Use of endothelial progenitor cell capture stent (Genous Bio-Engineered R Stent) during primary percutaneous coronary intervention in acute myocardial infarction: Intermediate- to long-term clinical follow-up

2008 ◽  
Vol 155 (1) ◽  
pp. 128-132 ◽  
Author(s):  
Melissa Co ◽  
Edgar Tay ◽  
Chi Hang Lee ◽  
Kian Keong Poh ◽  
Adrian Low ◽  
...  
Author(s):  
Shun Nishino ◽  
Nozomi Watanabe ◽  
Toshihiro Gi ◽  
Nehiro Kuriyama ◽  
Yoshisato Shibata ◽  
...  

Background: Recent animal studies have suggested that mitral valve (MV) leaflet remodeling can occur even without significant tethering force and that the postinfarct biological reaction would contribute to the histopathologic changes of the leaflet. We serially evaluated the MV remodeling in patients with anterior and inferior acute myocardial infarction (MI), by using 2- and 3-dimensional transthoracic echocardiography. Additional histopathologic examinations were performed to assess the leaflet pathology. Methods: Sixty consecutive first-onset acute MI (anterior MI, n=30; inferior MI, n=30) patients who underwent successful primary percutaneous coronary intervention were examined (1) before primary percutaneous coronary intervention, (2) at 6-month follow-up, and (3) at follow-up 1 year or later after onset. MV complex geometry including MV leaflet area and thickness was analyzed using dedicated software. Additional histopathologic study compared 18 valves harvested during surgery for ischemic mitral regurgitation (MR). Results: MV area and thickness incrementally increased during the follow-up period. MV leaflet area significantly increased (anterior MI: 5.59 [5.28–5.98] to 6.54 [6.20–7.26] cm 2 /m 2 , P <0.001; inferior MI: 5.60 [4.76–6.08] to 6.32 [5.90–6.90] cm 2 /m 2 , P <0.001), and leaflet thickness also increased (anterior MI: 1.09 [0.92–1.24] to 1.45 [1.28–1.60] mm/m 2 , P <0.001; inferior MI: 1.15 [1.03–1.25] to 1.44 [1.27–1.59] mm/m 2 , P <0.001); data represent onset versus ≥1 year. Larger annuls, larger tenting, and a reduced leaflet area/annular ratio with smaller coaptation index were observed in patients with persistent ischemic MR compared with those without significant ischemic MR. Histopathologic examinations revealed that MV thickness was significantly greater in chronic ischemic MR compared with acute ischemic MR (1432.6±490.5 versus 628.7±278.7 μm; P =0.001), with increased smooth muscle cells and fibrotic materials. Conclusions: MV leaflet remodeling progressed both in area and thickness after MI. This is the first clinical study to record the longitudinal course of MV leaflet remodeling by serial echocardiography.


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