Chronic stable angina revascularization percutaneous coronary intervention
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Chronic stable angina Microchapters | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
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Editors-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753; Cafer Zorkun, M.D., Ph.D. [2]; Associate Editors-In-Chief: John Fani Srour, M.D.; Smita Kohli, M.D.
Percutaneous Coronary Intervention(PCI)
Percutaneous coronary intervention began in 1977 as PTCA, a strategy in which a catheter-borne balloon was inflated at the point of coronary stenosis. The advantages of PCI for the treatment of CAD are many and include a low level of procedure-related morbidity, a low procedure-related mortality rate in properly selected patients, a short hospital stay, early return to activity, and the feasibility of multiple procedures. The disadvantages of PCI are that it is not feasible for many patients, there is a significant incidence of restenosis in lesions that are successfully treated, and there is a risk of acute coronary occlusion during PCI.
Ideal candidates for PTCA/PCI have stable angina, are under 75 years of age, with single-vessel, single-lesion CAD, without a history of diabetes. Lesions that are best for these procedures are short (<10 mm), concentric, discrete, and readily accessible. The risk of morbidity and mortality from the procedure is increased, particularly in patients with long (>20 mm), tortuous, irregular, angulated, calcified, severely stenotic (>90% stenosis) lesions and when more than one such lesion is present in an artery. Other important factors include operator volume and the presence or absence of on site cardiovascular surgeon. The 2005 ACC/AHA/SCAI guidelines for percutaneous coronary intervention made recommendations about hospital and operator volume and the importance of onsite cardiac surgery for both elective and primary PCI.
Primary success of coronary interventions is generally defined as an absolute increase of 20 percentage points in luminal diameter and a final diameter obstruction less than 30%. Such angiographic success can be anticipated in more than 90% of properly selected patients.
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[1]. 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[2], 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.
See Also
Sources
- The ACC/AHA/ACP–ASIM Guidelines for the Management of Patients With Chronic Stable Angina [3]
- TheACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina [4]
- The 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina [5]
References
- ↑ 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
- ↑ Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999) ACC/AHA/ACP-ASIM 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
- ↑ 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. 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. DOI:10.1161/CIRCULATIONAHA.107.187930 PMID: 17998462