Notes: From 1988 to 1990 chronic coronary occlusions were treated with a newly developed slowly rotating angioplasty system (ROTACS), which is designed for atraumatic passage of arterial obstructions. In all 152 patients (mean age 55 years, ranging from 29 to 78 years) attempts to recanalize the coronary occlusion with conventional guidewire systems had failed. In 74/152 patients the age of the occlusion could be estimated because of a previous angiogram or clinical event. It ranged from 1–192 months (median 6 months, mean value 14 months; in 20% of patients it was 1–3, in 37% 4–6, in 28% 7–12, and in 15% 〉 12 months). The occlusion was localized in the right coronary artery (RCA) in 86 cases, in the left anterior descending coronary artery (LAD) in 37 cases, and in the circumflex branch of the left coronary artery in 17 cases. Eleven bypass occlusions were treated. One patient had a LAD and RCA occlusion. Out of 152 patients 84 could be recanalized. The success rate rose with experience from 30% to 60%. It was 55% in the LAD, 52% in the RCA, 70% in the circumflex branch, and 63% in bypass grafts. The success rate in relation to the age of the occlusion was 93% in occlusions of 1–3 month duration, 74% in occlusions of 4–6 months duration, 52% in occlusions of 6–12 months duration, and 8% in occlusions older than 12 months. Seventy-six of the successfully treated patients underwent follow-up angiography after 4 months. In 56/76 (74%) the vessel remained open. Twenty-two patients (29%) had restenosis that was successfully dilated in 21 patients. Twenty patients (26%) had reocclusion. Thus, the angiographically determined long-term success rate was 72%. Emergency operation was necessary in two patients in whom reopening of the LAD was attempted although the occlusion was located directly at the take-off of the LAD from the left main. Since this type of occlusion was consequently considered a contraindication, no further serious complications occurred. There was one myocardial infarction, no death, no vessel wall perforation or other complications in the 152 patients. It is concluded that low speed ROTACS is a safe technique that can be applied in chronic coronary occlusions even if the duration of occlusion exceeds 6 months. (J Interven Cardiol 1991; 4:15–165)

Notes: There is evidence that an inflammatory microglial reaction participates in the pathophysiology of dopaminergic neuronal death in Parkinson's disease and in animal models of the disease. However, this phenomenon remains incompletely characterized. Using an in vitro model of neuronal/glial mesencephalic cultures, we show that the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+) stimulates the proliferation of microglial cells at concentrations that selectively reduce the survival of DA neurones. The mitogenic action of MPP+ was not the mere consequence of neuronal cell demise as the toxin produced the same effect in a model system of neuronal/glial cortical cultures, where target DA neurones are absent. Consistent with this observation, the proliferative effect of MPP+ was also detectable in neurone-free microglial/astroglial cultures. It disappeared, however, when MPP+ was added to pure microglial cell cultures suggesting that astrocytes played a key role in the mitogenic mechanism. Accordingly, the proliferation of microglial cells in response to MPP+ treatment was mimicked by granulocyte macrophage colony-stimulating factor (GM-CSF), a proinflammatory cytokine produced by astrocytes and was blocked by a neutralizing antibody to GM-CSF. Thus, we conclude that the microglial reaction observed following MPP+ exposure depends on astrocytic factors, e.g. GM-CSF, a finding that may have therapeutic implications.