Mechanism of edge recurrence following brachytherapy treatment of in-stent restenosis: a serial intravascular ultrasound study.
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Publications and source records attributed to MK Hong.
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Restenosis occurs after 30% to 50% of transcatheter coronary procedures; its mechanisms remain incompletely understood. Intravascular ultrasound (IVUS) studies were analyzed in 360 nonstented native coronary artery lesions in which follow-up quantitative angiographic and/or IVUS data was available. Pre-intervention, post-intervention, and follow-up, the external elastic membrane (EEM) and lumen cross-sectional areas (CSA) were measured; plaque+media (P+M=EEM Ð lumen CSA), and cross-sectional narrowing (CSN=P+M/EEM CSA) were calculated. The anatomic slice selected for serial analysis had an axial location within the lesion at the smallest follow-up lumen CSA. At follow-up, 73% of the decrease in lumen CSA was due to a decrease in EEM CSA; 27% was due to an increase in P+M CSA. The change in lumen CSA correlated more strongly with the change in EEM CSA than with the change in P+M CSA. The change in EEM CSA was bidirectional; 47 lesions (22%) showed an increase in EEM CSA. Despite a greater increase in P+M CSA, lesions exhibiting an increase in EEM CSA had (1) no change in lumen CSA, (2) decreased restenosis, and (3) a 49% frequency of late lumen gain. The independent clinical, angiographic, and IVUS predictors of angiographic restenosis (³ 50% diameter stenosis at follow-up) were the IVUS reference lumen CSA, angiographic pre-intervention diameter stenosis, and post-intervention IVUS CSN. Restenosis appeared to be determined primarily by the direction and magnitude of the change in EEM CSA. An increase in EEM CSA was adaptive while a decrease in EEM CSA contributed to restenosis. The most powerful predictor of restenosis was the IVUS post-procedural CSN. The importance of the post-procedural CSN was related to the change in EEM CSA as a mechanism of restenosis.
In recent studies, the technique of high pressure balloon dilation for stent optimization has been shown to improve procedural success and to reduce subacute closure after stenting. The late clinical outcome, however, is still uncertain after stenting with high pressure balloon dilation. Therefore, we evaluated the effect of high pressure balloon dilation on the subsequent clinical course in patients after intracoronary stenting. One-hundred ninety patients with 197 lesions were treated with Palmaz-Schatz stent implantation. Intracoronary stenting without high pressure balloon dilation and with anticoagulation was performed in 55 patients with 55 lesions (phase 1), whereas intracoronary stenting with high pressure balloon dilation, without anticoagulation was done in 135 patients with 142 lesions (phase 2). We compared the angiographic and clinical results immediately and at follow-up in both phase 1 and phase 2. Coronary angiography was repeated at 6 months in 147 patients (79%) and 150 lesions (77%). The overall incidence of angiographic restenosis was 24% (31% in phase 1 and 21% in phase 2). Angiographic restenosis occurred in 18% of elective stenting on de novo lesions (23% in phase 1 and 15% in phase 2). The target lesion revascularization rate was 19% (26% in phase 1 and 16% in phase 2). The restenosis rate was significantly reduced with high pressure balloon dilation in the infarct-related artery and for a stent size of ³ 4.0 mm (p < 0.05). In conclusion, intracoronary stenting using high pressure balloon dilation technique without anticoagulation has good immediate results, negligible stent thrombosis and may have a tendency towards lower rates of restenosis.
Restenosis occurs after 30% to 50% of transcatheter coronary procedures; its mechanisms remain incompletely understood. Intravascular ultrasound (IVUS) studies were analyzed in 360 non-stented native coronary artery lesions in which follow-up quantitative angiographic and/or IVUS data was available. Pre-intervention, post-intervention, and follow-up, the external elastic membrane (EEM) and lumen cross-sectional areas (CSA) were measured; plaque + media (P + M = EEM - lumen CSA), and cross-sectional narrowing (CSN = P + M/EEM CSA) were calculated. The anatomic slice selected for serial analysis had an axial location within the lesion at the smallest follow-up lumen CSA. At follow-up, 73% of the decrease in lumen CSA was due to a decrease in EEM CSA; 27% was due to an increase in P+M CSA. The change in lumen CSA correlated more strongly with the change in EEM CSA than with the change in P + M CSA. The change in EEM CSA was bidirectional; 47 lesions (22%) showed an increase in EEM CSA. Despite a greater increase in P + M CSA, lesions exhibiting an increase in EEM CSA had (1) no change in lumen CSA, (2) decreased restenosis, and (3) a 49% frequency of late lumen gain. The independent clinical, angiographic, and IVUS predictors of angiographic restenosis (³ 50% diameter stenosis at follow-up) were the IVUS reference lumen CSA, angiographic pre-intervention diameter stenosis, and post-intervention IVUS CSN. Restenosis appeared to be determined primarily by the direction and magnitude of the change in EEM CSA. An increase in EEM CSA was adaptive while a decrease in EEM CSA contributed to restenosis. The most powerful predictor of restenosis was the IVUS post-procedural CSN. The importance of the post-procedural CSN was related to the change in EEM CSA as a mechanism of restenosis.
To investigate the strategy of ÒdebulkingÓ in complex lesions before stent implantation (stent synergy) to improve procedural safety and achieve optimal acute and long-term results, we reviewed our experience in 389 patients with 504 lesions undergoing a combined stent procedure (45% rotational atherectomy, 24% laser angioplasty, 20% directional atherectomy, and 11% transluminal extraction atherectomy before stent implantation). Procedural success was achieved in 94.5%, with 4% major ischemic complications (1.1% death, 1.9% Q-wave myocardial infarction, and 2.3% emergency coronary artery bypass surgery). Overall, subacute stent thrombosis occurred in 1.5% of patients. Target-lesion revascularization during follow-up was required in 9.8% of the patients. We conclude that a strategy of selective pre-stent atheroablation in complex lesion subsets results in excellent procedural outcomes with acceptable complications and favorable long-term results.
Currently, surgical carotid endarterectomy has been the standard therapy for symptomatic and asymptomatic patients with significant carotid artery stenoses. However, there are high surgical risk and other patient subsets, wherein a Òlesser invasiveÓ catheter-based procedure may be worthwhile. Carotid stent-assisted angioplasty (CSSA) is a percutaneous interventional treatment approach for appropriately selected patients with common and internal carotid artery lesions. The present report discusses preliminary technique-related, angiographic, and intravascular ultrasound observations of CSSA. Five symptomatic patients (with six carotid stenoses) with other co-morbid states were treated by a multidisciplinary team under the aegis of an approved protocol using conventional equipment and available Palmaz tubular slotted stents. On-line quantitative angiography and intravascular ultrasound imaging was performed to guide stent insertion and monitor results. There were no procedure-related complications and angiographic results were excellent (final mean diameter stenosis 5%). Intravascular ultrasound imaging was feasible and safe. In two cases, the findings obtained from ultrasound images assisted in subsequent operator decisions. Thus far, there have been no additional clinical sequelae in these patients (@ 30 days). This preliminary experience with CSSA indicates that interventional neurovascular therapies may provide a useful alternative for selected patients requiring endoluminal reconstruction of carotid stenoses. Extensive additional studies are required to establish the appropriate clinical application of this technique.
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