Abrupt coronary artery occlusion during percutaneous transluminal coronary angioplasty

Abrupt coronary artery occlusion during percutaneous transluminal coronary angioplasty Pim J. de Feyter, MD, Peter P. T. de Jaegere, MD, Edward S. Murphy, Patrick W. Serruys, MD. Rotterdam, The Netherlands

Despite significant advances in operator skill and equipment, percutaneous transluminal coronary angioplasty (PTCA) continues to be plagued by two major problems: abrupt coronary artery occlusion during PTCA and late restenosis. Abrupt coronary artery occlusion during PTCA occurs in 4.4 % to 7.3 % of all procedures and is associated with major procedural complications including death, myocardial infarction, and emergency bypass surgery.ls In an individual patient the occurrence of abrupt coronary artery occlusion is often unpredictable, and it is the main reason for the requirement of in-hospital availability of surgical revascularization.lp 3y6y7 Approaches to the management of acute coronary artery occlusion usually have been limited to repeat balloon angioplasty and, in case of failure, emergency surgery; however, new interventional devices and techniques are being used or are being developed in an attempt to solve this problem. The purpose of this article is to review the incidence, prevention, prediction, detection, and management of abrupt coronary artery occlusion during PTCA. New technology will also be discussed. DEFINITION

AND INCIDENCE

The definition of abrupt coronary artery occlusion varies in the different reports,1-12 although they all have in common that there should be a critical reduction in coronary blood flow resulting in myocardial ischemia. For practical clinical reasons we propose that abrupt coronary artery occlusion be de-

From Received

the Thoraxcenter, for publication

University Nov.

Hospital 7, 1991;

accepted

Rotterdam. Dec.

Reprint requests: Pim J. de Feyter, MD, Catheterization raxcenter Bd 432, University Hospital Rotterdam-Dijkzigt, 3000 DR Rotterdam, The Netherlands. 4/l/36462

30, 1991. Laboratory, PO Box

Tho1738,

MD, and

fined as follows: a complete or critical reduction in coronary blood flow at the site of the dilated segment during or after PTCA with clinical or ECG evidence of myocardial ischemia. The event may occur while a patient is in the catheterization laboratory (immediate occlusion) or in the hospital after the procedure (early occlusion). The reduction in coronary blood flow is defined according to the angiographic criteria of the Thrombolysis in Myocardial Infarction (TIMI) trial where complete reduction in flow was related to TIM1 grade 0 and critical reduction to TIM1 grades 1 and 2. Included in this definition is acute occlusion resulting from direct mechanical trauma induced by manipulation during attempts to cross the lesion with a guide wire or balloon catheter. The incidence of this event appears to be low, especially after the introduction of (very) low-profile balloon catheters. At our institution we reviewed the records from 1423 consecutive PTCAs performed between 1986 and 1988. The incidence of acute predilation occlusion was 0.3% as opposed to an incidence of 7.3 % for abrupt coronary artery occlusion after dilation during the same period. Excluded from this definition are instances of side branch closure or distal embolization in which the ischemic syndrome resulted solely from compromised blood flow to a side branch or was attributed solely to the consequences of distal embolization. The reported incidence of abrupt coronary artery occlusion is highly dependent on the definition used in relation to the timing of the event. An incidence of abrupt coronary artery occlusion of 0.5 % to 3.1% has been reported if the event occurred after the patient had left the catheterization laboratory,3-11 and this incidence was higher, from 2.0 % to 5.6%) if abrupt coronary artery occlusion occurred during the procedure (while the patient was in the catheterization laboratory)3-7; of course the incidence was highest, 1633

1634

de Feyter

Table

et al.

1. Incidence

American

of abrupt

coronary

Reference

of event in/out catheterization laboratory

Ellis et a1.l Meyerovitz et aL2 Sinclair et a1.3 Steffenino et al.* Goldbaum et a1.5 Detre et al.‘j de Feyter et al.7 Sinclair et aL3

In + out In + out In In In In In out

Steffenino

out

artery occlusion*

Timing

et aL4

Goldbaum et a1.5 Detre et a1.6 de Feyter et a1.7 Hollman et a1.s Simpfendorfer et a1.g Gabliani et al.1° Gaul et al.‘lt

out out out out Out out out

Total number of patients with PTCA

Incidence abrupt occlusion (5%)

4,172 514 1,801 500 917 1,801 1,423 1,160

4.4 6.4 4.9 4.4 2.0 4.9 5.6

500

1.7

917 1,801 1,423 935 1,500 1,238

0.5 1.9 1.7 2.7 2.0 1.8

714

3.1

1.0

*Excluded were patients with PTCA in the setting of acute myocardial infarction; selected were studies that reported on patients with more than 500 attempted PTCA procedures. tIncidence of abrupt coronary artery occlusion after successful multiple-lesion coronary angioplasty.

from 4.4 % to 7.3 % , if the occlusion occurred in either situationle7 (Table Il. MECHANISMS OCCLUSION

OF ABRUPT

CORONARY

ARTERY

The mechanisms of abrupt coronary artery occlusion are multifactorial and include mechanical obstruction as a result of intimal flap, elastic recoil after dilatation, platelet adhesion and aggregation with ensuing intracoronary thrombus formation, subintima1 hemorrhage under the plaque, and vasoconstriction.13-20 It is not always possible to distinguish between these mechanisms by angiography, and they often occur in combination. However, we believe occlusive dissection after dilatation accounts for the vast majority of all cases of abrupt coronary artery occlusion. Elastic recoil, produced by the relaxation of an overstretched disease-free wall of an eccentric plaque or possibly also of “elastic” parts of the diseased arterial wall, may contribute to abrupt occlusion. Recently it has been shown that nearly 50% of the potential gain in cross-sectional area after balloon dilatation is lost shortly after dilatation as a result of elastic recoil.20 Also vasoconstriction or even frank spasm of the disease-free wall has been shown to contribute.17 Nonocclusive fibrin-platelet thrombus frequently layers the angioplasty site, but occlusive thrombus formation is usually associated with a flow-obstruc-

June 1992 Heart Journal

tive intraluminal flap or a deep medial injury and may therefore be considered a secondary phenomenon. Intraluminal thrombus formation may play a more significant role if the initial dilatation result is “suboptimal.” The residual stenosis produces local high-shear stress, which favors platelet activation and deposition on the affected area.21 This may allow for a more gradual closure of the vessel by additional thrombus formation particularly in patients after they have left the catheterization laboratory.iO Furthermore, when plaque fissuring with associated intraluminal thrombus is present before dilatation, the additional mechanical injury of the plaque induced by balloon inflation, together with remaining parts of the distorted thrombus, which is known to be a potent platelet aggregation stimulus, may lead to significant platelet and clotting activation. This may explain the high rate of abrupt occlusion (range 7”;, to 10.5%) in patients with acute coronary syndromes.229 23 These concerns of “suboptimal” results, deep medial injury, plaque fissuring, and thrombus, all emphasize the potential role of effective anticoagulation and the search for even more effective antithrombotic strategies.24 PREDICTORS OCCLUSION

OF ABRUPT

CORONARY

ARTERY

Although it is impossible to predict exactly who among individual patients will have an abrupt coronary artery occlusion, it appears possible to identify high-risk groups. l, 3s6, 7 For optimal clinical decision making and patient counseling it is appropriate to identify preprocedural and procedural high-risk groups. In a study by Ellis et al.,l which included 4772 procedures, multivariate analysis of 16 clinical variables disclosed female sex to be an independent factor, and analysis of 35 angiographic variables identified stenosis length of at least twice the luminal diameter, stenosis at a bend point of 45 degrees or more, stenosis at a branch point, stenosis-associated thrombus, other stenoses in the same vessel, and multivesse1 disease as independent risk factors. The 1985-1986 Percutaneous Transluminal Coronary Angioplasty Registry6 analyzed 1801 patients and disclosed that baseline patient factors independently associated with abrupt occlusion rates included triple-vessel disease, high-risk status for surgery, and acute coronary insufficiency and that lesion characteristics included diffuse or multiple discrete morphology, intracoronary thrombus, and collateral tlow from the dilated vessel. In a study by de Feyter et a1.,7 which included 1423 consecutive patients with attempted PTCA with an abrupt coronary artery occlusion rate of 7.3%) it has been shown that inde-

Volume Number

Table

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Abrupt

II. Factors predictive of abrupt coronary occlusion*

occlusion

during

PTCA

1635

III. Factors predictive of death associated with abrupt coronary occlusion* Table

Factors Preprocedural Clinical factors Female sex Unstable angina Angiographic factors Multivessel disease Multiple lesions in same vessel Collateral flow from the lesion Lesion factors Intracoronary thrombus Severe narrowing Long lesion Ulcerated lesion Lesion at branch point Lesion at bend point (>45 degrees) Postprocedural Angiographic factors Tear or dissection Postdilation lesion factors Remaining stenosis gradient 20 mm *Abstracted 1988;77:372; 1990;82:739;

from the following studies: Detre KM et al. 1985-1986 de Feyter Pd et al. Circulation

Factors Clinical factors Female sex Age >65 years Unstable angina Congestive heart failure Angiographic factors Left main coronary artery disease Three-vessel disease Left ventricular ejection fraction <30 % *Abstracted from: Ellis SG et al. J Am Co11 Cardiol1988;11:211; Holmes DR et al. J Am Co11 Cardiol 1988;12:1149; Park DD et al. J Am Co11 Cardiol 1988;11:237.

Hg or more

Ellis SG et al. Circulation PTCA Registry. Circulation 1991;83:927-36.

pendent preprocedural variables were unstable angina pectoris, multivessel disease, and complex lesions. Procedural factors associated with abrupt occlusion included post-PTCA percentage of stenosis, intimal tear or dissection, use of prolonged heparin infusion, and post-PTCA gradient of 20 mm Hg or more according to the study of Ellis et al.,r and the 1985 1986 PTCA Registry study disclosed that intimal tear and dissection were very strongly associated with abrupt occlusion.6 From these studies it appears that sex (female), symptomatic status (unstable angina), and severity, extent, and complexity of coronary artery lesions are important preprocedural factors (Table II). The risk associated with the absence or presence of one or more of these factors emphasizes) the low probability of abrupt coronary artery occlusion in patients without risk factors and the addictive effect of these risk factors such that the probability of abrupt coronary artery occlusion is approximately 25% if three risk factors are present. FACTORS AFFECTING THE RISK OF DEATH ASSOCIATED WITH ABRUPT CORONARY ARTERY OCCLUSION

When abrupt coronary artery occlusion occurs, there are several factors that are predictive of increased procedural mortality (Table III). Ellis et al.,12 who analyzed the results of more than 8000 procedures at Emory University and the San Francisco

Heart Institute, found female sex, multivessel disease,and collaterals from the dilated vessel to predict independently an adverse outcome after abrupt occlusion. Holmes et al.,25 reporting on the 1800 patients in the 1985-1986 National Heart, Lung, and Blood Institute PTCA Registry, found that a history of congestive heart failure, age 165 years, triple-vessel or left main coronary artery disease, and female sex each predicted a higher probability of death after abrupt occlusion. Park et al.,26reporting on experiences with more than 5000 casesat the Mid-America Heart Institute, found left ventricular ejection fraction 70 years, multivessel disease, and unstable angina to independently predict death. It appears that procedural death is closely associated with the presence of a large amount of ischemic myocardium at risk during the procedure, while taking into account the amount of preexisting nonviable myocardium. AVOIDING ABRUPT Patient selection.

CORONARY

ARTERY

OCCLUSION

Most important in avoiding the occurrence of abrupt coronary artery occlusion is the selection of patients. The selection process should take into account not only the chance of successful PTCA and avoidance of complications but also the consequences if complications occur. Recently the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures has provided guidelines for PTCA that use a lesion-specific classification of the morphologic characteristics of vesselsto be considered for balloon dilatation.27 Type A lesions are defined as those in which the anticipated success rate is 85% or higher and the risk of abrupt coronary artery occlusion is low (<4 %)). Type B lesions are those in which the anticipated success rates range from 60% to 85%) the risk of abrupt oc-

1636

de Feyter et al.

Table

American

IV. Studies of antiplatelet agentsto reduce acute complication

Reference

Barnathan

Design

et a1.2g

No. of patients

Retrospective

220

Retrospective

500

rate in patients

Treatment

ASA ASA + DIP None

Kent et a1.30

ASA None

White et a1.31

Prospective

333

Schwartz et a1.32

Prospective Controlled Prospective Controlled

376

Bertrand et a1.33 ASA,

Table

266

ASA + DIP Ticlopidine Placebo ASA Placebo Ticlopidine Placebo

undergoing

Acute major complications f%)

1.8 0 10.7 1.3 6.5 5.0 2.0 14.0 1.6 6.9 5.1

coronary

June 1992 Heart Journal

angioplasty

Significance p = 0.005 p = 0.001 p < 0.001 p < 0.005 p < 0.005 p = 0.01

p < 0.01

16.2

Aspirin; DIP, dipyridamole.

V. Various reasonsnot to perform redilatation Expected problems in recrossing lesion Tortuositylcalcificationlangulation Unstable guiding catheter Expected unfavorable redilatation outcome Diffuse disease Long spiral dissection Small-caliber vessel Severe angulation High risk of damage to left main coronary artery Additional significant (nondilatable) lesions

elusion is moderate (<8 % ), or both. Type C lesions are those in which the anticipated successrate is less than 60 9%)the risk of a procedural complication is high (X3%), or both. Attempts to dilate type C lesions were not recommended. Recently the Multivessel Angioplasty Prognosis Study group28 refined this classification and stratified group B into two subgroups: those with type B1 (one type B characteristic) and those with type Bz (two or more type B characteristics). These investigators reported a success rate of 76% and a complication rate of 10% in type B2 lesions versus an 84 % successrate and a 4 % complication rate in type B1 lesions (whereas C lesions had a 61% successrate and a 21% complication rate). They concluded that patients with multivessel diseasetype B2 or C lesions should be seriously considered for surgical revascularization in lieu of PTCA. Pharmacologic pretreatment. Pharmacologic modification of the platelet-fibrin response to vascular injury is possible and favorably influences the immediate outcome of the procedure. Results of several studies2gW33 have clearly shown that pretreatment with platelet inhibitor agents significantly reduces

the incidence of abrupt coronary artery occlusion (Table IV). Thus it is evident that elective coronary angioplasty should not be performed without prior antiplatelet therapy. The optimal dose (high or low) of aspirin is still unknown. Mufson et a1.34reported no difference in the likelihood of ischemic complications between patients randomly assigned to receive 80 mg or 1500 mg of aspirin daily starting the day before the procedure. The use of intravenous heparin for the prevention of acute thrombotic complications during or after coronary angioplasty has not been tested in randomized trials. However, it is common clinical practice to treat patients undergoing PTCA with intravenous heparin, often in combination with aspirin. This practice is supported by experimental evidence that the use of adequate doses of heparin during the procedure limits the formation of platelet aggregates and thrombosis.35 Data from three uncontrolled clinical trials of heparin treatment 1 to 7 days before attempted PTCA in patients with unstable angina pectoris or evidence of intracoronary thrombus also have suggested a beneficial effect.36-38 The rate of acute major procedural complications (myocardial infarction, emergency surgery, or death) was decreased in those patients pretreated with heparin. The utility of routinely prolonged heparin infusion after PTCA is controversial. Ellis et a1.3greported that the administration of 18 to 24 hours of postprocedural intravenous heparin after a standard dose of heparin was given during the procedure itself did not reduce ischemic complications after uncomplicated coronary angioplasty compared with a group randomly assigned to receive dextrose. However, it seems good clinical practice to treat “suboptimal PTCA results” (large dissection or filling defects)

Volume Number

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with prolonged heparin infusion.1° It is important to note that patient responses to heparin are highly variable, and close monitoring of heparin therapy with repeated measurements of activated clotting time or partial thromboplastin time is highly recommended.40T 41 A level 2.5 to 3 times the normal value is recommended to prevent abrupt occlusion. The use of nitrates (either intravenous or intracoronary) is advocated to prevent the occasional occurrence of abrupt occlusion resulting from spasm seen in this setting.17 In addition, nitrates also exert a beneficial antiplatelet effect.42 Calcium entry blockers may decrease myocardial ischemia and coronary spasm in association with PTCA. Although many physicians give calcium entry blockers to all patients before, during, and after PTCA, there is no firm scientific evidence to support this.43 Currently we practice the liberal use of intracoronary nitroglycerin, and we have abandoned the routine use of calcium entry blockers before and during PTCA; however, we still continue to give calcium entry blockers for 24 hours after PTCA in the hope of diminishing the role of spasm in abrupt occlusion. Results of pretreatment with thrombolytic agents to reduce the incidence of procedural complications in patients with unstable angina have been conflicting.44,45 Top01 et a1.44 in a randomized study observed a lower but nonsignificant incidence of complications after pretreatment with recombinant tissue plasminogen activator (rTPA), whereas van den Brand et a1.45 in their randomized study could not demonstrate any beneficial effects of pretreatment with rTPA. Therefore pretreatment with thrombolytic agents currently is not recommended, and further studies are needed to establish a specific role in this setting. However, this recommendation is based on the failure of rTPA to prevent abrupt occlusion, because other thrombolytic agents have not been tested in this setting. The preventive role of the routine use of thrombolytic treatment during PTCA has not been established either. Concomitant intracoronary infusion of urokinase during PTCA, tested in a randomized study of 251 consecutive patients, did not significantly reduce the frequency of acute complications.46 Use of alternative intervention techniques. The rate of abrupt occlusion may be decreased with the use of new techniques: directional atherectomy,47) 48 excimer laser,4g or stent implantation.50-53 Although currently no definitive evidence is available to clearly establish the merits of these new techniques, the following suggestions have been made. Direct atherectomy might be associated with a decreased rate of abrupt occlusion when used in eccentric lesions or in

occlusion during PTCA

Abrupt

1637

very proximal lesions of the left anterior descending artery. 47,48 It has been suggested that excimer laser angioplasty will yield better results and fewer acute complications when used in long lesions.4g It is expected that primary stent implantation will prevent abrupt occlusion resulting from dissection; however, this would be counterbalanced by the occurrence of acute and early thrombotic occlusions within the stent.50-53 Multicenter randomized studies currently are being performed (Coronary Angioplasty Vs Excisional Atherectomy Trial [CAVEAT], BElgiumNEtherland STENT [BENESTENT], AMsterdamROtterdam study [AMRO]) to determine whether these new devices will be superior to balloon angioplasty (CAVEAT: to compare directional atherectomy with PTCA; BENESTENT: stent vs PTCA; AMRO: excimer laser vs PTCA). DETECTION OCCLUSION

OF ABRUPT

CORONARY

ARTERY

The most reliable indicator of abrupt coronary artery occlusion is the recurrence of angina pectoris, which has the same characteristics before and during PTCA and is associated with specific ECG changes. ECG changes during balloon inflation should be noted at the time of angioplasty, because if these changes are identical during recurrence of angina after the procedure, then reocclusion of the vessel is almost certain, Other nonspecific ECG changes occur in up to 20% of patients, but they do not often herald the occurrence of abrupt coronary artery occlusion

54355

MANAGEMENT OCCLUSION Established

OF ABRUPT

CORONARY

ARTERY

techniques. The key to the management of abrupt coronary artery occlusion is to limit the duration of ischemia. The longer the time between acute occlusion and reperfusion, with ensuing hemodynamic deterioration, the worse the outcome. Therefore antegrade coronary blood flow and ischemia should be restored as soon as possible. Intracoronary nitroglycerin is given as a first step, and this will occasionally result in reopening of the vessel. This should be followed by a quick attempt at redilatation with the same or an oversized balloon (including longer inflation durations). Immediate repeat dilatation has been shown to be successful in 35% to 51% of all patients32 6, 7 If this is unsuccessful, placement of an autoperfusion catheter across the lesion has been proved helpful to stabilize patients and to serve as a “bridge” to emergency surgery. 56157 Recently an autoperfusion dilatation balloon catheter has become available that allows for

1638

de Feyter

et al.

American

June 1992 Heart Journal

VI. Overall outcome of managementof abrupt coronary artery occlusionwith a combination of pharmacologic intervention, redilatation, and emergencysurgery Table

Management

Overall

in-hospital

outcome

Failure with complications (7 i

Reference Sinclair et a1.3 Detre et a1.6$ de Feyter et aL7

Period 1981-1986 19851986 1986-1988

Consecutive PTCA patients 1,160 1,801 1,423

Abrupt occlusion patients f%) 54 (4.7) 122 (6.8) 104 (7.3)

Medical (%) 26 16 5

Initial attempt? Repeat PTCA (%) 80 84 91

Emergency CABG (%) 33 35 30

Success mo) 57 49 54

*

Failure with no complications (%I 15 7 4

MI (Si)

Death (%J

35 39 36

1.9 5.0 6.0

*Success is defined as reopening with repeat PTCA or surgery without major complication. tIf repeat PTCA was unsuccessful, the majority of these patients were referred for emergency surgery. SAlso included were patients in whom abrupt occlusion occurred during attempt to cross lesion.

prolonged inflation duration (at low balloon pressure, up to 30 minutes) and has the potential to “tack” the dissection.58>5gHowever, the use of the autoperfusion catheter may be problematic for several reasons: (1) Excessive tortuosity, severe angulation, or small caliber of the vessel and a higher profile of catheter may prevent placement of the catheter; (2) adequate systolic pressure is required; (3) the catheter has a high likelihood of thrombotic occlusion; or (4) the catheter may obstruct significant side branches or in the case of very proximal placement in the left anterior descending artery it may obstruct the circumflex artery. If restoration of coronary blood flow is not possible within a reasonable period of time for a variety of reasons (Table V), it is important to know when to stop and not waste valuable time by repeatedly attempting to recross and redilate the lesion or by using other new techniques @tent, direct atherectomy, or laser balloon welding). Instead immediate measures should be taken to relieve pain and anxiety and refer the patient for emergency bypass surgery. In selected cases, where thrombus formation was presumed to have played an important role in the occurrence of abrupt occlusion during PTCA, intravenous thrombolytic treatment has been given as an adjunctive treatment.7, 18,60,61 We have shown that this strategy was clinically successful in 53 % (with no death, myocardial infarction, or need for emergency surgery) and reduced the need for surgery in this highly select group of patients (up to 15%), but it could not prevent progression to myocardial infarction in 38% and cardiac death in 6 % .7 In a recent study of 48 patients with intracoronary thrombus accumulation complicating PTCA, the angiographic

success rate after administration of intracoronary urokinase was 90% and there was no procedurerelated myocardial infarction or death.61 The outcome in both studies differs significantly in favor of the latter study. Patient selection may have played a significant role, but it is also possible that urokinase is more effective than streptokinase in dissolving post-PTCA intracoronary thrombi. In casesof severe hemodynamic collapse intraaortic balloon pump support is necessary to stabilize the patient and improve the mortality and morbidity of subsequent acute surgery. Until recently a combination of various pharmacologic interventions (nitroglycerin and thrombolytic agents), repeat dilatations, use of an intraaortic balloon pump in the case of hemodynamic deterioration, and emergency surgery was the only approach available for treatment of abrupt occlusion. This overall approach was associated with a substantial rate of myocardial infarction and cardiac death (Table VI).3,6v 7 Emergency surgery after unsuccessful PTCA has been shown to be associated with a Q wave myocardial infarction rate ranging from 11% to 46 % and a mortality rate ranging from 1.4% to 11% (Table VII).62-67 The main feature that correlated best with periprocedural death and myocardial infarction was ongoing ischemia with ensuing hemodynamic instability.63* 66 New techniques. The overall poor results of these different treatment regimens have prompted the research for new alternative methods of providing definite nonsurgical reversal of abrupt coronary artery occlusion or a method that could relieve ischemia and stabilize the patient as a bridge to semielective surgery. Although the latter method does not provide definitive treatment, it would signify an enormous

Volume

123

Number

6

improvement for several reasons. First, the results of surgery after unsuccessful PTCA in nonischemic stable patients are comparable to the results of elective surgery.66 In addition, an unscheduled operation is taxing for medical and surgical personnel and may cause deviation from a routine technical plan so that fewer arterial grafts are used in emergency surgery after unsuccessful angioplasty. Finally, surgery in nonischemic patients may also allow the use of internal mammary artery grafts.66 Development of technology to decrease or completely ameliorate coronary ischemia subsequent to abrupt occlusion ideally should have the following features: have a high success rate, be simple, easy, and quick to use, have no other associated complications, and be low cost and widely available. Stent implantation, directional atherectomy, and laser balloon welding have the potential to improve results after unsuccessful angioplasty. Perhaps the greatest potential for the management of balloon-refractory abrupt occlusion to date has been the use of stents.68>6g Inasmuch as abrupt occlusion is largely a mechanical phenomenon of dissection and plaque displacement, a stent can reattach those dissections and provide for a smooth luminal surface with no impediment to forward flow. Several problems remain regarding emergency implantation of stents. First, because of the relatively high profile they cannot be delivered in all instances (vessels with diameters <2.5 mm, severe angulation point, or severe tortuosity). Second, because of the high degree of thrombogenicity of current stents, it is probably not wise to implant stents in the setting of acute myocardial infarction and recent unstable angina or if intracoronary thrombosis appears to be a predominant mechanism in abrupt occlusion. Third, stent implantation should not be performed in patients with contraindications for intensive treatment with anticoagulants and antiplatelets. Fourth, because of intensive anticoagulant treatment there is an increased risk of fatal bleeding and other bleeding complications, particularly at the puncture site. Fifth, the relatively short stents currently available fail to cover the often longer dissections. Therefore not all patients with abrupt occlusion are suitable for stent implantation. Retrospective analysis of 36 patients with refractory acute coronary occlusion disclosed that 69% (25 patients) were potentially suitable candidates for emergency stent implantation.6g In addition, specific problems in placing a stent in the setting of abrupt occlusion may arise: (1) Correct positioning of a stent is difficult because of the lack of visible side branches that act as landmarks as a result of the absence of adequate antegrade flow, and (2) it may be difficult to choose a stent size because acute

Abrupt

occlusion

during

PTCA

1639

Table VII. In-hospital results of emergency bypass surgery after unsuccessful PTCA* Total group No.

Reference

Cowley et al.62 Golding et a1.63 Killen et al.64 Reul et a1.65 Talley et al.‘j6 Greene 67 CABG, *Selected procedures.

Coronary were

3,079 1,831 3,000 518 7,246 1,214

Emergency CABG No. f%)

202 (7) 81 (4.5) 115 (4)

70 (13.5) 430 (6.0) 53

Q wave MI No. (%)

52 37 50 8

(26) (46) (44) (11.4)

91 (21)

27 (51)

artery bypass graft; MI, myocardial studies that included patients with

infarction. more than

Mortality No. (%)

13 2 13 4 6 2

(6.5) (2.5) (11)

(5.7) (1.4) (4.0)

500 PTCA

coronary artery occlusion is often associated with a smaller reference vessel segment as a result of spasm and absence of antegrade flow. Whether emergency stent implantation should be considered as definitive treatment or as a bridge to surgery depends on the estimated risk of acute thrombotic occlusion and ensuing obstruction of flow in a main vessel or a major side branch. We believe it is prudent to refer patients for semielective surgery after stent implantation if abrupt occlusion occurs in patients with unstable angina who already have activation of platelets and the clotting system, if the stent is positioned in the left main stem or a major side branch, if the results of stent implantation are suboptimal (no smooth appearance), and if intensive anticoagulant treatment cannot be continued for various reasons. Direct coronary atherectomy can be used successfully to treat abrupt occlusions in up to 87 % of patients.70y 71 The potential of atherectomy is excision of an occluding intraluminal dissection or intraluminal defects and a debulking effect, which diminishes the effects of excessive recoil. Because of the features of the catheter, bail-out atherectomy is restricted to proximal lesions in large vessels. Furthermore, it should not be used in cases of spiral dissection because of the danger of perforation. A valuable indirect intervention is percutaneous femoral-femoral cardiopulmonary bypass.71, 72 In cases of hemodynamic collapse, the cardiopulmonary support system is more effective than intraaortic balloon counterpulsation. The system can be rapidly initiated within the catheterization laboratory. It provides adequate systemic perfusion, and marked unloading of the left ventricle leads to a very low rate of myocardial oxygen consumption. This device does not result in myocardial perfusion of the area subserved by the occluded artery, but it buys some time for management of abrupt occlusion in an attempt to achieve a sufficient definitive result or otherwise sta-

1640

de Feyter et al.

bilize the patient to allow for transfer in stable condition for coronary bypass surgery. Its use is limited by the large size of the indwelling catheters and its ensuing morbidity. SHOULD ALL PATIENTS WITH REFRACTORY ABRUPT CORONARY ARTERY OCCLUSION AND MYOCARDIAL ISCHEMIA BE REFERRED FOR EMERGENCY SURGERY?

It may be argued that patients with abrupt occlusion of a smallIcaliber vessel and a small amount of myocardium at risk or with sufficient collateral circulation and no additional significant lesions in other vessels can be managed medically, thereby accepting the fact that the occlusion will result in a (small) myocardial infarction. The outcome of this approach should be weighed against the total burden of major surgery in these patients, and the fact that emergency surgery in these situations does not completely prevent the progression to myocardial infarction because of the inevitable delay between abrupt occlusion and revascularization. FUTURE

DIRECTIONS

Direct restoration of forward flow by autoperfusion (balloon) catheter, stent, or direct coronary atherectomy represents a substantial improvement in the management of abrupt occlusion. Currently the definite role and indication of each strategy or combination is not yet completely known and will require more studies. It is to be expected that refinements of the previously described techniques will further increase their usefulness. Future technology may provide us with less thrombogenetic stents by using newer alloys, coating with anticoagulant substances or endothelial cells, or using self-absorbable materials. Local application with intravascular devices (sweating balloon) of substances to “tack” tears and dissection, to prevent recoil, platelet adhesion and aggregation, and thrombus formation, might further enhance the management of acute coronary artery occlusion. New more specific antithrombotic agents such as hirudin, a specific thrombin inhibitor, or antiplatelet agents such as an inhibitor of platelet thromboxane As and synthesis, monoclonal antibodies against adhesive glycoproteins IIIB/IIA or vWF, or platelet membrane receptor-inhibitors may prove to be more effective. Potentially direct visualization (angioscopy) or indirect visualization (intravascular echocardiography) techniques might be useful to aid, select, and correct placement and employment of different interventional techniques or devices. However, there appears to be a paradox. Unstable, complex, eccentric, or long lesions located at severe angulation or at bifurcations

American

June 1992 Heart Journal

and lesions in tortuous or small-caliber vessels are at highest risk of abrupt occlusion, and yet they are the least amenable to successful reintervention with the devices now available. It is to be expected that also in the future the previously described techniques will not be consistently effective and emergency coronary bypass surgery will remain an important option in the management of abrupt occlusion. CONCLUSIONS

Abrupt coronary artery occlusion after PTCA is a major complication, and it is the predominant cause of procedure-related mortality and morbidity. The best strategy is to try to prevent it by careful patient selection. It has been shown to occur in 5 ‘?Gto 10 % of patients, and when it does occur it can be reversed with repeat PTCA in f 50 9%of all patients without subsequent sequela. If refractory to redilatation, ischemia should be controlled by immediate placement of a perfusion (balloon) catheter. If this is not possible prompt surgery is recommended. If ischemia can be controlled, a long inflation might definitively “tack” the dissection. If this is unsuccessful stent implantation, either as definitive therapy or as a bridge to “semielective” surgery, or alternatively in selected casesdirect coronary atherectomy, can solve the problem. In hemodynamically unstable or lifethreatening situations (left main artery occlusion, very proximal left anterior descending artery), institution of percutaneous extracorporeal support can stabilize the patient to permit a definite “workup” of abrupt occlusion or to serve as a safe bridge until emergency surgery. In our opinion currently the requirements for a hospital with a coronary interventional program are (1) the availability of (immediate) cardiac surgery backup, (2) the availability of an autoperfusion (balloon catheter), and (3) preferably the availability of a new device of which stent implantation or direct coronary atherectomy appears to have the greatest promise in the setting of management of abrupt coronary artery occlusion. We thank assistance.

Claudia

Sprenger

de Rover

for excellent

secretarial

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