Management of acute angioplasty complications

Management of acute angioplasty complications

REVISITATION SERIES strated in the first 1500 patients. Although the clinical benefits of c7E3 were sustained, even with the lower dose of heparin u...

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strated in the first 1500 patients. Although the clinical benefits of c7E3 were sustained, even with the lower dose of heparin used, the rate of hemorrhagic complications was not significantly different from placebo. Several other powerful antiplatelet agents directed against the glycoprotein IIb/IIIa receptor are also being investigated both as primary therapy for unstable coronary syndromes and as adjunctive therapy for PTCA. The results of these studies as well as those of the EPBXPILOG trials may have a profound effect on the management of AMI. In those patients treated by thrombolysis who have evidence for ongoing or recurrent ischemia, urgent cardiac catheterization is indicated. Rescue angioplasty for failed reperfusion in anterior wall myocardial infarctions has been shown to decrease the combined clinical endpoints of death or severe heart failure from 17% to 6%, while increasing exercise ejection fraction from 38% to 43%. In the GUSTO-I trial, cardiogenic shock occurred in 7.2% of patients, most often developing after hospital admission. Those patients who developed shock had the same high mortality (55%) as those initially presentingwith shock (57%), regardless of the thrombolytic regimen utilized. Only those patients subsequently treated with PTCA had a significantly lower 30 day mortality.

After Early Management The routine use of beta-blockers after MI, as well as the withdrawal of calcium channel blockers in patients with significant left ventricluar dysfunction is well established. Similarly, the benefit of angiotensin converting enzyme (ACE) inhibitors in those patients with residual severe left ventricular dysfunction is clear. However, the early initiation of ACE inhibitors in AM1 remains controversial. Finally, the Cardiac Arrhythmia Suppression Trials (CAST) failed to demonstrate beneficial effects of antiarrythmic therapy after MI, even in those patients with left ventricular dysfunction and high degrees of ambient ventricular ectopy. These trials indicated a possible increase in mortality with the use of those antiarrythmic agents tested. However, several studies have now shown that amiodarone therapy following MI may be used safely, without the increased risk of proarrythmic events or mortality. Whether amiodarone therapy can reduce either the incidence of sudden death or total mortality after MI remains unclear. The justification for its use routinely in this setting awaits the result of larger, randomized clinical trials. Address correspondence and reprint requests to Frank S. Saltiel, MD, MacNeal Cardiology Group, 3231 S. Euclid Avenue, Suite 201, Berwyn, IL 60402.

From ACC Current Journal Review: January/February 1994

REVZSZTATZON David P. Faxon, HD, Los Angeles, California

Management of Acute Angioplasty Complications

The major complications of PTCA have remained unchangedover the last few years,with acutevesselclosurethe most important and most responsiblefor AMI, hemodynamic collapse, emergency bypass surgery, or emergency PTCA. Abrupt closure continues to account for nearly 50% of the acute mortality of angioplasty. However, with advancesin technology, particularly coronary stent placement, thesecomplicationsare significantly lessfrequent than they were severalyearsago (1,2). As a result, a higher percentage of patients with complex anatomy are now undergoing angioplasty with improved successratesand similar overall complications rates. The expansion of the indications of angioplasty is in large part due to the increasedsafety of the procedure and improved managementof the major complications of angioplasty.

Davii P. Faxon, MD, Uniiersitj of Southern California, Department of Medicine, Division of Cardiology, Los Angeles, California

Summary

of Original

Article

The major complications of percutaneoustransluminal coronary angioplasty (PTCA) are acute vessel closure, acute myocardial infarction (AMI) and hemodynamic collapse. Advances in their prevention or managementhave reduced the need for emergency coronary artery bypass grafting (CABG) and made PTCA feasible for more high-risk patients. Editor’s Note: Becauseof the remarkable changesthat have occurred in the managementof the major complications after PTCA, ACC CurrentJournal Review haschosennot to reprint the original material. The revisitation is significantly updated by Dr. Faxon. ACC 0 1996 by the Amencan College of Card~?lqy Published by Elsewr Saence lnc

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Acute Closure Acute vesselclosure occurs in approximately 5 to 10% of patientsand is due to coronary dissection,acute thrombosis or, infrequently, atherosclerotic emboli (1,2>. The major

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change in management of acute closure over the last several years has been the widespread use of intracoronary stenting. The Gianturco-Roubin was first stent available for this purpose, however, with the availability of the J&J stent in the United States and numerous stent designs in Europe and the rest of the world, the management of acute vessel closure associated with coronary dissection is bailout stenting (3,4). The current use for this indication approximates the incidence of acute closure, namely, 5 to 10% of all cases. In several large reviews of bailout stenting and in several recent single center reports, the use of bailout stenting has dramatically reduced complications of angioplasty by reducing the need for emergency bypass surgery by 75% and in turn, reducing the incidence of AM1 by one-third and the overall mortality rate by 80% (1). While perfusion balloon catheter inflations are effective in 50 to 70°b of patients, stents are easier to use, highly effective, and associated with a low complication rate (>95% successful). For these reasons, bailout stenting is currently the preferred treatment for this problem.

randomized trials are evaluating other glycoprotein IIb/IIIa antagonists, however, preliminary reports indicate that these other agents may be less effective than 7E3 in reducing acute complications. One of the difficulties in optimally deciding who should require a stent to begin with or who should be pretreated with ReoPro, is that the angiographic criteria to identify high risk patients for acute closure are poor. Intravascular ultrasound may provide additional useful information. Patients with soft plaque and extensive calcification may be at particularly high risk of coronary dissection and many practitioners now place intracoronary stents in these patients as a primary strategy to reduce acute complications. Acute Myocardial

Bailout stenting is currently the preferred treatment for acute vessel closure. Antithrombotic

Use

Antithrombotic strategies have also been studied. Intracoronary thrombolytic agents have been shown to have some benefit in patients with intracoronary thrombosis, however, routine use in patients with unstable angina has been shown to be detrimental (5). In addition, several trials have indicated no clear long-term benefit to the direct antithrombin agents hirudin or hirulog, although short term complications were reduced (6,7). Recent studies using the glycoprotein IIb/IIIa receptor antagonist 7E3 (ReoPro) have, however, shown significant reductions in complications in patients undergoing high and low risk procedures, including recent MI, unstable angina, or stable angina (8). The overall reduction in complications has ranged between 58 and 78% in the recently reported Evaluation of PTCA to Improve Long-term Outcome by c7E3 GPIIb/IIIa receptor blockade (EPILOG) trial. In this study, the combined use of stenting and ReoPro further reduced complications by 78% in patients with abrupt closure. Many practitioners are now using stenting and/or ReoPro routinely in order to prevent major complications, including abrupt closure in high risk patients, particularly those with a visible clot on angiography. An alternative approach is the use of stenting and/or ReoPro when complications ensue. The disadvantage of this approach is that the combination of high dose heparin and ReoPro has been associated with an increased bleeding complication rate, which can be avoided by pretreatment with ReoPro and lower dose heparin use. A number of ongoing ACC CURRENT

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Infarction

The incidence of AM1 is currently less than 2%, primarily as a result of the improved management of abrupt vessel closure. Side branch occlusion or embolization of atherosclerotic material or thrombosis continues to be a significant issue, particularly with bifurcation lesions and in old degenerated saphenous vein grafts. Current management of these problems includes recognition of the potential for side branch occlusion, particularly from intravascular ultrasound images, and protection of the side branch by guidewire placement prior to balloon inflation. Embolization risk is increased in old saphenous vein grafts that show significant ulcerations and degeneration on angiography. Again, intravascular ultrasound can be useful in identifying patients at high risk for this complication. Currently, long stents appears to have some value in tacking the pliable atherosclerotic plaque against the arterial wall, but embolization remains a problem. Hemodynamic

Collapse

The incidence of hemodynamic instability and hypotension during balloon inflations is also less common today than it was several years ago, as a result of improved management of acute closure. The primary use of the perfusion balloon continues to be an appropriate and helpful means of reducing hemodynamic instability in patients with a large area of myocardium at jeopardy. Intra-aortic balloon counter-pulsation continues to be routinely used in high risk patients, however, temporary cardiopulmonary bypass is much less frequently used. Summary Over the last two years, tremendous changes have occurred in the management of major complications after PTCA. This is principally due to the use of coronary stenting as a bailout technique in the presence of coronary dissection or as a primary dilation strategy. It is likely that as newer stent designs become available and new, powerful antiplatelet agents such as 7E3 are more frequently used, complications of angioplasty will continue to decrease.

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6. Bitt1 JA, Strony J, Bnnker JA, et al. Treatment with bivalirudin (htrulog) as compared with heparin during coronary angioplasty for unstable or postinfarction angina. Himlog Angioplasty Study Investigators. N Engl J Med 1995;333:764-9

REFERENCES 1. Danchm M, Dachin V, Juilliere Y, Dibor 0, Bischott N, Pinelli G, Guilier M, Chennier F. Changes in patient treatment after abrupt closure complicating percutaneous transluminal coronary angioplasty: A historical perspective Am Heart J 1995;130:1158-63.

7. Serruys PW. Herrman JP, Simon R. et al. A comparison of hirudin with hepann m the prevention of restenosis after coronary angioplasty. Helvetica Investigators. N Engl J Med 1995,333:757-63.

2. Scott NA, Weintraub WS, Carlin SF, et al. Recent changes in the management and outcome of acute closure after percutaneous coronary angioplasty. Am J Cardiol 1993;71:1159-63.

8. Top01 EJ, Calif RM, Weisman HF, et al. Randomized trial of coronary intervention with antibody against platelet IIb/IIIa integrin for reduction of climcal restenosis: results at six months. The EPIC Investigators. Lancet 1994.343:881-6.

3. Stauffer JC, Eckhart E, Vogt P, Koppenberan L, Guy JJ. Stand-by versus stent-by during elective percutaneous transluminal coronary angioplasty. Amer Heart J 1995;130:21-6. 4. Roubin GS. Cannon AD, Agrawal SK, et al. lntracoronary stenting for acute and threatened closure complicating percutaneous transluminal coronary angioplasty. Circulation 1992;85:916-27. 5. Ambrose JA, Almeida OD, Sharma SK, et al. Adjunctive thrombolytic therapy during angioplasty for ischemic rest angina. Results of the TAUSA Trial. TAUSA Investigators. Thrombolysis and Angioplasty in Unstable Angina Trial. Circulation 1994;90:69-77.

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Address correspondence and repnnt requests to Davtd P. Faxon, MD, Division of Cardiology, USC School of Medicine, 1355 San Pablo St., AMC-117, Los Angeles, CA 90033.

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