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{{CMG}}, {{AOEIC}}: Bhaskar Purushottam, M.D. [mailto:bpurushottam@gmail.com]
{{CMG}}, {{AOEIC}}: Bhaskar Purushottam, M.D. [mailto:bpurushottam@gmail.com]
==Overview==
==Overview==
'''Restenosis''' literally means the ''re''occurrence of ''[[stenosis]]''. This is usually restenosis of an [[artery]], or other [[blood vessel]], but possibly any hollow organ that has been "unblocked". This term is common in [[vascular surgery]], [[cardiac surgery]], [[interventional radiology]], or [[interventional cardiology]] following [[angioplasty]], all branches of [[medicine]] that frequently treat stenotic lesions.  
'''Restenosis''' literally means the ''re''occurrence of ''[[stenosis]]''. This is usually restenosis of an [[artery]], or other [[blood vessel]], but possibly any hollow organ that has been "unblocked". This term is common in [[vascular surgery]], [[cardiac surgery]], [[interventional radiology]], or [[interventional cardiology]] following [[angioplasty]], all branches of [[medicine]] that frequently treat stenotic lesions. In simple words, coronary re-stenosis can be considered as the reduction in the lumen diameter after a percutaneous coronary intervention (PCI). It can be defined based on angiography or as clinical restenosis. By angiography, the term 'Binary Angiographic Re-stenosis' is defined as > 50% luminal narrowing at follow-up angiography. However, the most widely accepted and relevant definition would be a 'Clinical Re-stenosis', which is defined as need for a repeat target lesion revascularization (TLR) due to symptomatic coronary ischemia from the previously intervened vessel (proposed by the Academic Research Consortium). Therefore, this definition needs angiographic narrowing as well as clinical correlation. If the lesion does not meet angiographic criteria, but meets the criteria for a physiologically significant lesion by fractional flow reserve (FFR) or anatomically by intravascular ultrasound (IVUS) with the appropriate clinical context, it is still considered 'Clinical Re-stenosis'. PCI has evolved significantly from plain balloon angioplasty to the development of biodegradable stents in the last few decades. Currently, almost all coronary interventions use a bare metal stent (BMS) or more so a drug eluting stent (DES). Hence, the discussion in the following paragraphs will focus on in-stent re-stenosis of drug eluting and bare metal stents.


==Coronary Restenosis==
==Coronary Restenosis==

Revision as of 04:51, 26 January 2012

Restenosis Microchapters

Home

Patient Info

Overview

Historical Perspective

Pathophysiology

Epidemiology & Demographics

Risk Factors

Screening

Causes of Restenosis

Differentiating Restenosis from other Diseases

Natural History, Complications & Prognosis

Diagnosis

History & Symptoms

Physical Examination

Lab Tests

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Restenosis On the Web

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Most cited articles

Review articles

CME Programs

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MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Restenosis

CDC on Restenosis

Restenosis in the news

Blogs on Restenosis

Directions to Hospitals Treating Restenosis

Risk calculators and risk factors for Restenosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-In-Chief:: Bhaskar Purushottam, M.D. [2]

Overview

Restenosis literally means the reoccurrence of stenosis. This is usually restenosis of an artery, or other blood vessel, but possibly any hollow organ that has been "unblocked". This term is common in vascular surgery, cardiac surgery, interventional radiology, or interventional cardiology following angioplasty, all branches of medicine that frequently treat stenotic lesions. In simple words, coronary re-stenosis can be considered as the reduction in the lumen diameter after a percutaneous coronary intervention (PCI). It can be defined based on angiography or as clinical restenosis. By angiography, the term 'Binary Angiographic Re-stenosis' is defined as > 50% luminal narrowing at follow-up angiography. However, the most widely accepted and relevant definition would be a 'Clinical Re-stenosis', which is defined as need for a repeat target lesion revascularization (TLR) due to symptomatic coronary ischemia from the previously intervened vessel (proposed by the Academic Research Consortium). Therefore, this definition needs angiographic narrowing as well as clinical correlation. If the lesion does not meet angiographic criteria, but meets the criteria for a physiologically significant lesion by fractional flow reserve (FFR) or anatomically by intravascular ultrasound (IVUS) with the appropriate clinical context, it is still considered 'Clinical Re-stenosis'. PCI has evolved significantly from plain balloon angioplasty to the development of biodegradable stents in the last few decades. Currently, almost all coronary interventions use a bare metal stent (BMS) or more so a drug eluting stent (DES). Hence, the discussion in the following paragraphs will focus on in-stent re-stenosis of drug eluting and bare metal stents.

Coronary Restenosis

There are probably several mechanisms that lead to restenosis. An important one is the inflammatory response, which induces tissue proliferation around an angioplasty site.

Cardiologists have tried a number of approaches to decrease the risk of restenosis. Stenting is becoming more commonplace; replacing balloon angioplasty. During the stenting procedure, a metal mesh (stent) is deployed against the wall of the artery revascularizing the artery. Other approaches include local radiotherapy and the use of immunosuppressive drugs, coated onto the stenting mesh. Analogues of rapamycin, such as tacrolimus (FK-506), sirolimus and more so everolimus, normally used as immunosuppressants but recently discovered to also inhibit the proliferation of vascular smooth muscle cells, have appeared to be quite effective in preventing restenosis in clinical trials. Antisense knockdown of c-myc, a protein critical for progression of cell replication, is another approach to inhibit cell proliferation in the artery wall and has been through preliminary clinical trials using Morpholino oligos.

Related Chapters

References

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