Biomedical subjects
P Erne
Publications and source records attributed to P Erne.
Right ventricular myxoma mimicking recurrent pulmonary embolism after primary ligament reconstruction.
Recurrent pulmonary emboli may be due to numerous causes and deep vein thrombosis are not an unusual source of pulmonary emboli following surgery. In this case report, the diagnostic approach and implications of a right ventricular myxoma as a rare source in a young patient is described. A 27-year old healthy woman presented scintigraphically proven recurrent pulmonary emboli after primary ligament reconstruction. Following a long period of diagnostic work-up for thromboembolism after surgery, a transthoracic and transoesophageal echocardiography was performed to document a right ventricular myxoma. Both transthoracic and transoesophageal echocardiography are powerful diagnostic means in a cardiac work-up and were used in this patient for the documentation of a right ventricular myxoma mimicking deep vein thromboembolism after surgery. As consequence of this case report we recommend to investigate patients with recurrent pulmonary embolism and no detectable venous thrombosis by echocardiography and a need for cardiac catheterization is restricted to patients with possible coexisting coronary artery disease. Furthermore, this case report demonstrates a myxoma in the right ventricle occurring only in 3-4% of all myxomas.
[Transthoracic echocardiography--indications for modern color Doppler echocardiography].
Transthoracic echocardiography as a pillar of modern cardiology has become the most important cardiac examination following the assessment of patients history and clinical status. By this it is possible to judge clinical problems of the heart and all forms of heart disease appropriately, reproducibly and noninvasive. With use of two-dimensional echocardiography morphological and functional data of the anatomy of the heart and the great vessels can be obtained, but even a quantitative approach with measurement of left ventricular function is possible. Together with conventional doppler and colour doppler sonography this method is able to replace many diagnostic catheter evaluations, since ventricular function, stenotic lesions, insufficiences, shunt lesions and pulmonary artery pressures can be quantitated. Data from echodopplersonography are of great importance to establish the prognosis and risk of mortality of individual patients. Thus, echocardiography is increasingly used as diagnostic tool. In consequence, there is need for definitions of appropriate yield to warrant echocardiography on the basis of clinical and cost-effectiveness criteria and a quality control of continuing education to guarantee the outstanding value of this method. This article summarizes the recommendations for the use of doppler echocardiography in cardiovascular diseases according to the actual executive summary of the classification system used of the American College of Cardiology and the American Heart Association.
[What is your diagnosis? Right ventricular dysplasia].
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[Aortic valve abscess with perforation in the right atrium].
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[What is your diagnosis? Multifocal atrial tachycardia].
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[What is your diagnosis? WPW syndrome].
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Characterization of the human and mouse cDNAs coding for S100A13, a new member of the S100 protein family.
Here we report the characterization of the human S100A13 cDNA coding for a novel calcium-binding protein belonging to the S100 protein family. The predicted S100A13 protein shows sequence homologies to other S100 proteins between 50.5% (to S100A5) and 59.3% (to S100A12). High mRNA amounts were found in skeletal muscle, heart, kidney, ovary, small intestine and pancreas. Since twelve S100 genes are clustered on human chromosome 1q21, we determined the chromosomal localization of the human S100A13. It co-localizes with S100A1 on the cluster. Furthermore, we characterized the cDNA sequence coding for the mouse homolog of S100A13. Similar to the putative human protein, mouse S100A13 is composed of 98 amino acids displaying a homology of 86.7% compared to human S100A13.
Altered expression of the Ca(2+)-binding protein S100A1 in human cardiomyopathy.
The Ca(2+)-binding protein S100A1 displays a tissue-specific expression pattern with highest levels in myocardium and has been shown to interact with SR-proteins regulating the Ca(2+)-induced Ca(2+)-release. We, therefore, hypothesized that changes in S100A1 gene expression might correlate with the pathognomonic finding of altered SR Ca(2+)-transients in human end stage heart failure. To test this hypothesis, we established a specific and sensitive method to analyse S100A1 expression in cardiac tissues by employing hydrophobic interaction-chromatography and reversed-phase high performance liquid chromatography (RP-HPLC) coupled with Electron-Ionisation-Mass-Spectrometry (ESI-MS). Porcine myocardium showed a differential expression of S100A1 with relative protein concentrations of 62 +/- 8% in the right ventricle (RV), 57 +/- 9% in the right atrium (RA), and 25 +/- 15% in the left atrium (LA) as compared to the left ventricle (LV) (100 +/- 10%; P < 0.001). Northern blot analyses confirmed a likewise distribution of porcine S100A1 mRNA implying a regulation on the transcriptional level. Analyses of left ventricular specimen of patients with end stage heart failure (CHF, n = 6; CHD, n = 6) revealed significantly reduced S100A1 protein levels, while integration of S100A1 peaks after RP-HPLC yielded two groups of patients with < 76% (69 +/- 7%, n = 6) and < 35% (23 +/- 12%, n = 6) respectively as compared to controls (100 +/- 8%, n = 3). These data demonstrate for the first time that S100A1 is differentially expressed in myocardium and that in human cardiomyopathy a reduced expression of S100A1 may contribute to a compromised contractility.
Ca2+ channel blockers modulate metabolism of collagens within the extracellular matrix.
The extracellular matrix (ECM) is an intricate network composed of an array of macromolecules capable of regulating the functional responsiveness of cells. Its composition greatly varies among different types of tissue, and dysregulation of its metabolism may contribute to vascular remodeling during the pathogenesis of various diseases, including atherosclerosis. In view of their antiatherosclerotic effects, the role of Ca2+ channel blockers in the metabolism of ECM was examined. Nanomolar concentrations of the five Ca2+ channel blockers amlodipine, felodipine, manidipine, verapamil, or diltiazem significantly decreased both the constitutive and platelet-derived growth factor BB-dependent collagen deposition in the ECM formed by human vascular smooth muscle cells and fibroblasts. The drugs inhibited the expression of fibrillar collagens type I and III and of basement membrane type IV collagen. Furthermore, Ca2+ channel blockers specifically increased the proteolytic activity of the 72-kDa type IV collagenase as shown by gelatin zymography and inhibited the transcription of tissue inhibitor of metalloproteinases-2.
Involvement of protein kinase C in hypoxia-induced desensitization of the beta-adrenergic system in human endothelial cells.
In order to better understand the mechanisms whereby oxygen deficiency promotes blunting of the endothelial beta-adrenergic receptor (beta-AR) system we examined the effects of hypoxia on beta-AR, adenylate cyclase (AC) activity and phosphoinositide turnover in cultures of human pulmonary artery and umbilical vein endothelial cells. 1 hr of hypobaric hypoxia (290 mm Hg) increased basal levels of inositol mono-, bis-, and tris-phosphate to those following histamine stimulation under normoxia. Basal and isoproterenol-stimulated AC activities were lowered after 1 hr of hypoxia. beta-AR density was decreased after 2-3 hrs of hypoxia and after treatment of EC with histamine, platelet activating factor or phorbol myristate acetate (PMA). In protein-kinase C (PK-C)-downregulated EC, neither hypoxia nor PMA influenced beta-AR density or AC activity. Hypoxia-induced desensitization of beta-AR signal transduction in EC may involve hypoxia-stimulated phosphoinositide turnover and subsequent PK-C activation.
[What is your diagnosis? Ventricular tachycardia].
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[What is your diagnosis? Right bundle-branch block].
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[What is your diagnosis? Ebstein Anomaly with additionally hemodynamically relevant left-right shunt in type II atrial septal defect].
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[What is your diagnosis? Atrial septal defect].
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