Percutaneous Balloon Angioplasty and General Coronary Intervention

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.


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

Table 28.1 Recommended Duration of Dual Antiplatelet Therapy Following Stent Implantation


Bare-metal stent:


For stable coronary artery disease patients, a minimum of 1 mo and ideally up to 12 mo of clopidogrel 75 mg (unless the patient is at increased risk of bleeding, in which case it should be given for a minimum of 2 wk)c .


For acute coronary syndrome, at least 12 mo after PCI. Options include clopidogrel 75 mg daily, prasugrel 10 mg dailya , and ticagrelor 90 mg twice dailyb . If the risk of significant bleeding outweighs the anticipated benefit, earlier discontinuation should be consideredc .


Drug-eluting stents:


For stable coronary artery disease patients, clopidogrel 75 mg daily for 12 mo, if patient not at high risk of bleeding.


For acute coronary syndrome, at least 12 months after PCI. Options include clopidogrel 75 mg daily, prasugrel 10 mg dailya , and ticagrelor 90 mg twice dailyb .

a Prasugrel should not be administered to patients with a prior history of stroke or transient ischemic attack.


Use with aspirin 81 mg daily.


Use of proton pump inhibitors is indicated in patients with a prior history of gastrointestinal bleeding, and reasonable for those at increased risk (e.g., advanced age, concomitant use of warfarin, steroids, NSAIDs, Helicobacter pylori infection).

Continuation of dual antiplatelet therapy beyond 12 months may be considered in a few patients undergoing DES implantation and in patients with left main and bifurcation (2 stent) stenting.

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.


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.

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

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).

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Jun 26, 2016 | Posted by in CARDIOLOGY | Comments Off on Percutaneous Balloon Angioplasty and General Coronary Intervention

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