SUMMARY Samples from 34 patients were studied both histologically and immunocytochemically by the indirect biotin-avidin peroxidase technique to analyse the distribution of the extracellular matrix components (type IV collagen, fibronectin, types I and III collagens) in dissection of the aorta. Most showed defects in type IV collagen around medial smooth muscle cells. Defects in smooth muscle cell basement membrane were found throughout the media in cystic medial degeneration and in medionecrosis, whereas in atherosclerosis such unlabelled areas were found only above advanced atherosclerotic plaques. In aortitis other defects in the smooth muscle cell basement membrane were found in areas of inflammatory infiltrates. In all of these conditions similar defects in fibronectin expression were also found. No defects in the expression of interstitial collagens type I and III were seen in the dissecting aortas. Moreover, cystic medial degeneration, medionecrosis, and atherosclerosis were characterised by intense staining of these interstitial matrix components. In the pathogenesis of the aortic dissection local changes in the basement membranes of the medial layer may be important.Aortic dissection is the most common and often lethal catastrophy that occurs in the aorta.' Controversy surrounds its pathogenesis. 1 2 Recent studies emphasised the role of haemodynamic factors, especially hypertension, in its pathogenesis.26 Some connective tissue and metabolic diseases, however, increase the risk of aortic dissection at an early age.' [7][8][9]
Mycoplasma hominis infections are easily missed because conventional methods for bacterial detection may fail. Here, 8 cases of septic mediastinitis due to M. hominis are reported and reviewed in the context of previously reported cases of mediastinitis, sternum wound infection, pleuritis, or pericarditis caused by M. hominis. All 8 patients had a predisposing initial condition related to poor cardiorespiratory function, aspiration, or complications related to coronary artery surgery or other thoracic surgeries. Mediastinitis was associated with purulent pleural effusion and acute septic symptoms requiring inotropic medication and ventilatory support. Later, the patients had a tendency for indolent chronic courses with pleuritis, pericarditis, or open sternal wounds that lasted for several months. M. hominis infections may also present as mild sternum wound infection or as chronic local pericarditis or pleuritis without septic mediastinitis. Treatment includes surgical drainage and debridement. Antibiotics effective against M. hominis should be considered when treating mediastinitis of unknown etiology.
Post-mortem analysis with castangiography was performed on 54 patients who died within 30 days of coronary artery bypass surgery. Myocardial failure was the cause of 85% of the deaths. There were 215 coronary anastomoses (4.0 +/- 1.1/patient), 24% of which were non-functioning. Most of the occlusions were due to various technical failures. The most striking features were 1) high occlusion rate (25%) in sequential vein grafts and 2) disastrous complications of coronary endarterectomies. Compared with preoperative angiographic data, only 15 (28%) of the 54 patients were found to have 'complete' revascularization, with patent grafts and all stenosed coronary arteries bypassed. The need for recognition and avoidance of technical complications is stressed: Failures of surgical technique constitute a major risk factor in coronary artery surgery.
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