CHAPTER 29 Percutaneous Catheter-Based Treatment of Coronary and Valvular Heart Disease

Although catheter-based therapy for the management of obstructive vascular disease in humans began with the pioneering work of Dotter and Judkins,¹ the extension and application of catheter-based therapy to the management of obstructive coronary artery disease (CAD) is properly credited to Gruntzig, working in Switzerland, and Myler, working in the United States. The mid-to-late 1970s were a period of intense efforts toward the miniaturization of catheter design along with feasibility studies beginning with a canine model and extending to the operating room setting and, finally, the cardiac catheterization laboratory.²^,³ With Gruntzig’s move from Zurich, Switzerland, to Atlanta, Georgia, in 1980, the technique and technology of what was then termed percutaneous transluminal coronary angioplasty (PTCA) developed rapidly.

First-generation angioplasty balloon catheters were crude (and hazardous) by today’s standards—generally 2 mm in diameter and “guided” into the target vessel by large-bore (9F to 10F) stiff guide catheters. The range of these early PTCA catheters was severely limited by the lack of optimal directional control and the large profile of the balloon catheter itself. Consequently, over the next several decades, the promise of this noninvasive approach to the management of patients with symptomatic coronary heart disease was realized with an explosion in the technology of catheter materials and manufacturing. Without such advances, the indications for this procedure would remain limited to clinically stable patients who are suitable for coronary artery bypass graft (CABG) surgery, and in whom a discrete, proximal, concentric, noncalcified, nonangulated stenosis in a large epicardial vessel was identified as the cause of disease (Fig. 29-1A).⁴

FIGURE 29-1 The “ideal” lesion for percutaneous transluminal coronary angioplasty (PTCA). A, An “ideal” lesion for PTCA is a discrete, concentric, noncalcified stenosis in the proximal portion of the left anterior descending coronary artery (arrow). B, Arterial pressure recordings from the guiding catheter (upper tracing) and distal lumen of the PTCA catheter (lower tracing) in a nonstenotic arterial segment. C, Translesional pressure gradient recording with PTCA catheter distal to stenosis. The gradient represents the hemodynamic severity of the stenosis. D, On balloon deflation, translesional pressure gradient begins to decrease (left-hand side) to control levels noted in B; this indicates improvement in the hemodynamic severity of the stenosis. E, Confirming the hemodynamic results in A, coronary angiogram shows virtual elimination of stenosis (arrow).

The early double-lumen design allowed for distal coronary artery pressure monitoring (Fig. 29-1B through D), enabling immediate assessment of the hemodynamic result of PTCA, and the large-bore guide catheter allowed for the injection of contrast material to assess the result fluoroscopically (Fig. 29-1E). As the popularity of PTCA grew, and the clinical and anatomic spectrum of disease encountered in diagnostic angiography laboratories expanded, it became clear, however, that (1) “lower profile” PTCA catheters would be necessary to treat many stenoses, and (2) improved “manipulability” and “directionality” were mandatory. PTCA catheter systems were modified with quantum leaps in technology—elimination of the double-lumen design (with consequent loss of ability to monitor distal pressure) and the creation of a (re)movable PTCA guidewire (in contrast to the fixed balloon–short wire design of prototypic catheters). These two fundamental changes, along with continued modifications in catheter and guidewire design, allowed for the explosive growth in PTCA procedures over the last 30 years. The development of “niche” devices,⁵^,⁶ each designed for a specific anatomic situation, allowed for broader application in a wider spectrum of lesions and patients. During this explosive growth period in primarily nonballoon catheter technology, the procedure assumed a new name—percutaneous coronary intervention (PCI).

This chapter primarily reviews percutaneous catheter-based treatments of CAD in adults. The emerging application of percutaneous catheter-based management of valvular heart disease is briefly discussed at the end of the chapter.

PROCEDURE

Description and Special Anatomic Considerations

Birfurcation-Type Lesions

When plaque is present at, around, or within the ostium of a significant side-branch (i.e., bifurcation [Fig. 29-2]), the chances of short-term and long-term ischemic complications are increased. There is much debate on the best way to approach these lesions. When the side-branch is small (<1.5 mm in diameter or subtending a small vascular territory), simply stenting over that side-branch is sufficient. In this situation, the chances of possible ischemic complications of displacing plaque into the side-branch, causing acute occlusion, are relatively small, and do not warrant increased procedural complexity and duration. When the side-branch approaches the diameter of the main branch or has a large vascular territory that it supplies, the ischemic complications of such plaque shift become significant. Myriad approaches to catheter-based management of bifurcation lesions have been described,⁷^,⁸ which reflect the anatomic diversity of this category. Despite the use of stents and potent anticoagulant and antiplatelet regimens, however, clinical outcomes in patients with such anatomy remain suboptimal.⁹

FIGURE 29-2 Bifurcation coronary artery lesions. A, Complex bifurcation lesion at the origin of a large diagonal artery. Note disease of native left anterior descending (LAD) artery, disease of diagonal artery, and disease of LAD artery distal to bifurcation (outlined by box). B, Bifurcation lesion in a different patient from A, in whom target lesion is in mid-LAD artery (arrow) after the origin of a diagonal artery. C, After percutaneous transluminal coronary angioplasty of LAD artery, there is plaque shift from the target area into the origin of the aforementioned diagonal artery (arrow). D, Because of occlusive behavior in diagonal artery (arrow), the latter is “treated” as well.

Saphenous Vein Bypass Grafts

With the half-life of saphenous vein bypass grafts generally around 8 to 10 years, the number of post-CABG patients needing intervention continues to grow. Lesions in such older grafts (Fig. 29-3) present difficult issues: The veins themselves are characterized by diffuse fibrointimal hyperplasia even when nonobstructive—the vascular disease process continues to varying degrees, and a complex plaque consisting of platelets, thrombin, fibrin, inflammatory cells, and cholesterol crystals adheres to the endoluminal surface. Debris from large, bulky atherosclerotic plaque during PCI is frequently “liberated” downstream¹⁰; this often results in a “no-flow” phenomenon wherein such embolization results in occlusion of the distal vasculature with dramatic clinical consequences. Subsequently, it was found that the risk of peri-procedural ischemic complications during saphenous vein graft PCI can be reduced by up to 50% with the use of distal protection devices (Fig. 29-4).¹¹

FIGURE 29-3 An 8-year-old aorto–right coronary artery saphenous vein bypass graft. Note irregular borders consistent with endoluminal deposits of atherosclerotic debris and fibrointimal hyperplasia.

FIGURE 29-4 Saphenous vein bypass graft. A, Use of distal protection device during intervention on a saphenous vein bypass graft stenosis (arrow). B, Arrow indicates collection system distal to balloon segment of percutaneous transluminal coronary angioplasty catheter. C, Up arrow indicates distal collecting portion of the catheter (see B), whereas down arrow indicates lesion appearance after percutaneous coronary intervention with stent placement.

Complex Lesions, Angulated Lesions, and Lesions Distal to Proximal Vessel Tortuosity

Complex lesions, angulated lesions, and lesions distal to proximal vessel tortuosity (Figs. 29-5 through 29-7) also characterize “high-risk” anatomic subsets. Although especially true in the PTCA era, negotiation of severe tortuosity and proximal curvatures is still a challenge for even the most “low-profile” devices. Similarly, complex lesions, generally encountered in the setting of acute coronary syndromes, remain unpredictable in their response to PCI.

FIGURE 29-5 Complex lesion in mid-circumflex coronary artery extending proximal and distal to tortuous segment of circumflex artery proper (arrow).

FIGURE 29-6 Complex “lesion on a bend” involving proximal left circumflex artery.

FIGURE 29-7 Complex lesion in circumflex marginal artery (horizontal arrow) distal to a sharp bend in artery (up arrow).

A key to working in tortuous arteries is having proper guide catheter support (i.e., adequate support to enable the PCI instrument to reach, and cross, the distal or postcurvature target lesion). The hazard here is dissection of the proximal vessel by the tensile forces exerted by the guide and, in some instances, propagation of the proximal vessel with complete occlusion. Advances in guidewire technology have vastly improved the ability to deliver various devices into or through excessively angulated arteries. The additional support provided by stiffer wires or wires specifically designed to decrease friction (by moving the balloon catheter or stent away from the arterial wall) has been a major advance in these difficult situations. Perhaps the most important improvements in these situations have been in stent design. Over the past decade, coronary stents have gone from very stiff and bulky catheter designs to designs that provide more flexibility and, consequently, deliverability. Not only are stents easier to pass to the lesion distal to a tortuous segment, but they are now also able to conform to angulated lesions with a minimal loss of radial force (Fig. 29-8).

FIGURE 29-8 Complex coronary artery lesion. A, “Lesion on a bend” in proximal portion of right coronary artery. B, Apparent “straightening” of arterial segment after stent placement.

Chronic Total Occlusions

Chronic total occlusion (Fig. 29-9), one of the last frontiers of interventional cardiology, refers to a native coronary artery (or vein graft) that has been occluded for at least 2 weeks. Such totally occluded vessels are commonly found during diagnostic catheterization. Although they may or may not be associated with a discernible myocardial infarct in the subtended territory, such anatomy still may predispose to symptoms of coronary insufficiency that medical therapy cannot treat adequately. In this setting, an attempt at recanalization is often contemplated.

FIGURE 29-9 Chronic total occlusion of distal circumflex marginal artery. A, Arterial occlusion begins at the horizontal arrow. Down arrow indicates branch filling of the distal vessel via intracoronary collaterals. B, Recanalization of total occlusion in A with stent placement. Arrows indicate same areas as defined in A.

Historically, successful recanalization of a chronic total occlusion was achieved in only 50% to 70% of attempts even with very experienced operators. The difficulty arises from the nature of the lesion itself. The usual process of passing a soft, flexible guidewire distal to the target lesion (to pass balloons and stents) becomes considerably more troublesome with no patent lumen to follow. Until a wire can be passed beyond the obstruction, no other devices can be used to treat the lesion. Often a fibrotic and calcified cap forms on the occluded end of the vessel, which can be very difficult to penetrate. Even when penetration is successful, entry into the distal lumen can be problematic, and dissection of the distal vessel is common. This inability to traverse the occlusion with a guidewire is still the most common mode of failure when treating a chronic total occlusion. The advent of newer “coated,” stiffer, and tapered-tip wires and the use of techniques such as simultaneous bilateral coronary angiography have increased success rates modestly. Other, more innovative (and aggressive) techniques under study are a subject requiring more in-depth discussion.

When a wire is across the occluded segment, there can still be difficulty in getting the catheter into position. Even with immediate procedural success, chronic total occlusions are characterized by higher rates of restenosis compared with similar procedures in initially patent arteries. Currently, the presence of a chronic total occlusion is often the deciding factor in the decision to refer a patient to surgery rather than attempt a PCI, particularly when complete revascularization is desired in the setting of multivessel disease.¹²

Long Lesions and Diffuse Disease

The presence of diffuse disease (i.e., >20 mm in length [Fig. 29-10]) within a vessel was always one of the biggest dilemmas for PCI, and remains one of the largest contributing factors for restenosis. Restenosis rates after PTCA in long lesions can be 80%. Although stenting these lesions was often necessary for more angiographically acceptable immediate results, persistent rates of (in-stent) restenosis of 40% temper enthusiasm for this subset of lesions. The advent of drug-eluting stents has enabled these lesions to be successfully treated with dramatically reduced restenosis rates. These stents have successfully reduced restenosis rates and the need for repeat revascularization in patients with diffuse disease to the 9% to 20% range.¹³

FIGURE 29-10 Long segment (diffuse) coronary artery disease. A, Long, diffusely diseased segment of the left anterior descending artery beginning at top arrow and terminating at bottom arrow. B, Same region of artery as in A after placement of multiple stents.

Left Main Coronary Artery Disease

Traditionally, significant disease of the left main coronary artery (Figs. 29-11 and 29-12) has been one of the firmest indications for CABG surgery.¹⁴ When “protected” by a previous bypass graft to either the left anterior descending artery or the circumflex artery, these procedures can be done with a minimum of risk and high likelihood of success. In the unprotected state, however, the complexity of anatomy (typically a bifurcation or trifurcation) and the amount of myocardium at risk make these procedures high risk for the short-term and mid-term. In the United States, Canada, and most of Europe, left main coronary artery PCI remains a procedure used only for patients who have a prohibitive risk for CABG surgery. In parts of Asia and certain other countries in Eastern Europe and South America, these procedures have continued to be used on a wider basis.¹⁵ The main issues that have continued to limit wider acceptance of this procedure are the ramifications of the complications of in-stent restenosis and stent thrombosis (see later). When ongoing procedural and technologic modifications (e.g., designs to “fit” a bifurcation specifically) are established, PCI extended to this previously contraindicated group may become more frequent.¹⁶

FIGURE 29-11 Left main coronary artery disease. A, High-grade stenosis of the ostium of the left main coronary artery. B, High-grade stenosis of the distal portion of the left main coronary artery.

FIGURE 29-12 Left main coronary artery disease. A, Percutaneous coronary intervention for a stenosis in the body of the left main coronary artery (before intervention). B, A cutting balloon is used to “prepare” the fibrotic lesion for stent placement. C, A bare-metal stent is successfully deployed at the target lesion. D, Satisfactory final angiographic result.

(Courtesy of Raoul Bonan, MD.)

ST Segment Elevation Myocardial Infarction

The most dramatic clinical presentation for a patient with CAD is ST segment elevation myocardial infarction (STEMI). Prompt triage, diagnosis, medical stabilization, and reperfusion are the mainstays of treatment. Considerable effort has been expended in developing and optimizing the care that these patients receive. The goal for successful reperfusion (“door-to-balloon” time) is as quickly as possible, but at least no more than 90 minutes. In settings where a cardiac catheterization laboratory is not immediately available, the choice is clear—prompt thrombolytic therapy should be initiated in patients who are eligible within 30 minutes. These patients should be transferred to a PCI-capable facility for further care, especially if there is evidence of ongoing ischemia, heart failure, significant arrhythmias, or lack of clinical reperfusion.

“Primary” PCI is considered the gold standard for treatment and has been compared with thrombolytic therapy multiple times.¹⁷ Traditionally, the preferred procedural method has been to perform an initial balloon angioplasty followed by stent placement for definitive recanalization. Only when a large thrombus burden was obvious was thrombectomy with either an aspiration or rheolytic device considered necessary (Fig. 29-13). Poor myocardial tissue level perfusion despite the apparently “normal flow” in the epicardial vessel has continued to be a significant problem, however, which has been linked to distal embolization of thrombus, plaque, or both. This problem has led to a resurgence in the use of aspiration or rheolytic thrombectomy devices (Fig. 29-14) as a means of initial reperfusion followed by stenting for definitive recanalization.¹⁸

FIGURE 29-13 Total occlusion of the proximal portion of the left anterior descending artery is found in this patient presenting with an acute ST segment elevation myocardial infarction. Notice the presence of thrombus in the segment of artery immediately proximal to the occlusion (arrow).

FIGURE 29-14 Thrombotic occlusion. A, Total (thrombotic) occlusion in the proximal portion of a saphenous vein bypass graft. Notice the abrupt disappearance of the column of contrast material within the proximal portion of the vessel (arrow). B, Immediately after extraction thrombectomy, prompt restitution of flow is noted in the large vascular bed supplied by this bypass graft.

Stent Thrombosis

Stent thrombosis (Fig. 29-15) is a dramatic event that can occur immediately, acutely (within 24 hours), subacutely (within 30 days), late (within 1 year), or very late (after 1 year). Stent thrombosis can be a devastating event, which frequently manifests with STEMI. Risk factors for early, acute, and subacute stent thrombosis include inadequate (or resistance to) antithrombotic or antiplatelet therapy, untreated dissection at the site of implant, prothrombotic substrate, and premature cessation of dual antiplatelet therapy. The treatment is emergent recatheterization, removal of thrombus with aspiration thrombectomy, or balloon angioplasty. It is also generally recommended to perform intravascular ultrasound to ensure that no mechanical complications, such as undetected dissection, undersized or underdeployed stents, or residual obstructive plaque proximal or distal to the stent, are present. These complications must be dealt with appropriately by ensuring proper expansion, using further stenting, maximizing medical therapy, and ensuring compliance. With the present armamentarium of devices, medications, and adjunctive procedures, stent thrombosis is a rare event (overall risk by 1 year approximately 1%).