Identifying the High-Risk PCI Patient

Retrospective studies and databases have been utilized to identify risk factors for adverse events occurring during PCI.

ACC, American College of Cardiology; AHA, American Heart Association.

^{Table 12-2} Lesion Characteristics and the Increased Risk of Ischemic Complications (Based on Multivariate Analysis)

Adapted from Ellis SG, Guetta V, Miller D, et al. Relation between lesion characteristics and risk with percutaneous intervention in the stent and glycoprotein IIb/IIIa era. Circulation 1999;100:1971–1976.

The ACC/AHA Lesion Classification Scheme has since been modified in that lesions with one “type B” characteristic are designated as “type B1” while lesions with two or more “type B” characteristics are designated as “type B2” lesions. Since this classification was first implemented in 1988, significant advances in PCI techniques have allowed treatment of more complex lesions with lower risks. In the current era of coronary stenting, it is primarily the type C lesions that are associated with lower success and higher complication rates.

In the mid-1990s, an era in which coronary stents and platelet glycoprotein IIb/IIIa inhibitors were frequently utilized, Ellis and coworkers analyzed a large database of patients undergoing PCI. Ten angiographic factors were identified that correlated with greater risk of complication. The two factors associated with the greatest increased risk were degenerated saphenous vein grafts (relative risk 4.18) and nonchronic total occlusion (relative risk 4.74). Other factors included long lesions, lesions with large filling defects, calcified angulated lesions, eccentric lesions, and old saphenous vein grafts (Table 12-2). The finding of marked increased risk in degenerated vein grafts supports the practice of using distal protection devices during PCI of such lesions.

Angiographic Risk Assessment Using the SYNTAX Score

The SYNTAX score, an angiographic grading tool to determine the complexity of coronary artery disease (CAD), was derived from pre-existing risk assessment classifications from numerous studies and expert consensus. The SYNTAX score is the sum of the points assigned to each individual lesion identified in the coronary tree with >50% diameter narrowing in vessels >1.5 mm diameter. The coronary tree is divided into 16 segments according to the AHA classification (see Fig. 12-1). Each segment is given a score of 1 or 2 based on the presence of disease, and this score is then weighted based on a chart, with values ranging from 3.5 for the proximal left anterior descending artery (LAD) to 5.0 for left main, and 0.5 for smaller branches. The branches <1.5 mm in diameter, despite having severe lesions, are not included in the SYNTAX score. The percent diameter stenosis is not a consideration in the SYNTAX score, only the presence of a stenosis from 50% to 99% diameter, <50% diameter narrowing, or total occlusion. A multiplication factor of 2 is used for non-occlusive lesions and 5 is used for occlusive lesions, reflecting the difficulty of PCI. Further characterization of the lesions adds points. (Fig. 12-1 shows the diagram of vessel segments used in the SYNTAX score.)

Figure 12-1 Definition of the coronary tree segments from the SYNTAX study

1. RCA (right coronary artery) proximal: from the ostium to one half the distance to the acute margin of the heart.

2. RCA mid: from the end of first segment to acute margin of heart.

3. RCA distal: from the acute margin of the heart to the origin of the posterior descending artery.

4. Posterior descending artery: running in the posterior interventricular groove.

5. Left main: from the ostium of the LCA (left coronary artery) through bifurcation into left anterior descending and left circumflex branches.

6. LAD (left anterior descending) proximal: proximal to and including first major septal branch.

7. LAD mid: LAD immediately distal to origin of first septal branch and extending to the point where LAD forms an angle (RAO [right anterior oblique] view). If this angle is not identifiable, this segment ends at one half the distance from the first septal to the apex of the heart.

8. LAD apical: terminal portion of LAD, beginning at the end of previous segment and extending to or beyond the apex.

9. First diagonal: the first diagonal originating from segment 6 or 7.

9a. First diagonal a: additional first diagonal originating from segment 6 or 7, before segment 8.

10. Second diagonal: originating from segment 8 or the transition between segment 7 and 8.

10a. Second diagonal a: additional second diagonal originating from segment 8.

11. Proximal circumflex artery: main stem of circumflex from its origin of left main and including origin of first obtuse marginal branch.

12. Intermediate/anterolateral artery: branch from trifurcating left main other than proximal LAD or LCX (left circumflex). It belongs to the circumflex territory.

12a. Obtuse marginal a: first side branch of circumflex running in general to the area of obtuse margin of the heart.

12b. Obtuse marginal b: second additional branch of circumflex running in the same direction as 12.

13. Distal circumflex artery: the stem of the circumflex distal to the origin of the most distal obtuse marginal branch, and running along the posterior left atrioventricular groove. Caliber may be small or artery absent.

14. Left posterolateral: running to the posterolateral surface of the left ventricle. May be absent or a division of obtuse marginal branch.

14a. Left posterolateral a: distal from 14 and running in the same direction.

14b. Left posterolateral b: distal from 14 and 14a and running in the same direction.

15. Posterior descending: most distal part of dominant left circumflex when present. It gives origin to septal branches. When this artery is present, segment 4 is usually absent.

16. Posterolateral branch from RCA: posterolateral branch originating from the distal coronary artery distal to the crux.

16a. Posterolateral branch from RCA: first posterolateral branch from segment 16.

16b. Posterolateral branch from RCA: second posterolateral branch from segment 16.

16c. Posterolateral branch from RCA: third posterolateral branch from segment 16.

(From Sianos G, Morel MA, Kappetein AP, et al. The SYNTAX Score: an angiographic tool grading the complexity of coronary artery disease. EuroIntervention 2005;1:219–227.)

The SYNTAX score algorithm then sums each of these features for a total SYNTAX score. Table 12-3 summarizes the SYNTAX grade categories. A computer algorithm (available online at www.syntaxscore.com) is then queried, and a summed value is produced. Figure 12-2 shows two patients each with three-vessel CAD but very different PCI risk based on SYNTAX scores.

^{Table 12-3} The SYNTAX Score Algorithm

Reprinted from Sianos G, Morel MA, Kappetein AP, et al. The SYNTAX score: an angiographic tool grading the complexity of CAD. EuroIntervention 2005;1:219–227.

Figure 12-2 Angiographic examples of SYNTAX scores in patients undergoing PCI. Selected angiograms.

(Reprinted from Sianos G, Morel MA, Kappetein AP, et al. The SYNTAX score: an angiographic tool grading the complexity of CAD. EuroIntervention 2005;1:219–227 with permission.)

In patients with SYNTAX score <33, equal outcomes after revascularization were obtained with regard to major adverse cardiac events for both PCI and CABG. For higher SYNTAX scores, CABG had fewer adverse events than PCI. The conclusion of the SYNTAX study showed that the overall safety outcomes (death, cerebrovascular accident, MI) were similar in CABG and PCI patients at 12 months (7.7 vs. 7.6%). There was a higher rate of revascularization in the PCI group (13.7 vs. 5.9%), balanced by a higher rate of cerebrovascular accident in the CABG group (2.2 vs. 0.6%). Of note, the overall PCI major adverse cardiac and cerebrovascular event rate (MACCE) was higher (17.8 vs.12.1%) primarily due to an excess need for repeat revascularization. If one accepts a repeat revascularization as part of the natural history of PCI and not an adverse event, then the difference between revascularization strategies becomes even less (Fig. 12-3).

Figure 12-3 Outcomes of SYNTAX study by SYNTAX scores. Rates of major adverse cardiac or cerebrovascular events among the study patients, according to treatment group and SYNTAX score category. Kaplan-Meier curves are shown for the percutaneous coronary intervention (PCI) group and the coronary artery bypass grafting (CABG) group for major adverse cardiac or cerebrovascular events at 12 months. The 12-month event rates were similar between the two treatment groups for patients with low SYNTAX scores (0–22) (A) or intermediate SYNTAX scores (23–32) (B). Among patients with high SYNTAX scores (=33, indicating the most complex disease), those in the PCI group had a significantly higher event rate at 12 months than those in the CABG group. SYNTAX scores were calculated at the core laboratory. The I bars indicate 1.5 SE. P values were calculated with the use of the chi-square test.

(Reprinted from Serruys PW, Morice, MC, Kappetein AP, et al. Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med 2009;360(10):961–972.)

Based on angiographic assessment and the operators’ experience in the cath lab, the number and type of complex anatomic lesions determines which revascularization approach might be selected. However, the physiology of coronary lesions and stenting are strongly related to outcomes. A recent publication by Tonino et al. from the FAME study group reported on what truly constituted three-vessel and two-vessel CAD, making clear that one cannot equate angiographic three-vessel CAD with physiologic three-vessel CAD. Fractional flow reserve thus has important implications for the decision-making process in patients with multivessel disease.

Patient-Related Factors

Several clinical factors can be utilized to identify high-risk PCI, such as the presence of multivessel disease, angioplasty to more than one lesion, suboptimal activated clotting time (ACT), residual stenosis above 30%, depressed ejection fraction, old age (>65 years), unstable angina and recent MI (Table 12-4). A retrospective study from the Mayo Clinic, examining the risk of PCI with the use of glycoprotein IIb/IIIa inhibitors and coronary stents, found that clinical factors such as left main or multivessel disease, an ejection fraction below 35%, or a recent MI were more important than angiographic factors for predicting complications. Other studies have identified the presence of diabetes mellitus and renal disease as indicators of high-risk patients (Table 12-5).

^{Table 12-4} Patient and Clinical Factors Associated With Higher Risk PCI

PCI, percutaneous coronary intervention.

^{Table 12-5} Elective PCI Patient and Lesion High-Risk Characteristics

CHF, congestive heart failure; SVG, saphenous vein graft.

Modified from King SB, III, Walford G, for the New York State Cardiac Advisory Committee. Percutaneous coronary interventions in New York State, 2005–2007. Albany: New York State Department of Health, April 2010;1–52; and Dehmer GJ, Blankenship J, Wharton TP, Jr., et al. The current status and future direction of percutaneous coronary intervention without on-site surgical backup: an expert consensus document from the Society for Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv 2007;69:471–478.

Specific High-Risk Subsets

PCI for AMI

PCI for AMI can be performed before (primary PCI) or after thrombolysis (facilitated or rescue PCI). Primary PCI is the approach of choice for acute ST-segment elevation MI, but is not available in all facilities. Primary PCI for AMI is indicated in patients who present within 12 hours from the onset of symptoms and in whom the infarct vessel can be recanalized within 90 minutes of presentation. Primary PCI is also indicated for patients in whom thrombolytics are contraindicated and for patients in cardiogenic shock. Figure 12-4 shows angiograms of PCI for AMI.

Figure 12-4 Angiograms of patient with acute inferior myocardial infarction (MI) with thrombus in the right coronary artery (RCA) (top left,A).B shows post balloon dilation, C, during stent implantation, and D, final result with no significant residual narrowing.

(Courtesy of Drs. Wil Suh and Igor Palacios.)

The advantages of primary PCI include early and complete reperfusion, early identification of associated CAD, and reduced bleeding complications relative to thrombolytic therapy. The disadvantage is the delay in reperfusion therapy caused by on-call services. Primary PCI should not be performed in asymptomatic patients who present more than 12 hours after symptom onset and are hemodynamically and electrically stable.

PCI for AMI after thrombolysis for patients with continuing or recurrent myocardial ischemia is termed rescue PCI. Rescue PCI has resulted in higher rates of early infarct artery patency, improved regional infarct zone, wall motion, and greater freedom from adverse in-hospital and clinical events compared to a strategy of repeat thrombolysis. The REACT (Rescue Angioplasty Versus Conservative Treatment of Repeat Thrombolysis) trial was a randomized study that demonstrated significantly lower MACCE rates at 1 year in patients randomized to rescue PCI after failed thrombolysis. Improvement in the TIMI grade flow from 2 to 3 may offer additional clinical benefit.

PCI in AMI patients immediately after successful thrombolysis (called facilitated PCI) has shown no benefit with regard to salvage of jeopardized myocardium or prevention of reinfarction or death. In some studies, this approach was associated with increased adverse events, including bleeding, recurrent ischemia, emergency coronary artery surgery, and death. Routine PCI immediately after thrombolysis may increase the chance of vascular complications at the access site and hemorrhage into the infarct related vessel wall (Table 12-6).

^{Table 12-6} Key Points for Acute Myocardial Infarction PCI

In contrast to trials of facilitated PCI, in which PCI occurred within 2 hours after thrombolysis at a PCI-capable facility, two recent trials (CARESS-in-AMI and TRANSFER-AMI) have addressed the management of patients who present to a non-PCI facility and receive thrombolytics. In these trials, ST-segment elevation MI patients with any high-risk features (e.g., anterior MI, extensive or >2 mm ST-segment elevation or depression, congestive heart failure, or low ejection fraction) were randomized to immediate transfer to a PCI-capable facility for planned PCI (within 6 hours), or to transfer only if rescue PCI was required. Patients transferred immediately after thrombolysis for a PCI had a reduction in MACCE, with a number needed to treat of 16-17 in both trials, and demonstrated no increase in bleeding. As a result, PCI performed as part of a pharmacoinvasive strategy for high-risk AMI patients has received a IIa ACC/AHA guideline recommendation.

Transvenous Pacing

Prophylactic pacemaker insertion is determined by (1) the patient’s risk of developing a bradyarrhythmia and (2) the patient’s ability to tolerate the arrhythmia should it occur. Conditions in which a prophylactic pacemaker may be considered include:

A balloon-tipped pacing catheter reduces the potential for right ventricular perforation.

Hemodynamic Support

In patients with hypotension, mitral regurgitation, multivessel disease, or decreased left ventricular function, hemodynamic support should be instituted before the procedure begins. After successful PCI for acute infarction, IABP is associated with reduced recurrent ischemia. Other percutaneous hemodynamic support devices such as TandemHeart and Impella have been used for high-risk PCI, but the ease and speed of placing the IABP still makes it the most attractive device for AMI procedures.

Intra-aortic Balloon Pump (IABP)

IABP counterpulsation increases myocardial oxygen supply and decreases myocardial oxygen demand. IABP balloon inflation at the onset of diastole (at the dicrotic notch on the central arterial pressure tracing) results in augmentation of diastolic pressure, which increases coronary artery (and systemic) perfusion. Deflation of the balloon just before systole (end diastole on the arterial pressure tracing) results in decreased ventricular afterload, which decreases myocardial oxygen consumption and increases cardiac output. These effects are illustrated in Figure 12-5. An example of the arterial waveform during correctly timed intra-aortic balloon counterpulsation is shown in Figure 12-6.

Figure 12-5 Arterial waveforms during 2:1 intra-aortic balloon pump (IABP) counterpulsation. A, one complete cardiac cycle; B, unassisted aortic end-diastolic pressure; C, unassisted aortic systolic pressure; D, dicrotic notch (balloon inflation); E, diastolic augmentation; F, assisted aortic end-diastolic pressure; G, assisted systole.

Figure 12-6 Hemodynamic simulator-predicted coronary flow enhancement (blue line) with the Impella (right) compared to the baseline (left) and intra-aortic balloon pump (IABP) (center). Diastolic augmentation of IABP increases coronary artery perfusion while deflation of the balloon just before the onset of systole decreases afterload, which results in decreased myocardial oxygen demand, decreased cardiac workload, and increased cardiac output.

Adapted from Hunziker 2006, as reproduced in Weber DM, Raess DH, Henriques J, Siess T. Principles of Impella Cardiac Support. Cardiac Interventions Today, August/September 2009: 3–16.

With an IABP, there appears to be a 20% to 30% increase in cardiac output in patients with low-output syndromes and a significant amount of afterload reduction as demonstrated in reduction of mitral regurgitation. Direct measurement of coronary blood flow during IABP function has demonstrated augmentation in nondiseased and post-angioplasty vessels, but no increase in vessels distal to significant stenosis.

The indications and contraindications for IABP counterpulsation during high-risk PCI are shown in Table 12-9. Before a diagnostic cardiac catheterization or interventional procedure, the patient should be treated medically to optimize hemodynamics and reduce myocardial ischemia. Hypotension (not responding to volume loading or intravenous vasopressors) and medically refractory angina are important indications for IABP placement. Contraindications to IABP placement must be factored into decisions on whether to proceed with a high-risk PCI.

^{Table 12-9} Indications and Contraindications for IABP Counterpulsation During High-Risk PCI

IABP, intra-aortic balloon pump; PCI, percutaneous coronary intervention; TIMI, thrombolysis in myocardial infarction.

In unstable patients and very high–risk patients, an IABP may be required before proceeding with the catheterization; however, there is scant evidence that routine prophylactic IABP insertion reduces complications. In the BCIS-1 trial, 301 patients with low ejection fraction (EF) (<30%) and extensive myocardium at risk were randomized to routine or bailout IABP insertion, and no difference in MACCE was seen. Bailout IABP was required in 12% of control patients.

Routine IABP support after PCI is also not indicated. In a prospective randomized study of 1100 patients with AMI (437 of which were high risk), Stone et al. found that routine IABP support for 36 to 48 hours after PCI did not improve the combined end point of death, reinfarction, infarct-related artery reocclusion, stroke, new-onset heart failure, or sustained hypotension compared to patients in the control arm.

Although routine insertion may not be indicated, the ACC/AHA guidelines give IABP support a Class I recommendation for refractory cardiogenic shock, so the ability to rapidly initiate support during high-risk PCI is required.

Notes on the IABP insertion technique:

Recall that the normal puncture site should be about 2 cm below the inguinal ligament (or centered near the middle of the femoral head). For IABP insertion, a puncture slightly more proximal than a standard femoral puncture for cardiac catheterization may be helpful. A puncture lower than the prescribed site may introduce the balloon into a superficial femoral artery too small to accept the large IABP catheter.

As discussed previously, iliac-femoral angiography (or distal aortic angiography with runoff) should be performed at the time of diagnostic catheterization, or at least, preceding high-risk PCI. The IABP balloon is inserted into either groin using standard Seldinger technique, as described in detail by Kern (2011). The Cardiac Catheterization Handbook, 5th edition. Some manufacturers are making small caliber or “sheathless” IABP balloon catheters, which are especially useful in the elderly and those with peripheral vascular disease. Fluoroscopic observation of the balloon inflated above the renal arteries confirms optimal placement.

Complications of IABP most commonly result from a low puncture site, perforation of the superficial femoral artery, or forceful advancement of the catheter damaging the arterial entry site. The most serious complication of IABP is lower extremity ischemia, which occurs in approximately 5% to 10% of patients. Prolonged intra-aortic balloon counterpulsation is also associated with hemolysis and platelet destruction, and thus the blood counts of patients should be closely monitored.

Despite the use of IABP during angioplasty in high-risk patients, there remains an in-hospital mortality of 6% to 19%, with a rate of vascular complications of 2% to 14%.

Impella LV Support Device

The Impella LV support device is an alternative to IABP and cardiopulmonary support. The Impella 2.5 is a minimally invasive, catheter-based cardiac assist device which directly unloads the left ventricle, reduces myocardial workload and oxygen consumption, and increases cardiac output and coronary and end-organ perfusion.

The Impella 2.5 can be inserted into the left ventricle over a 0.018-inch stiff guidewire through the femoral artery, across the aortic valve and into the left ventricle. The tip of the catheter has a “pigtail” that facilitates safe positioning in the left ventricle. The impeller motor draws blood into the cannula and expels it into the aorta, thereby generating pressure, and flows up to 2.5 L/min (Fig. 12-7). This compares with the IABP, which provides 0.2-0.4 L/min of support. A 13F femoral sheath is required for insertion of the Impella 2.5. Peripheral vascular disease and aortic valve disease are contraindications to the Impella.

Figure 12-7 Impella system. 13F catheter is shown with ports for infusion to cool impeller. Insert shows the inflow and outflow ports with their protective cages, cannula structure, and impeller motor.

Unloading of the LV by the Impella increases aortic and intracoronary pressure, hyperemic flow velocity, and coronary flow velocity reserve, and decreased microvascular resistance. The Impella-induced increase in coronary flow probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance.

Clinical trials comparing the IABP with the Impella 2.5 have demonstrated improvements in hemodynamic parameters but no improvements in survival or MACE. In the ISAR-SHOCK trial of 26 patients with AMI and cardiogenic shock, when compared with patients receiving IABP patients with Impella had increases in mean arterial pressure and cardiac index, and decreases in lactate levels, but no difference in 30-day mortality. Recently, the PROTECT-II trial of Impella 2.5 versus IABP for high-risk PCI was stopped halfway (305 patients) due to futility.

Despite these early setbacks, based on its relative ease of use and high level of circulatory support, the Impella remains a promising device for use in selected patients for high-risk PCI or refractory shock.

The TandemHeart Pump System

The TandemHeart percutaneous ventricular assist device is designed for short-term mechanical LV support. The TandemHeart involves the placement of a 21F catheter inserted into the left atria from the femoral vein via a transseptal puncture. Blood is withdrawn from the left atrium by an external centrifugal pump and infused into the femoral artery via a 14–19F catheter. The TandemHeart can provide up to 4.5 L/min of cardiac support. As with IABP and Impella, iliac-femoral angiography must be performed prior to canula insertion. Figure 12-8 shows the TandemHeart system.

Figure 12-8 A, TandemHeart system. B, C, Arterial and venous canula system in right femoral artery and vein with centrifugal pump secured on thigh. D, Canula after removal from leg to show different lengths and sizes. E, TandemHeart console.

Like the Impella, compared with the IABP the TandemHeart has been shown to improve hemodynamic parameters in two small trials. However, there is a high rate of complications with its use, including bleeding, tamponade, and vascular complications. The complexity of its insertion (30–45 minutes) and higher complication rate compared with the Impella or IABP likely will limit the role of the TandemHeart to patients with aortic valve disease, or to severe cardiogenic shock refractory to IABP support.

Management of Complications in High-Risk PCI Patients

Bradyarrhythmias and Heart Block

Bradyarrhythmias may occur as a result of ischemia of the sinus node (most commonly supplied via the right coronary artery). Symptomatic sinus bradycardia can initially be treated with atropine (0.5–1.0 mg IV), with repeat doses every 3 to 5 min as indicated, up to a usual total maximal dose of 2.0 mg (see Table 12-8).

Heart block may occur as a result of occlusion of the “dominant” artery (either the right coronary artery or the left circumflex artery) that supplies the atrioventricular node. Although there are no data to support this, intuitively one might believe that a patient with abrupt closure of the right coronary artery is more likely to develop heart block if the left circumflex artery is already occluded (and vice versa). Complete heart block with a slow ventricular escape rhythm should not be treated with atropine. Dopamine (initial infusion 5 mcg/kg/min) may, in certain circumstances, ameliorate sinus bradycardia or heart block.

Patients on beta blockers or calcium channel blockers can be treated with glucagon (1 mg) or calcium chloride (1 ampoule, 13.6 mEq), although the effects of such therapy are more theoretical than established. For both bradycardia and heart block, severely symptomatic patients can be treated with transcutaneous or transvenous pacing. Ultimately, the treatment for these conditions includes restoration of the compromised coronary artery blood flow.

Ventricular Tachyarrhythmias

Ventricular tachycardia (VT) and ventricular fibrillation (VF) may result from severe myocardial ischemia. Patients who develop VT and are hemodynamically stable can first be treated with intravenous antiarrhythmic therapy, specifically amiodarone and lidocaine (see Table 12-8). Stable patients not responding to antiarrhythmic therapy can be treated with synchronized cardioversion (beginning at 100 J and increasing stepwise up to 360 J as necessary).

Patients who develop unstable or pulseless VT or VF have been treated with a precordial thump. However, immediate defibrillation is indicated (at 200 J biphasic energy). Chest compressions are indicated to support coronary perfusion pressure and should be continued with minimal interruptions. Patients who do not convert after defibrillation should be treated with epinephrine (1 mg IV, repeated every 3–5 min) or vasopression (40 units IV × 1) and repeat defibrillation afterward. Patients who still do not respond can then be treated with amiodarone (300 mg IV bolus after dilution in 20 mL fluid) or lidocaine (1.0–1.5 mg/kg IV bolus). The advanced cardiac life support (ACLS) algorithm for the treatment of pulseless VT/VF is presented in Figure 12-9.

Figure 12-9 An ACLS algorithm for the treatment of pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF).

During resuscitative efforts, coronary access, as well as guidewire position across the lesion, should be maintained to complete the ultimate coronary recanalization. It is unknown how defibrillation affects the coronary artery with the guidewire in place.

Pulselessness

Asystole is usually the result of extensive myocardial ischemia. Asystole should be confirmed in two leads because it can be difficult to distinguish fine ventricular fibrillation from asystole. If the diagnosis is unclear, one should assume that fine ventricular fibrillation is present and treat it accordingly. Atropine (1 mg) and epinephrine (1 mg) should be given and can be repeated every 3 to 5 minutes if necessary. Metabolic abnormalities, including hyperkalemia or severe pre-existing acidosis, may contribute to the arrhythmia and may respond to the use of buffers.

Electromechanical dissociation (also called pulseless electrical activity [PEA]) is a condition that is almost uniformly fatal unless the underlying cause can be identified and immediately treated. General treatment includes the use of epinephrine (1 mg every 5 min). Bicarbonate may be considered. If PEA or asystole is refractory, emergency cardiopulmonary bypass may be considered.

Underlying causes of PEA include:

Pulmonary Edema

Pulmonary edema during high-risk PCI may be the result of ischemia-induced depression of myocardial function and/or volume overload due to intravenous fluids. Initial measures may include administration of furosemide 20 to 40 mg intravenously (which initially acts as a venodilator well before its diuretic actions become significant) and/or intravenous nitroglycerin (which also acts primarily via venodilation). Inotropic support can be considered utilizing dobutamine (2.5 advanced cardiac life support (ACLS 10 mcg/kg/min). Patients refractory to these measures, particularly those with severely compromised left ventricular function, may require intubation, IABP support, or intravenous afterload reduction.

Anaphylactoid Reactions

Anaphylactoid reactions to contrast agents may include hypotension and shock. Although such reactions are exceedingly rare during PCI procedures, the operator should understand the treatment of this life-threatening condition. Recommendations by the Society for Cardiac Angiography and Intervention for treatment include intravenous epinephrine with large volumes of normal saline, diphenhydramine, hydrocortisone, and, if unresponsive to therapy, an H₂ blocker and dopamine. Specific dosing regimens are given in Table 12-10.

Abrupt Vessel Closure and Thrombosis (Fig. 12-10)

Abrupt vessel closure is an uncommon complication since the introduction of stents. It is often due to dissection in association with intracoronary thrombosis. In these cases, immediate relief of the dissection with stenting of the inflow flap is indicated. In other cases, acute stent thrombosis may occur as a result of an inadequate anticoagulation or antiplatelet regimen, or from suboptimal stent deployment.

Figure 12-10 Angiogram of acute stent thrombosis.

Although multiple studies have demonstrated that initiation of platelet IIb/IIIa inhibitor therapy at the time of PCI decreases ischemic complications, there are no data on the degree of benefit from the “bailout” use of platelet IIb/IIIa inhibitors once a complication such as abrupt vessel closure has occurred. Nevertheless, the pathophysiology of abrupt vessel closure supports initiating platelet IIb/IIIa therapy. In patients who are may require emergency CABG, the operator should balance the benefit of IIb/IIIa inhibitors against the possibility that CABG will be delayed or precluded by their use.

In addition to thrombosis aspiration, the operator must ensure adequate anticoagulation. ACT should be checked in patients being treated with either unfractionated heparin or bivalirudin and, if it is low, the heparin dose should be repeated. The ACT does not reflect the degree of anticoagulation in patients who have been treated with enoxaparin. Patients who have received a subcutaneous dose of enoxaparin (1 mg/kg) within the previous 8 hours usually have therapeutic levels of anti-factor-Xa activity. Those who have received their last dose 8 to 12 hours prior to intervention may benefit from an additional dose (0.3 mg/kg IV, if they have not already received this “booster” dose at the time of PCI).

The data on administration of intracoronary thrombolytic therapy are conflicting. This route is rarely used in current practice, particularly given the availability of platelet IIb/IIIa inhibitors.

Slow Flow and No Reflow

Slow flow refers to the phenomenon in which blood flow (as assessed by contrast dye flow) in a treated and non-occluded artery decreases from TIMI 3 to TIMI 1 or 2 after intervention. No reflow refers to TIMI grade 0 flow after PCI. The occurrence of slow flow during PCI is usually accompanied by severe chest pain, ST-segment elevations, and sometimes hemodynamic and/or electrophysiological deterioration. The mechanisms for no reflow or slow reflow are only partially understood but appear to involve a variable combination of:

Treatment recommendations for slow or no reflow are as follows. Given the contribution of platelets and thrombus to slow flow (and no reflow), rescue or emergent administration of a platelet IIb/IIIa inhibitor is prudent (despite few if any data). The ACT should be rechecked and additional boluses of antithrombin therapy given if the ACT is subtherapeutic. (However, there are again no data that show that this benefits slow flow or no reflow.)

Vasodilator therapy directed at the coronary microcirculation can include one or more of the following agents administered intracoronary:

Preparation and administration of these medications is given in Table 12-11.

^{Table 12-11} Preparation and Administration Guidelines for Intracoronary Vasodilators Used for “Slow Flow” and “No Reflow”

Atherosclerotic emboli appear to play a major role in the slow-flow phenomenon during treatment of degenerated saphenous vein grafts. Distal protection devices (FilterWire, Spider) decrease the incidence of complications during saphenous vein graft PCI. A proximal protection device (Proxis) has been shown to reduce complications on the same order as distal protection devices and is indicated when graft anatomy precludes distal protection. These devices should be considered for prophylactic use when possible. However, there is no role for these devices once atheroembolization has occurred.

Coronary Perforation

Coronary perforation becomes of major clinical significance when it leads to cardiac tamponade. Treatment begins with prolonged inflation of a PTCA (percutaneous transluminal coronary angioplasty) balloon at the perforation site. Placement of a coronary stent graft to “seal” the perforation may ultimately be needed. Proximal balloon inflation relative to the perforation may also work provided there are no large distal collaterals. Continued brisk flow from a perforation despite these interventions may require placement of a covered stent graft (Jomed).

Treatment of cardiac tamponade requires pericardiocentesis. Reversal of anticoagulation may facilitate hemostasis at the site of perforation and efflux of blood into the pericardium, but this benefit must be balanced against the risk of thrombosis occurring in the coronary artery being treated.

Major Bleeding

Decisions as to whether to “reverse” anticoagulation and antiplatelet therapy in patients with major bleeding complications must balance the risk of further bleeding with the risk of coronary arterial thrombosis. The anticoagulant effects of unfractionated heparin can be reversed with protamine sulfate (1 unit protamine per 100 units heparin). Protamine should be used with caution in patients who have received NPH insulin or are postvasectomy. Protamine partially reverses the anticoagulant effects of low-molecular-weight heparin. Patients who have been treated with subcutaneous enoxaparin can be treated with 1 mg protamine per 1 mg enoxaparin when the last enoxaparin dose is within 0 to 8 hours of PCI, and 0.5 mg protamine per 1 mg enoxaparin when the last enoxaparin dose was 8 to 12 hours prior to PCI. Protamine is not effective in patients treated with a direct thrombin inhibitor (such as bivalirudin).

Both aspirin and clopidogrel are irreversible platelet inhibitors whose antiaggregatory effects can be reversed only with platelet transfusion. As abciximab is an antibody fragment that binds tightly to the IIb/IIIa receptor, and as less free abciximab molecules are in circulation than molecules of tirofiban or eptifibatide, the effects of abciximab on platelet aggregation are reversed to a greater degree with platelet transfusion than those of either tirofiban or eptifibatide.

Summary

Careful evaluation of angiographic, patient-related, and clinical factors can identify the high-risk PCI patient. Use of pharmacologic and mechanical therapies may serve to decrease the risks of major complications during high-risk PCI. Adequate planning and laboratory preparation are essential to quickly address complications when they occur. Familiarity with both pharmacotherapy and mechanical therapy is essential when attempting high-risk PCI.