APLA ומסתמים

האם נכון ש-APLA גורמת לבעיות מסתם?ואם כן ,האם יתכן שלאחר טיפול בקומדין והפרין כשנה יש הטבה בפעילות המסתם? תודה.

ראשית, אם כבר,הקשר הוא כנראה הפוך. לא הנוגדנים גורמים לבעיית מסתמים, אלא יש שכיחות גבוהה של היווצרות נוגדנים כשיש בעיית מסתם. שנית, יתכן שאותה מחלה שגורמת לנוגדנים גורמת גם בעיית מסתמים (כמו לופוס, למשל): (הציטוט מתייחס לשתי הנקודות הראשונות) Int J Cardiol 1995 Sep;51(2):117-26 Cardiac valve involvement in systemic lupus erythematosus and primary antiphospholipid syndrome: lack of correlation with antiphospholipid antibodies. Gabrielli F, Alcini E, Di Prima MA, Mazzacurati G, Masala C Department of Cardiovascular and Respiratory Sciences, University La Sapienza, Rome, Italy. The aim of this study was to determine the prevalence of cardiac valve disease in systemic lupus erythematosus or in patients with primary antiphospholipid syndrome and to assess the role of the antiphospholipid antibodies as risk factor for endocardial lesions. We studied 39 consecutive patients with systemic lupus erythematosus (mean age 34 +/- 12 years, 38 female and one male), 20 women with primary antiphospholipid syndrome (mean age 32 +/- 4 years) and 20 normal subjects (mean age 35 +/- 8 years, 15 female and five male). All patients with primary antiphospholipid syndrome had increased levels of serum anticardiolipin antibodies and recurrent fetal abortions; some of them also had arterial and/or venous thrombosis and/or thrombocytopenia. M-mode, two-dimensional and Doppler echocardiography were performed in all patients. IgG anticardiolipin antibodies were measured by an enzyme-linked immunosorbent assay. Valvular lesions were observed in 15 patients (38%) with systemic lupus erythematosus. These abnormalities included: mitral valve thickening or vegetation, mitral valve prolapse and aortic valve vegetation; mitral, aortic and tricuspid regurgitation; mitral stenosis. None of the patients with primary antiphospholipid syndrome and of the normal subjects was found to have valvular abnormalities. In systemic lupus erythematosus, high levels of anticardiolipin antibodies were detected in 73% of the patients with valvular lesions and in 67% of the patients without valvular lesions (P > 0.05). We conclude that valvular involvement is frequent in patients with systemic lupus erythematosus but it is apparently unrelated to antiphospholipid autoimmunization. שלישית, יתכן מצב של אוטם שריר הלב בגלל הנוגדנים, ובגלל האוטם עלולות להיווצר וגטציות על המסתמים. אלה עשויות להעלם לאחר טיפול אנטיקואגולנטי: J Am Soc Echocardiogr 1997 Oct;10(8):877-80 Resolution of vegetations with anticoagulation after myocardial infarction in primary antiphospholipid syndrome. Agirbasli MA, Hansen DE, Byrd BF 3rd Division of Cardiology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. We report here a case of primary antiphospholipid syndrome with all three clinical features with acute myocardial infarction. Echocardiography showed large vegetations at both mitral valve leaflets. Laboratory evaluation showed presence of antiphospholipid antibodies. High-intensity anticoagulation was begun, and repeat echocardiographic study in 4 months showed disappearance of the mitral valve vegetations יכול גם להיות מצב של היווצרות קרישים על מסתם מלאכותי בגלל הנוגדנים.

שימי לב לכך שהציטוטים באנגלית נקראים מלמטה למעלה (בתוך כל פיסקה)..... זה בהחלט מעצבן...... אבל כך בנוי האתר הזה. עוד ציטוט Am Heart J 1993 Apr;125(4):1123-9 A comparison of cardiac valvular involvement in the primary antiphospholipid syndrome versus anticardiolipin-negative systemic lupus erythematosus. Gleason CB, Stoddard MF, Wagner SG, Longaker RA, Pierangeli S, Harris EN Department of Medicine, University of Louisville, KY 40292. Recurrent thrombosis and pregnancy loss are well-recognized features of the antiphospholipid syndrome. Uncertainty exists, however, as to whether other reported features of the antiphospholipid syndrome such as cardiac valvular vegetations are truly part of this disorder or more reflective of associated systemic lupus erythematosus (SLE). Several recent studies have concluded that patients with antiphospholipid antibodies have a higher risk of developing Libman-Sacks endocarditis. This study was performed to determine whether antiphospholipid antibodies are the only risk factors for cardiac valvular disease in patients with primary antiphospholipid syndrome (PAPS) or SLE. Ten patients with PAPS were matched with 20 patients with SLE and 20 healthy control subjects by sex. All participants were tested for anticardiolipin (aCL) antibodies by means of a standardized enzyme-linked immunosorbent assay technique, and all underwent two-dimensional and color-flow Doppler echocardiography. The echocardiograms were interpreted by two cardiologists blinded to the patients' underlying disease. Sixty percent of the PAPS group had cardiac valvular involvement compared with 40% of the SLE group (p = NS). We conclude that cardiac valvular vegetations are common both in aCL-negative patients with SLE and in patients with PAPS. This suggests that aCL antibodies either play no causative role or are not the only risk factors in the development of cardiac valvular vegetations J Am Coll Cardiol 1992 Nov 1;20(5):1127-34 Systemic lupus erythematosus valve disease by transesophageal echocardiography and the role of antiphospholipid antibodies. Roldan CA, Shively BK, Lau CC, Gurule FT, Smith EA, Crawford MH Department of Veterans Affairs Medical Center, Albuquerque, New Mexico 87108. OBJECTIVES. The aims of this study were to better characterize valve disease in systemic lupus erythematosus and to determine its association with antiphospholipid antibodies. BACKGROUND. Estimates of the prevalence of valve disease in systemic lupus erythematosus have been higher in autopsy series than in clinical studies using transthoracic echocardiography. Antiphospholipid antibodies have been suggested to be a primary pathogenetic factor. METHODS. Transesophageal echocardiography was performed on 1) 54 patients with lupus erythematosus, 22 of them with (group I) and 32 without (group II) antiphospholipid antibody; 2) on 10 patients with antiphospholipid syndrome (group III); and 3) on 35 normal subjects (group IV). RESULTS. Patients in groups I and III had similar types and concentrations of antibodies. Leaflet thickening was found in 50% of group I, 47% of group II, 10% of group III and 9% of group IV patients (group I or II vs. group III or IV, p < 0.03). Leaflet thickening in patients with lupus erythematosus was diffuse; it usually involved the mitral and aortic valves and was associated with valve regurgitation (73%) or valve masses (50%). Valve masses were observed in 41% of group I, 25% of group II, 10% of group III and in none of group IV patients (group I or II vs. group IV, p < 0.002). Most valve masses in patients with lupus erythematosus were located near the base on the atrial side of the mitral valve or on the vessel side of the aortic valve, had variable size (0.2 to 0.85 cm2), shape and echodensity. Valve regurgitation was observed in 64% of group I, 59% of group II, 10% of group III and 20% of group IV patients (group I or II vs. group III or IV, p < 0.006). Moderate or severe regurgitant lesions were noted in 27% of group I and 25% of group II patients. CONCLUSIONS. Lupus erythematosus valve disease is frequent (74%) regardless of the presence or absence of antiphospholipid antibodies. Therefore antiphospholipid antibodies may not be a primary pathogenetic factor. The characteristic appearance of leaflet thickening and masses in patients with lupus erythematosus may be unique.