Bibliothek

Notizen: Mitral valve replacement was performed in 21 patients using a surgical technique that preserves the entire papillary muscle and chordal apparatus. With this technique, the anterior mitral leaflet is split from the center of the free edge toward the annulus. Bilateral incisions are made from the proximal end of this split to the two mitral commissures, detaching the anterior leaflet from the annulus. These two halves of the leaflet, with all chordae intact (corresponding to the anterolateral and posteromedial papillary muscles), are judiciously trimmed to remove areas of leaflet untethered by chordae tendineae and (when necessary) fibrous thickening; then swung posteriorly and sutured to the posterior mitral annulus using mattress sutures with pledgets. This surgical technique is expected to favor the preservation of left ventricular function and avoid occurrence of irreversible left ventricular dilation/dysfunction, and has been used successfully for calcific and degenerative etiologies, using both tilting disc valves and porcine bioprostheses. It is especially useful in the implantation of tilting disc and bileaflet mechanical prostheses because anterior subvalvular chordae tissue may interfere with the disc excursion and relocated to the posterior leaflet annulus.

Notizen: The timing of surgical intervention in asymptomatic or mildly symptomatic patients with mitral regurgitation has always been a difficult clinical dilemma, especially with current options of valve replacement or valve repair. Symptomatic status should be carefully assessed and may depend upon either atrial fibrillation or progressive left ventricular dysfunction. Many patients may claim to be asymptomatic, but have profound limitations to their functional capacity and impairment of contraction indices. Because of this, every effort should be made to objectively follow the asymptomatic patient and schedule surgical intervention before irreversible left ventricular dysfunction. Left ventricular ejection fraction continues to be an inappropriate parameter, for the regurgitant fraction increases the preload to the left ventricle, and the regurgitant orifice reduces left ventricular after load with increase In ejection fraction. End-diastolic dimension of volume is dependent upon such preload, and hence not accurate. End-systolic diameter is a better prognostic index; an end-systolic dimension of 4.5 cm (2.6 cm/m2) and a calculated end-systolic volume of 50 mL/m2 seem to be reasonable discriminators of outcome following surgery. More recent investigations suggest that left ventricular dP/dt, measured from a Doppler profile of mitral regurgitation, is perhaps a better predictor. In the asymptomatic patient, it is difficult to justify a role for intense medical therapy. The patient who develops atrial fibrillation does require a long-term anticoagulation therapy, and valve repair might be considered in this patient. Sinus rhythm may be restored with early surgical intervention, thereby reducing complications of throm-boemboiism or anticoagulant therapy. But there is little evidence that the atrial dysrhythmia predisposes to progressive left Ventricular dysfunctlon. Vasodilator therapy In asymptomatic patients may delay the progression of left ventricular dysfunction in aortic regurgitation, but there is little evidence that such therapy in patients with mitral regurgitation will delay left ventricular dysfunction and surgical intervention. (J Card Surg 1994;9[Suppl]:248–251)

Notizen: Abstract: A comprehensive study was carried out to clarify the chemical compositions of spinal cord, cord myelin, and myelin subfractions of multiple sclerosis (MS). The protein compositions of normal-appearing cerebral white matter and cerebral plaque and periplaque tissues were also analyzed for comparison. MS whole cord samples were found to contain higher amounts of water compared with normal samples. The total lipid contents were below normal. Among the individual lipids, cholesterol content remained unchanged, whereas cholesteryl esters appeared increased in MS cords. The acidic phospholipid concentrations were found to be lower than normal. Glycolipids, such as cerebrosides GM4, GM1, and GD1b, which are abundant in myelin, were all decreased. However, the concentrations of GM3 and GD3, which are more characteristic of reactive astrocytes, were highly elevated. The total protein content of MS cord samples was decreased, and the decrease was attributable to the loss of myelin proteins as evidenced by the low recovery of myelin. The concentrations of myelin-specific proteins, such as proteolipid protein and myelin basic protein, were significantly reduced. Other changes in the protein compositions included the accretion of two low molecular weight proteins of approximately 11,000 and 12,000, and the appearance of a periodic acid-Schiff-positive protein with the same electrophoretic mobility as the P0 protein. Analysis of the isolated myelin indicated that it had a grossly normal protein composition. However, the two low molecular weight proteins and the P0 protein appeared to be enriched in an upper-phase cord subtraction. We attribute the appearance of the two low molecular weight proteins to the breakdown of proteolipid protein and/or myelin basic protein as a result of demyelination, and the appearance of P0 to the involvement of PNS myelin. The latter finding provides the first biochemical evidence that in MS cord, remyelination can be achieved in part by invading Schwann cells and/or by the small number of Schwann cells that may be present in the cord.