Chapter 20. Myocardial Revascularization with Percutaneous Devices

At its height, the popularity of surgical coronary revascularization spurred improvement in catheter-based technology—first for imaging quality and later for attempted therapy. In 1974, Andreas Gruentzig completed development of the double-lumen balloon catheter that was miniaturized for use in coronary arteries. Soon afterward, techniques for percutaneous transluminal coronary angioplasty (PTCA) expanded as technical breakthroughs were applied to subselective catheters, devices, guidewires, balloon materials, and lastly, coronary stents. Presently trial evidence attests that percutaneous therapy is useful as a treatment in patients with unacceptably controlled angina whose anatomy does not imply a survival benefit from revascularization or for patients with uncontrollable, unstable symptoms. However, surgical and percutaneous revascularization cannot be considered equivalent.1

Principles

In the early balloon angioplasty era, several technical limitations restricted percutaneous techniques to low-risk patients with proximal, discrete coronary artery stenoses, and procedural outcomes lacked predictability. As advances in tools and techniques were developed, higher-risk patients became candidates for percutaneous therapy. Over time, several principles for safety and success were recognized (Table 20-1).

Tools

Guiding Catheters

Guiding catheters differ from diagnostic catheters in that a wire-braid supports a thin catheter wall, allowing for a larger central lumen and providing enough rigidity to support the advance of subselective catheters to the distal regions of the coronary bed. The anatomy of the ascending aorta and the origin of the treated coronary artery determine the shape of the guiding catheter that will provide the most secure positioning (Fig. 20-1). The choice of guiding catheter often is the deciding factor for success when approaching challenging anatomy or when complications increase procedural difficulty. Guiding catheter manipulation is a common cause of procedural complications that necessitate urgent transition to coronary artery bypass surgery.

Guidewires

When the guiding catheter position remains secure, the guidewire allows control of the distal vessel. Different wires vary in stiffness, coatings, diameter, and design of the distal steering tip. For most procedures, the chosen wire is a 190- to 300-cm monofilament that is 0.0254 to 0.0356 cm in diameter, with either a graded tapering segment welded to the tip or a gradual taper of the monofilament. The central wire core at the tip is “plastic,” or malleable, and may be shaped by the operator. In many wire designs, a wire coil wrapped around the central filament projects a blunter, less traumatic tip to the vessel that it must traverse. Generally, the softest tip is the safest tip. However, in certain situations, such as treatment of a chronic total occlusion, a stiffer wire tip with a bonded, hydrophilic coating, rather than the wire coil, is frequently most effective. Although increasing the likelihood of crossing the lesion successfully, these stiffer, “slicker” wires also increase the risk of complications, such as creation of a subintimal wire course, dissection or perforation of the vessel (Fig. 20-2).

Tools for Lumen Expansion

The vast bulk of subselective devices for coronary artery manipulation are balloon inflation catheters or some variation of this theme. Balloon catheter designs vary in the placement of the proximal opening of the central lumen. The “on the wire” design has a central lumen extending the length of the catheter. This design affords the best trackability and capability for maneuvering through difficult anatomy but requires an assistant to manipulate the wire during device advance. The “monorail” design has a central lumen extending only through the distal balloon shaft of the catheter. The remaining catheter shaft communicates only with the balloon lumen. This design, although less trackable, allows the procedure to be performed without the need for an assistant.

Properties of the angioplasty balloon include compliance, maximally tolerated pressure, profile, and friction coefficient. Compliance, or growth under pressure, and maximally tolerated pressure are a function of balloon wall thickness and material. Compliance is divided into three categories: noncompliant, semicompliant, and compliant, depending upon the growth of the balloon under pressure. The thin-walled, compliant balloon has the lowest deflated profile, allowing the device to pass through the most severely occluded vessels. However, the balloon may not expand uniformly or lengthen when exposed to high pressures, such as pressures in excess of 20 atm (15,200 mm Hg), which are required to dilate hard and heavily calcified stenoses or stents. A variety of balloon coatings may be used to reduce the friction coefficient or protect from abrasion (as in passing a stent).

Antithrombotic Therapy

During an angioplasty procedure, blood may stagnate in the guiding catheter or near the treated lesion when a wire or device is placed within the lumen of the target lesion. In addition, metallic components of the guidewire or other devices attract fibrinogen, thus stimulating thrombosis. Therefore, a thrombus may form easily unless prevented with intense anticoagulation therapy (Table 20-2). Most angioplasty procedures are performed with unfractionated heparin (UFH) titrated to an activated clotting time (ACT) value of more than 300 seconds.2 Alternative anticoagulants, such as low-molecular-weight heparins and direct antithrombin antagonists, may be used.3–7 The DTI may be associated with reduced risk for major bleeding complications but are not reversible in the event of need for emergency surgical referral.8 Antiplatelet therapy also reduces the risk of thrombosis at the treated lesion. In addition to aspirin and thienopyridines, glycoprotein IIb/IIIa (GP IIb/IIIa) complex inhibitors may be employed in specific circumstances. The GP IIb/IIIa complex inhibitors are unique in their ability to impair platelet–platelet aggregation, regardless of the type or intensity of stimulus. Anticoagulation is titrated to a lower intensity (an ACT of 200 to 250 seconds) when GP IIb/IIIa inhibitors are used.

Mechanisms

Balloon angioplasty transmits increased intraluminal pressures circumferentially to the rigid intimal surface of the diseased vessel. Because atherosclerotic lesions typically are heterogeneous in their circumferential distribution and physical characteristics, the nondiseased or less diseased wall may be overstretched during balloon inflation. In most instances, the lesion segment with the greatest structural integrity is a focal point for applied stress. Adjacent regions of the vascular wall can shift, and the diseased, inelastic intima can fracture. Although this mechanism allows balloon expansion and an increase in luminal diameter, extension of the fracture into the intima–media border creates a dissection plane, the growth of which will be determined by the mechanical characteristics of the lesion and the amount of force applied. If growth of the dissection plane results in significant displacement of the diseased intima, the vessel will close. This event, termed abrupt or acute occlusion, complicates about 10% of balloon angioplasty procedures. Overstretching the minimally diseased or nondiseased wall without creating plaque fracture typically results in early recoil of the treated lesion to its original state.

After balloon deflation, a small amount of thrombus accumulates, providing the stimulus and framework for colonization by inflammatory cells and myofibroblasts and the eventual, local synthesis of temporary (intimal hyperplasia) and permanent (collagen-rich) connective tissue. In addition, mechanical injury to the media and adventitia results in scar formation. The scar's contracture may reduce vessel cross-sectional area—a phenomenon termed negative remodeling. 9,10 During vascular healing, the encroaching intimal hyperplasia that peaks in volume at about 3 months, combined with negative remodeling, results in restenosis after 40% to 50% of balloon angioplasty procedures.11–13

Outcomes

In approximately 2 to 10% of balloon angioplasty procedures, intimal dissection, thrombosis, and perhaps medial smooth muscle spasm combine to produce abrupt closure.14,15 Abrupt closure may be treated successfully with repeat balloon inflation but is treated more commonly with stent implantation.16 The specter of abrupt closure and myocardial infarction (MI) or emergency bypass surgery and its complications historically has limited the application of balloon angioplasty.

In patients with stable angina, mortality from a balloon angioplasty procedure is 1% at 1 month.17 About half the deaths are the result of a procedural complication, and most are related to low cardiac output (Table 20-3).18 Although the incidence of restenosis (>50% diameter stenosis during follow-up) is 40 to 50% within 6 to 9 months of a PTCA procedure,11,13,19 only 25% of patients report recurrent angina that warrants further investigation.20 Patients with restenosis have an increased risk of MI and coronary artery bypass surgery.21

Stents

The two failure modes of balloon angioplasty, abrupt closure and restenosis, have stimulated development of myriad devices, all with the goal of reducing the risk of the procedure, the risk of restenosis, or both. Only coronary stents have been shown to be advantageous over balloon angioplasty, except in cases of severely calcified lesions (Table 20-4). There are numerous coronary stent designs, but the majority of those in current use consist of a stainless steel (or alloy, such as cobalt chromium) cylinder that has been “carved,” creating a so-called slotted-tube design. Stent expansion creates a series of interlocking cells, resembling a cylindrical meshwork (Fig. 20-3). Stents are thus deformable, but when expanded, they maintain sufficient rigidity to act as scaffolding after deflation of the angioplasty balloon. Intimal disruption is contained and far less likely to propagate and occlude the treated vessel. In addition, the rigid framework left behind becomes part of the vessel wall, addressing the issue of remodeling, which is one of the mechanisms of restenosis.

Stents allow safe expansion of the vessel beyond that typically achieved with PTCA at the time of balloon expansion; however, stent use increases thrombotic and inflammatory responses of the vessel wall. The increased injury and a foreign-body response to stent struts result in a more intense and prolonged local inflammatory response.22 As a result, stent placement paradoxically exacerbates intimal hyperplasia.23,24 Using the late (6- or 9-month) loss in lumen diameter after stent implantation as a measure of intimal hyperplasia, even the most modern stent designs fall within a range of about 0.8 mm, more than twice the loss incurred after PTCA (0.32 mm). As a result, when examining restenosis after angioplasty, the impact of stent for percutaneous coronary revascularization (PCR) is rather small in comparison with that of PTCA.23,24 The bulk of intimal hyperplasia and risk of restenosis are functions of the size of the treated lumen on completion of the procedure, length of the treated lesion, and presence of unstable angina, hypertension, and diabetes mellitus (Table 20-5).25–27 Long-term follow-up studies suggest that a stent that does not reocclude during the first 6 to 9 months after implantation is not subject to late, rapid disease progression.28–32

By reducing the likelihood of both abrupt closure requiring emergency coronary artery bypass surgery and restenosis, stent-assisted angioplasty is more effective than routine balloon angioplasty for virtually any type of coronary artery lesion. Registry data describe a risk for emergency surgery of only 0.3 to 1.1%, and a procedural mortality of less than 1%.33–36 The likelihood of procedural complications may be estimated on the basis of lesion characteristics (Table 20-6).37 Depending on lesion characteristics and the number of lesions treated, after 1 year, 5 to 10% of patients require coronary artery bypass surgery, and 15 to 20% undergo a second PTCR procedure.38–41 After 5 years, 10 to 15% of patients require another revascularization procedure because of the development of severe stenosis at an untreated site.32 Diabetes increases the risk for adverse outcomes by increasing the risk of restenosis and disease progression at untreated sites.

As noted in the description of the guidewire, iron components of stent struts attract fibrinogen and offer a site for platelet attachment and thrombosis. The increased risk of thrombosis at the treated site persists until endothelialization is complete. As a result, more intense antithrombotic therapy is required during the procedure and for up to 1 year afterward.42,43

Stents may be used as a drug-delivery system. However, rather than simply applying a drug to the stent surface, from which it will dissipate quickly, drug delivery is controlled by using a surface polymer or by altering the design or the material used to construct the stent.44 This method of drug delivery, called a drug-eluting stent (DES), allows the drug to be applied at high concentrations at the site of interest and reduces the probability of systemic toxicity.

Drug-eluting stents reduce the primary determinant of restenosis by 50 to 100%, as determined by quantitation of late lumen loss after angioplasty (Fig. 20-4). Studies examining the efficacy of the DES introduced new nomenclature to the follow-up end points. The most useful follow-up end point is termed target vessel failure (TVF), signified by cardiac death, MI, or repeat revascularization of the treated vessel. One year after the procedure, TVF is reduced from 19.4 to 21% with a bare-metal stent (BMS) to 8.8 to 10% with a paclitaxel or sirolimus DES.38,41

Reduced rates of repeat intervention after DES placement have been reported for every type of lesion studied, except bifurcation lesions, in which the risk of restenosis remains significant, and the risk of potentially fatal early thrombosis is as high as 3.5% (Table 20-7).38,45–52 However, the impact of DESs on failure of long-term treatment and repeat procedures does not translate to a reduced risk of procedure-related complications.53 In addition, incomplete healing, a response to the eluting polymer, or both, confer an increased risk of stent thrombosis that extends beyond 1 year. As a result, dual antiplatelet therapy should be continued for at least 1 year after the procedure in all patients and indefinitely in patients with complex lesions.

Other Devices

Perfusion Balloons

Before the routine use of coronary stents, abrupt closure owing to dissection could be treated with repeat balloon inflation and, if unsuccessful, coronary artery bypass surgery. Prolonged balloon inflation generally was necessary for successful restoration of patency, but in the event of failure, transport for emergency surgery often was accompanied by severe ischemia of the treated territory. As a result, balloon catheters with a short third-lumen opening just proximal and distal to the balloon were developed. These catheters, or “perfusion balloons,” allowed for prolonged balloon inflation with far less ischemia and could be used to ameliorate the severity of ischemia during transport for surgery after an unsuccessful procedure. Since the introduction of the coronary stent, perfusion balloons rarely are used.

Atherectomy

When introduced, the concept of reducing the bulk of the obstructing atheroma was quite attractive. The idea was to reduce vessel wall thickness or “debulk,” allowing for balloon expansion at a lower pressure. With less force applied for lumen expansion, theoretically the likelihood of abrupt closure would be reduced, as would the degree of arterial injury at the time of treatment. Several devices used for debulking have been developed and studied, including directional coronary atherectomy, percutaneous transluminal rotational ablation, and laser ablation. Unfortunately, when subjected to rigorous examination, debulking devices provide no incremental gain over plain balloon angioplasty in achieving procedural success or avoiding restenosis.54–57 Although each device has developed a specific niche (see Table 20-4), their routine use generally is associated with an increased risk of procedural complications, including perforation and MI.57–59

Rotational atherectomy requires additional discussion because, unlike the other types of atherectomy, it is still commonly used. The Rotablator (Boston Scientific Corporation, Natick, MA) is an olive-shaped device that is coated with diamond chips. It is attached to an electrical motor, which causes the device to rotate at high speeds. The device is designed to abrade a rigid atherosclerotic intima, creating microemboli that are small enough to pass through the coronary microcirculation without incident. It is also useful as an initial treatment method for very rigid, heavily calcified lesions. However, the concept is not without failings. Microembolization is likely to exacerbate ischemia and therefore is contraindicated when there are thrombotic lesions, if there is impaired microcirculatory flow associated with a recent MI, or if the treated vessel is the last remaining patent vessel. Use of this device is also associated with an increased risk of perforation in highly angulated lesions.

Aspiration Devices

A number of coronary aspiration devices are available to reduce the risk of distal embolization and diminish the local concentration of prothrombotic and vasoactive substances. These devices range from a simple end-hole catheter attached to a syringe to a complex suction catheter with or without an associated mechanical disrupter. These devices forcibly extract components of the thrombus or atheroma.60 Their use may improve flow after treatment of thrombus-laden lesions or saphenous vein grafts (Fig. 20-5).61

Embolic Protection Devices

During balloon angioplasty, mechanical dissolution of thrombus, if present, may result in macroembolization and distal vessel occlusion. The high-pressure manipulation of an atheromatous lesion also may free cholesterol crystals and other components of the lesion, resulting in distal microembolization, thrombosis, and slow- or no-reflow phenomenon. Several devices have been developed to reduce the frequency or impact of distal embolization. These devices may be placed distal or proximal to the treated lesion. Distal devices are mounted on the guidewire and use either a suspended micropore filter to trap particulate matter of 100 to 150 μm or larger or balloon occlusion of the treated vessel with posttreatment aspiration to capture embolized material. Proximally placed devices temporarily interrupt flow and aspirate the treated vessel. The PercuSurge GuardWire Plus (Medtronic, Minneapolis, MN) is a balloon occlusion and aspiration device that underwent testing in vein grafts in the Saphenous Vein Graft Angioplasty Free of Emboli Randomized (SAFER) trial.62 The trial demonstrated a 42% reduction in creatine kinase (CK) elevations and more than a 50% reduction in the no-reflow phenomenon.62 Unfortunately, these results did not apply to patients with MI.63

Imaging Devices

Angiographic imaging allows imaging of the coronary lumen but may be unreliable in the setting of severe calcification, difficult branching patterns, or previously placed coronary stents. Furthermore, a thrombus that may increase the risk of PCR may go undetected by standard angiographic imaging. Therefore, a number of alternative imaging methods have been developed to improve diagnosis, plan revascularization efforts, and evaluate the success of such efforts. Angioscopy or fiberoptic imaging requires occlusion of the imaged vessel and perfusion with saline. Although a useful tool to investigate the presence or components of thrombus within coronary vessels, angioscopy has not been a useful adjunct to PCR. In contrast, intracoronary ultrasound imaging has proved especially useful. Ultrasound imaging allows accurate determination of vessel size, luminal reduction, lesion components, and progress associated with revascularization attempts. Ultrasound guidance for stent implantation is associated with a greater than 30% reduction in the need for repeat procedures.64 Of equal importance, intracoronary ultrasound is an invaluable research tool used to investigate the accuracy of contrast angiography and the impact of mural lesion components on complications and outcomes after angioplasty.

Devices that Measure Lesion Severity

The hemodynamic significance of coronary lesions, the appropriateness of a treatment, and the success of treatment may be determined by the following two means: a guidewire that measures the velocity of blood flow within coronary arteries or a calculation that measures pressure distal to a coronary lesion.

A miniaturized Doppler-equipped guidewire with a 12-MHz transducer uses a pulsed interrogation that samples 5.2 mm beyond the guidewire tip at an angle of 14 degrees on either side. Assuming that the cross-sectional area of the interrogated vessel remains constant during all measurements, the ratio of velocities measured reflects the ratio of blood flow between any two measurements. The most important and reliable parameter that a flow probe measures is the ratio of resting flow to vasodilated coronary flow, a value known as coronary flow reserve. When measured using the Doppler probe, the value is termed coronary velocity reserve (CVR). As a coronary lesion becomes flow limiting, attempts to normalize tissue perfusion by autoregulation result in arteriolar dilatation at rest. Therefore, the administration of an arteriolar vasodilator such as adenosine will have little additional effect on flow velocity. The absence of an appropriate increase in velocity during adenosine- or dipyridamole-induced arteriolar vasodilation produces abnormal flow reserve. A CVR less than 2.0 indicates hemodynamically significant lesions.

CVR measurement reflects changes in flow relative to an assumed normal baseline state but is subject to error when baseline flow is abnormal. Examples of abnormal states include left ventricular (LV) hypertrophy, fibrosis, and perhaps anemia. In addition, abnormally large or small driving pressure gradients may fall outside the range of normal coronary autoregulation, altering the basal-to-hyperemic ratio. Failure to achieve arteriolar dilatation in response to adenosine or dipyridamole will produce an abnormal calculated flow reserve. Examples that affect arteriolar dilatation include diabetes mellitus, amyloidosis, and recent caffeine or theophylline ingestion.

An alternative to flow measurement is pressure measurement, proximally and distally to the lesion in question. Under normal conditions, epicardial vessels present little detectable resistance to flow. Therefore, driving pressure (PAo) and arteriolar resistance pressure (PRA) determine maximal coronary blood flow. The presence of a flow-limiting coronary lesion will cause some of the driving pressure to be lost, so maximal flow will depend on the distal coronary pressure (Pd) -to-PRA gradient and arteriolar resistance. Therefore, the fraction of maximal basal flow that remains possible in the presence of the lesion is

Canceling resistance and assuming that right atrial pressure remains constant results in a very simple relationship:

This ratio, called the myocardial fractional flow reserve (FFR), is obtained after the administration of adenosine. An FFR of 0.75 or less identifies a hemodynamically significant lesion. Routine use of FFR to ensure the necessity of PCI reduces the risk of adverse events both immediately and at 1 year.65

Before the advent of DESs, restenosis after angioplasty or stent implantation could be treated by medical therapy, repeat angioplasty, or coronary artery bypass surgery. The frequency of restenosis led to a large population of patients with multiple treatment failures, intractable symptoms, and prohibitive risks for surgical treatment. Because a proportion of the cell population colonizing a treated lesion and contributing to restenosis arose from the media of the treated lesion, radiation therapy to prevent cell replication was proposed. The well-recognized dangers of high-dose, external-beam radiation limited dosing to local application, but this therapy still was seen as a substantial risk. Although a source of increased adverse events when used as a treatment for de novo coronary lesions, radiation brachytherapy for the treatment of refractory in-stent restenosis has met with limited success.66,67

Performance of a percutaneous revascularization procedure includes an obligatory period of ischemia in the treated region. The duration of ischemia may be prolonged in the event of abrupt closure or distal embolization, and recovery may be incomplete or delayed for a period of days, as in the treatment of acute MI. For patients with depressed LV systolic function or those in whom the treated territory is large, there is a risk for developing cardiogenic shock during and after the procedure. This risk substantially increases the possibility of acute renal failure, stroke, and death. The likelihood of shock complicating an angioplasty procedure may be predicted by using a scoring method that incorporates the extent and severity of systolic dysfunction present before the procedure and the extent that can be expected as a result of the procedure (Table 20-8).37 Elective placement of an intra-aortic balloon pump (IABP) is associated with a reduced risk of hypotension and major complications.68

The percutaneous left ventricular assist device (PLVAD) is a miniaturized axial-flow pump that is being used increasingly for support of patients in shock or during high-risk angioplasty procedures.69 The PLVAD is capable of providing up to 4 L of additional blood flow per minute. Although it can provide superior circulatory support, the PLVAD has not shown any survival advantage when compared with the IABP, and vascular access-site complications are more frequent with the PLVAD.70

In addition to abrupt closure and restenosis, there are several other potential complications of PCR that may influence the risk:benefit ratio for an individual patient. These complications include bleeding, vascular access–site complications, stroke, radiocontrast nephropathy, and MI owing to distal embolization.

Hemorrhage

Bleeding that requires transfusion or results in hemodynamic instability occurs in 0.5 to 4% of PCR procedures, depending on patient variables (eg, age, gender, and presence of peripheral vascular disease), procedural variables (eg, location of femoral arteriotomy and duration), and pharmacologic variables (eg, intensity of antithrombotic therapy).2 A number of devices have been designed to improve femoral hemostasis after sheath removal, but none has proved superior to standard compression hemostasis.71 With the availability of lower-profile equipment, the radial artery is being used with greater frequency, which results in a reduction in bleeding and access-site complications.72

Ischemia

Stroke complicates approximately 0.18% of PCR procedures.73 Its occurrence is associated with increased age, depressed left ventricular ejection fraction (LVEF), diabetes mellitus, saphenous vein graft intervention, and complicated or prolonged procedures requiring the placement of an intra-aortic balloon pump.74

Myocardial infarction complicates 5 to 30% of PCR procedures, depending on the definition of infarction.75 Using a definition of new Q wave, the incidence is 1%.76 When any elevation of the MB fraction of CK (CK-MB) is used as the definition, as many as 38% of patients have a periprocedural MI.75 Use of more stringent definitions of infarction, such as greater than three or 10 times the upper limit of normal, reduces the reported values to 11% to 18% or 5%, respectively.76–78 Actually, any elevation carries prognostic significance, but elevation above three times the upper limit of normal is accepted as a definition of periprocedural MI.

Elevated markers of myocardial injury may be seen after apparently uncomplicated procedures.75 One mechanism for such events is microscopic distal embolization. When severe, microscopic distal embolization of a coronary artery creates the angiographic appearance of slow vessel filling, it is termed no - or slow-reflow. No-reflow is seen most often in the setting of saphenous vein graft angioplasty, but also may complicate rotational atherectomy and primary PCR for acute MI. Methods of quantifying abnormal flow after PCR include a subjective estimation of flow velocity, the Thrombolysis in Myocardial Infarction (TIMI) flow rate (III, normal; II, slow; I, minimal contrast material flow beyond the treated site; and 0, no flow), and the more objective method of corrected TIMI frame count. Individual frames of the angiographic image are counted from the time of contrast material entry into the treated vessel until a predetermined distal landmark is reached. No-reflow may be a brief and self-limiting phenomenon, but when prolonged, it is associated with increased mortality.79 Pharmacologic manipulations, including intracoronary verapamil, adenosine, and nitroprusside, may be used in an attempt to prevent or treat no-reflow phenomenon (see Table 20-2).

Perforation of the coronary artery complicates 0.5% of angioplasty procedures,80 and its frequency increases almost 10-fold when ablation devices are used (1.3% for ablation versus 0.1% for PTCA; p < .001). Coronary artery perforation occurs more frequently in elderly and female patients (Table 20-9).80,81

Pericardial tamponade is frequently but not invariably associated with coronary artery perforation. The overall incidence of tamponade after PCI is 0.12% and doubles when ablation devices are used. PCI-associated tamponade is recognized 55%82 of the time during or after the procedure while the patient is still in the catheterization laboratory and 45% of the time after the patient leaves the laboratory. A minority of episodes of late tamponade (13%) are associated with recognized coronary artery perforation. Tamponade requires surgical treatment in 39% of patients, is closely associated with MI complicating PCR, and carries a mortality rate of 42%.82

The covered stent that was developed for, but failed to reduce the risk of, saphenous vein graft restenosis83 presently is used as a rescue device after coronary artery perforation or for the treatment of coronary or saphenous vein graft aneurysms (Fig. 20-7).84 When a covered stent is used for the treatment of coronary artery perforation, the need for emergency surgery is reduced, and the outcome of coronary artery perforation is improved. A small number of patients, however, still will require surgery.85

Toxicity

Acute renal failure after exposure to radiocontrast material, or radiocontrast nephropathy (RCN), is poorly understood. Its occurrence is a function of age, congestive heart failure, hemodynamic instability, diabetes mellitus, preexisting renal insufficiency, anemia, peripheral vascular disease, and the amount of contrast material administered.86–88 The incidence of RCN after coronary angiography is 5 to 6%, with the nadir of renal function occurring 3 to 5 days after the procedure.89 Even a transient decline in renal function leads to an increased risk of ischemic cardiovascular events during follow-up, and renal failure requiring hemodialysis is seen in about 10% of patients with RCN, increasing both short- and long-term mortality.86,87,90

The only methods for reducing the risk of RCN are the use of iso-osmolar contrast, volume expansion, and, perhaps, acetylcysteine administration. Iodixanol, an iso-osmolar nonionic contrast agent, reduced the incidence of RCN after noncardiac angiography.91 Giving four oral doses (600 mg each of N-acetylcysteine; two doses on the day before and two on the day of the procedure) has met with varied outcomes in several studies but appears to be beneficial.92,93 Administering crystalloid solution in volumes sufficient to maintain brisk urine flow, perhaps aided by alkalinization of urine pH, is the most effective intervention to ensure an adequate volume state.94

Acute Coronary Syndromes (ACS)

Successful PTCA and stent implantation (in most instances) within the first 6 hours of ST-segment elevation MI is at least as effective as, and perhaps more effective than, thrombolytic agents in limiting myocardial damage and improving in-hospital survival.95–97 The routine use of coronary stents for acute MI is associated with a restenosis rate of 17% and a 6-month event-free survival of 83 to 95%98–101 The use of DESs reduces the risk of any adverse event from 17 to 9.4% at 300 days.49 After failed attempts at thrombolysis or for patients with cardiogenic shock who received thrombolysis, stent revascularization increases myocardial salvage and reduces the risk of death, heart failure, or reinfarction.102–105

Previous Coronary Artery Bypass

Stent implantation with the assistance of embolic protection devices is the preferred method for percutaneous treatment of saphenous vein grafts.62,103 The use of distal embolic protection reduces the risk of periprocedural MI from 14.7 to 8.6%.62 Unfortunately, diseased grafts have a high probability of developing new lesions, reducing long-term event-free survival. After stent implantation, overall survival is 79% at 4 years, but survival free of MI or another revascularization procedure is only 29%.106–110 Drug-eluting stents reduce the risk of restenosis after saphenous vein graft PCR but will not affect the likelihood of progression elsewhere in the diseased graft.47

The future of interventional cardiology lies in reducing procedural risk and extending treatment durability. For many patients, the goal of providing durable treatment success has been very nearly achieved with the introduction of DESs, an approach that has yet to be fully explored. However, a DES does not reduce procedural risk, and problems remain for patients with diffuse atherosclerosis, diabetes mellitus, bifurcation lesions, and acute coronary syndromes. The suggestion that poor outcomes may be expected after PCI and that surgical revascularization may be more appropriate have been recognized and can be measured objectively using the SYNTAX score.111 Its adoption, utilization, and regular refinement will be difficult but necessary in order to match the right patient to the right treatment.112

Ironically, the goal of reducing procedural risk has been pursued most effectively for saphenous vein graft revascularization with the development of distal embolic protection devices. However, for native-vessel interventions, particularly during acute coronary syndromes, further advances likely will be pharmacologic rather than technical. Drawing on observations made in ischemic preconditioning, modification of myocardial energy metabolism with drugs, such as ranolazine, perhexiline maleate, and others, represents a means of improving the heart's ability to withstand ischemia, thus temporizing the impact of temporary vascular occlusion and macroembolization or microembolization.113–115 In addition, inhibitors of the protein kinase family of enzymes, central to intracellular signaling, also may improve the heart's ability to withstand ischemia and reduce the severity of reperfusion injury.

Local drug delivery has met with great success in reducing the problem of restenosis. However, there are numerous methods of modifying the physiology driving intimal hyperplasia after stent implantation. New DES platforms offer the alternative of eluting multiple drugs at different rates, reducing the need for systemic medical therapy, such as prolonged dual antiplatelet therapy. In addition, complex molecules that can be absorbed by the body are being developed as stent platforms. The use of such a stent, one that delivers antithrombotic and antiproliferative drug therapy, could conceivably allow PCR protection from acute closure, recoil, thrombosis, and restenosis, without contributing to vessel rigidity that increases the difficulty of subsequent procedures.

A growing number of patients who are surviving longer with severe multivessel coronary artery disease remain hampered by severe angina pectoris. In many instances, years of slow, steady disease progression have left extensive collateral vessels that prevent infarction and the near or complete loss of major branch vessels. These patients currently have no option for percutaneous or surgical revascularization. For this population, the use of stem cells, perhaps the most efficient producers of cytokines and growth factors in their proper sequence, has met with early success. Direct injection of stem cells into regions of ischemic myocardium improves walking time and reduces the frequency of angina attacks.116

1. Percutaneous revascularization is best used as a treatment for unacceptable symptom control in patients who do not have anatomic indications for revascularization for prolonging survival.

2. Stent implantation substantially improves the safety of PCI, and the use of drug-eluting stents reduces the likelihood of long-term treatment failure. However, the use of drug-eluting stents requires that patients be candidates for long-term, dual antiplatelet drug therapy.

3. Measurement of the fractional flow reserve (FFR) is crucial for determining the necessity of PCI. Its routine use for the evaluation of moderate lesions results in a reduced risk of major complications of intervention compared with angiographic analysis alone.

4. When possible, all saphenous vein graft interventions should be performed with distal protection devices in place.

5. In patients who, for clinical reasons, can be treated by percutaneous or surgical means, the SYNTAX score should be used to ensure objective measurement of the most appropriate therapy.

Chrissie Chambers provided editorial support for this chapter.