Percutaneous Balloon Angioplasty and General Coronary Intervention
Abhiram Prasad
David R. Holmes
Dotter and Judkins1 were the first to propose the concept of transluminal angioplasty—enlargement of the lumen of a stenotic vessel by a catheter—technique in 1964. Their technique used a spring-coil guidewire over which a series of progressively larger rigid dilators were advanced to dilate the atherosclerotic arterial stenosis. While the Dotter technique proved effective in peripheral arteries, the need to insert large-caliber rigid dilators through the arterial puncture (and the high shear forces applied by the dilators as they crossed the atherosclerotic lesion) ultimately restricted its clinical application. Gruentzig’s pioneering work in 19742 replaced the rigid dilators with an inflatable nonelastomeric balloon mounted on a comparatively smaller catheter shaft which could be introduced percutaneously, advanced across a vascular stenosis in its smaller (collapsed) state, and then inflated with sufficient force to enlarge the stenotic lumen. Although others had speculated about the possibility, Gruentzig was the first to refine balloon angioplasty into a usable clinical tool, through a series of experiments in animals, cadavers, peripheral arteries, and the coronary arteries of patients undergoing bypass surgery. This culminated in the first percutaneous transluminal coronary angioplasty (PTCA) of a stenotic coronary artery in a conscious human (September 16, 1977).3
Balloon angioplasty remained the only catheter-based revascularization technique in widespread use until the mid-1990s, when other modalities including atherectomy and stents (see Chapters 29 and 31) were introduced. Accordingly, the technique is now more commonly referred to as percutaneous coronary intervention (PCI). This chapter will review the basic equipment, techniques, and results of coronary angioplasty as a historical and conceptual foundation for the entire field of catheter-based PCI.
HISTORY
Gruentzig’s new technique of balloon angioplasty was initially met with a great deal of skepticism by many cardiologists, but a small group around the world recognized its great potential.4 In 1979, these early adopters met to form a registry of all coronary angioplasty cases worldwide under the sponsorship
of the National Heart, Lung, and Blood Institute (NHLBI) which had enrolled 3,000 cases by 1981. Over time, progressive improvements in equipment and technique have produced dramatic growth in PTCA and transformed it into the dominant form of coronary revascularization (Figure 28.1). In 2009, approximately 596,000 PCI (in-patient) procedures were performed in the United States5; also it is one of the most common procedures used worldwide.
of the National Heart, Lung, and Blood Institute (NHLBI) which had enrolled 3,000 cases by 1981. Over time, progressive improvements in equipment and technique have produced dramatic growth in PTCA and transformed it into the dominant form of coronary revascularization (Figure 28.1). In 2009, approximately 596,000 PCI (in-patient) procedures were performed in the United States5; also it is one of the most common procedures used worldwide.
Over the past 15 years or so, the role of balloon dilation has become much less prominent as a stand-alone treatment. In current practice, it serves predominantly as an adjunctive therapy for preparing (i.e., predilating) or optimizing (i.e., postdilating) stent placement. Despite the fact that PCI is being performed in increasingly more complex lesions and patients, the advent of the stents and other new interventional devices, as well as adjunctive antithrombotic pharmacology (see Chapter 5), has improved the procedural success rate of PCI to approximately 95%, the procedural mortality to approximately 1%, and the emergency bypass rate to <0.5% among an unselected cohort.6
EQUIPMENT
A coronary angioplasty system consists of three basic components (Figure 28.2): (a) a guiding catheter, which provides stable access to the coronary ostium, a route for contrast administration, and a conduit for the advancement of the equipment; (b) a guidewire that can be passed through the guiding catheter, across the target lesion into the distal coronary vasculature to provide a rail over which therapeutic devices can be advanced; and (c) a balloon dilatation catheter filled with contrast medium.
Guiding Catheters
The original guiding catheters were thick-walled 10F- or 11F-outer diameter tubular structures that had small lumens, minimal torque control, and traumatic edges. In contrast, current guiding catheter designs more closely emulate the performance of diagnostic coronary angiographic catheters. To allow passage of therapeutic instruments, however, guiding catheters must have a lumen diameter at least twice that of a typical diagnostic catheter (e.g., 0.076 inch [2 mm] versus 0.038 inch [1 mm]). To achieve this lumen in a catheter of outer diameter as small as 6F, the catheter walls must be very thin (<0.12 mm, or 0.005 inch). Yet the catheter must still incorporate a Teflon liner to reduce friction, metal or plastic braid to transmit torque and provide sufficient stiffness to offer backup support during device advancement, and a smooth outer coating to resist thrombus formation. The complexity of this design goal requires use of special materials the properties of which are typically varied along the length of the catheter to optimize the balance between support and flexibility at each point. Most guiding catheters now also include a very soft material in the most distal 2 mm of the catheter to reduce the chance of vessel trauma during engagement of the nontapered tip.
Guiding catheters are available in virtually all of the conventional Judkins and Amplatz curves, as well as in a wide range of custom shapes (extra backup (XB), hockey stick, multipurpose, Voda, etc.) designed to ease engagement or provide better support during balloon advancement. As thinwall technology has improved and balloon shaft diameters have decreased, the size of the guiding catheters needed to perform PCI has fallen progressively. In the 1980s and 1990s, 9F and 8F/7F guiding catheters predominated, respectively. Although larger guiding catheters are sometimes still needed for rotational atherectomy, or treatment of bifurcation lesions (7F for kissing balloons and 8F for two stents) or chronic total occlusions, most procedures in current practice can be completed through 6F guiding catheters. Also available are 5F guiding catheters, but they offer no major advantage and are not routinely used.
To function adequately, the guiding catheter must be able to selectively engage the ostium. This requires the selection of an appropriate catheter shape and the ability to manipulate the catheter under fluoroscopic guidance (see Chapter 15). Engagement of the desired vessel, however, should not interfere with arterial inflow. This is routinely possible in the left coronary artery, but damping of the guiding catheter pressure when the right coronary artery ostium is engaged was once a common and vexing problem. This has been overcome by the smaller-diameter (e.g., 6F) guiding catheters and by the introduction of guiding catheters equipped with side holes that allow ongoing perfusion despite wedged engagement. Since the guiding catheter is also used to deliver small boluses of contrast medium into the target vessel (as needed to visualize vascular side branches and the target lesion for angioplasty), contrast flow out of such side holes may increase the total contrast volume used during a procedure. Also, use of catheters with side holes may provide a false sense of security by showing a normal pressure tracing in the face of reduced coronary perfusion. For these reasons, their use should be minimized.
A second important function of the guiding catheter is to provide adequate support for advancement of interventional devices across the target stenosis. This support is derived from the intrinsic stiffness of the guiding catheter, the shape that allows it to buttress against the opposite aortic wall, and deep engagement of the guiding catheter into the coronary ostium (Figure 28.3). While deep engagement of the guiding catheter is sometimes required in challenging cases, it is also well-recognized as a potential cause of complications (e.g., ostial or proximal coronary dissection). This complication has become far less frequent with incorporation of an atraumatic tip on most guiding catheters and the performance of deep engagement only by relying on coaxial advancement over the balloon catheter. After a deeply engaged guiding catheter has been used to position a dilatation balloon or other device across the lesion, it is important to then withdraw the guiding
catheter back to avoid its migration into an even deeper position as the device is withdrawn. In this sense, the ability to actively use the guiding catheter constitutes one of the important skills required for effective management of the overall angioplasty equipment system.
catheter back to avoid its migration into an even deeper position as the device is withdrawn. In this sense, the ability to actively use the guiding catheter constitutes one of the important skills required for effective management of the overall angioplasty equipment system.
 Figure 28.1 Trends in cardiovascular procedures, United States: 1979-2009. PCI indicates percutaneous coronary intervention. Note: Inpatient procedures only. Source: National Hospital Discharge Survey, National Center for Health Statistics, and National Heart, Lung, and Blood Institute. (Roger et al. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation 2012;125:e12-e230.) |
Guidewires
The original dilatation balloon designed by Gruentzig had a short fixed segment of guidewire (spring coil) attached to its tip to lead the balloon in the vessel lumen and help avoid subintimal passage as the catheter was advanced across the stenosis (see Figure 28.2). These devices provided the operator no control over whether the catheter followed the desired path or was diverted into one or more side branches proximal to the lesion, because neither the shape nor the orientation of the leading wire could be modified. In the early 1980s, Simpson designed a movable guidewire system in which a 0.018 inch Teflon-coated wire extended and moved freely through a central lumen within a coaxial dilatation catheter.7 If this guidewire selected the desired vessel, it was advanced until it crossed the target lesion. If the guidewire instead selected a more proximal side branch, the balloon catheter was advanced to a point just before the side branch and the wire was withdrawn and reshaped in an effort to choose the desired path beyond. By a series of such iterative advancements of wire and dilatation catheter, many lesions could be crossed by the guidewire and then by the dilatation catheter. In 1983, this concept was advanced further with the introduction of the first steerable guidewires, the rotational orientation of which could be controlled precisely using a “torquer” (pin vise) attached to the proximal end of the wire.
In contrast to crude early guidewires, modern guidewires are designed to combine tip softness, trackability around curves, radiographic visibility, and precise torque control, which together allow the guidewire to be steered past vascular side branches and through tortuous or stenotic segments. With these refinements, crossing a subtotal lesion with the guidewire has become a task that takes seconds rather than minutes to hours, opening up all portions of the epicardial
coronary circulation to a variety of interventional devices. The basic guidewire consists of a solid core (stainless steel or superelastic nitinol) that is ground to a progressive taper in its distal portion. This taper helps retain torque control when the wire is steered around the series of bends located in the guiding catheter and proximal coronary anatomy and allows the stiffer proximal portions of the wire to follow the soft tip into side branches. This core is generally covered by a spring
coil, and a coating (e.g., Teflon, Silicone) is generally applied to the body of the wire. Radiopaque platinum is often applied to the distal 3 to 25 cm. A family of hydrophilic polymer covered tip guidewires are also available to aid in crossing vessels with extreme tortuosity, calcification, side branches through stent struts, and total occlusion. It must be remembered that hydrophilic wires allow reduced tactile feel and are more likely to cause dissections or perforations.
coronary circulation to a variety of interventional devices. The basic guidewire consists of a solid core (stainless steel or superelastic nitinol) that is ground to a progressive taper in its distal portion. This taper helps retain torque control when the wire is steered around the series of bends located in the guiding catheter and proximal coronary anatomy and allows the stiffer proximal portions of the wire to follow the soft tip into side branches. This core is generally covered by a spring
coil, and a coating (e.g., Teflon, Silicone) is generally applied to the body of the wire. Radiopaque platinum is often applied to the distal 3 to 25 cm. A family of hydrophilic polymer covered tip guidewires are also available to aid in crossing vessels with extreme tortuosity, calcification, side branches through stent struts, and total occlusion. It must be remembered that hydrophilic wires allow reduced tactile feel and are more likely to cause dissections or perforations.
 Figure 28.2 Components of the coronary angioplasty system. The original Gruentzig fixed guidewire balloon (A) is compared with the steerable guide wire system (B). Although both are advanced through a guiding catheter positioned in the coronary ostium, neither the wire shape nor its orientation could be changed once the original Gruentzig catheter was introduced, whereas the steerable design allows the guidewire to be advanced, withdrawn, and reshaped, and steered independently of the balloon catheter to select the desired vessel. Once in place in the distal vessel beyond the target lesion, the guidewire serves as a rail over which the angioplasty balloon or other device can be advanced. |
 Figure 28.3 Use of deep guiding catheter engagement to facilitate coronary intervention. Left. Complex lesion in the right coronary artery including aneurysm (dark arrow) and diffuse distal disease (open curved arrow). Center. Left Amplatz guiding catheter (AL-1) is deeply engaged to provide optimal support for stent placement. Right. After stent placement, the vessel is widely patent, but replacement of the Amplatz catheter with a conventional right Judkins catheter (JR4) shows how effective the Amplatz has been in straightening out a severe upward bend (shepherd’s hook) in the proximal right coronary artery. Although progressive improvement in device profile and trackability has made such deep engagement less necessary, the technique is still of great value in selected cases. Deep seating of the guiding catheter needs to be done with great care and by coaxial advancement of the guiding catheter over a balloon catheter to avoid injuring the proximal coronary artery. |
There is substantial choice of tip stiffness, driven by the way the tapered core wire is attached to the outer coil at the wire tip. In soft wires, the tapered core is generally welded to the coil via a flattened intermediary shaping ribbon that allows the operator to kink or bend the tip of the wire into a shape that is appropriate for navigating the vessel features it must pass while maintaining the required level of atraumatic softness. Even with soft “work horse” wires, it is still important to heed the advice of Dotter and Judkins1 that “the guidewire is passed across the atheromatous block more by the application of judgment than of force.” Wires with preshaped tips are generally used for the majority of cases in contemporary practice, but the tips may be manually shaped, particularly to meet the challenges of anatomic navigation. Longer primary tips or a secondary bend are used for large-diameter arteries and for entering tortuous segments. Short and lessangulated tips are best suited for entering diffusely diseased and chronically occluded arteries.
When larger probing force is required (e.g., for crossing a chronic total occlusion), stiffer tip designs are available. These “core-to-tip” guidewires are often graded by the force that the straight guidewire tip can apply to a strain gauge from a distance of 1 cm. Wires are available with force increments of 3, 4.5, 6, 9, and 12 g in the United States, though wires with even higher tip stiffness are available in other countries. The core-to-tip design also provides better torque control. Use of these stiff-tip guidewires requires a high degree of skill and feel to avoid unintentional vessel injury (dissection or perforation), and in general, less experienced operators are well advised to start with softer guidewires and work up to the stiffer wires progressively.
Independent of the tip stiffness, advancing certain devices around bends may take more shaft support from the guidewire. This is provided by extra-support wires, which have a thicker and firmer inner core. Alternatively, some operators prefer to place a second guidewire across the lesion in parallel (a “buddy” wire) to straighten vessel bends and facilitate device passage. With the wide variety of choices in 0.014 inch guidewires, it is currently rare to use larger-diameter guidewires in coronary work, although wires of 0.016 and 0.018 inch were previously used for this purpose (requiring, of course, the use of matching devices with larger internal lumen diameters). Guidewires with a diameter of <0.014 inch offer little advantage except with certain devices such as the 0.009 inch Rotablator wire (see Chapter 29), but some specialty chronic total occlusion guidewires have a tapered tip (0.014 inch to 0.009-0.012 inch) to help penetrate the plaque and find microchannels.
Standard coronary guidewires are approximately 190 cm long, that is, some 50 cm longer than the average balloon
catheter shaft. This allows the wire to be advanced across the lesion while the balloon catheter remains in the guiding catheter, but does not generally offer sufficient length for exchange of one “over-the-wire” (OTW) device for another. Most guidewires are therefore also available in a 300 cm exchange length, or are extendable to that length by attachment of an extension. Such wires can be passed through the guiding catheter and across the target lesion and remain in place as a series of OTW devices (balloons, rotational atherectomy burrs, stents) are delivered or removed without the need for recrossing the lesion.8 OTW devices have largely been replaced by rapid-exchange (Rx) or monorail balloon catheters and stent delivery systems compatible with shorter guidewires.
catheter shaft. This allows the wire to be advanced across the lesion while the balloon catheter remains in the guiding catheter, but does not generally offer sufficient length for exchange of one “over-the-wire” (OTW) device for another. Most guidewires are therefore also available in a 300 cm exchange length, or are extendable to that length by attachment of an extension. Such wires can be passed through the guiding catheter and across the target lesion and remain in place as a series of OTW devices (balloons, rotational atherectomy burrs, stents) are delivered or removed without the need for recrossing the lesion.8 OTW devices have largely been replaced by rapid-exchange (Rx) or monorail balloon catheters and stent delivery systems compatible with shorter guidewires.
Dilatation Catheters
The dilatation catheters for coronary angioplasty have undergone radical evolution since 1977. As described above, the original Gruentzig catheters were designed with a short segment of guidewire permanently affixed to the catheter tip to decrease the risk of subintimal passage during advancement down the coronary tree. The shaft of these catheters had two lumens—one for inflation and deflation of the balloon and one for distal pressure measurement and/or contrast injection. This reflected the initial reliance on monitoring trans-stenotic (i.e., aortic root to distal coronary) pressure gradient as a way of assessing lesion severity, since it was very difficult to perform adequate contrast injections through small-lumen guiding catheters around the large (4.3F, 1.3 mm) shafts of early balloon catheters. In contrast, contemporary catheters are delivered over independently movable and/or steerable guidewires (see Figure 28.2). The central lumen of such dilatation catheters must have a sufficient caliber to allow free movement of the guidewire, but are no longer used for either pressure measurement or contrast injection. However, it is of interest that the measurement of trans-stenotic pressure gradients to evaluate the significance and completeness of correction of coronary stenoses has evolved into pressure measurement guidewires (see “Fractional Flow Reserve,” Chapter 24).
An important characteristic of the dilatation catheter is the diameter of the smallest opening through which the deflated balloon can be passed (its profile). The original Gruentzig catheters had a 0.060 inch (1.5 mm) profile, but current dilatation catheters have profiles as small as 0.020 inch (0.5 mm). To preserve the best balloon profile, a “negative” or “aspiration” preparation should be performed in which a contrast-filled 20 mL syringe is attached to the balloon inflation hub, the plunger is pulled back to apply a vacuum, and gently released to allow the balloon to draw in a small volume of dilute (1:2 dilution with saline) contrast. The crossing profile increases significantly after a balloon is used, and this may be relevant when one attempts to reuse a previously inflated balloon to cross a second lesion and finds that the secondary (or rewrap) profile is far less satisfactory than the primary (prior to inflation) profile.
Balloon angioplasty catheters are available either as OTW catheters in which the guidewire runs through a central lumen in the shaft throughout its entire length or as monorail Rx catheters in which the wire is contained within the balloon shaft only over its distal 25 cm and then runs outside the balloon shaft more proximally. The latter type of catheters can be exchanged quickly by a single operator over a standard-length (190 cm) guidewire and generally have smaller shaft profiles to allow better contrast injection or simultaneous placement of two balloons for the treatment of bifurcation lesions. Fixed-wire devices, which consisted of a balloon mounted directly on a steerable wire core (deflated profile of 0.020 inch or 0.5 mm), were widely used in the late 1980s, but are no longer in use today.
Although profile is important, the ability of the balloon to bend so as to advance easily through tortuous vascular segments (trackability) and the presence of sufficient shaft stiffness (pushability) to force it through the stenosis are also important. Delivery of the balloon is also aided by the incorporation of a friction-resistant coating to improve surface lubricity. Specialized balloon catheters include perfusion balloon catheters, which have a series of side holes in the shaft proximal and distal to the balloon segment or a spiral channel within the balloon to allow ongoing antegrade blood flow and thereby mitigate myocardial ischemia during prolonged balloon inflations. In an era when stents provide definitive control of elastic recoil and dissection, however, the use of perfusion balloons has become rare except for controlling hemorrhage from a coronary perforation without producing severe distal myocardial ischemia (see Chapter 4). Some special balloons exploit the concept of focused force angioplasty, in which a wire (Angiosculpt balloon, AngioScore, Fremont, CA) or microblades on the balloon surface (cutting balloon, Boston Scientific, Natick, MA) concentrate the delivery of dilating force from the balloon to the lesion to lower stenosis resolution pressure and reduce balloon slippage forward or backward during inflation (the so-called watermelon seeding effect). These technologies have not, however, improved the long-term patency as compared with conventional PTCA,9,10 and the cutting balloon carries a small but real risk of perforation when oversized. These devices have been promoted for use in ostial lesions or in-stent restenosis owing to neointimal proliferation, but there is no definitive evidence that they improve procedural outcomes.
Other than these factors, the most important characteristic of the dilatation catheter is its ability to inflate to a precisely defined diameter despite application of pressures that average 10 to 16 atm. This was not possible with early balloons manufactured from polyvinyl chloride (PVC); their compliance led to balloon oversizing and rupture at pressures as low as 6 atm. More suitable performance can be readily achieved today using balloons manufactured from high-density polyethylene, polyethylene terephthalate (PET), or nylon, despite balloon wall thicknesses as low as 0.0003 to 0.0005 inch (7.62 to 12.7 µm). Based on material and wall thickness, each balloon has an individual compliance characteristic reflecting
the pressure at which the balloon reaches its specified (nominal) diameter and how much that diameter increases as the balloon is inflated to even higher pressures. More compliant balloon materials tend to reach their nominal diameter at 6 atm and then grow by ≤20% above their nominal size (i.e., a 3.0 mm balloon growing to 3.5 mm) at 10 atm. Semicompliant balloon materials such as high-density polyethylene or nylon grow by <10% over this pressure range, whereas truly noncompliant balloon materials such as PET can retain their defined diameter up to 20 atm to allow dilatation of calcific stenoses or full expansion of coronary stents (Figure 28.4).
the pressure at which the balloon reaches its specified (nominal) diameter and how much that diameter increases as the balloon is inflated to even higher pressures. More compliant balloon materials tend to reach their nominal diameter at 6 atm and then grow by ≤20% above their nominal size (i.e., a 3.0 mm balloon growing to 3.5 mm) at 10 atm. Semicompliant balloon materials such as high-density polyethylene or nylon grow by <10% over this pressure range, whereas truly noncompliant balloon materials such as PET can retain their defined diameter up to 20 atm to allow dilatation of calcific stenoses or full expansion of coronary stents (Figure 28.4).
Balloon compliance characteristics must be kept in mind especially when inflating a compliant or semicompliant balloon to pressures above nominal (usually roughly 6 to 10 atm) to avoid overdistending the adjacent normal vessel. Noncompliant balloons are desirable when high pressure inflation is needed (resistant lesions and postdilation of stents) so that the dilating force is applied to treat the stenosis rather than in enlarging the balloon.
Regardless of which balloon type is used, it is important to stay within the stated range of inflation pressures in order to avoid balloon rupture. This pressure range is specified in terms of the rated burst pressure (i.e., an inflation pressure at which the probability of balloon rupture is <0.1%). Taking any balloon catheter above its rated burst pressure (usually 16 to 20 atm) increases the risk of balloon rupture, with the potential for air embolization (if the balloon was incompletely purged), vessel rupture, local dissection, or difficulty in removing the balloon from an incompletely dilated lesion.11 This risk grows further with pressures above the rated burst pressure to which the balloon is inflated, until it reaches 50% risk of rupture when the maximum burst pressure is reached. Instead of relying solely on high balloon inflation pressures, we recommend the use of rotational atherectomy for treating resistant lesions which are invariably associated with severe calcification. An uncommon exception to this rule is stent postdilatation in a calcified or fibrotic lesion that has not been adequately predilated or pretreated with rotational atherectomy before stent placement, and where there is no alternative for achieving full stent expansion.
Various manufacturers currently provide dilatation catheters that meet these design specifications with inflated diameters of 1.25, 1.5, 2.0, 2.5, 3.0, 3.5, and 4.0 mm to match the size of the coronary artery in which the stenosis is located. Larger balloons (i.e., 4.5, 5.0, and 6.0 mm) are occasionally needed for treatment of large right coronary arteries or saphenous vein grafts. Quarter-sized balloons (e.g., 2.25, 2.75, and 3.25 mm) are also available, but that degree of precision probably exceeds the operator’s ability to gauge vessel size, and stocking quarter-sizes tends to unfavorably increase the size of a laboratory’s balloon inventory. The typical lesion requires a predilation balloon that is 12 to 15 mm long, but balloons are also available for shorter (8 mm for dilating or postdilating focal lesions) or longer (20 or 30 mm for dilation of a diffusely diseased segment) diffuse lesions.12 Although most lesions can be dilated effectively with balloon catheters from any of the several manufacturers, subtle differences in performance characteristics can make the difference between success and failure; therefore, each interventional laboratory still needs to stock a variety of balloon types. Although balloon prices were once nearly $700, competition and widespread use have brought current prices down to approximately $150,
giving little incentive for resterilization and reuse, with the risk of infection, prolonged procedure time, and device failures with resterilized products.13,14
giving little incentive for resterilization and reuse, with the risk of infection, prolonged procedure time, and device failures with resterilized products.13,14
 Figure 28.4 Successful dilatation of a rigid calcific lesion (arrows). This rigid lesion (top) in the midleft anterior descending coronary artery of a postbypass patient (note surgical clips) resisted dilatation at 300 lb/in2 (20 atm), but yielded to an inflation pressure of 330 lb/in2 (22 atm; middle two views) with reduction in the stenosis (bottom). Such pressures are obtainable only with high-pressure noncompliant balloons. In current practice, such “nondilatable” lesions would most appropriately be treated by rotational atherectomy (see Chapter 29). |
PROCEDURE
A coronary angioplasty procedure bears a superficial resemblance to diagnostic cardiac catheterization in that catheters are introduced percutaneously under local anesthesia. However, since angioplasty involves selective cannulation of coronary arteries with guidewires and balloon catheters, temporary occlusion of antegrade coronary arterial flow, as well as manipulation of the culprit lesion by balloon inflation and/ or stent deployment, the procedure is significantly more complicated and entails approximately 10-fold higher risk (i.e., 1% versus 0.1%) as compared with a diagnostic catheterization.15 However, the risks of coronary angioplasty vary widely with the baseline clinical condition of the patient, the characteristics of the lesion to be treated, and the techniques used (see “Complications” below and Chapter 4).
When obtaining informed consent, the estimated individual risks together with the potential benefits, alternatives, and goals should be discussed in detail with the patient and family prior to the procedure. To mitigate the very real risks of major complications, angioplasty should be attempted only by experienced personnel and generally only in a setting where full cardiac surgical and anesthesia support is available.16 One exception is the performance of primary PCI for the treatment of acute ST-elevation myocardial infarction (STEMI), where the need for rapid revascularization has led to the allowance of such procedures in approved catheterization laboratories staffed by experienced interventional operators, even when onsite cardiac surgery is not available. An expert consensus document from the Society for Cardiovascular Angiography and Interventions details the requirements for establishing a PCI program without onsite surgical backup.17 The practice of elective angioplasty without onsite surgery, however, remains outside the recommendations of PCI guidelines at this time, though it is performed in some hospitals in the United States and Europe that have appropriate program development using clinical and angiographic criteria for patient selection.16,18
Historically patients were admitted the night before elective angioplasty, but currently elective patients are admitted on the morning of the procedure. Details of patient evaluation, informed consent, and preprocedure laboratory work will thus generally have been completed in a separate outpatient visit or be compressed into a very brief encounter immediately prior to the procedure. This is particularly true for patients who come to catheter-based intervention at the conclusion of what began as a diagnostic catheterization that progressed to coronary intervention (the so-called ad hoc PCI).19 Although a major proportion of PCI is now performed in the ad hoc fashion, consideration of staging is important in case of the following situations: (a) high anticipated procedural risk or technical complexity (e.g., chronic total occlusion) making surgical consultation or additional discussions with the patient and family desirable before proceeding with a nonemergency intervention; (b) Nonavailability of PCI at the diagnostic catheterization facility; and (c) the likelihood of the combined procedure leading to a large volume of contrast being used. Similar considerations apply to the decision to stage a complex multivessel procedure into two or more sessions (e.g., patient tolerance, clinical stability, total contrast load, stability of the initial treatment results), but current techniques generally make staging (between diagnostic and interventional procedures, or between treatment of some lesions and others) an uncommon clinical necessity. Finally, patients should be counseled on the need for and risks of dual antiplatelet therapy before placement of intracoronary stents, especially drug eluting stents, and alternative therapies should be pursued if patients are unwilling or unable to comply with the recommended duration of dual antiplatelet therapy.
Oral intake should be restricted after midnight on the evening prior to the procedure, and the patient should be pretreated with aspirin 325 mg/day to diminish platelet deposition on the disrupted endothelium.20 Patients not on aspirin therapy should be given nonenteric aspirin 325 mg, while those already taking daily aspirin therapy should receive 81 to 325 mg before PCI. In the aspirin-allergic patient requiring an elective PCI, a graded aspirin desensitization protocol21 may be considered prior to the procedure. An oral platelet ADP-receptor antagonist (such as clopidogrel, prasugrel, ticagrelor) should generally be administered prior to the procedure,22 supplemented by intravenous platelet glycoprotein IIb/IIIa receptor antagonists in patients with acute coronary syndromes,23 to reduce the incidence of periprocedural myocardial infarction or repeat emergency revascularization for vessel closure or stent thrombosis. Since aspirin reduces late cardiac mortality in patients with coronary disease, it is generally continued indefinitely after the procedure. Similar data now exist for longer-term clopidogrel treatment, and hence ADP-receptor antagonists may be used as an alternative to aspirin in patients with aspirin allergy.24 Statins appear to have some benefits when pretreatment is initiated from 7 days to just prior to PCI, especially in statin naïve patients. Hence, it is reasonable to administer a high dose of statin before PCI to reduce the risk of periprocedural MI.25 Patients with a past history of an hypersensitivity reaction to contrast media should receive steroid and antihistamine prophylaxis; this prophylaxis is not beneficial in patients with a prior history of allergic reactions to shellfish or seafood.26 Finally, patients should be assessed for risk of contrast-induced acute kidney injury (nephropathy). Important risk factors for contrastinduced acute kidney injury include advanced age, chronic kidney injury, diabetes mellitus, congestive heart failure, and the volume of contrast used during the procedure. The risk may be estimated using a scoring system.27 Adequate hydration and minimizing the volume of contrast administered are
the only interventions demonstrated to reduce the risk of contrast-induced acute kidney injury (see Chapter 4). It is most important to do so in patients with creatinine clearance of <60 mL/minute. There is now good evidence demonstrating that administration of N-acetylcysteine is not beneficial.
the only interventions demonstrated to reduce the risk of contrast-induced acute kidney injury (see Chapter 4). It is most important to do so in patients with creatinine clearance of <60 mL/minute. There is now good evidence demonstrating that administration of N-acetylcysteine is not beneficial.
The 2011 PCI guidelines advocate that a “time-out” is performed before all PCI to verify that the correct patient is having the intended procedure.16 The aim of this process is to improve patient care by collective discussion of the case immediately prior to the procedure. The timeout may be checklist driven or conversational, depending on each laboratory’s established practice.28
PCI is performed either via the femoral or via the radial approach, based on considerations about potential complications related to vascular access, as well as operator and patient preference. The 2011 PCI guidelines state that it is reasonable to use radial artery access to decrease access site complications. However, femoral access remains the most commonly used approach in the United States. Vascular complications via the femoral approach may be minimized by the use of fluoroscopic landmarks or ultrasound guidance. Low punctures are associated with hematomas and other vascular complications while high punctures increase the risk of retroperitoneal hemorrhage. Most catheter-based interventions are performed safely without right heart catheterization, but occasionally venous access is also required for the initiation of ventricular pacing, although placement of a prophylactic pacemaker is seldom needed except in cases of rotational atherectomy of the right coronary artery or rheolytic thrombectomy (see Chapter 29). In addition, there are some high-risk procedures in which measurement of right heart pressures may aid in fluid management.
After placement of the arterial sheath, intravenous antithrombin therapy is initiated (see Chapter 5). The most common agent is still unfractionated heparin (70 U/kg), which may be reduced to 50 U/kg when there is concomitant administration of a platelet glycoprotein IIb/IIIa receptor antagonist. Alternatives include low-molecular weight heparin (e.g., enoxaparin) in patients who have been on such agents preprocedure29 or a direct thrombin antagonist (e.g., bivalirudin [Angiomax, the Medicines Company, Parsippany, NJ]).30,31 If unfractionated heparin is used, it should be noted that there is wide patient-to-patient variability in heparin binding and activity. So, ACT (activated clotting time) should be measured and additional heparin administered as needed to prolong the ACT to 275 to 300 seconds (reduced to 250 seconds if a platelet glycoprotein IIb/IIIa receptor blocker is to be given) before any angioplasty devices are introduced. Additional doses or an infusion of the antithrombotic agent may be required to maintain the ACT at this level throughout the case—ACTs <250 seconds are associated with a marked increase in the incidence of occlusive complications unless an adjunctive IIb/IIIa receptor blocker is used, whereas ACTs >300 to 350 seconds tend to increase the risk of bleeding.32 ACTs may also be used to monitor the effect of direct thrombin inhibitors such as bivalirudin, which have found increasing use during PCI based on more predictable dose-response characteristics than that of heparin, greater efficacy against clotbound thrombin, reduced platelet activation, less bleeding, and lack of cross-reactivity in patients with heparin-induced thrombocytopenia (HIT, Chapter 5). Since low-molecular weight heparin has relatively more activity against factor Xa than against thrombin, it causes less prolongation of the ACT so that specialized anti-Xa assays are required to monitor lowmolecular weight heparin effects.
Baseline angiograms are then obtained of one or both coronary arteries using either a standard diagnostic catheter or the angioplasty guiding catheter. Baseline angiography serves to (a) evaluate any potential changes in angiographic appearance (interval development of total occlusion, thrombus formation) since the previous diagnostic catheterization, (b) permit the selection of the angiographic views that allow optimal visualization of the stenoses, and (c) aid in planning of the detailed interventional strategy. Coronary injections should be repeated after the administration of sublingual or intracoronary nitroglycerin to demonstrate that spasm is not a significant component of the target stenosis and to minimize the occurrence of coronary spasm during the subsequent angioplasty. Occasionally, unnecessary intervention is avoided when the intended target of a catheter-based intervention resolves with nitroglycerin (coronary spasm)! This is more frequent with lesions of the ostium of the RCA. In this setting, at the time of diagnostic angiography catheterinduced spasm may occur. If the patient returns at a later time for intervention, this ostial “stenosis” may prove to have been unrecognized catheter spasm.
The best working views that show the target lesions and the adjacent side branches most clearly and with the least foreshortening are recorded and transferred to the roadmap monitor for reference during the procedure. The approximate reference diameter and length of each target lesion is estimated by comparing it to the diagnostic catheter (generally 5F or 1.65 mm) or selected guiding catheter. Decisions are then made regarding the sequence of lesions to be approached (integrating lesion severity, myocardial territory involved, and noninvasive test data) and the specific interventional approach that will be used. For example, a bifurcation lesion that may require kissing balloon inflations and/or a two-stent approach (see Chapter 31) may warrant use of a guiding catheter that is larger than 6F.
The appropriate guiding catheter is connected to the pressure manifold (see Chapter 15) by way of an extension tube and a rotating hemostatic valve (e.g., Tuohy-Borst valve), and positioned in the appropriate coronary ostium. The hemostatic valve contains an adjustable O-ring that allows introduction and free movement of the PCI devices while maintaining a sufficient seal around the shaft to permit pressure measurement and contrast injection while minimizing blood loss. The angioplasty guidewire is first introduced into the guiding catheter, either through a needlelike guidewire introducer (bare-wire technique for Rx systems) or, less frequently, loaded into an OTW balloon or support catheter,
and then steered across the target lesion. The guidewire is advanced across the lesion with the aid of puffs of contrast material through the guiding catheter as the vessel is imaged fluoroscopically in a projection that shows the desired path free of foreshortening or overlapping side branches. Once the position of the wire tip in the distal vasculature has been confirmed by contrast angiography, the desired angioplasty balloon or other device is selected.
and then steered across the target lesion. The guidewire is advanced across the lesion with the aid of puffs of contrast material through the guiding catheter as the vessel is imaged fluoroscopically in a projection that shows the desired path free of foreshortening or overlapping side branches. Once the position of the wire tip in the distal vasculature has been confirmed by contrast angiography, the desired angioplasty balloon or other device is selected.
Optimal stand-alone angioplasty results are obtained using a balloon with a diameter that closely approximates the diameter of a presumably nondiseased reference segment adjacent to the site being treated (balloon/artery ratio 0.9:1.1).33,34 Slightly larger balloons (approximately 1.1 to 1.2 times the size of the reference lumen) may be used if intravascular ultrasound (see Chapter 25) is used and shows that the outer vessel (external elastic membrane [EEM]) diameter in the reference segment is significantly larger than the reference lumen (diffuse disease without a true normal reference segment). On the other hand, slightly smaller initial balloons are used when it is difficult to estimate the correct reference size of a diffusely diseased or rapidly tapering vessel, when difficulty is anticipated in crossing the lesion, or if the risk of complications must be minimized in a patient who cannot receive a stent. In the era when stenting (especially drug-eluting stenting) has become the definitive treatment, however, it is routine to predilate the target lesion with a balloon that is slightly undersized relative to the reference vessel and roughly the same length as the target lesion (see Chapter 31). Modern low-profile stents can often be delivered without predilation of the target lesion (the so-called direct stenting), but predilation makes delivery and accurate placement of the stent within the lesion easier, facilitates the selection of the correct stent diameter and length (by comparison with the diameter and length of the inflated predilating balloon), and ensures that lesion compliance is sufficient to allow full expansion of the stent without pretreatment by rotational atherectomy (see Chapter 29). Predilation is particularly important if a short stent is used, to avoid “missing” the lesion during stenting if “watermelon seeding” is felt likely.
Once the dilatation catheter has been positioned within the target stenosis, the balloon is inflated progressively using a screw-powered hand-held inflation device equipped with a pressure dial. At low pressures (i.e., 2 to 4 atm), the balloon typically exhibits an hourglass appearance owing to central constriction by the coronary stenosis being treated. In soft lesions, this constriction (or “waist”) may expand gradually as the inflation pressure is increased, allowing the balloon to assume its full cylindrical shape. In more rigid lesions, the constriction may remain prominent until the balloon expands abruptly at a stenosis resolution pressure that may be as high as 20 atm.35 Some operators prefer to increase pressure rapidly until all balloon deformities resolve, but this increases the risk of dissection when a fibrotic or calcified plaque yields suddenly or when the ends of a somewhat compliant balloon grow to excessive diameter on either side of the resistant lesion. If a calcified plaque resists balloon expansion at 10 to 14 atm, one may thus prefer to consider use of a Rotablator (see Chapter 29) rather than inflating the balloon to the very high pressures (≥20 atm, Figure 28.4) that may be required for full dilation.
At the other extreme, elastic (usually eccentric) stenoses may allow full balloon expansion at low pressures but then tend to recoil promptly once the balloon is deflated. This type of lesion was once treated by repeated inflations, cautious use of oversized balloons, or directional atherectomy, but stent implantation is now the routine treatment. Focused force dilation (with a cutting balloon or the Angiosculpt balloon) may also be helpful in dilating the fibrotic or elastic lesion effectively (see below). There is little objective evidence that slower speed of inflation or prolonged (1 minute or more) inflations offer more benefit than offered by the 30-second inflations.36
Whatever inflation strategy is adopted, the response of each lesion to balloon dilation must then be assessed individually so that the dilation protocol can be tailored to achieve the best possible result. The most common way to assess lesion response to balloon dilation is repeat angiography. Complete normalization of the vessel lumen would be the ideal end result of coronary angioplasty, but a typical result of even a successful angioplasty is a 30% residual diameter stenosis (i.e., a 1.9 mm lumen in a 3 mm vessel) with some degree of intimal disruption (reflected as localized haziness, filling defect, or dissection). Although this once created a dilemma about whether to persist with additional balloon inflations (weighed against the risk of creating a vessel dissection), the need to obtain a perfect result with balloon angioplasty is now moot in the stent era—any lesion that can be stented is generally stented. In the current view, the best position for standalone balloon angioplasty is thus in lesions that are poorly suited to stenting owing to vessel size below 2 mm or branch ostial disease where bifurcation stenting is not contemplated.
Given the importance of achieving the best acute angiographic result, and the uncertainty inherent in angiographic assessment of the irregular lumen postangioplasty, a number of other techniques have been used to grade the quality of an angioplasty result. Initially, PTCA operators relied heavily on the trans-stenotic gradient as an index of dilatation adequacy, seeking a postdilation pressure difference of <15 mmHg between the aortic pressure (measured through the guiding catheter) and the distal coronary artery pressure (measured through the tip of the dilatation catheter). In practice, such measurements were complicated by the presence of the dilatation catheter within the stenosis and the small size of the dilatation catheter lumen, which led to abandonment of the gradient measurement by 1988.37 There has been some recent reawakened interest based on the availability of newer solid state pressure-measuring guidewires that can be used to assess the trans-stenotic gradient at baseline flow and during maximal hyperemia38 (see Chapter 24). The goal is to achieve a fractional flow reserve (FFR)—defined as the ratio of distal mean coronary pressure to aortic mean pressure during adenosine-induced hyperemia—of >0.95 in a successful
PCI. Physiologic assessment can also be done using Doppler flow-measuring guidewires to assess the coronary flow reserve (CFR) as an index of baseline lesion significance and a confirmation of adequate dilation. However, this technique is no longer used in PCI owing to the superiority of FFR as index of stenosis severity, which unlike CFR, is generally not impacted by the presence of microvascular dysfunction. Alternatively, intravascular ultrasound (IVUS; see Chapter 25) or optical coherence tomography (OCT) can more accurately measure lumen diameter and cross-sectional area after dilation, and can detect vessel dissection or hematoma more accurately. Although IVUS has provided important mechanistic insights into balloon angioplasty, it is not used in more than 5% to 10% of routine clinical cases because of the added procedural time and expense. In most laboratories, the postdilation angiogram thus remains the gold standard to assess whether or not an adequate result has been obtained.
PCI. Physiologic assessment can also be done using Doppler flow-measuring guidewires to assess the coronary flow reserve (CFR) as an index of baseline lesion significance and a confirmation of adequate dilation. However, this technique is no longer used in PCI owing to the superiority of FFR as index of stenosis severity, which unlike CFR, is generally not impacted by the presence of microvascular dysfunction. Alternatively, intravascular ultrasound (IVUS; see Chapter 25) or optical coherence tomography (OCT) can more accurately measure lumen diameter and cross-sectional area after dilation, and can detect vessel dissection or hematoma more accurately. Although IVUS has provided important mechanistic insights into balloon angioplasty, it is not used in more than 5% to 10% of routine clinical cases because of the added procedural time and expense. In most laboratories, the postdilation angiogram thus remains the gold standard to assess whether or not an adequate result has been obtained.
Once adequate dilatation is deemed to have been achieved, it is common to withdraw the balloon catheter completely from the guiding catheter, leaving the guidewire across the dilated segment to allow observation of the treated vessel for signs of angiographic deterioration. With more predictable interventions such as stenting, however, a single set of postprocedure angiograms in orthogonal views with the guidewire removed is usually sufficient to document a suitable result in the treated lesion and the absence of dissections, branch occlusions, or guidewire perforations in the adjacent portions of the vessel. At that point, other significant lesions may be dilated, if needed, or the procedure may be concluded and the patient transferred to the recovery area.
Radiation safety is an integral component of PCI, and processes to minimize exposure of the patient and staff must be stringently followed39 (see Chapter 2). The informed consent process ought to include a discussion on the potential adverse effects of radiation, particularly for those likely to receive high doses from complex procedures. Following the procedure, the patient’s radiation dose (e.g., cumulative skin dose, fluoroscopy time, number of cine images) should be recorded. It is recommended that, for the management of patients who receive a high procedural radiation dose, each laboratory define a threshold dose above which follow-up protocols are initiated.
POSTPROCEDURE MANAGEMENT
Postprocedure management after PCI has been progressively streamlined.15 It was once common to leave the arterial sheath in place overnight with continued heparin infusion, while perfusing the sheath lumen and monitoring for distal limb ischemia. This practice allowed prompt vascular reaccess should delayed abrupt closure occur.40 With the advent of stenting and glycoprotein IIb/IIIa receptor antagonists, such delayed abrupt closures occur so infrequently that the practice shifted to removal of the sheaths later the same day as soon as the heparin effect wore off (ACT <160 seconds), with no postprocedure heparin infusion.41,42 In fact, now with the wide adoption of femoral puncture site closure devices and radial access, it is common to remove the arterial sheath in the catheterization laboratory at the end of the interventional procedure, despite a fully anticoagulated state.
After sheath removal, the patient typically remains at bed rest for 6 hours and then ambulates before discharge. The time to ambulation is reduced significantly, however, if a femoral closure device has been used. If a glycoprotein IIb/IIIa receptor antagonist is used intraprocedurally, it is commonly infused for approximately 18 hours postprocedure, though there is a trend toward shorter infusions in order to reduce the risk of bleeding.43 Aspirin (81 to 325 mg/day) is continued indefinitely, and patients who have received a stent are given clopidogrel 600 mg (or Prasugrel 60 mg, Ticagrelor 180 mg) as a loading dose (300 mg with 24 hours of fibrinolytics) during or prior to the procedure. If Ticagrelor is used, typically the dose of aspirin is reduced (see Chapter 5). The duration of dual antiplatelet therapy varies depending on type of stent, technical factors (left main or bifurcation stenting), clinical factors (stable versus acute coronary syndrome), and the potential risk of bleeding16,22,24 (Table 28.1; see also Chapter 5). Patients should be counseled on the importance of compliance with dual antiplatelet therapy and that therapy should not be discontinued without consultation with their cardiologist. Proton pump inhibitors should be used in patients with a history of prior gastrointestinal bleeding who require dual antiplatelet therapy, and it is reasonable to prescribe those for patients at increased risk for bleeding. If the risk from bleeding outweighs the potential benefit of the recommended duration of dual antiplatelet therapy, earlier discontinuation is reasonable.16
With a good angiographic result in the treated lesions, marked relief of ischemic symptoms should be expected unless other significant disease has been left untreated. In the patient with significant multivessel disease (see below), it may thus be particularly helpful to measure the FFR across any indeterminate lesion using a pressure wire at the time of the procedure or perform a maximal exercise test in a few weeks after discharge. Earlier (i.e., predischarge) exercise testing was once performed on a routine basis, but has now been abandoned owing to the potential of groin rebleeding, delay of discharge, or the small risk of precipitating thrombotic closure of the dilatation site. Patients may return to full activity within 72 hours, by which time the groin puncture site should have healed sufficiently to allow even brisk physical activity.
Patients should expect to have no or minimal anginal symptoms early after discharge—ongoing anginal symptoms after discharge suggest persistent untreated disease or a poor result at the treatment site. A good initial result, with recurrent symptoms within the first weeks or 1 to 2 months may suggest subacute stent thrombosis, which usually presents as an acute STEMI requiring emergency recatheterization. On the other hand, initial symptomatic relief followed by recurrence
of symptoms between 2 and 6 months suggests restenosis of the dilated segment. (Clinically significant restenosis has been reduced markedly from 30% with PTCA to 15% with baremetal stenting and to <5% with drug-eluting stenting.) When symptoms recur 1 or more years after successful angioplasty, it generally suggests progression of disease at another site.44
of symptoms between 2 and 6 months suggests restenosis of the dilated segment. (Clinically significant restenosis has been reduced markedly from 30% with PTCA to 15% with baremetal stenting and to <5% with drug-eluting stenting.) When symptoms recur 1 or more years after successful angioplasty, it generally suggests progression of disease at another site.44
Table 28.1 Recommended Duration of Dual Antiplatelet Therapy Following Stent Implantation | ||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||
Along with educating the patient and family regarding these possibilities and their proposed management (including additional catheter intervention or bypass surgery, as needed), the acute angioplasty admission should also be viewed as an opportunity to educate about changes in lifestyle (smoking cessation, exercise, weight loss) or drug therapy (for hypertension and/or hyperlipidemia) to reduce the risk for the progression of atherosclerotic disease.45 Current lipid guidelines call for achieving a LDL level of <70 mg/dL in patients with proven coronary artery disease, as would be the case for the post-PCI patient.46 Medically supervised exercise programs (cardiac rehabilitation) should be recommended to patients after PCI, particularly for patients at moderate to high risk. Treadmill exercise testing is reasonable for patients entering a formal cardiac rehabilitation program after PCI, but routine periodic stress testing of asymptomatic patients after PCI without specific clinical indications should not be performed.
MECHANISM OF PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY
According to the original explanation proposed by Dotter and Judkins1 and by Gruentzig et al.,3 the enlargement of the vessel lumen following angioplasty was ascribed to compression of the atheromatous plaque—akin to footprints in the snow. In fact, true plaque compression accounts for a minority of the observed improvement.47 Extrusion of liquid components from the plaque does permit some compression of soft plaques but contributes minimally to improvement in more fibrotic lesions, even when balloon inflation is prolonged to 1 minute. In the absence of significant reduction in plaque volume, most of the luminal improvement following PTCA seems to result from plaque redistribution—more like footprints in wet sand. Some of this takes place by longitudinal displacement of plaque upstream and downstream from the lesion, but maximum improvement in the lumen following balloon angioplasty or stenting results from controlled overstretching of the entire vessel segment by the PTCA balloon. This stretching leads to fracture of the intimal plaque and partial disruption of the media and adventitia, with consequent enlargement of both the lumen and the overall outer diameter of the vessel47 (Figure 28.5).
Although use of a full-sized balloon (balloon/artery ratio of 1:1) should theoretically eliminate all narrowing at the treatment site, the overstretched vessel wall invariably exhibits elastic recoil48,49 following balloon deflation and some degree of local vasospasm.50 These processes typically leave the stretched vessel with a residual stenosis. A typical balloon angioplasty result also shows evidence of localized trauma to more superficial plaque components as an almost universal haziness of the lumen.51 Higher degrees of disruption are reflected by intimal filling defects (Figure 28.6 ), contrast caps outside the vessel lumen, or spiral dissections that may interfere with antegrade blood flow (Figure 28.7). Such local disruption has been seen on IVUS, angioscopy, and histologic examination of postmortem angioplasty specimens, and its extent correlates with the risk of an occlusive complication.52 In contrast, stenting or directional atherectomy reduces or even eliminates this elastic recoil, dissection, and vascular tone, and thereby provides lower (0% to 10% rather than 30%) postprocedural residual stenosis, and a smooth
and uniform lumen by angiography or IVUS, with less chance of acute or delayed closure.
and uniform lumen by angiography or IVUS, with less chance of acute or delayed closure.
 Figure 28.5 Proposed mechanism of angioplasty. A. Deflated balloon positioned across stenosis. B. Inflation of the balloon catheter within the stenotic segment causes cracking of the intimal plaque, stretching of the media and adventitia, and expansion of the outer diameter of the vessel. C. Following balloon deflation, there is partial elastic recoil of the vessel wall, leaving a residual stenosis and local plaque disruption that would be evident as haziness of the lumen contours on angiography. |
Given the amount of vascular injury that takes place during balloon dilation, it is remarkable that dislodgment and clinically evident distal embolization of plaque fragments seem to be infrequent both in experimental studies53 and in most clinical angioplasty procedures. There is increasing evidence, however, that subclinical distal atheroembolization during balloon angioplasty and stent placement occurs frequently. This is most clearly established in patients undergoing dilatation of a saphenous vein bypass graft or patients with large thrombi adherent to the lesion. Distal embolization of large (>1 mm) plaque elements is usually manifest as an abrupt cutoff of flow in the embolized distal vessel.54 In contrast, microembolization of plaque debris or adherent thrombus may contribute to postprocedure chest pain, enzyme
elevation, or the no-reflow phenomenon in which there is dramatic reduction in antegrade flow with manifestations of severe ischemia (chest pain and ST-segment elevation), in the absence of epicardial vessel stenosis, dissection, or macroembolic cutoff.55 No-reflow can usually be improved by distal intracoronary injection of an arterial vasodilator (adenosine 12-60 µg; nitroprusside 100 µg; verapamil 100 µg; diltiazem 250 µg; nicardipine 200 µg—but not nitroglycerin, which is more of an epicardial than arteriolar vasodilator). But such treatment does not prevent periprocedural myocardial infarction. In contrast, the use of a distal embolic protection system in vein graft interventions (see Chapter 29) recovers atheroembolic debris and reduces the incidence of these complications by nearly half. The SAFER trial of vein graft stenting thus showed that such enzyme elevations occurred in 17% of lesions, with evidence of no-reflow in 8% of lesions, which were reduced to 9.7% and 3.3%, respectively, through the use of distal embolic protection.56 Similar benefits have now been seen with distal embolic filter devices,57 and in other vascular beds (carotid). However, they have not been shown to improve outcomes in native coronary arteries, but are selectively used by some interventionists in the presence of a large thrombus burden at the site of the culprit lesion.58
elevation, or the no-reflow phenomenon in which there is dramatic reduction in antegrade flow with manifestations of severe ischemia (chest pain and ST-segment elevation), in the absence of epicardial vessel stenosis, dissection, or macroembolic cutoff.55 No-reflow can usually be improved by distal intracoronary injection of an arterial vasodilator (adenosine 12-60 µg; nitroprusside 100 µg; verapamil 100 µg; diltiazem 250 µg; nicardipine 200 µg—but not nitroglycerin, which is more of an epicardial than arteriolar vasodilator). But such treatment does not prevent periprocedural myocardial infarction. In contrast, the use of a distal embolic protection system in vein graft interventions (see Chapter 29) recovers atheroembolic debris and reduces the incidence of these complications by nearly half. The SAFER trial of vein graft stenting thus showed that such enzyme elevations occurred in 17% of lesions, with evidence of no-reflow in 8% of lesions, which were reduced to 9.7% and 3.3%, respectively, through the use of distal embolic protection.56 Similar benefits have now been seen with distal embolic filter devices,57 and in other vascular beds (carotid). However, they have not been shown to improve outcomes in native coronary arteries, but are selectively used by some interventionists in the presence of a large thrombus burden at the site of the culprit lesion.58
 Figure 28.6 Normal healing of PTCA-related coronary dissection. As compared with the baseline angiogram (A), the immediate post-PTCA angiogram (B) shows enlargement of the left anterior descending (LAD) lumen with two small filling defects typical of an uncomplicated coronary dissection (arrow). Follow-up angiogram 3 months later (C) shows preservation of luminal caliber with complete healing of the localized dissection (arrow). (From Baim DS. Percutaneous transluminal coronary angioplasty. In Braunwald E, ed. Harrison’s Principles of Internal Medicine: Update VI. New York: McGraw-Hill; 1985.) |
 Figure 28.7 Coronary dissection leading to abrupt closure. The appearance of a right coronary stenosis prior to (A) and immediately following (B) coronary angioplasty, with an evident localized dissection. Within 15 minutes following removal of the dilatation catheter, the patient experienced chest pain associated with inferior ST-segment elevation and angiographic evidence of progressive dissection with impeded antegrade flow (C). Standard management in 1980 (when this case was done) consisted of emergency bypass surgery, which was accomplished without complication. Current practice is to attempt to recross the lesion and treat the dissection with angioplasty and stents. (From Baim DS. Percutaneous transluminal angioplasty—analysis of unsuccessful procedures as a guide toward improved results. Cardiovasc Intervent Radiol 1982;5:186.) |
Although it is a theoretical possibility with sufficient local stretching trauma, frank vessel rupture fortunately has turned out to be a rare consequence during conventional balloon angioplasty, barring the use of significantly oversized balloons.59 Vessel perforation is actually more common (approximately 1% incidence) when atherectomy devices are used60 (see Chapter 29), when stents are postdilated at high pressure (>18 atm) with oversized (>1.1:1) balloons, or when stiff or hydrophilic wires are advanced into small distal branches. Local vessel perforation or distal guidewire perforation in a patient treated with a glycoprotein IIb/IIIa antagonist usually constitutes a medical emergency requiring prompt occlusion of the perforation site with a balloon, drainage of hemopericardium if cardiac tamponade is present, and definitive sealing of the perforation site with prolonged balloon inflation, a covered stent, an embolic coil, or emergency surgery60,61 (see Chapters 4 and 44).
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
