Assays which detect the release of platelet-specific proteins and of peptides during thrombogenesis and are considered markers of activation of platelets and the coagulation system have recently been developed. This study was designed to utilize these haemostasis-related markers to test the hypothesis that a prethrombotic state is related to the presence, aetiology and severity of heart failure. Seventy patients with heart failure were evaluated and data were compared with 36 normal volunteers and 41 patients with coronary artery disease without heart failure (CAD). Thrombogenesis was documented using assays which measure platelet function, thrombin activity and fibrinolysis. Platelet function was measured by determining plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (BTG). Thrombin-antithrombin III complexes (TAT) and fibrinopeptide A (FPA) were determined to evaluate thrombin activity. Fibrinolytic activity was assessed by measuring D-Dimer levels. Patients with heart failure, when compared to normals, had increased plasma levels of BTG (89 +/- 62 IU.ml-1 vs 50 +/- 59 IU.ml-1, P < 0.01), TAT (4.6 +/- 4.3 micrograms.l-1 vs 2.3 +/- 0.64 micrograms.l-1, P < 0.005), and D-Dimer levels (506 +/- 444 IU.ml-1 vs 191 +/- 144 IU.ml-1, P < 0.0001). Patients with heart failure, when compared to the CAD group, had increased plasma levels of D-Dimer (506 +/- 444 ng.ml-1 vs 191 +/- 144 ng.ml-1, P < 0.05). Aetiology of heart failure did not affect these measurements. Patients with severe heart failure, as determined by high plasma norepinephrine concentration or low ejection fraction, were more likely to have activation of platelets and the coagulation system.(ABSTRACT TRUNCATED AT 250 WORDS)

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The results suggest that EM after one burr-hole surgery prevents postoperative complications without increasing the risk of recurrence in CSDH patients > or =65 years of age.

This study was undertaken to evaluate the histological reaction of cultured endothelial cells to endovascular embolic materials in vitro. Endothelial cells were isolated and cultured from a canine carotid artery. Embolic materials (platinum microcoils, polyvinyl alcohol particles, silicon balloons, or silk threads), either in their normal state or after having been coated with type 1 collagen, fibronectin, or laminin, were placed on endothelial cells and cocultured for 6, 12, and 24 hours and 2, 3, 7, 14, and 21 days. The cocultures were investigated histologically using a scanning electron microscope. Endothelial cells were not found on any uncoated embolic materials, even at 21 days. On the materials coated with fibronectin or laminin, endothelial cells began to proliferate in 7 days, covering the materials extensively in 14 days. On the other hand, endothelial cells began to proliferate on the collagen-coated materials in 3 days, covering them extensively in 7 days and reaching confluence with a cobblestone pattern in 21 days. The densities of endothelial cells on collagen-coated materials were much higher than those observed on the materials coated with other extracellular matrices. Future advantages of the clinical use of collagen-coated embolic materials in interventional treatment are discussed.

Nineteen patients with massive lobar haemorrhage without angiographic lesions received direct or stereotactic surgery, and biopsy specimens were examined histologically. Ten patients (53%) were found to have vessels positive for Congo-red staining, and demonstrating amyloid angiopathy. In the patients with amyloid angiopathy, CT scan and surgical findings were investigated. Subarachnoid haemorrhage (9/10), irregularly shaped haematoma (9/10) and fluid-blood density level in the haematoma cavity (7/10) were frequently found on CT scan. The characteristic surgical findings in patients treated by direct surgery were subarachnoid haemorrhage adjacent to intracerebral haematoma (8/8) and the existence of a tangle of vessels in the haematoma cavity (4/8). Evacuation of haematomas was relatively easy, and difficulty of haemostasis was not encountered during surgery.

Two cases of primary angiitis of the central nervous system with subarachnoid hemorrhage are reported. One patient was admitted with very thin and localized sulcal subarachnoid hemorrhage, followed by the development of multiple parenchymal edema. Although the first angiography showed only a mild narrowing of an artery, the second angiography demonstrated multiple segmental narrowings of arteries. An open biopsy failed to show histological changes. The second patient suffered from sylvian subarachnoid hemorrhage along with multiple intracerebral hemorrhages, with angiography that was diagnostic for angiitis. In both cases, predonine was initiated and further angiography clearly demonstrated a resolution of the angiitis. The usefulness of serial angiography for diagnosis in comparison with surgical biopsy and for monitoring the treatment of this disease is discussed. The occurrence of subarachnoid hemorrhage in this disease is also reviewed.

MRA may help prompt the noninvasive diagnosis in certain cases of Tolosa-Hunt syndrome with little inflammatory reaction in the cavernous sinus but with predominant intra- and juxta-cavernous periarteritis.