In-Stent Restenosis

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Roxana Mehran - One of the best experts on this subject based on the ideXlab platform.

  • in stent Restenosis in the drug eluting stent era
    Journal of the American College of Cardiology, 2010
    Co-Authors: George Dangas, Adriano Caixeta, Bimmer E. Claessen, Elias Sanidas, Gary S Mintz, Roxana Mehran
    Abstract:

    The introduction of the drug-eluting stent (DES) proved to be an important step forward in reducing rates of Restenosis and target lesion revascularization after percutaneous coronary intervention. However, the rapid implementation of DES in standard practice and expansion of the indications for percutaneous coronary intervention to high-risk patients and complex lesions also introduced a new problem: DES In-Stent Restenosis (ISR), which occurs in 3% to 20% of patients, depending on patient and lesion characteristics and DES type. The clinical presentation of DES ISR is usually recurrent angina, but some patients present with acute coronary syndrome. Mechanisms of DES ISR can be biological, mechanical, and technical, and its pattern is predominantly focal. Intravascular imaging can assist in defining the mechanism and selecting treatment modalities. Based upon the current available evidence, an algorithm for the treatment approaches to DES Restenosis is proposed.

  • Usefulness of the angiographic pattern of In-Stent Restenosis in predicting the success of gamma vascular brachytherapy.
    The American journal of cardiology, 2003
    Co-Authors: Costantino O. Costantini, George Dangas, Gary S Mintz, Roxana Mehran, Alexandra J. Lansky, Kazuyuki Shirai, Gregg W. Stone, Martin B. Leon
    Abstract:

    The prognostic role of the angiographic pattern of In-Stent Restenosis after gamma vascular brachytherapy was assessed from a pooled data set of 4 clinical trials comprising 295 irradiated patients with matched baseline and follow-up angiograms. The binary angiographic Restenosis rate increased with worsening In-Stent Restenosis patterns; however, target lesion revascularization and major adverse cardiac event rates increased for focal, diffuse, and proliferative patterns of In-Stent Restenosis but not for total occlusions.

  • Treatment of In-Stent Restenosis.
    Seminars in interventional cardiology : SIIC, 1998
    Co-Authors: G.s. Mintz, Ron Waksman, Lowell F Satler, Augusto D Pichard, Roxana Mehran, Kenneth M. Kent, Martin B. Leon
    Abstract:

    Although In-Stent Restenosis is the result of neointimal hyperplasia, mechanical problems (e.g. stent underexpansion) that occurred during implantation may result in Restenosis at follow-up. The treatment of In-Stent Restenosis, begins with identification of these occult mechanical problems. Thereafter, In-Stent Restenosis can be treated with PTCA, atheroablation, or additional stent implantation; it is nuclear which technique is superior. Not all In-Stent Restenosis lesions have a similar risk of recurrence. Recurrence appears to depend on several markers of biologic activity: focal vs diffuse In-Stent Restenosis, the first episode vs recurrent In-Stent Restenosis, and early vs late recurrence. Vascular brachytherapy has emerged as the most promising way to treat high-risk lesion subsets.

  • In-Stent Restenosis: the Washington Hospital Center experience.
    The American Journal of Cardiology, 1998
    Co-Authors: Gary S Mintz, Lowell F Satler, Augusto D Pichard, Roxana Mehran, Kenneth M. Kent, Rainer Hoffmann, Jeffrey J. Popma, Martin B. Leon
    Abstract:

    Abstract In-Stent Restenosis has become a significant clinical problem. In 1997 alone, it is estimated that up to 100,000 patients world-wide with In-Stent Restenosis were treated. Serial intravascular ultrasound (IVUS) analysis has shown that tubular-slotted stents almost never chronically recoil and that neointimal hyperplasia is responsible for In-Stent Restenosis. With the rapid recent explosion in stent use, information about In-Stent Restenosis has lagged behind, especially on the impact of new stent designs. For example, the true prevalence of In-Stent Restenosis (1) varies with the lesion and patient subset, being much higher in the "real world" than in the selected patients typically enrolled in many studies; and (2) depends on its definition (i.e., clinical vs angiographic, intralesion vs In-Stent). "Conventional" catheter-based treatments have included percutaneous transluminal coronary angioplasty (PTCA), rotational atherectomy, excimer laser coronary angioplasty, directional coronary atherectomy, and additional stent implantation. Rates of recurrence with these approaches are not known and vary considerably among series; however, certain lesions seem likely to recur regardless of the treatment modality. Recently, brachytherapy has emerged as the most promising way to treat In-Stent Restenosis.

Ron Waksman - One of the best experts on this subject based on the ideXlab platform.

  • In-Stent Restenosis: A Second Chance to Get It Right
    Journal of the American College of Cardiology, 2020
    Co-Authors: Evan Shlofmitz, Nauman Khalid, Ron Waksman
    Abstract:

    The DAEDALUS (Difference in Antirestenotic Effectiveness of Drug-Eluting Stent and Drug-Coated Balloon Angioplasty for the Occurrence of Coronary In-Stent Restenosis) investigators ([1][1]) conducted an important study demonstrating the challenge of In-Stent Restenosis (ISR) and the poor outcomes

  • Safety and efficacy of everolimus-eluting stents for bare-metal In-Stent Restenosis.
    Cardiovascular Revascularization Medicine, 2015
    Co-Authors: Michael Mahmoudi, William O Suddath, Rebecca Torguson, Lowell F Satler, Augusto D Pichard, Ron Waksman
    Abstract:

    Abstract Objective The aim of this study was to compare the safety and efficacy of the everolimus-eluting stents (EES) with the paclitaxel-eluting stent (PES) and sirolimus-eluting stent (SES) for the treatment of bare-metal In-Stent Restenosis. Background The optimal treatment for bare-metal In-Stent Restenosis remains controversial. Methods The study cohort comprised 322 consecutive patients (543 lesions) who presented with bare-metal In-Stent Restenosis to our institution and underwent coronary artery stent implantation with EES (114 patients; 181 lesions), PES (65 patients; 116 lesions) and SES (143 patients; 246 lesions). The analyzed clinical parameters were the 1-year rates of death, Q-wave myocardial infarction (MI), target lesion revascularization (TLR), target vessel revascularization (TVR), definite stent thrombosis (ST) and major adverse cardiac events (MACE) defined as the composite of death, MI, or TLR at 1-year. Results The three groups were well matched for the conventional risk factors except for age and chronic kidney disease. The 1-year analyzed clinical parameters were similar in the three groups: death (EES = 3.5%, PES = 4.6%, SES = 4.2%; p = 0.94), MI (EES = 3.5%, PES = 6.3%, SES = 2.1%; p = 0.31), TLR (EES = 9.8%, PES = 9.5%, SES = 5.7%; p = 0.42), TVR (EES = 14.3%, PES = 11.1%, SES = 11.3%; p = 0.74), definite ST (EES = 0.9%, PES = 3.1%, SES = 3.5%; p = 0.38) and MACE (EES = 14.0%, PES = 15.4%, SES = 10.5%; p = 0.54). Male gender (hazard ratio = 0.47; 95% confidence interval = 0.25–0.88) and number of treated lesions (hazard ratio = 1.47; 95% confidence interval = 1.06–2.05) were found to be independent predictors of MACE. Conclusion The results of the present study indicate that EES may provide similar safety and efficacy as first generation DES for the treatment of patients presenting with bare-metal In-Stent Restenosis.

  • In-Stent Restenosis of drug-eluting stents
    Future cardiology, 2013
    Co-Authors: Sa'ar Minha, Augusto D Pichard, Ron Waksman
    Abstract:

    Drug-eluting stents (DES) have emerged as an improved alternative to bare-metal stents by demonstrating reduced rates of Restenosis and target lesion revascularization. This emergence has led to the unrestricted use of DES for various indications and lesions, and subsequently revealed DES In-Stent Restenosis as a novel interventional therapeutic dilemma. Recent insights regarding the patho-physiological processes and therapeutic alternatives have added to the accumulated knowledge regarding the appropriate approach to this phenomenon. This review aims to detail the mechanism and clinical presentation of, and therapeutic strategies for, the treatment of DES in In-Stent Restenosis.

  • Clinical trials of intracoronary gamma radiation therapy for In-Stent Restenosis.
    The Journal of invasive cardiology, 2002
    Co-Authors: Dong-hun Cha, Andrew E. Ajani, Edouard Cheneau, Ron Waksman
    Abstract:

    The only gamma emitter used in clinical trials for In-Stent Restenosis is 192Iridium (192Ir). The efficacy of intracoronary gamma radiation therapy in reducing clinical and angiographic Restenosis in patients with In-Stent Restenosis has been established. This review is intended to give an overview of the clinical trials utilizing gamma vascular brachytherapy in patients with In-Stent Restenosis and give insight into the future of intracoronary radiation therapy.

  • Treatment of In-Stent Restenosis.
    Seminars in interventional cardiology : SIIC, 1998
    Co-Authors: G.s. Mintz, Ron Waksman, Lowell F Satler, Augusto D Pichard, Roxana Mehran, Kenneth M. Kent, Martin B. Leon
    Abstract:

    Although In-Stent Restenosis is the result of neointimal hyperplasia, mechanical problems (e.g. stent underexpansion) that occurred during implantation may result in Restenosis at follow-up. The treatment of In-Stent Restenosis, begins with identification of these occult mechanical problems. Thereafter, In-Stent Restenosis can be treated with PTCA, atheroablation, or additional stent implantation; it is nuclear which technique is superior. Not all In-Stent Restenosis lesions have a similar risk of recurrence. Recurrence appears to depend on several markers of biologic activity: focal vs diffuse In-Stent Restenosis, the first episode vs recurrent In-Stent Restenosis, and early vs late recurrence. Vascular brachytherapy has emerged as the most promising way to treat high-risk lesion subsets.

Martin B. Leon - One of the best experts on this subject based on the ideXlab platform.

  • Usefulness of the angiographic pattern of In-Stent Restenosis in predicting the success of gamma vascular brachytherapy.
    The American journal of cardiology, 2003
    Co-Authors: Costantino O. Costantini, George Dangas, Gary S Mintz, Roxana Mehran, Alexandra J. Lansky, Kazuyuki Shirai, Gregg W. Stone, Martin B. Leon
    Abstract:

    The prognostic role of the angiographic pattern of In-Stent Restenosis after gamma vascular brachytherapy was assessed from a pooled data set of 4 clinical trials comprising 295 irradiated patients with matched baseline and follow-up angiograms. The binary angiographic Restenosis rate increased with worsening In-Stent Restenosis patterns; however, target lesion revascularization and major adverse cardiac event rates increased for focal, diffuse, and proliferative patterns of In-Stent Restenosis but not for total occlusions.

  • Treatment of In-Stent Restenosis.
    Seminars in interventional cardiology : SIIC, 1998
    Co-Authors: G.s. Mintz, Ron Waksman, Lowell F Satler, Augusto D Pichard, Roxana Mehran, Kenneth M. Kent, Martin B. Leon
    Abstract:

    Although In-Stent Restenosis is the result of neointimal hyperplasia, mechanical problems (e.g. stent underexpansion) that occurred during implantation may result in Restenosis at follow-up. The treatment of In-Stent Restenosis, begins with identification of these occult mechanical problems. Thereafter, In-Stent Restenosis can be treated with PTCA, atheroablation, or additional stent implantation; it is nuclear which technique is superior. Not all In-Stent Restenosis lesions have a similar risk of recurrence. Recurrence appears to depend on several markers of biologic activity: focal vs diffuse In-Stent Restenosis, the first episode vs recurrent In-Stent Restenosis, and early vs late recurrence. Vascular brachytherapy has emerged as the most promising way to treat high-risk lesion subsets.

  • In-Stent Restenosis: the Washington Hospital Center experience.
    The American Journal of Cardiology, 1998
    Co-Authors: Gary S Mintz, Lowell F Satler, Augusto D Pichard, Roxana Mehran, Kenneth M. Kent, Rainer Hoffmann, Jeffrey J. Popma, Martin B. Leon
    Abstract:

    Abstract In-Stent Restenosis has become a significant clinical problem. In 1997 alone, it is estimated that up to 100,000 patients world-wide with In-Stent Restenosis were treated. Serial intravascular ultrasound (IVUS) analysis has shown that tubular-slotted stents almost never chronically recoil and that neointimal hyperplasia is responsible for In-Stent Restenosis. With the rapid recent explosion in stent use, information about In-Stent Restenosis has lagged behind, especially on the impact of new stent designs. For example, the true prevalence of In-Stent Restenosis (1) varies with the lesion and patient subset, being much higher in the "real world" than in the selected patients typically enrolled in many studies; and (2) depends on its definition (i.e., clinical vs angiographic, intralesion vs In-Stent). "Conventional" catheter-based treatments have included percutaneous transluminal coronary angioplasty (PTCA), rotational atherectomy, excimer laser coronary angioplasty, directional coronary atherectomy, and additional stent implantation. Rates of recurrence with these approaches are not known and vary considerably among series; however, certain lesions seem likely to recur regardless of the treatment modality. Recently, brachytherapy has emerged as the most promising way to treat In-Stent Restenosis.

Wang Lei - One of the best experts on this subject based on the ideXlab platform.

  • The Renin-angiotensin System and In-Stent Restenosis
    Advances in Cardiovascular Diseases, 2006
    Co-Authors: Wang Lei
    Abstract:

    The renin-angiotensin system (RAS) can regulate smooth muscle cell (SMC) proliferation and migration, and play an important role in In-Stent Restenosis. There are contradictory effects of preventing In-Stent Restenosis to inhibit RAS by angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers. This review discusses the pathophysiology of In-Stent Restenosis, the role of the RAS in In-Stent Restenosis, and the possible role of RAS intervention in the prevention of In-Stent Restenosis.

Wiek H. Van Gilst - One of the best experts on this subject based on the ideXlab platform.

  • Renin-angiotensin system intervention to prevent In-Stent Restenosis: an unclosed chapter.
    Journal of cardiovascular pharmacology, 2005
    Co-Authors: Bas Langeveld, Anton J.m. Roks, René A. Tio, Adriaan A. Voors, Felix Zijlstra, Wiek H. Van Gilst
    Abstract:

    The occurrence of In-Stent Restenosis is a major drawback of percutaneous transluminal coronary angioplasty with stent placement. Target vessel revascularization is necessary in 15% of patients who receive a stent. Recent advances in the development of drug-eluting stents have reduced these numbers tremendously. However refinement of antirestenotic therapies remains obligatory. The emerging interest in more physiological antirestenotic therapies might unchain an interest in the well-known inhibitors of the rennin-angiotensin system (RAS), the angiotensin-converting enzyme inhibitors, and the angiotensin II type I receptor blockers. Contradictory results overshadow the discussion of whether intervention in the RAS could prevent In-Stent Restenosis. This review discusses the pathophysiology of In-Stent Restenosis, the role of the RAS in In-Stent Restenosis, and the possible role of RAS intervention in the prevention of In-Stent Restenosis.