Search

We present the case of a 75-year-old woman with a medical history of rheumatoid arthritis treated with hydroxychloroquine, who was admitted with acute left-sided heart failure due to a hydroxychloroquine-induced cardiomyopathy as supported by endomyocardial biopsy.

To determine whether superhydrophobic modification of small diameter expanded polytetrafluoroethylene (ePTFE) vascular grafts improves the performance of these grafts, we assessed neointima formation and platelet deposition in standard and superhydrophobic modified ePTFE grafts. Standard and superhydrophobic vascular grafts were implanted in the carotid arteries of two rabbits and two pigs. Furthermore, standard and superhydrophobic vascular patches were implanted in the carotid arteries of seven pigs. After 4 weeks of implantation all patches were removed and histomorphometric data were analyzed. The early thrombotic effect of superhydrophobic modification was examined by quantifying platelet glycoprotein receptor IIIa deposition onto each type of vascular graft after 15 min of in vitro circulation with human blood. All superhydrophobic and standard ePTFE vascular grafts occluded 15 min to 1 h after implantation in both rabbit and pig carotid arteries. All implanted patches remained patent and were completely covered by endothelium. Superhydrophobic modification of ePTFE vascular grafts did not lead to less neointima formation and resulted in significantly more platelet deposition than did standard ePTFE vascular grafts. Thus, superhydrophobic modification does not improve the performance of small diameter ePTFE vascular grafts.

Platelets and leucocytes are important participants in the response of the body to small diameter vascular grafts implanted into the arterial circulation. A sensitive and quick method for measuring platelet and leucocyte deposition contributes to material evaluation. With a newly developed fluorescence labeling method we examined the deposition of platelets and leucocytes onto vascular grafts in vitro. Human platelets and leucocytes were isolated and labeled with the fluorescence label Europium trichloride (EuCl3). After reconstitution of the labeled cells in plasma their functionality appeared intact and competitive with unlabeled cells. Eu-labeled platelets or leucocytes were then incubated with expanded polytetrafluoroethylene (ePTFE), Dacron and polyurethane (PU) vascular grafts in autologous plasma. Beta-thromboglobin and thromboxane release from platelets and beta-glucuronidase release from leucocytes during the incubation experiments were measured. Platelets and leucocytes deposited significantly less onto ePTFE compared to Dacron and polyurethane (P < 0.01). Our results are in accordance with results of in vivo studies using radio-active labeling to study platelet and leucocyte deposition. However, a new finding was that this reduced cell deposition may in part be due to possible toxic effects of ePTFE, shown by increased haemolysis and beta-thromboglobin release.

Objectives: To use the autologous gastroepiploic artery (GEA) as arterial bypass graft for peripheral revascularisation. We compared the development of intimal hyperplasia and nitric oxide (NO) capacity in GEA and internal jugular vein (IJV) implanted as peripheral grafts., Materials and Methods: In pigs the GEA was implanted into the right peripheral circulation as a femoropopliteal bypass graft. In the left peripheral circulation the IJV was implanted as a femoropopliteal graft. After 21 days all grafts were harvested. Vascular rings of each graft before and after operation were studied for NO capacity. The distal half of each graft was prepared for histomorphometric studies., Results: Administration of bradykinin to IJV and GEA induced relaxation. After implantation bradykinin resulted in contraction in IJV grafts, whereas in GEA grafts relaxation was reduced. In IJV grafts extensive intimal hyperplasia was formed, whereas in GEA grafts only small areas of intimal hyperplasia were formed., Conclusions: The functional studies lost NO capacity in IJV grafts, whereas NO capacity in GEA grafts remained intact. Intimal hyperplasia in IJV grafts was extensive, whereas GEA grafts demonstrated preservation of pre-existent intimal architecture. These results may encourage the application of the human GEA as bypass graft for reconstruction of arteries in the lower limb or foot.

Purpose: The purpose of this study was to determine whether the wall thickening observed in vein grafts after they were placed into the arterial circulation could be inhibited by periadventitial delivery of an insoluble sulfated polymer of beta-cyclodextrin (P-CDS) capable of tightly binding heparin binding growth factors., Methods: Thirty-four New Zealand white rabbits underwent implantation of reversed autologous jugular vein interposition grafts in the common carotid artery and were randomized to receive either 20 mg P-CDS (n = 18) topically around the graft or no additional therapy (n = 16). Before being killed at 28 days, animals were given bromodeoxyuridine to assess smooth muscle cell proliferation. Histomorphometric analyses were performed after perfusion fixation., Results: Compared to controls, treatment with P-CDS was associated with reduced mean intimal thickness (24 +/- 3 vs 38 +/- 4 microns; mean SEM, p < 0.01) and intimal area (0.25 +/- 0.03 vs 0.54 +/- 0.09 mm2; p < 0.01). There was also significantly less medial thickness in the P-CDS group (45 +/- 3 vs 63 +/-3, p < 0.001). There was no significant difference in intimal or medial smooth muscle cell proliferation between P-CDS-treated and control vein grafts at 28 days. The polymer persisted in the adventitia with a mild foreign body reaction., Conclusion: Periadventitial placement of P-CDS, a novel, insoluble, sulfated carbohydrate polymer, inhibits intimal and medial thickening of vein bypass grafts in this model of vein grafting. The persistence of P-CDS in vivo for prolonged periods, and the ease of topical application of P-CDS during vascular bypasses may have important implications for its future use in vascular surgery.

The origin of the noradrenergic innervation of the preganglionic autonomic nuclei in the medulla oblongata and spinal cord is still controversial. In this investigation descending connections of the locus coeruleus to the dorsal motor vagus nucleus in the rat are studied with Phaseolus vulgaris leucoagglutinin and horseradish peroxidase as neuroanatomical tracers. Locus coeruleus projections in the motor vagus nucleus are found in the medial part at rostral levels and in the lateral part at intermediate levels of this nucleus. The terminal labeling in the lateral intermediate part of the vagus nucleus appears in an area where possibly preganglionic parasympathetic cardiac neurons are located, suggesting that the locus coeruleus might be involved in regulation of cardiovascular functions. After small iontophoretic injections of horseradish peroxidase in the motor vagus nucleus, retrogradely labeled cells are found in the ventral part of the locus coeruleus and occasionally in the dorsal part of the nucleus. The results show that the locus coeruleus-dorsal motor vagus nucleus pathway may participate in the inhibition of the cardiac preganglionic neurons in the dorsal motor vagus nucleus by the hypothalamic paraventricular nucleus.