnosis of malignant pericardial effusion is not well established. The aim of this study was to measure the concentrations of the tumor markers CEA, CA 19-9, CA 72-4, SCC and NSE in malignant and non-malignant pericardial effusions and to assess their diagnostic utility in differentiating malignant from benign pericardial effusion. METHODS: We investigated the pericardial fluid of 29 patients with proven malignant pericardial effusion and 25 patients with non-malignant pericardial effusion. The etiology of the pericardial effusion was defined by pericardial cytology, epicardial histology and PCR for cardiotropic viruses from pericardial and epicardial tissue acquired by pericardioscopy. The group with non-malignant pericardial effusion comprised 15 patients with autoreactive effusion and 10 patients with viral pericardial effusion. We analyzed the following tumor markers in the pericardial fluid: carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 19-9, carbohydrate antigen (CA) 72-4, squamous cell carcinoma (SCC) antigen and neuron-specific enolase (NSE). RESULTS: Of the tumor markers tested the mean concentrations of the CEA, CA 72-4 and CA 19-9 were significantly higher in malignant pericardial effusions than in non-malignant effusions (CEA 450.66 ±1620.58 µg/l vs. 0.72 ±1.49 µg/l, p<0.001; CA 19-9 1331.31 ±3420.87 kU/l vs. 58.85 ±17.53 kU/l, p=0.04; CA 72-4 707.90 ±2397.55 kU/l vs. 0.48 ±2.40 kU/l, p<0.001). ROC curve analysis showed that pericardial fluid CA 72-4 yielded an area under the curve (AUC) of 0.85 (95% confidence interval 0.74-0.95), followed by CEA with 0.80 (95% confidence interval 0.68-0.92). Pericardial fluid CA 72-4 levels >1.0 kU/l had 72% sensitivity (95% confidence interval 53%-87%) and 96% specificity (95% confidence interval 80%-99.9%) and CA 72-4 levels >2.5 kU/l had 69% sensitivity (95% confidence interval 49%-85%) and 96% specificity (95% confidence interval 80%-99.9%) in differentiating malignant pericardial effusions from effusions due to benign conditions. CONCLUSION: Malignant pericardial effusions are associated with significantly higher pericardial concentrations of the tumor markers CEA, CA 72-4 and CA 19-9. Of the tested tumor markers, measurement of CA 72-4 levels in pericardial fluid offered the best diagnostic accuracy. Based on our data evaluation of every patient with unexplained pericardial effusion and negative pericardial fluid cytology should include the measurement of pericardial fluid CA 72-4 levels. Under these circumstances the elevation of pericardial fluid CA 72-4 levels should include malignancy as a probable diagnosis.

[New possibilities of diagnostics and therapy of pericarditis]. / Neue Möglichkeiten der Diagnostik und Therapie der Perikarditis.

Pericarditis is an inflammatory disorder of the pericardium with or without an associated pericardial effusion. The diagnosis is based on the clinical manifestations and typical ECG changes. Echocardiography is essential to reveal the size of the pericardial effusion and to determine its hemodynamic significance. The precise etiology of pericarditis may be established by pericardiocentesis, pericardioscopy and targeted biopsy and consecutive pericardial fluid and biopsy analysis by molecular biology, cytology, microbiology and immunological techniques. Non steroidal anti-inflammatory drugs and/or colchicine are the mainstay of anti-inflammatory treatment of pericarditis. Systemic corticoid treatment should be restricted to patients with associated autoimmune disorder, relapsing pericarditis and as a complementary therapy in tuberculous pericarditis. In autoreactive pericarditis intrapericardial instillation of triamcinolone is effective with few side effects. In malignant pericarditis the intrapericardial administration of cisplatin prevents early recurrences.

[Recurrent autoreactive pericardial effusion. Impact of an aetiological classification of pericarditis]. / Rezidivierender autoreaktiver Perikarderguss. Bedeutung einer ätiologischen Klassifikation der Perikarditis.

HISTORY: A 36 year-old man suffered from fever, fatigue, pleurodynia and precordial discomfort. His family physician suspected febrile tracheobronchitis and treated it with ampicillin for 5 days. Because symptoms persisted an ECG was done which suggested acute myocardial infarction. The patient underwent an emergency coronary angiography which excluded coronary artery disease and aortic dissection. Pericarditis was suspected and the patient put on aspirin, 500 mg/d. Because of persisting cardiac symptoms an echocardiography was performed which revealed systolic separation between epi- and pericardium, characteristic of a small pericardial effusion after acute pericarditis. The symptoms improved after one week of treatment with diclofenac and the ECG had become normal. Two months later the patient was seen at our cardiac outpatient clinic. He had night sweats, sporadic precordial pain and severe dyspnoe. INVESTIGATIONS: Further investigations revealed tachycardia (120/min), hypotension (95/70 mm Hg), pulsus paradoxus and jugular vein sustension. Echocardiography revealed a large pericardial effusion ("swinging heart"), which explained the low voltage and the electrical alternans in the ECG. TREATMENT AND COURSE: Pericardiocentesis was carried out the same day to relieve the tamponade. It was followed by pericardioscopy and epi- as well as pericardial biopsy. 485 ml of a serous effusion were drained. Cytology and histology demonstrated a lymphocytic fibrinous pericarditis. Polymerase chain reaction (PCR) on viral and bacterial RNA and DNA of potentially cardiotropic agents remained negative. The pigtail catheter was left in place and 80 mg of gentamycin were given intrapericardially on day 1 and 2, followed by 500 mg of crystalloid triamcinolone acetate after the PCR was found to be negative. Oral treatment with 0.5 mg colchicine three times a day (off-label use) was started and maintained for 6 months. After 9 months no effusion was detected and the patient was free of symptoms. CONCLUSIONS: After exclusion of bacterial and viral pericardial infection, a high single dose of intrapericardial triamcinolone combined with long-term oral colchicine has proven to be a highly efficacious treatment of autoreactive pericarditis which will avoid relapses in most cases.

Invasive techniques--from diagnosis to treatment.

Invasive diagnostic and therapeutic techniques are indispensable for the diagnosis and interventional treatment of coronary artery disease, valvular involvement and, in particular, if the specific components of the inflammatory or degenerative processes in rheumatic disease are to be identified in the different components of the heart. Although impairment of cardiac function and ischaemia can be suspected also by non-invasive techniques, coronary involvement needs the final proof by angiography. Endomyocardial or epicardial biopsy identifies the key players of autoreactivity: the infiltrating cells and the bound and circulating antibodies. Before corticoid treatment is started, a viral or microbial aetiology has to be excluded at the site of cardiac inflammation. This again can only be done by the analysis of cardiac tissue samples.