American heart journal · 2007
Histopathological evaluation of left atrial appendage thrombogenesis removed during surgery for atrial fibrillation.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Saito Tsunenori, Tamura Koichi, Uchida Daisuke, Saito Tomonari, Nitta Takashi, Sugisaki Yuichi
Аннотация
BACKGROUND: In this study, we histopathologically assessed left atrial appendages (LAAs) resected during surgical treatment for atrial fibrillation (AF) to elucidate the mechanism of intra-LAA thrombus formation in valvular AF.
METHODS: The clinicopathological study of resected LAA was made on 56 valvular AF cases: 28 with mitral regurgitation (MR), 3 with mitral stenosis, and 25 with mitral stenosis and MR. Pathological findings of thrombi in LAA were compared with clinical features, including history of valvular diseases and embolism, and findings of echocardiography. Results were analyzed using chi2 test, Fisher exact method, or Welch t test.
RESULTS: Two types of mural thrombi were found in LAA: membranous (M)-thrombi and polypoid-shape (P)-thrombi. M-thrombi were found on LAA endocardium in 48 (86%) patients. All of the P-thrombi were observed on preexisting M-thrombi. More patients showed thrombi in the LAA orifice than in the tip (P < .001), especially in cases of MR (21 patients; P < .01). By echocardiography, MR flow was classified into 3 directions: toward the roof, anteroseptal, or posterolateral wall of the left atrium. Patients with MR jet flow against the posterolateral wall near the LAA entrance had a higher risk of LAA thrombi (P = .007).
CONCLUSIONS: Instability of M-thrombi, including surface rupture before complete organization, relates to P-thrombi formation that results in high incidence of embolism in AF patients.
METHODS: The clinicopathological study of resected LAA was made on 56 valvular AF cases: 28 with mitral regurgitation (MR), 3 with mitral stenosis, and 25 with mitral stenosis and MR. Pathological findings of thrombi in LAA were compared with clinical features, including history of valvular diseases and embolism, and findings of echocardiography. Results were analyzed using chi2 test, Fisher exact method, or Welch t test.
RESULTS: Two types of mural thrombi were found in LAA: membranous (M)-thrombi and polypoid-shape (P)-thrombi. M-thrombi were found on LAA endocardium in 48 (86%) patients. All of the P-thrombi were observed on preexisting M-thrombi. More patients showed thrombi in the LAA orifice than in the tip (P < .001), especially in cases of MR (21 patients; P < .01). By echocardiography, MR flow was classified into 3 directions: toward the roof, anteroseptal, or posterolateral wall of the left atrium. Patients with MR jet flow against the posterolateral wall near the LAA entrance had a higher risk of LAA thrombi (P = .007).
CONCLUSIONS: Instability of M-thrombi, including surface rupture before complete organization, relates to P-thrombi formation that results in high incidence of embolism in AF patients.