The St. Jude Medical (SJM) prosthetic cardiac valve is a low-profile, bileaflet mechanical valve with an excellent record of durability and a low overall complication rate.1–3 Mechanical failure is a rare occurrence with this valve.4 We report a case of mechanical failure of a SJM prosthesis due to leaflet fracture with subsequent embolization.

There is evidence that peptide neurotransmitters (e.g., substance P, neurokinin A, vasoactive intestinal peptide, calcitonin gene-related peptide) from sensory nerves play a part in vasoregulation. We examined the effect of neonatal treatment with capsaicin, a procedure that causes permanent impairment of primary sensory neurons, on a recently described arteriolar response to inflammation, focal arteriolar insudation (FAI). FAI occurs at a distance from the site of injury, in arterioles supplying that area, and is first observed 6 hr after onset of inflammation and maximally at 24 hr; the affected arterioles show dilation, with increased endothelial permeability and occasional smooth muscle cell damage. In our model, inflammation is induced by implanting a sterile plastic disk in the connective tissue superficial to the rat cremaster muscle. When carbon black is injected intravenously 24 hr later, FAI in the cremaster arterioles can be detected on light microscopy as areas of carbon extravasation; and the length of affected segments is morphometrically measured. The capsaicin-pretreated group showed a marked decrease in FAI compared to the controls. Mean FAI in the capsaicin group (12 animals) was 1.8 +/- 2.4 (SD) mm/cremaster compared to 5.6 +/- 5.1 for the control group (12 animals). P less than 0.003. These results provide evidence that this arteriolar response to inflammation is modulated in part by capsaicin-sensitive neurons.

The local injection of pure inflammatory mediators induces venular leakage. To test the effect of endogenous mediators from dying tissue on vascular leakage, the authors devised an experimental model simulating an infarct, whereby living vessels would be exposed to fragments of organs undergoing aseptic necrosis. Tissues from donor rats were implanted aseptically in the cremasteric sac. Control rats were implanted with materials deemed to be as close as possible to nonirritating: boiled tissues and spheres of Teflon or glass. At different points the rats were injected intravenously with carbon black and killed an hour later. Whole cremaster mounts showed that vascular labeling was strictly venular up to 8 hours, mixed with capillary labeling between 12 and 24 hours, and mainly or exclusively capillary at 48 hours. Histology showed an acute inflammatory infiltrate in the labeled areas. A similar but weaker labeling pattern accompanied by milder inflammation was seen in controls. These results indicate that the vascular leakage in aseptic inflammation is biphasic, first venular, then capillary; and that the capillary phase is induced by the inflammatory reaction itself, possibly through a form of diffuse angiogenesis.

Intimal changes were quantitated in several rat models of arterial hypertension. One kidney-one clip rats drinking water (1K-1C-water), one-kidney rats treated with deoxycorticosterone acetate and drinking 1% NaCl (1K-DOCA-salt), and two-kidney rats drinking 1% NaCl (2K-salt) were studied after 1 to 8 weeks. The thoracic aorta was examined en face and by electron microscopy. Surprisingly, all 2K-salt, most 1K-DOCA-salt (17 out of 19), and two-thirds of 1K-1C-water rats (12 out of 18) had normal arterial pressure at sacrifice. In these normotensive 2K-salt, 1K-1C-water, and 1K-DOCA-salt animals, intimal mononuclear cells (which emigrated from the blood) increased between three- and ninefold. In these same normotensive 1K-1C-water and 1K-DOCA-salt rats, endothelial cell mitoses increased three- to sixfold with a corresponding increase in endothelial cell numbers. In the latter two groups, there was no evidence of endothelial cell denudation or changes in aortic circumference, and the subendothelial space widened mainly with reticular basement membrane presumably synthesized by the endothelium. In normotensive 1K-DOCA-salt rats, most of the endothelial cells were thick and there were several intercellular gaps. Endothelial proliferation, synthesis of macromolecules, and gap formation, as well as increased mononuclear cell emigration, indicate functional changes in mononuclear cells and in endothelial cells. We suggest that the experimental procedures designed to produce hypertension also generate factor(s) which activates mononuclear cells and/or endothelial cells. This cellular activation leads to intimal changes independent of hypertension.

The subcutaneous insertion of sterile, inert plastic pellets over the cremaster muscles of rats induces characteristic focal lesions of the arterioles at a distance from the pellets. These lesions appear with a delay of about 6 hours; by light microscopy they are characterized by a focal dilatation accompanied by endothelial damage and increased permeability. They are more severe if the pellets are loaded with histamine and are inhibited if the pellets are loaded with serotonin. Electron microscopy shows interendothelial gaps; the media is massively infiltrated with blood components and fibrin. The medial smooth muscle cells are stretched and at times necrotic; inflammatory cells are scarce. On the basis of these features the lesion was named focal arteriolar insudation (FAI). Although its pathogenesis is not yet clear, the data at hand suggest that it is caused by endogenous mediators affecting the smooth muscle cells and/or the endothelium. FAI appears to be a specific arteriolar response to chronic nonspecific irritation.