Periprocedural complications of percutaneous transluminal coronary angioplasty

Robert C Stoler, MD
Joseph P Carrozza, MD
Donald S Baim, MD
 May 1, 2000

The various forms of therapeutic cardiac catheterization, such as percutaneous transluminal coronary angioplasty (PTCA) and newer techniques, have all of the adverse events associated with other invasive cardiac procedures such as coronary angiography. (See "Complications of diagnostic cardiac catheterization"). In addition, PTCA has unique, primarily coronary complications that occur both in the short-term and, with restenosis, over the long-term.

This card will review most of the periprocedural complications associated with PTCA. Two other major complications, acute vessel closure and restenosis, are discussed separately. (See "Acute vessel closure after percutaneous transluminal coronary angioplasty" and see "Restenosis after percutaneous transluminal coronary angioplasty").

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY ！ The use of larger guiding catheters and sheaths make damage to the proximal coronary artery or peripheral site of insertion more likely. In addition, the advancement of guidewires and catheters into diseased coronary arteries may lead to vessel injury and the routine use of postprocedural heparin is associated with an increase risk of bleeding and vascular complications.

Mortality ！ Mortality rates for balloon angioplasty reported in large series from experienced operators range from 0.5 to 1.7 percent [1,2,3,4], similar to the 1.1 percent reported in the second NHLBI percutaneous transluminal coronary angioplasty registry [5]. In one review of angioplasties performed in 12,232 patients, procedural complications accounted for 54 percent of all post angioplasty deaths while a preexisting acute cardiac condition accounted for 34 percent [6]. The most common mode of death was low output failure (66 percent), while other less common causes were ventricular arrhythmia, stroke, renal failure, bleeding, ventricular rupture, respiratory failure, pulmonary embolism, and infection.

The ACC has recommended that to maintain optimal proficiency for coronary interventions, hospitals should have a volume of at least 400 procedures per year and physicians should be performing greater than or equal 75 procedures per year [7,8]. In addition to the experience of the operator, and the number of procedures performed at the institution, the risk of mortality with PTCA is also associated with a number of clinical and angiographic features (show table 1). Age was the most important correlate of in-hospital mortality in one study of 21,516 patients [9]. Mortality increased from 0.28 percent in those less than 50 years of age to 3.45 percent in patients 80 years or older. In other studies, additional risk factors were whether or not the patient has had a myocardial infarction (MI) (3.8 versus 0.7 percent in those without an infarct) [4] and body mass index (body weight [kg]/height [m2]) with the risk of mortality after PTCA being increased 2.7 to 7.4 fold in patients who are underweight (BMI <25) or overweight (BMI >35) [10].

Contrast media concerns ！ There may also be an increased risk of thrombosis with the use of nonionic as opposed to ionic contrast media. One study randomized 211 patients with an acute MI or unstable angina to receive either nonionic or ionic low osmolar contrast media [11]. Patients who received ionic media were less likely to have decreased blood flow during angioplasty (8.1 versus 17.8 percent), recurrent ischemic episodes requiring repeat catheterization (3.0 versus 11.4 percent), or repeat angioplasty (1.0 versus 5.8 percent). Similar results were seen in the GUSTO IIb trial, which randomized 454 patients with an acute MI undergoing angioplasty to either nonionic or ionic contrast media [12]. Although there was a trend favoring ionic contrast, the differences were not statistically significant after adjusting for imbalances in baseline characteristics [12].

Another study performed intracoronary angioscopy after angioplasty in 30 patients with unstable angina and reported that the use of nonionic contrast medium was associated with significantly more frequent development of angioscopically visible new thrombus (74 versus 33 percent for an ionic contrast medium) [13].

While some feel that this issue remains unresolved, there are two randomized trials involving a total of 3411 patients undergoing elective or urgent PTCA. These reports found no difference in the rate of abrupt closure or clinical outcome (myocardial infarction, need for emergency bypass surgery, or cardiac death) after PTCA with ionic compared to nonionic contrast media [14,15]. However, other less severe complications such as hypersensitivity reactions and adverse drug reactions were more frequent with the ionic contrast medium. At present, we tend to favor the use of nonionic contrast media in patients who are less able to tolerate the potential hemodynamic and electrophysiologic effects of ionic contrast (eg, those with severe left ventricular dysfunction or bradycardia induced by contrast injection).

Chest pain ！ Chest pain within 48 hours after PTCA (with or without stenting) is common and results from abrupt vessel closure, transient coronary spasm, nonocclusive thrombus, side branch occlusion, or distal embolization. In the EPISTENT trial of 2399 patients, the incidence was 11.4 percent and associated ECG changes were seen in 12 percent of these patients [16]. Although the occurrence of chest pain with ECG changes was associated with an increased risk of a cardiac event (death, all myocardial infarction, repeat revascularization) compared to the absence of chest pain (42.4 versus 4.6 percent), the risk of a cardiac event was also increased in those with chest pain who do not have ECG changes (12.7 percent). (See "Natural history of unstable angina" and see "Overview of the management of unstable angina").

Arterial dissection ！ Major complications of balloon angioplasty relate in large part to coronary arterial dissection and abrupt closure. While dissections may result from overly vigorous attempts at guidewire passage, most are due to the "controlled injury" induced by inflation of the dilatation catheter. Dissections are found in up to 50 percent of patients immediately after angioplasty [17]. The occurrence of dissection cannot be predicted by preinterventional analysis of lesion morphology or plaque composition by intracoronary ultrasound [18].

Intimal tears or dissections following PTCA have been arbitrarily divided into types I to III or types A to F (show figure 1) [19,20].

  •  Type A ！ Luminal haziness
  •  Type B ！ Linear dissection
  •  Type C ！ Extraluminal contrast staining
  •  Type D ！ Spiral dissection
  •  Type E ！ Dissection with reduced flow
  •  Type F ！ Dissection with total occlusion

Follow-up angiography of mild dissections as soon as six weeks after the procedure often demonstrates complete healing, although occasional late localized aneurysm formation has been described [17]. In contrast, larger dissections are associated with an increased risk of progression to total occlusion (abrupt closure) of the treated arterial segment [21,22]. In one series of 691 dissections following PTCA, 543 were type B; these patients had a course similar to those without dissections [22]. In comparison, the patients with type C to F dissections had high incidence of acute vessel closure (31 percent), myocardial infarction (13 percent), and emergency CABG (37 percent).

The increased risk of abrupt closure and myocardial infarction associated with a large dissection has lead to the routine use of stenting for any dissection; however a stent may not be necessary for a nonocclusive dissection. (See "Acute vessel closure after percutaneous transluminal coronary angioplasty"). As an example, one study compared the outcome of 45 patients with 49 nonocclusive dissections (type A to D) and good distal flow (TIMI grade 3) who did not received a stent with 60 patients who underwent stenting for a dissection [23]. At six months there were no clinical adverse events in the unstented group and the restenosis rate was lower than those who underwent stenting (12 versus 25 percent). Since the use of stents has increased to 70 to 80 percent of all coronary interventions, it is rare for a patient to leave the catheterization laboratory with a significant coronary dissection.

Acute closure ！ Acute closure occurs in 4 to 9 percent of cases and was historically associated with a ten-fold increase in mortality to about 1 percent [1,2,19,20,21,22]. It is also responsible for two other major complications of angioplasty: nonfatal MI (less than 5 percent), and emergency coronary artery bypass graft. Most cases of abrupt closure occur within minutes of the final balloon inflation, subacute closure may occur up to hours later in 0.5 to 1.0 percent of cases, typically as the heparin anticoagulation wears off [19,21]. (See "Acute vessel closure after percutaneous transluminal coronary angioplasty"). The problem of acute closure and emergency surgery have both decreased substantially in recent years, to less than one-half percent, since most lesions, including all those with a poor mechanical result from another therapy, undergo stent placement; a lesion with a poor result that cannot be stented or which persist after stenting is usually treated with intravenous platelet IIb/IIIa receptor blocking agent. (See "Use of intracoronary stents for acute vessel closure").

Myocardial infarction ！ Transmural myocardial infarction (Q-wave MI) is seen in approximately 1 percent of patients undergoing PTCA, generally due to abrupt closure or loss of a major side branch [25]. When creatine kinase myocardial band (CK-MB) isoenzymes are routinely measured after the procedure, up to 10 percent of patients undergoing uncomplicated PTCA show some elevation consistent with a non-Q wave MI [26]. Some of the CK elevations are due to the "no reflow" phenomenon [27].

The risk of an ischemic complication is most strongly associated with low weight and preprocedural percent stenosis [28,29]. As an example, one study of 2256 patients who underwent preinterventional intracoronary ultrasound found that CK-MB elevation was associated with a greater lesion and reference segment plaque burden, cross sectional area narrowing, lesion arc of calcium, and positive remodeling [29]. Other factors include a history of hypertension, peripheral vascular disease, presence of a side branch, and lesion complexity [28]. (See "Technique and interpretation of intracoronary ultrasonography" and see "Clinical use of intracoronary ultrasonography").

It was initially suggested that CK elevations after angioplasty did not affect survival unless the CK-MB levels were at least two times the upper limit of normal or associated with new ST-T wave abnormalities [30]. In a retrospective analysis of 4664 patients undergoing PTCA or atherectomy, for example, 4 percent of patients had an elevation of creatine kinase (CK) that was at least two times control levels associated with a CK-MB above 4 percent [31]. After a mean follow-up of 36 months, cardiac enzyme elevations between two to five times control were significantly associated with cardiac death (risk ratio 2.19, p<0.0001) and a trend towards increased cardiac hospitalization.

The IMPACT-II trial prospectively obtained serum for CK-MB after angioplasty in 2341 patients [32]. Elevated serum CK-MB was associated with an increased 30 day and six month incidence of the combined endpoint of death, reinfarction, or emergency revascularization; the incidence was directly associated with the degree of elevation above normal, ranging from 3 and 25 percent when CK-MB was normal (which occurred in 76 percent of patients) to 18 and 44 percent when CK-MB was 10 times normal (show figure 2).

IMPACT-II also found that small elevations in CK-MB (between one and three times normal) were associated with an increased risk of short-term adverse outcomes. Similar results were noted in noncontrolled data from a single center [33]. Among 4484 patients with elevations of CK less than twice control, those with a CK-MB of more than 4 percent had a higher incidence of cardiac death and myocardial infarction (show figure 3), and a trend toward an increased need for revascularization and hospitalization [33].

The relationship between periprocedural MI and long-term (three year) survival was prospectively evaluated by the EPIC trial [34]. The risk ratio associated with a one, two, five, and ten fold increase in CK level was 1.47, 1.65, 2,16, and 2.40 respectively; however, the 95 percent confidence intervals for these odds ratios all overlap and are not statistically significant.

Further, the impact of post-procedure CK release on long-term outcome remains controversial, and has been challenged by other randomized trials such as the Balloon versus Optimal Atherectomy Trial (BOAT) [35]. This study randomized 1000 patients to PTCA or directional atherectomy plus adjunctive PTCA [35]. The one year mortality for directional atherectomy was lower (0.6 versus 1.6 percent for PTCA), despite a significantly higher incidence of CK-MB elevation to greater than three times normal in the atherectomy group (16 versus 6 percent). Similar lack of deleterious effect has been reported to three years in the BOAT study. Other reports have observed no differential effect of CK-MB elevation up to five times normal on survival [36]. Nor has, therapy with the glycoprotein IIb/IIIa receptor blockers, which are potent agents for decreasing the incidence of periprocedural CK-MB elevation, caused a significant improvement in late (one to three year) survival, as would be expected if there were a cause-and-effect relationship between CK-MB elevation and late events. It is thus entirely possible that the association between CK-MB elevation and late events observed in some studies relates to the more common elevation of CK-MB in patients undergoing treatment for diffuse coronary disease, with the increase in late events due to the presence of diffuse disease rather than the CK-MB elevation.

Serum troponin T may be a more sensitive marker of myocardial damage after PTCA than CK, as elevated concentrations are seen in as many as 21 percent of cases [37,38]. The clinical significance of these findings is uncertain given the controversy over the prognostic implications of small elevations in serum CK.

A review of over 10,000 patients undergoing percutaneous intervention made the following recommendations [39]:

  •  A preprocedural and postprocedural ECG should be obtained and the routine measurements of CK and CK-MB is recommended, ideally obtained at baseline and 8 to 16 hours after the procedure.

  •  Patients with elevations of threefold or more above the upper limit of normal should be treated as having a myocardial infarction, especially in the presence of a technical complication of the procedure.

  •  The significance of elevations of less than thrice normal are more uncertain, although any evidence of clinical instability should prompt caution in discharge and activity.

Another problem is that 2 to 4 percent of patients treated for a recent MI or for stenosis in a saphenous vein graft will experience intense vasospasm of the distal microcirculation, possibly due to the release of vasoactive substances such as serotonin [30]. This can often be treated successfully with intracoronary calcium channel blockade (diltiazem or verapamil), but prolonged episodes may lead to overt infarction [27].

The other potential cause of an MI after the treatment of saphenous vein graft disease is distal embolization of friable plaque constituents. (See "Indications for percutaneous transluminal coronary angioplasty in the management of stable angina pectoris-I"). The use of embolus containment systems has shown recovery of plaque constituents (cholesterol crystals, foam cells) and marked diminution in the frequency of infarction. This technique is now under investigation in a randomized clinical trial.

  Impact on restenosis ！ Although elevations of CK after PTCA are associated with an increase in mortality, the EPIC study found that patients with elevated CK were less likely to develop restenosis as measured by a decreased need for target vessel revascularization [40]. Late target vessel revascularization was performed in 29.8 percent of patients with no CK elevation, in 24.8 percent of those with CK >3 times normal and in 16.9 percent of patients with elevations >10 times normal. A possible explanation for this is a reduction in angina, the clinical symptom leading to target vessel revascularization, as a result of myocardial necrosis in the territory of restenosis.

Occlusion of branch vessels ！ Occlusion of branch vessels occurs in up to 14 percent of cases [5,25,41] from what has been termed the "snowplow effect". This complication can be avoided at times using simultaneous dilatation of two vessels ("kissing balloon" technique) or directional atherectomy [17]. (See "Indications for percutaneous transluminal coronary angioplasty in the management of stable angina pectoris-I").

Vascular complications ！ Vascular complications make up a significant portion of the morbidity associated with percutaneous coronary interventions and can be seen in up to 3.2 percent of angioplasty cases [42,43,44]. Major hematomas and pseudoaneurysms are most frequent followed by arterial laceration, retroperitoneal hematoma, arteriovenous fistula, arterial occlusion, and local infection with or without sepsis (see below) [42,44]. (See "Complications of diagnostic cardiac catheterization"). Perforation or frank rupture of coronary arteries has also been described [25,41]. Transfusions have been required in up to 13 percent of cases in some series [44].

Variables associated with higher rates of vascular complications include: age over 65 years, arterial sheath size (>7 French), periprocedural heparin or thrombolytic therapy, severe obesity, unstable angina, recurrent ischemia or repeat procedure, low platelet count, presence of peripheral vascular disease, duration of sheath of more than 15 hours, presence of more than two risk factors for coronary artery disease, and use of the intraaortic balloon pump (IABP) [31,42,43].

Vascular access site complications are more frequent when antiplatelet drugs are used. For example, the EPIC trial of 2058 patients reported that minor or major bleeding occurred in 22 percent of patients receiving abciximab compared with 9 percent of placebo patients (p<0.001) [45]. However, the need for vascular surgery was equivalent (1.5 versus 1 percent). The occurrence of a major or minor vascular site hemorrhage prolonged the median hospital stay by two days, while the need for vascular surgery prolonged hospitalization by four days.

The use of a collagen vascular hemostasis device (VasoSeal) is effective for controlling the bleeding at the femoral artery puncture site after diagnostic catheterization or PTCA. Absorbable bovine collagen is incorporated into a delivery device that is placed at the femoral artery puncture site. In one study of 305 patients who underwent PTCA, the device reduced mean hemostasis time (8 versus 19 minutes for manual compression) and mean immobilization time (8 versus 13 hours); over 50 percent of patients could be mobilized by six hours [46].

  Dislodgement of aortic debris ！ The use of stiff, large-bore guiding catheters can result in aortic trauma and the "scraping" of atheromatous debris from the aortic wall, providing a potential source of systemic embolism. One series of 1000 patients found that 51 percent had aortic atheromatous material retrieved from the catheter after back flow of blood; the incidence ranged from 24 to 65 percent depending upon the shape of the catheter [23]. However, there were no associated in-hospital ischemic complications, probably due to sufficient withdrawal of blood containing the debris prior to the injection of contrast.

  Postprocedural heparin ！ Heparin is almost always used during PTCA to reduce the risk of abrupt closure, but administering it after the procedure complicates the ability to achieve hemostasis at the site of arterial access. Several studies have found that the routine use of postprocedural heparin after elective PTCA or PTCA for unstable angina was unnecessary and increased the risk of bleeding and vascular injury, prolonged the hospital stay, and increased cost [47,48]; its omission reduced the incidence of bleeding and length of hospitalization without increasing the incidence of in-hospital or one month ischemic events [48].

  Use of low molecular weight heparin ！ Low molecular weight heparin has a lower affinity for plasma proteins, a greater bioavailability, and a longer half-life than unfractionated heparin; it also possesses a more predictable dose response, which eliminates the need to monitor for anticoagulant effect. (See "New anticoagulants" and see "Clinical use of heparin and low molecular weight heparin"). As an example, one study randomized 60 patients to intravenous enoxaparin (1 mg/kg bolus dose) or unfractionated heparin (to an activated clotting time of 300 second) at the time of catheterization [49]. The antithrombotic properties of the two drugs were comparable and there was no difference in PTCA success rates, in-hospital ischemia, bleeding, or vascular complications.

Infection ！ Although PTCA is performed under sterile conditions, bacteremia and sepsis can occur. In one study of 4217 PTCAs in 3473 patients, the incidence of bacteremia was 0.64 percent and the most common organisms were staphylococcus aureus, coagulase-negative staphylococcus, and group B streptococcus [50]. Septic complications (femoral artery mycotic aneurysm, arthritis, and thrombosis) occurred in 0.24 percent. Risk factors for PTCA related bacteremia were duration of the procedure, number of catheterizations at the same access site, difficult vascular access, and arterial sheath in place for more than one day.

Myocardial stunning ！ Short periods of myocardial ischemia induced by PTCA, which are too brief to cause myocardial necrosis, may be followed by long-lasting periods of impaired contractile function, a phenomenon known as myocardial stunning. In one series of 50 patients monitored by transesophageal echocardiography during PTCA and stenting, significant myocardial contractile dysfunction in previously ischemic and nonischemic myocardium occurred 15 minutes after successful dilatation [51]. This was associated with a significant reduction in coronary artery blood flow; both the vasoconstriction and left ventricular dysfunction were counteracted by the administration of alpha-adrenergic blockers.

Increased risk in patients with peripheral vascular disease ！ Patients with peripheral vascular disease (PVD) appear to be at an increased risk for periprocedural complications after PTCA. This was illustrated by data from the BARI trial, which compared the outcome of 550 patients with PVD to that of 1770 patients without PVD [52]. There were no differences in coronary anatomy or PTCA success rates between the two groups; however, patients with PVD had a higher incidence of a major complication (death, MI, stroke, coma, or emergency revascularization) after PTCA (11.7 versus 7.8 percent for those without PVD), even after controlling for baseline differences.

Increased risk associated with signs of inflammation ！ Preprocedural activation of inflammatory cells may play a role in the modulation of vessel wall response to balloon injury; evidence suggests that acute phase reactants and proinflammatory cytokines promote leukocyte and endothelial smooth muscle activation, resulting in an increase in procoagulant activity, metalloproteinase release and neointimal proliferation. C-reactive protein (CRP) is an easily measurable acute phase reactant, synthesized in response to proinflammatory cytokines. (See "Acute phase proteins"). One study of 121 patients with stable or unstable angina found that the preprocedural level of CRP was a powerful predictor of adverse events after PTCA [53]. Intraprocedural and in-hospital complications were more frequent in patients with high serum levels (>0.3 mg/dL) of CRP (22 versus 0 percent for normal CRP levels). After a one year follow-up, clinical restenosis developed more frequently in those with high serum levels of CRP (63 versus 27 percent). (See "Restenosis after percutaneous transluminal coronary angioplasty").

Timing of adverse events ！ The timing of adverse events after a percutaneous coronary intervention can impact on the duration and intensity of postprocedural care and monitoring. This was evaluated by the IMPACT-II trial, which randomized 4010 patients to eptifibatide or placebo during an intervention [54]. Ten percent of patients experienced an adverse event (death, myocardial infarction, repeat nonelective intervention, nonelective bypass surgery, or stenting for abrupt closure), and 66 percent of these events occurred within six hours of the intervention. By nine hours, there was no increased risk of an event. Independent predictors of an event within six hours were dissection, preprocedural and postprocedural coronary blood flow, side-branch occlusion, use of a thrombolytic agent during the procedure, previous bypass surgery, unstable angina, and hyperlipidemia.

PROPHYLACTIC USE OF INTRAAORTIC BALLOON COUNTERPULSATION ！ Intraaortic balloon counterpulsation (IABP) has been used in high risk or complicated PTCA, including patients with cardiogenic shock, and its use improves 30 day survival. (See "Intraaortic balloon pump counterpulsation"). Its role for preventing periprocedural complications associated with primary PTCA as treatment for an acute myocardial infarction was evaluated in a study of 1490 patients [55]. IABP used before PTCA reduced the incidence of periprocedural events (ventricular fibrillation or tachycardia, cardiopulmonary arrest, or prolonged hypotension requiring support) in patients with cardiogenic shock (15 versus 35 percent for those not treated with an IABP) and in those with congestive heart failure or low ejection fraction (0 versus 15 percent) [55]. The use of an IABP was a significant independent predictor or freedom from catheterization laboratory events (odd ratio 0.48), suggesting that it may have a role as prophylactic therapy for infarction patients with poor left ventricular function.

EMERGENCY CORONARY BYPASS GRAFTING FOR FAILED PTCA ！ Improvement in catheter design and the use of stents have reduced the incidence of emergency bypass surgery after failed PTCA to less than 1 percent [4,56,57]. In one study of 21,519 patients, the need for emergency bypass surgery was lower in patients over 70 years of age than in younger patients [9]. The operative mortality in patients in whom PTCA has failed remains high, approaching 14 percent in one series of 117 patients [58]. Patients who have had a myocardial infarction are also increased risk [4]. An ACC/AHA Task Force has published guidelines for the use of CABG after failed PTCA (show table 2) [59].

Stenting prior to bypass surgery ！ Although stenting has significantly reduced the need for emergency bypass surgery, a small percentage of patients still require bypass surgery after stenting because of persistent coronary occlusion or dissection resulting in ischemia. However, stenting has a favorable impact on the outcome of surgery. As an example, one nonrandomized study of 60 patients who did or did not receive a stent found that stenting reduced the incidence of perioperative myocardial infarction (19 versus 50 percent without stenting) and mortality (0 versus 17.6 percent) [60].

1. Fischman, DL, Leon, MB, Baim, DS, et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994; 331:496.
2. Serruys, PW, De Jaegere, P, Kiemeneij, F, et al. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994; 331:489.
3. Topol, EJ, Leya, F, Pinkerton, CA, et al for the CAVEAT Study Group. A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease. N Engl J Med 1993; 329:221.
4. Maynard, C, Chapko, MK, Every, NR, et al. Coronary angioplasty outcomes in the Healthcare Cost and Utilization Project, 1993-1994. Am J Cardiol 1998; 81:848.
5. Dorros, G, Cowley, MJ, Simpson, J, et al. Percutaneous transluminal coronary angioplasty: Report of complications from the National Heart, Lung, and Blood Institute PTCA registry. Circulation 1983; 67:723.
6. Malenka, DJ, O'Rourke, D, Miller, MA, et al, for the Northern New England Cardiovascular Disease Study Group. Cause of in-hospital death in 12,232 consecutive patients undergoing percutaneous transluminal coronary angioplasty. Am Heart J 1999; 137:632.
7. Hirshfeld, JW Jr, Ellis, SG, Faxon, DP. Recommendations for the assessment and maintenance of proficiency in coronary interventional procedures: Statement of the American College of Cardiology. J Am Coll Cardiol 1998; 31:722.
8. Malenka, DJ, McGrath, PD, Wennberg, DE, et al, for the Northern New England Cardiovascular Disease Study Group. The relationship between operator volume and outcomes after percutaneous coronary interventions in high volume hospitals in 1994- 1996: the northern New England experience. Northern New England Cardiovascular Disease Study Group [In Process Citation]. J Am Coll Cardiol 1999; 34:1471.
9. Taddei, CF, Weintraub, WS, Douglas, JS Jr, et al. Influence of age on outcome after percutaneous transluminal coronary angioplasty. Am J Cardiol 1999; 84:245.
10. Ellis, SG, Elliott, J, Horrigan, NM, et al. Low-normal or excessive body mass index: Newly identified and powerful risk factors for death and other complications with percutaneous coronary intervention. Am J Cardiol 1996; 78:642.
11. Grines, CL, Schreiber, TL, Savas, V, et al. A randomized trial of low osmolar ionic versus nonionic contrast media in patients with myocardial infarction or unstable angina undergoing percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1996; 27:1381.
12. Batchelor, WB, Granger, CB, Kleiman, NS, et al. A comparison of ionic versus nonionic contrast medium during primary percutaneous transluminal coronary angioplasty for acute myocardial infarction (GUSTO IIb). Am J Cardiol 2000; 85:692.
13. Qureshi, NR, den Heijer, P, Crijns, HJGM. Percutaneous coronary angioscopic comparison of thrombus formation during percutaneous coronary angioplasty with ionic and nonionic low osmolality contrast media in unstable angina. Am J Cardiol 1997; 80:700.
14. Schrader, R, Esch, I, Ensslen, R, et al. A randomized trial comparing the impact of a nonionic (iomeprol) versus an ionic (ioxaglate) low osmolar contrast medium on abrupt closure and ischemic complications after coronary angioplasty. J Am Coll Cardiol 1999; 33:395.
15. Bertrand, ME, Esplugas, E, Piessens, J, Rasch, W. Influence of a Nonionic, Iso-Osmolar Contrast Medium (Iodixanol) Versus an Ionic, Low-Osmolar Contrast Medium (Ioxaglate) on Major Adverse Cardiac Events in Patients Undergoing Percutaneous Transluminal Coronary Angioplasty: A Multicenter, Randomized, Double-Blind Study. Circulation 2000; 101:131.
16. Robbins, MA, Marso, SP, Wolski, K, et al. Chest pain--a strong predictor of adverse cardiac events following precutaneous intervention (from the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting Trial [EPISENT]).] [In Process Citation]. Am J Cardiol 1999; 84:1350.
17. Baim, DS, Grossman, W. Complications of cardiac catheterization. In: Cardiac Catheterization, Angiography and Intervention, Baim, DS, Grossman, W (Eds), Williams & Wilkins, Baltimore, 1996, p.17.
18. Athanasiadis, A, Haase, KK, Wullen, B, et al. Lesion morphology assessed by pre-interventional intravascular ultrasound does not predict the incidence of severe coronary artery dissections. Eur Heart J 1998; 19:870.
19. Black, AJR, Namay, DL, Niederman, AL, et al. Tear of dissection after coronary angioplasty: Morphologic correlates of an ischemic complication. Circulation 1989; 79:1035.
20. Matthews, BJ, Ewels, CJ, Kent, KM. Coronary dissection: A predictor of restenosis? Am Heart J 1988; 115:547.
21. Ellis, SG, Roubin, GS, King, SB 3rd, et al. Angiographic and clinical predictors of acute closure after native vessel coronary angioplasty. Circulation 1988; 77:372.
22. Huber, MS, Mooney, JF, Madison, J, Mooney, MR. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am J Cardiol 1991; 68:467.
23. Cappelletti, A, Margonato, A, Rosano, G, et al. Short- and long-term evolution of unstented nonocclusive coronary dissection after coronary angioplasty [In Process Citation]. J Am Coll Cardiol 1999; 34:1484.
24. Keeley, EC, Grines, CL. Scraping of aortic debris by coronary guiding catheters: A prospective evaluation of 1000 cases. J Am Coll Cardiol 1998; 32:1861.
25. Holmes, DR Jr., Holubkov, R, Vliestra, RE, et al. Comparison of complications during percutaneous transluminal coronary angioplasty from 1977 to 1981 and from 1985 to 1986: The NHLBI PTCA registry. J Am Coll Cardiol 1988; 12:1149.
26. Klein, L, Kramer, B, Howard, E, Lesch, M. Incidence and significance of transient creatine kinase elevation and the diagnosis of non-Q-wave myocardial infarction associated with coronary angioplasty. J Am Coll Cardiol 1991; 17:621.
27. Piana, R, Paik, GY, Moscucci, M, et al. Incidence and treatment of "no reflow" after percutaneous coronary intervention. Circulation 1994; 89:2514.
28. Thel, MC, Califf, RM, Tcheng, JE, et al. Clinical risk factors for ischemic complications after percutaneous coronary interventions: Results from the EPIC trial. Am Heart J 1999; 137:264.
29. Mehran, R, Dangas, G, Mintz, GS, et al. Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions : intravascular ultrasound study of 2256 patients [In Process Citation]. Circulation 2000; 101:604.
30. Kugelmass, AD, Cohen, DJ, Moscucci, M, et al. Elevation of the creatine kinase myocardial isoform following otherwise successful directional coronary atherectomy and stenting. Am J Cardiol 1994; 74:748.
31. Abdelmeguid, AE, Ellis, SG, Sapp, SK, et al. Defining the appropriate threshold of creatine kinase elevation after percutaneous cornary interventions. Am Heart J 1996; 131:1097.
32. Tardiff, BE, Califf, RM, Tcheng, JE, et al. Clinical outcomes after detection of elevated cardiac enzymes in patients undergoing percutaneous intervention. IMPACT-II Investigators. J Am Coll Cardiol 1999; 33:88.
33. Abdelmeguid, AE, Topol, EJ. The myth of the myocardial "infarctlet" during percutaneous coronary revascularization procedures. Circulation 1996; 94:3369.
34. Topol, EJ, Ferguson, JJ, Weisman, HF, et al, for the EPIC Investigator Group. Long-term protection from myocardial ischemic events in a randomized trial of brief integrin ß3 blockade with percutaneous coronary intervention. JAMA 1997; 278:479.
35. Baim, DS, Cutlip, DE, Sharma, SK, et al, for the BOAT Investigators. Final results of the Balloon vs Optimal Atherectomy Trial (BOAT). Circulation 1998; 97:322.
36. Klein, L, Kramer, B, Howard, E, Lesch, M. Incidence and significance of transient creatine kinase elevation and the diagnosis of non-Q-wave myocardial infarction associated with coronary angioplasty. J Am Coll Cardiol 1991; 17:621.
37. Johansen, O, Brekket, M, Stromme, JH, et al. Myocardial damage during percutaneous transluminal coronary angioplasty as evidenced by troponin T measurements. Eur Heart J 1998; 19:112.
38. Shyu, K-G, Kuan, P-L, Cheng, J-J, et al. Cardiac troponin, creatine kinase, and its isoform release after successful percutaneous transluminal coronary angioplasty with or without stenting. Am Heart J 1998; 135:862.
39. Califf, RM, Abdelmeguid, AAE, Kuntz, RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol 1998; 31:241.
40. Nairns, CR, Miller, DP, Califf, RM, et al. The relationship between periprocedural myocardial infarction and subsequent target vessel revascularization following percutaneous coronary revascularization: Insights from the EPIC trial. J Am Coll Cardiol 1999; 33:647.
41. Detre, K, Holubkov, R, Kelsey, S, et al. Percutaneous transluminal coronary angioplasty in 1985-1986 and 1977- 1981. The National Heart, Lung, and Blood Institute Registry. N Engl J Med 1988; 318:265.
42. Muller, DWM, Shamir, KJ, Ellis, SG, Topol, EJ. Peripheral vascular complications after conventional and complex percutaneous coronary interventional procedures. Am J Cardiol 1992; 69:63.
43. Carrozza, JP, Baim, DS. Complications of directional coronary atherectomy: Incidence, causes, and management. Am J Cardiol 1993; 72:47E.
44. Popma, JJ, Satler, LF, Pichard, AD, et al. Vascular complications after balloon and new device angioplasty. Circulation 1993; 88:1569.
45. Blackenship, JC, Hellkamp, AS, Aguirre, FV, et al, for the EPIC Investigators. Vascular access site complications after percutaneous coronary intervention with abciximab in the Evaluation of c7E3 for the Prevention of Ischemic Complications (EPIC) trial. Am J Cardiol 1998; 81:36.
46. Brachmann, J, Ansah, M, Kosinski, EJ, et al. Improved clinical effectiveness with a collagen vascular hemostasis device for shortened immobilization time following diagnostic angiography and percutaneous transluminal coronary angioplasty. Am J Cardiol 1998; 81:1502.
47. Friedman, HZ, Cragg, DR, Glazer, SM, et al. Randomized, prospective evaluation of prolonged versus abbreviated intravenous heparin therapy after coronary angioplasty. J Am Coll Cardiol 1994; 24:1214.
48. Rabah, M, Mason, D, Muller, DWM, et al. Heparin after percutaneous intervention (HAPI): A prospective multicenter randomized trial of three heparin regimens after successful coronary intervention. J Am Coll Cardiol 1999; 34:461.
49. Rabah, MM, Premmereur, J, Graham, M, et al. Usefulness of intravenous enoxaparin for percutaneous coronary intervention in stable angina pectoris [In Process Citation]. Am J Cardiol 1999; 84:1391.
50. Samore, MH, Wessolossky, MA, Lewis, SM, et al. Frequency, risk factors, and outcome for bacteremia after percutaneous transluminal coronary angioplasty. Am J Cardiol 1997; 79:873.
51. Gregorini, L, Marco, J, Palombo, C, et al. Postischemic left ventricular dysfunction is abolished by alpha-adrenergic blocking agents. J Am Coll Cardiol 1998; 31:992.
52. Rihal, CS, Sutton-Tyrrell, K, Guo, P, et al. Increased incidence of periprocedural complications among patients with peripheral vascular disease undergoing myocardial revascularization in the Bypass Angioplasty Revascularization Investigation. Circulation 1999; 100:171.
53. Buffon, A, Liuzzo, G, Biasucci, LM, et al. Preprocedural serum levels of C-reactive protein predict early complications and late restenosis after coronary angioplasty. J Am Coll Cardiol 1999; 34:1512.
54. Thel, MC, Califf, RM, Tardiff, BE, et al. Timing of and risk factors for myocardial ischemic events after percutaneous coronary intervention (IMPACT-II). Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis. Am J Cardiol 2000; 85:427.
55. Brodie, BR, Stuckey, TD, Hansen, C, Muncy, D. Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces catheterization laboratory events in high-risk patients with an acute myocardial infarction. Am J Cardiol 1999; 84:18.
56. Wang, N, Gundry, SR, Van Arsdell, G, et al. Percutaneous transluminal coronary angioplasty failures in patients with multivessel disease: Is there an increased risk? J Thorac Cardiovasc Surg 1995; 110:214.
57. Boylan, MJ, Loop, FD, Lytle, BW, et al. Have PTCA failures requiring emergent coronary bypass changed? Ten-year experience with 253 patients. Ann Thorac Surg 1995; 59:283.
58. Lazar, HL, Jacobs, AK, Aldea, GS, et al. Factors influencing mortality after emergency coronary artery bypass grafting for failed percutaneous transluminal coronary angioplasty. Ann Thorac Surg 1997; 64:1747.
59. Eagle, KA, Guyton, RA, Davidoff, R, et al. ACC/AHA guidelines for coronary artery bypass graft surgery: executive summary and recommendations: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee to revise the 1991 guidelines for coronary artery bypass graft surgery). Circulation 1999; 100:1464.
60. Lazar, HL, Bao, Y, Lancaster, D, et al. Favorable impact of stents after emergent coronary artery bypass for failed angioplasty. Ann Thorac Surg 1999; 68:1644.