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自評
闡釋，在過度表現 Annexin VI 的老鼠研究中發現，Annexin VI 之過度表現，會降低細胞 內鈣離子濃度降低去極化後鈣離子流，最後導致細胞收縮之功能降低，有趣的是在 Annexin VI 完全去除之老鼠心室心肌細胞，發現會增加細胞質內鈣離子之移除，也影響到收縮功能。此兩個研究顯示正常的 Annexin VI 表現對於心肌細胞細胞內鈣離子調控扮演非常重要 的角色。
相反的，在心室組織中在心臟衰竭初期 Annexin VI 表現則明顯降低，然而在末期心臟 衰竭，Annexin VI 的表現則維持不變或者降低，顯示心室 Annexin VI 的表現跟心臟病理 發現之嚴重程度有關，然而，在末期心臟衰竭，Annexin VI 在右心房的表現則沒有變化，
相反的，本研究顯示慢性心房顫動會導致 Annexin VI 在左、右心房心耳組織中 Annexin VI 之表現大大降低。這樣的差異可以由 Li 等人的研究來做解釋，在此研究中作者發現心臟衰 竭不像心房顫動並不一定合併心房之有效不反應期或者動作定位之降低，我們的研究顯 示，心房組織中 Annexin VI 之降低可能是在人類之心房顫動鈣離子調控異常之上游缺陷，
然而 Annexin VI 在鈣離子調控之真正機轉及作用點則仍有待進一步釐清。
二、 Annexin VI 在心房組織中之分佈
Annexin VI 與心肌細胞相關蛋白質之相關空間關係的釐清，將有助於了解 Annexin VI 在心房所扮演的角色，本研究藉由雙染免疫定位研究發現，在心房組織中 Annexin VI 主要 分佈於心房心肌細胞膜上，與鈉鈣交換蛋白質及 L 型鈣離子通道有完全重疊之現象，相反 的，Annexin VI 的分佈與細胞質內之 ryanodine 接受體則完全沒有重疊現象，顯示 Annexin VI 在心房心肌細胞鈣離子調控，可能主要經由鈉鈣交換蛋白質及 L 型鈣離子通道，對於肌 漿網之鈣離子釋放，及回收作用可能是間接的。
三、
本研究限制
本研究中所有的病人皆具有嚴重之冠狀動脈病變，因此心房組織之缺氧可能造成某些 影響，此外，我們雖然假設 Annexin VI 之降低可能導致心房鈣離子調控之異常，但我們並 未提供直接證據顯示，Annexin VI 之降低到底是心房顫動之因或者是果，因此必須進一步 研究來釐清心肌缺氧對 Annexin VI 表現之影響並決定心房顫動之時程與心房 Annexins VI 降低之關係，並確定 Annexin VI 調控鈣離子之真正作用點。
本研究已經撰寫成論文正在投稿當中。