Chronic stable angina revascularization percutaneous coronary intervention
|
Chronic stable angina Microchapters | ||
|
Classification | ||
|---|---|---|
| ||
| ||
|
Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
|
Diagnosis | ||
|
Alternative Therapies for Refractory Angina | ||
|
Discharge Care | ||
|
Guidelines for Asymptomatic Patients | ||
|
Case Studies | ||
|
Chronic stable angina revascularization percutaneous coronary intervention On the Web | ||
|
FDA on Chronic stable angina revascularization percutaneous coronary intervention | ||
|
CDC onChronic stable angina revascularization percutaneous coronary intervention | ||
|
Chronic stable angina revascularization percutaneous coronary intervention in the news | ||
|
Blogs on Chronic stable angina revascularization percutaneous coronary intervention | ||
|
to Hospitals Treating Chronic stable angina revascularization percutaneous coronary intervention | ||
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3] Phone:617-632-7753; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [4]; John Fani Srour, M.D.; Jinhui Wu, M.D.; Lakshmi Gopalakrishnan, M.B.B.S.
Overview
Percutaneous coronary intervention for coronary artery disease first began in 1977, as a valuable mode of revascularization, wherein at the point of coronary stenosis a catheter-borne balloon is inflated to relieve the stenosis. The advantages of PCI for the treatment of CAD are many and include a low level of procedure-related morbidity and mortality rate in properly selected patients, a shorter hospital stay, early return to activity, and the feasibility of multiple procedures. The risk of acute coronary occlusion during PCI and increased incidence of restenosis in lesions that were successfully treated limits the use of PCI.[1][2]
Ideal candidates for PTCA/PCI include patients with stable angina less than 75 years of age, with single-vessel and/or single-lesion CAD, without a history of diabetes. Objective large ischemia, in particular, lesions less than 10 mm, readily accessible, concentric, and discrete are best suited for revascularization by PCI. On the contrary, chronic total occlusions that cannot be crossed, lesions greater than 20 mm, tortuous, irregular, angulated, calcified, severely stenotic with one or more lesion greater than 90% stenosis present in an artery are associated with an increased risk of morbidity and mortality from the procedure. In addition, PCI is used with reservation in diabetics with multi-vessel disease and in patients with unprotected left main stenosis. Other important factors include the operator volume and the presence or absence of onsite cardiovascular surgeon.[3]
Primary success of coronary intervention is generally defined as an absolute increase of 20% points in the luminal diameter and a final diameter obstruction of less than 30%. Such angiographic success can be anticipated in more than 90% of properly selected patients.
Over the years, alternative methods of percutaneous treatment developed include the use of intracoronary brachytherapy for in-stent restenosis,[4][5] cutting balloon with metal razors to avoid the spillage and subsequent reduction in the incidence of vessel trauma, burr rotablation that pulverizes the atheromatous material[6] and intracoronary stents designed to maintain the lumen size.
Complications of percutaneous coronary intervention
The improvements in devices, the use of stents, and aggressive antiplatelet therapy have significantly reduced the incidence of major procedural complications of PCI over the past 2 decades despite the increasing complexity of cases. However, as with any invasive procedure, complications can occur. The major complications of PTCA/PCI include coronary artery dissection and acute closure, intramural hematoma, coronary artery perforation, and occlusion of branch vessels: Dissections are found in up to 50 percent of patients immediately after PTCA. Intimal tears or dissections following PTCA have been arbitrarily divided into types A to F.
- Type A — Luminal haziness
- Type B — Linear dissection
- Type C — Extraluminal contrast staining
- Type D — Spiral dissection
- Type E — Dissection with reduced flow
- Type F — Dissection with total occlusion
These problems are now much less frequent since stent placement is performed in most percutaneous coronary procedures. Abrupt closure is most often due to arterial dissection and is manifested as acute ischemic chest pain and ECG changes. The incidence of abrupt closure with conventional balloon angioplasty (PTCA) is approximately 5% and is associated with a 10-fold increase in mortality to about 1 percent and nonfatal MI. The frequency of this complication, however, has now been greatly reduced by pretreatment with the platelet glycoprotein IIb/IIIa receptor blockers and by the insertion of an intracoronary stent. If stenting does not restore adequate flow, emergency CABG can be performed.
Coronary artery intramural hematoma is defined as an accumulation of blood within the medial space displacing the internal elastic membrane inward and the external elastic membrane outward, with or without identifiable entry and exit points. It is identified in 6.7 percent of procedures by intravascular ultrasound (IVUS).
Coronary artery perforation in the stent era is a rare but potentially disastrous complication.
Downstream embolization of thrombus or plaque contents with microvascular obstruction is common after PCI and occlusion of side branches has been reported in up to 19 percent of cases in which a stent was placed across a major side branch.
Stent thrombosis is catastrophic complication that usually leads to death or ST segment elevation MI. It is therefore a medical emergency. Stent thrombosis can occur acutely (during or soon after the PCI), subacutely (within 30 days after stent placement), or as a complication. Late stent thrombosis is associated with the cessation of aspirin or clopidogrel therapy. On the other hand, very late stent thrombosis, occurring after one year, is associated with drug-eluting stents.
Restenosis is the result of arterial damage with subsequent neointimal tissue proliferation. It is usually defined as a greater than 50% diameter stenosis. The incidence of angiographic restenosis is approximately 30% to 40% after PTCA. Intracoronary stents reduce the rate of angiographic and clinical restenosis and post-procedural myocardial infarction compared to percutaneous transluminal coronary angioplasty (PTCA) alone. Trials have demonstrated that the sirolimus and paclitaxel drug-eluting stents markedly reduced the incidence of in-stent restenosis and the rate of target lesion revascularization compared to bare metal stents. As a result, stents are currently utilized in nearly all percutaneous coronary interventions. However, the benefits of drug-eluting stents on restenosis must be weighed against rates of stent thrombosis, which often leads to death or MI, if dual antiplatelet therapy is prematurely discontinued. Restenosis occurs more frequently in diabetics, smaller arteries, among total occlusions, and in left anterior descending arteries, particularly proximal lesions. Since not all angiographic restenosis results in recurrent symptoms, the rates of clinical restenosis are lower than these angiographic estimates. Recurrent sever angina occurs in approximately half of the patients who develop angiographic restenosis and usually responds to stenting. In symptomatic patients with BMS restenosis, a repeat stenting using a DES is usually recommended. In symptomatic patients with intracoronary DES restenosis, there are insufficient data to suggest any specific treatment.
Clinical trial data: PTCA/PCI versus medical treatment in the management of stable angina pectoris
There are important limitations concerning the applicability of the results of older trials and even newer trials to the current clinical practice.
In early trials of percutaneous intervention versus medical therapy, the majority of patients underwent coronary angioplasty alone without stenting. For example, the benefits of PTCA have been compared to medical therapy in single vessel disease in the randomized Veterans Affairs Angioplasty Compared to Medicine (ACME) trial[7]. PTCA resulted in a reduction in anginal symptoms compared to medical therapy (50% angina free versus 24% at one month), however, while the benefit of PTCA was still significant at 6 months, the magnitude of this benefit was reduced (64% angina free versus 45%). Patients treated with PTCA also had an improvement of 2.1 3.1 minutes in exercise duration which was significantly greater than the 0.5 2.2 minutes experienced in the medical therapy group.
Other older trials compared PTCA to both limited (AVERT trial) and optimal medical interventions (RITA-2 and MASS II). The findings of these trials were that patients undergoing PTCA had similar rates of death and myocardial infarction as those on medical therapy and were less likely to have angina during the first few years.
More recent literature provides comparison between the use of stents and medical management, however, there is few data examining the extensive use of drug eluting stents and current extensive antithrombotic regimens (clopidogrel and GP IIb/IIIa inhibitors). In the most recent trial, COURAGE[8], drug-eluting stents were used in only 15 percent of patients. However, the COURAGE trial has the data most applicable to current practice. In this study 2287 patients were randomized to either aggressive medical therapy alone or aggressive medical therapy plus PCI with bare metal stenting. Patients were required to have both objective evidence of ischemia and significant CHD in a least one vessel; 87 percent were symptomatic and 58 percent had Canadian Cardiovascular Society CCS class II or III angina. Patients were excluded if they had CCS class IV angina, ≥50 percent left main disease, a markedly positive treadmill test (significant ST segment depressions and/or a hypotensive response during stage I of the Bruce protocol), an LVEF less than 30 percent, or coronary lesions deemed unsuitable for PCI. All patients received optimal medical therapy with beta blockers, calcium channel blockers, nitrates, antiplatelet therapy (either aspirin or clopidogrel), and aggressive lipid-lowering therapy with statin (attained median LDL-cholesterol was 72 mg/dL at five years). Exercise was recommended to achieve further improvements in the lipid profile when necessary. The results were published at a median follow-up of 4.6 years. There was no significant difference between the two treatment strategies for the primary end point of death from any cause and non-fatal MI. There was no significant difference in the rates of hospitalization for ACS. Patients in the PCI group underwent significantly fewer subsequent revascularization procedures (21 versus 33 percent, HR 0.60, 95% CI 0.51-71).
The issue of whether patients who receive PCI plus optimal medical therapy have a better quality of life and less angina than those who receive optimal medical therapy was addressed in COURAGE as well:
At baseline, 22 percent of patients were free of angina. At three months, significantly more patients who received PCI were angina free (53 versus 42 percent), but at 36 months there was no significant difference (59 versus 56 percent). Patients in both groups showed significant improvements from baseline values in various measures of quality of life. The percent of patients with clinically significant improvement in parameters such as physical limitation, angina stability, angina frequency, and overall quality of life was significantly higher in the PCI group by the sixth months. However, there was no significant difference in these rates at 36 months.
The results of COURAGE demonstrate that PCI with bare metal stents plus optimal medical therapy and initial, optimal medical therapy with revascularization as necessary are comparable strategies.
ACC/AHA Guidelines- Revascularization With PTCA (or Other Catheter-Based Techniques) and CABG (DO NOT EDIT) [9]
| “ |
Class I1. PTCA for patients with two- or three-vessel disease with significant proximal left anterior descending CAD, who have anatomy suitable for catheter-based therapy, normal LV function, and who do not have treated diabetes. (Level of Evidence: B) 2. PTCA or CABG for patients with one- or two-vessel CAD without significant proximal left anterior descending CAD but with a large area of viable myocardium and high-risk criteria on noninvasive testing. (Level of Evidence: B) 3. In patients with prior PTCA, CABG or PTCA for recurrent stenosis associated with a large area of viable myocardium and/or high-risk criteria on noninvasive testing. (Level of Evidence: C) 4. PTCA or CABG for patients who have not been successfully treated by medical therapy and can undergo revascularization with acceptable risk. (Level of Evidence: B) Class IIa1. Repeat CABG for patients with multiple saphenous vein graft stenoses, especially when there is significant stenosis of a graft supplying the left anterior descending coronary artery. PTCA may be appropriate for focal saphenous vein graft lesions or multiple stenoses in poor candidates for re-operative surgery. (Level of Evidence: C) 2. PTCA or CABG for patients with one- or two-vessel CAD without significant proximal left anterior descending CAD but with a moderate area of viable myocardium and demonstrable ischemia on noninvasive testing. (Level of Evidence: B) 3. PTCA or CABG for patients with one-vessel disease with significant proximal left anterior descending0 CAD. (Level of Evidence: B) Class IIb1. Compared with CABG, PTCA for patients with two- or three-vessel disease with significant proximal left anterior descending CAD who have anatomy suitable for catheter-based therapy and who have treated diabetes or abnormal LV function. (Level of Evidence: B) 2. PTCA for patients with significant left main coronary disease who are not candidates for CABG. (Level of Evidence: C) 3. PTCA for patients with one- or two-vessel CAD without significant proximal left anterior descending CAD who have survived sudden cardiac death or sustained ventricular tachycardia. (Level of Evidence: C) Class III1. PTCA or CABG for patients with one- or two-vessel CAD without significant proximal left anterior descending CAD who have mild symptoms that are unlikely due to myocardial ischemia or have not received an adequate trial of medical therapy and
2. PTCA or CABG for patients with borderline coronary stenoses (50% to 60% diameter in locations other than the left main) and no demonstrable ischemia on noninvasive testing. (Level of Evidence: C) 3. PTCA or CABG for patients with insignificant coronary stenosis (less than 50% diameter). (Level of Evidence: C) 4. PTCA in patients with significant left main CAD who are candidates for CABG. (Level of Evidence: B) |
” |
ESC Guidelines- Revascularization to improve prognosis (DO NOT EDIT) [10]
| “ |
Class IIa1. PCI or CABG for patients with reversible ischaemia on functional testing and evidence of frequent episodes of ischaemia during daily activities. (Level of Evidence: C) |
” |
ESC Guidelines- Revascularization to improve symptoms (DO NOT EDIT) [10]
| “ |
Class I1. PCI for one-vessel disease technically suitable for percutaneous revascularization in patients with moderate-to-severe symptoms not controlled by medical therapy, in whom procedural risks do not outweigh potential benefits. (Level of Evidence: A) 2. PCI for multi-vessel disease without high-risk coronary anatomy, technically suitable for percutaneous revascularization in patients with moderate-to-severe symptoms not controlled by medical therapy, in whom procedural risks do not outweigh potential benefits. (Level of Evidence: A) Class IIa1. PCI for one-vessel disease technically suitable for percutaneous revascularization in patients with mild-to-moderate symptoms which are nonetheless unacceptable to the patient, in whom procedural risks do not outweigh potential benefits. (Level of Evidence: A) 2. PCI for multi-vessel disease technically suitable for percutaneous revascularization in patients with mild-to-moderate symptoms which are nonetheless unacceptable to the patient, in whom procedural risks do not outweigh potential benefits. (Level of Evidence: A) |
” |
Vote on and Suggest Revisions to the Current Guidelines
Sources
- The ACC/AHA/ACP–ASIM Guidelines for the Management of Patients With Chronic Stable Angina [9]
- Guidelines on the management of stable angina pectoris: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology [10]
- TheACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina [11]
- The 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina [12]
References
- ↑ Bauters C, Banos JL, Van Belle E, Mc Fadden EP, Lablanche JM, Bertrand ME (1998) Six-month angiographic outcome after successful repeat percutaneous intervention for in-stent restenosis. Circulation 97 (4):318-21. PMID: 9468204
- ↑ Mehran R, Dangas G, Abizaid AS, Mintz GS, Lansky AJ, Satler LF et al. (1999) Angiographic patterns of in-stent restenosis: classification and implications for long-term outcome. Circulation 100 (18):1872-8. PMID: 10545431
- ↑ Smith SC, Feldman TE, Hirshfeld JW, Jacobs AK, Kern MJ, King SB et al. (2006) ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). Circulation 113 (1):156-75. DOI:10.1161/CIRCULATIONAHA.105.170815 PMID: 16391169
- ↑ Teirstein PS, Massullo V, Jani S, Popma JJ, Russo RJ, Schatz RA et al. (2000) Three-year clinical and angiographic follow-up after intracoronary radiation : results of a randomized clinical trial. Circulation 101 (4):360-5. PMID: 10653825
- ↑ Salomon R, Soreq H, Givon D, Sela I, Littauer UZ (1975) Proceedings: Enzymatic acylation of histidine to tobacco mosaic virus RNA. Isr J Med Sci 11 (11):1208-9. PMID: 1205798
- ↑ Kobayashi Y, Teirstein P, Linnemeier T, Stone G, Leon M, Moses J (2001) Rotational atherectomy (stentablation) in a lesion with stent underexpansion due to heavily calcified plaque. Catheter Cardiovasc Interv 52 (2):208-11. PMID: 11170330
- ↑ A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. Veterans Affairs ACME Investigators. Parisi AF, Folland ED, Hartigan P. N Engl J Med. 1992 Jan 2;326(1):10-6. PMID: 1345754
- ↑ Optimal medical therapy with or without PCI for stable coronary disease. Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS; COURAGE Trial Research Group. N Engl J Med. 2007 Apr 12;356(15):1503-16. Epub 2007 Mar 26. PMID: 17387127
- ↑ 9.0 9.1 Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999)guidelines for the management of patients with chronic stable angina: executive summary and recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina).Circulation 99 (21):2829-48. PMID: 10351980
- ↑ 10.0 10.1 10.2 Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367.
- ↑ Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS et al. (2003) ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina). Circulation 107 (1):149-58.[1] PMID: 12515758
- ↑ Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina. Circulation 116 (23):2762-72.[2] PMID: 17998462