Background. Aortic dissection still has a poor prognosis despite progress in therapy. Therefore, this prospective follow-up study was designed to determine whether the degree of communication between true and false lumen in relation to the type of dissection, analyzed by transesophageal echocardiography, influences the risk after initiation of medical or surgical therapy.

Background-Simvastatin, a 3-hydroxy-methylglutaryl coenzyme A reductase inhibitor, has been shown to lower serum cholesterol levels in clinical use. Moreover, statins exert beneficial effects in vascular diseases by inhibition of leukocyte rolling, adherence, and transmigration. The aim of this study was to determine if pretreatment with simvastatin attenuates Staphylococcus aureus ␣-toxin-induced increase in leukocyte-endothelial interactions during exotoxemia. Methods and Results-The effects of simvastatin on leukocyte-endothelial cell interactions were observed by intravital microscopy in the rat mesenteric microcirculation. Simvastatin (50 or 100 g/kg) was administered 18 hours before the study. Activation of microcirculation was induced by bolus administration of 40 g/kg S aureus ␣-toxin. Exotoxemia resulted in a significant and time-dependent increase in leukocyte rolling, adherence, and transmigration of leukocytes as well as P-selectin expression on the intestinal vascular endothelium. Pretreatment with simvastatin significantly inhibited exotoxin-induced leukocyte rolling from 71Ϯ10 to 14Ϯ4.7 cells/min (PϽ0.01) and adherence from 14Ϯ3.5 to 0.4Ϯ0.2 cells (PϽ0.01). In addition, simvastatin pretreatment significantly inhibited transmigration of leukocytes from 10.5Ϯ1.2 to 4.2Ϯ0.9 (PϽ0.05) cells. Immunohistochemical detection of endothelial cell adhesion molecule P-selectin showed a 50% decrease in endothelial cell surface expression after simvastatin treatment. Furthermore, simvastatin treatment resulted in enhanced expression of endothelial cell NO synthase III in the intestinal microcirculation. Conclusions-These results demonstrate that simvastatin interferes with exotoxin-induced leukocyte-endothelial cell interactions, which may be relevant in various infectious diseases. Statin treatment may offer a new therapeutic strategy for these clinical conditions.

Abstract-Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non-C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment were 0.07Ϯ0.01 and 0.08Ϯ0.01 (SEM), respectively. However, differences in atherosclerotic plaque formation were discernible macroscopically, with extensive aortic lesions being visible in all C6-competent animals and absent in all C6-deficient animals. Aortas were sectioned from thorax to abdomen, and 10 sections were stained from each aorta. Quantification of atherosclerotic lesions and lumen stenosis with the use of computer-based morphometry documented a dramatic protective effect of C6 deficiency on the development of diet-induced atherosclerosis. We conclude that the terminal complement sequence is centrally involved in atherosclerotic lesion progression. (Arterioscler Thromb Vasc Biol. 1998;18:1790-1795.)Key Words: complement activation Ⅲ atherosclerosis T he possible relevance of complement activation in atherogenesis has not received much attention to date, and only a few reviews are available on the topic. 1,2 The first immunohistochemical studies on complement deposition in atherosclerotic lesions appeared in 1985 to 1987, 3-5 and C5b-9 complexes were subsequently quantified by ELISA in detergent extracts of lesion homogenates. 6 In those studies, the stages of lesion development were not defined, so it could not be excluded that complement activation might have occurred subsequent to tissue damage. An experimental study was then performed in rabbits, leading to the clear demonstration that diet-induced deposition of lipids in the subendothelium was temporally associated with complement activation, which occurred before lesion infiltration by monocytes. 7 A directed search led to tentative identification of the complement-activating entity. Heterogeneously sized lipid droplets containing high amounts of free cholesterol were isolated from early lesions and were shown to be capable of spontaneously activating the alternative complement pathway. 8 The origin of this lipid, termed the lesion complement activator (LCA), was unknown, but the possibility that it represented an LDL derivative was obvious. To corroborate this assumption, attempts were undertaken to transform LDL in vitro into a complement-activating moiety. This was found to be possible by combined treatment of the lipoprotein with a protease, cholesterol-esterase, and neuraminidase, 9 enzymes that occur ubiquitously in lysosomes of mammalian cells and that are...

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Conclusions-S bovis endocarditis is a severe illness because of the more common involvement of multiple valves, and of the frequent occurrence of haemodynamically relevant valvar regurgitation and infectious myocardial infiltration. (Heart 1998;80:276-280)

Early diagnosis of primary pulmonary artery sarcomas can be improved by computed tomography and magnetic resonance scanning. Radical surgical resection probably presents the only chance for cure. The role of neoadjuvant or adjuvant treatment modalities has to be defined. Pulmonary artery sarcoma need not necessarily be a fatal diagnosis.

Follow-up of 18 patients with aortic dissection (five with type I, one with type II, 11 with type III dissection according to DeBakey) by transesophageal, two-dimensional and color-coded Doppler echocardiography showed a persistence of the false lumen in five of seven patients (71%) after surgery and in nine of 11 patients (82%) after medical therapy. In two patients treated with surgery, the dissected part of the aorta had been resected, whereas in two patients treated medically, a progressive and complete obliteration of the false lumen was observed. In the false lumen, thrombus formation was absent in four, localized in four, and progressive in six patients. Flow within the false lumen could be registered in 14 patients, and two distinct flow patterns were differentiated (laminar biphasic flow or slowly circulating flow). Persisting intimal tears were visualized by two-dimensional echocardiography in four patients, whereas colorcoded Doppler showed an additional one to three intimal tears in the descending aorta in 10 patients. Flow across these intimal tears was biphasic in 75% of patients; that is, systolic flow was directed from the true to the false lumen with diastolic flow reversal. Unidirectional flow was detected in 25% of the communications, directed in 20%o from the true to the false lumen, serving as an entry only and in one (5%) as reentry only. Additional information concerning complications like extension of the dissection (one of 18 patients), localized dilatation of the aorta (two of 18 patients), mediastinal hematoma (one of 18 patients), or aortic regurgitation (three of 18 patients) were detected by this method. Concerning the morphologic findings and the detection of flow characteristics, the transesophageal approach was superior to conventional echocardiography especially in the descending thoracic aorta. Thus, transesophageal twodimensional and color-coded Doppler echocardiography seems to be an ideal method not only for the easy detection of aortic dissection but also for follow-up. (Circulation 1989;80:24-33 Transesophageal echocardiography overcomes these methodologic limitations and is of great diagnostic value because of high-quality cross-sectional images of the ascending and descending thoracic aorta even in patients in shock or on mechanical ventilation.23-30 Surgery without further diagnostic investigation has been performed successfully in emergency cases.30 In combination with color-coded Doppler flow imaging, which superimposes flow information

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