Angiographic Results and Elastic Recoil Following Coronary Excimer Laser Angioplasty with Saline Perfusion

Recent experiments have demonstrated that pressure waves of several hundred atmospheres, which occur during excimer laser coronary angioplasty (ELCA), are reduced while ablating in saline in comparison to blood or contrast medium. We report the procedural outcome of ELCA (XeCI laser operating at 308 nm, 25–40 Hz, 40–60 mJ/mm² fluence, and 135 nsec/pulse) performed with a modified saline infusion protocol (two operator technique, flush, and continuous application of saline through the guiding catheter immediately prior and during the whole losing procedure). We studied 48 patients (34 males, 14 females; mean age: 61 ± 6 years; 18 occlusions, 30 stenoses [> 60% diameter stenosis]) with 10 type A, 17 type B, and 21 type C lesions. Laser success (> 20% increase in minimal luminal diameter [MLD]) was achieved in 41 patients (85.4%), and procedural success (< 50% residual stenosis) in 44 patients (91.6%). The MLD increased from 0.37 ± 0.12 to 1.63 ± 0.35 mm (P < 0.001) following laser ablation, and to 2.30 ± 0.34 mm (P > 0.01) after percutaneous transluminal coronary angioplasty (PTCA). The mean percentage stenosis decreased from 81%± 6% (baseline) to 48%± 12% (P < 0.001) after laser ablation, and to 29%± 10% (P < 0.01) following PTCA. The mean diameter of the laser-catheter (LC) was 1.54 ± 0.2 and the mean diameter of the inflated balloon at maximum pressure was 2.7 ± 0.25 mm. Thus, the elastic recoil (ER) following balloon deflation was 15%± 9%, and below the reported ER for PTCA. Two major dissections occurred following ELCA; one patient required bypass surgery and developed a Q wave myocardial infarction (Ml), and one patient was successfully treated with stent implantation following abrupt closure. There were no in-hospital deaths, further Q wave MIs, and/or perforation. In conclusion, ELCA with concomitant saline infusion is effective, safe, and easy to perform. The use of this ablation procedure reduces the rate of significant dissections, favors effective tissue ablation, and thus may in part be responsible for a reduced amount of elastic recoil following additional balloon angioplasty. (J Interven Cardiol 1996;9:9–18)     

Sclerosing lymphangitis of the penis: a lymphangiofibrosis thrombotica occlusiva*

Three patients with so-called non-venereal sclerosing lymphangitis of the penis are presented. Light and electron microscopy of one case revealed a lymphatic collecting vessel with a fibrin thrombus in the process of recanalization and vessel wall fibrosis due to hyperplasia of smooth muscle cells and fibroblasts. The term ‘lymphangiofibrosis thrombotica occlusiva’ is proposed. Lymph stasis is suggested as a provoking factor for the dilatation and clinically striking firm thickening of the affected collecting vessel. No microorganisms were recognized. Within the fibrin thrombus, sprouts of endothelial cells showed intracellular vacuoles, probably indicating the first identifiable step in lymph capillary lumen formation. Signs of collagen remodelling were encountered in the thickened vessel wall.     

DYSKERATOSIS IN BOWEN''S DISEASE: THE ULTRASTRUOTURE AND FATE OF KERATINOCYTES WITH ALTERED TONO-FILAMENT-DESMOSOME COMPLEXES

Summary.— The ultrastructure of dyskeratotic cells in Bowen's disease has been studied. It has been found that, in the suprabasal layers in some keratino-cytes, all tonofilament-desmosome complexes (TFDC), as well as many cytoplasmic organelles, are altered. The earliest stage of TFDG alteration con-sisted in the separation and retraction of tonofilaments from the desmosomes. The consequence of this was the disappearance of the desmosomes and acantholytic separation of the involved keratinocyte. Our findings indicate that this was followed by the disintegration of the involved keratinocyte apart from the tonofilaments. These were released into the intercellular space and finally into the corium through breaks In the basal lamina. The Langerhans and some other dendritic epidermal cells are likely to play a role in the latter process.     

ULTRASTRUCTURAL DIFFERENCES IN HUMAN MALIGNANT MELANOMATA

Summary.— Thirty-two human malignant melanomata have been investigated with the electron microscope. On the basis of the fine structure of the melano-mata and melanosomes we have distinguished 2 different tumour forms (Type A and Type B). The melanosomes of Type A appear cigar-shaped, whereas the premelanosomes have an internal helical structure exhibiting periodicity. Most of the mitochondria of this tumour type show an elongated from and numerous cristae. The nucleolus is usually very large and exhibits some vacuole-like structures which contain a fine granular substance. The nucleus is distinguished by the different extent of heteropyknotic chromatin and fre-quently has "nuclear bodies". The tumour cells of the other melanoma form (Type B) contain only spherical melanosomes, whereas the premelanosomes show no internal fibrillar structure. The mitochondria mostly appear spherical as well; their matrix is slightly electron dense. There is no marked difference between the nuclei of these 2 melanoma forms. Their pathogenesis is discussed.