Mapping of intim al proliferation in vessels with m ultiple palm azschatzstents :insight fro m an intravascular ultrasound study

studies indicated that restenosis rate was higher after multiple stents implantation than single stent. Restenosis following stent is mainly due to neointimal hyperplasia and takes place frequently at sites between the stents (In between) and at the central articulation (CA) of Palmaz Schatz stents. To understand this process, we compared serial [post intervention and follow up (FU, 6±2 months)] intravascular ultrasound studies in 86 stents implanted into 30 native and 11 saphenous vein graft lesions. Each lesion had more than one stent (16?mm long) placed closely to each other. Lumen and stent areas (mm 2) were measured; plaque (stent lumen) area, late lumen loss (D lumen area) and tissure growth (D plaque area) were calculated for the edges, bodys, In between, and CA of all stents. The lumen at sites between the stents and at the central articulation are smaller than at the bodys or edges of the stents because of slightly smaller stent area and superimposed prolapse of tissue through the sites between thestents and through the central articulation. Subsequent accumulation of neoimtimal tissue is uniformly throughout the stent. [BHDFG1*2,WK7,WK5,WK4。2,WK5,WK5W]EdgeBodyCAIn betweenANOVA P [BHDZG1*2,WK7ZQ,WK5,WK4。2,WK5,WK5ZQ*3/5W]Post stent area10.3±2.59.4±2.39.2±3.09.1±3.1<0.0?001[BHDWG1*2,WK7ZQ,WK5,WK4。2,WK5,WK5W]FU stent area9.7±3.19.3±3.19.0±3.58.9±3.70.001[BH,WK7ZQ,WK5,WK4。2,WK5,WK5W]Post lumen area10.1±2.69.3±3.29.0±3.98.6±4.1<0.0?001FU lumen area6.9±3.76.4±3.55.9±4.15.4±3.8<0.0?001Post plaque area0.0±0.20.0±0.00.5±1.10.7±1.4<0.0?001FU palque area2.9±2.13.1±1.93.2±2.43.4±2.50.002Late lumen loss3.2±2.12.9±2.03.1±2.83.3±2.6NSTissue growth2.7±2.52.8±2.32.8±2.52.9±2.6NS Serial intravascular ultrasound imaging shows that restenosis at the locations between the stents (compared to the edges or body) of Palmaz Schatz is the result of smaller initial lumen and tissue prolapse (similar as at CA) and not due to an increased neointimal tissue accumulation. Thus, long stent design may reduce stent restenosis.

Distribution ofintimal proliferation in long lesions covered with multiplestents:insightfrom an intravascular ultrasound study

Angiographic studies show higher restenosis rates in long lesions covered with multiple stents. To understand this process,we compared serial [post intervention and follow up (FU,6±3 months)] intravascular ultrasound (IVUS) studies in 155 various stents implanted into 65 native de novo lesions (>20?mm). Lumen and stent areas (2?mm) were measured; plaque (stent lumen) area,late lumen loss and tissue growth were calculated for the edges, bodys, and connection points (CP) of the stents. Two types of CP were identified: overlapping (OVL) and non overlapping (NOVL). The lumen areas at CP after stent were smaller than those at the bodys or edges because of smaller stent area (OVL) and prolapse of tissue through the sites between the stents (NOVL). Post stent area10.6±2.79.5±2.59.0±2.89.1±3.0<0.0?001FU stent area9.8±3.09.4±3.18.8±3.68.9±3.50.0029.8±3.09.4±3.18.8±3.68.9±3.50.0029.4±3.18.8±3.68.9±3.50.0028.8±3.68.9±3.50.0028.9±3.50.0020.0020.00210.3±2.79.4±3.38.5±4.18.7±3.7<0.0?001FU lumen area7.1±3.66.6±3.45.5±3.75.8±4.2<0.0?001Post plaque area0.0±0.30.0±0.00.0±0.00.6±1.0<0.0?001FU plaque area3.0±2.13.2±2.03.3±2.43.4±2.30.002Late lumen loss3.2±2.22.8±2.13.0±2.73.2±2.7NSTissue growth2.8±2.62.7±2.42.8±2.52.9±2.6NS Serial IVUS imaging shows that restenosis at the connection point is the result of smaller initial lumen (OVL and NOVL) and tissue prolapse (NOVL) and is not due to an increased neointimal accumulation. New design of long stent may reduce stent restenosis in long lesions.

Coronary microvascular dysfunction exists early after hearttransplantationand normalisation during followup :serial assessment with intracoronaryFlo Wire

In order to assess the vascular integrity after heart transplantation (HTx), intracoronary Doppler was performed in 13 patients within 3 months after HTx and at one year follow up in all the 3 epicardial coronary arteries (LAD, LCX, and RCA) For intracoronary Doppler flow mapping, a 0 014 inch,15 MHz FloWire (Cardiometrics) was used Coromary flow velocity reserve (CFR) was derived by calculating the ratio between average peak flow velocity (APV) at baseline and after intracoronary adenosine injection (LAD and LCX, 18?μg; RCA, 12?μg) All patients were found to have relatively normal coronary angiograms within 3 months and at one year follow up CFVR was increased significantly in LAD (2 87±0 59 vs 3 63±0 91, P <0 05) and LCX (2 38±0 76 vs 3 27±0 75, P <0 01) at 1 year follow up in comparison to the baseline No significant increase in the RCA was found (3 13±1 62 vs 3 33±1 10, P > 0 05) Reduction of CFR exists within 3 months after HTx and normalises within one year This indicates that microvascular dysfunction especially in LAD and LCX exists early after HTx which will be normalised at 1 year CFR of the RCA seems to recover early HTx