"Bow-tie" mitral valve repair: an adjuvant technique for ischemic mitral regurgitation.

BACKGROUND: Current techniques of mitral valve repair rely on decreasing valve area to increase leaflet apposition, but fail to address subvalvular dysfunction. A novel repair has been introduced with partial left ventriculectomy, which apposes the anterior leaflet to a corresponding point on the posterior leaflet creating a double-orifice valve, with reported adequate control of mitral regurgitation. METHODS: We started to use the "bow-tie" repair as an adjunct to posterior ring annuloplasty in cases in which mitral regurgitation was not adequately controlled by decreasing mitral valve area (n = 6), or when placement of an annuloplasty ring was impractical (n = 4). Mean follow-up was 336 days (range, 82 to 551 days) with no postoperative deaths. RESULTS: Mitral regurgitation decreased from 3.6+/-0.5 to 0.8+/-0.4 (p < 0.0001), with a concomitant increase in ejection fraction from 33%+/-13% to 45%+/-11% (p = 0.0156) before hospital discharge. Mitral valve area, measured by pressure half-time, decreased from a mean of 2.5+/-0.3 to 2.1+/-0.3 cm2, with a mean transvalvular gradient of 4.5+/-2.0 mm Hg. In patients whose mitral valve was repaired using the bow-tie alone, mitral regurgitation was reduced from 4+, to a trace to 1+. Postoperatively, mitral valve area increased from 1.9 to 2.5 cm2 during exercise, further supporting the concept that this technique preserves mitral valve annular function. CONCLUSIONS: These observations suggest that the bow-tie repair may offer advantages over conventional techniques of mitral valve repair and should be considered as an adjunct, especially in patients with impaired left ventricular function.

Cholesterol accumulation in human cornea: evidence that extracellular cholesteryl ester-rich lipid particles deposit independently of foam cells.

The cornea is a connective tissue site where lipid accumulates as a peripheral arcus lipoides. We found that cholesterol, in predominantly esterified form, progressively accumulated with age in the peripheral corneas of 20- to 90-yr-old individuals. Ultrastructural studies showed extracellular solid spherical lipid particles (< 200 nm in diameter) enmeshed between collagen fibers. Immunostaining showed significant apoE and apoA-I, but very little apoB in the peripheral cornea. Lipid particles were extracted from minced corneas into a buffer and subjected to isopycnic density gradient centrifugation. The lipid particles had a density < 1.02 g/ml, contained > 75% of their cholesterol in esterified form, and were distributed in two populations with average diameters of 22 +/- 5 nm (SD) and 79 +/- 26 nm. Gel-filtration chromatographic analysis of the corneal lipid particles showed that most cholesterol eluted with the larger particles and these larger particles lacked apoB. ApoA-I was associated with lipid particles the size of HDL. Most apoE was associated with lipid particles larger than the apoA-I-containing lipid particles and smaller than the large lipid particles that carried most of the corneal cholesterol. Thus, the cholesteryl ester-rich lipid particles that accumulate in the cornea are 1) similar to lipid particles previously localized within and isolated from human atherosclerotic lesions, 2) accumulate without foam cells, and 3) may be derived from low density lipoproteins that have lost their apoB and fused.