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خرید پکیج
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Periprocedural complications of percutaneous coronary intervention

Periprocedural complications of percutaneous coronary intervention
Literature review current through: Jan 2024.
This topic last updated: May 24, 2023.

INTRODUCTION — Complications seen during percutaneous coronary intervention (PCI) include those related to cardiac catheterization and diagnostic coronary angiography, or the intervention itself. The periprocedural complications related to PCI will be reviewed here. The complications of cardiac catheterization are discussed separately. (See "Complications of diagnostic cardiac catheterization".)

In this discussion, PCI refers to any therapeutic procedure during which a wire or catheter is inserted into a coronary artery and luminal enlargement is attempted.

INCIDENCE AND CAUSES OF EARLY MORTALITY — A 2013 report from the Cleveland (United States) Clinic's institutional PCI registry presented the incidence and causes of death within 30 days of 4078 PCIs performed between 2009 and 2011 [1]. The following findings were noted:

There were 81 deaths (2 percent), of which 58 percent were cardiac and 42 percent noncardiac. There were 19 deaths after the initial hospital discharge.

Only 42 percent of the deaths were attributable to PCI-related complications. Of these, 73 percent were attributable to definite or probable stent thrombosis, 12 percent to bleeding, 9 percent to coronary dissection, and 6 percent to renal failure.

Of the noncardiac causes of death, the most common were complications of infection or neurologic events.

PREDICTORS OF MORTALITY AND MAJOR COMPLICATIONS

Absence of on-site cardiac surgery — We and others believe it is reasonable to perform elective PCI at hospitals without on-site cardiac surgical services, as multiple studies have shown that outcomes are similar for stable patients undergoing PCI at hospitals with and without on-site cardiac surgical backup when measures of institutional and operator quality are evaluated (table 1 and table 2 and table 3) [2]. The best evidence comes from a 2011 meta-analysis and two subsequent randomized trials:

A 2011 meta-analysis of 11 studies that included over 900,000 patients found no increase in the average mortality rate (0.9 versus 0.8 percent, respectively; odds ratio [OR] 1.15, 95% CI 0.93-1.41) and no significant difference in the risk of emergency bypass surgery (OR 1.21, 95% CI 0.52-2.85) [3].

The noninferiority CPORT-E trial randomly assigned 18,867 patients with stable and unstable coronary disease in a 3:1 ratio to PCI at a hospital without or with on-site cardiac surgery [4]. Patients with ST-elevation MI, unprotected left main disease, or a left ventricular ejection fraction of less than 20 percent were excluded. There was no difference in the rates of the two co-primary outcomes at hospitals without or with cardiac surgery: mortality at six weeks (0.9 versus 1.0 percent, respectively; difference, -0.04 percentage points, 95% CI -0.31 to 0.23) or major adverse cardiac events at nine months (12.1 versus 11.2 percent, respectively; difference, 0.92 percentage points, 95% CI 0.04 to 1.80). However, the incidence of target vessel revascularization was significantly higher at non-SOS sites.

The MASS COMM trial randomly assigned, in a 3:1 ratio, 3691 patients with indications for nonemergency PCI who presented at Massachusetts hospitals without on-site cardiac surgery to undergo PCI at that hospital or a hospital with cardiac surgery services [5]. With regard to the co-primary composite end points of major adverse cardiac events (death, MI, repeat revascularization, or stroke) at 30 days (safety end point) and at 12 months (effectiveness end point), PCI procedures performed at hospitals without on-site cardiac surgery were noninferior (9.5 versus 9.4 percent; relative risk 1.00, 95% one-sided upper confidence limit, 1.22 and 17.3 versus 17.8 percent, relative risk 0.98, 95% one-sided upper confidence limit, 1.13).

The discussion of primary PCI at hospitals without on-site cardiac surgery is found elsewhere. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome", section on 'PCI without on-site cardiac surgery'.)

Short-term outcomes — A number of multivariable risk models have been developed to predict in-hospital mortality and major complications after PCI (table 4) [6-18]. Such models have typically been validated only within the institution at which they were developed, and some were based upon patient populations treated with balloon angioplasty alone.

In one analysis, five of these multivariable mortality models were compared for their ability to predict in-hospital mortality in 4448 patients in the National Heart, Lung, and Blood Institute Dynamic Registry who underwent PCI from 1997 to 1999 [6]. During the index hospitalization, 64 patients died (for an in-hospital mortality rate of 1.4 percent).

This outcome was closely approximated by three of the models: the New York state model [8,9], the Northern New England model [10], and the Cleveland Clinic model [11]. Two other models were less accurate: the University of Michigan model, which predicted 47 deaths (1.1 percent) [12], and the American College of Cardiology Registry model, which predicted 603 deaths (13.5 percent) [7].

The Mayo Clinic developed a risk score to identify patients at increased risk for major complications after PCI [14]. The score, derived from patients who underwent PCI between 1996 and 1999 and then validated in 2000, is relevant to current clinical practice since it was performed after stenting became routine, the patients were usually treated with clopidogrel or ticlopidine, and intravenous glycoprotein IIb/IIIa inhibitors were available [15].

A predictive point score was based upon eight clinical and angiographic variables, including a number of high-risk parameters such as shock, heart failure, urgent or emergent PCI, and left main or multivessel disease (table 5). Major complications were defined as in-hospital mortality, ST-elevation MI, urgent or emergent CABG, and stroke. In the validation cohort, the observed complication rates were comparable to the expected rates for all risk levels. Since this risk model includes three angiographic variables, a low score derived from the five clinical variables would not permit exclusion of high risk prior to intervention.

A subsequent study from the Mayo Clinic, using data from over 9000 PCIs performed between 2000 and 2005, developed two risk-prediction models, one for mortality alone and one for all major adverse cardiovascular events [16]. The model consisted of seven baseline clinical and noninvasive variables: age, MI within the past 24 hours, preprocedural shock, serum creatinine, left ventricular ejection fraction, heart failure, and peripheral artery disease. The two models successfully predicted the risk of adverse events during the index hospitalization. Limitations of the study include performance at a single referral center in a lower-risk patient population.

The risk models discussed above were derived from cohorts that included a high percentage of patients with a recent MI [17]. Whether a preprocedural cardiac troponin (cTn) elevation in patients with stable coronary artery disease is a predictor of adverse postprocedural outcome was addressed using the EVENT registry of 7592 unselected patients undergoing PCI with stenting [18]. Of the 2382 stable EVENT patients, 142 (6 percent) were found to have baseline cTn above the upper limit of normal. Compared with patients with normal cTn, the following findings were noted at hospital discharge:

There was a significantly higher rate of in-hospital death or MI (13.4 versus 5.6 percent). This was attributable in large part to an increase in periprocedural MI.

In multivariable analyses, baseline cTn elevation was an independent predictor of in-hospital death or MI (odds ratio, 2.1; 95% CI 1.2 to 3.8).

There was a trend toward a higher rate of urgent repeat PCI (1.4 versus 0.2 percent)

LONG-TERM MORTALITY

Mortality at one year — Myocardial infarction (MI) after percutaneous coronary intervention (PCI) predicts mortality at one year in patients who undergo PCI. A preprocedural elevation in cardiac troponin (cTn) also predicts adverse outcomes. In the EVENT registry discussed in the preceding section, a preprocedural elevation in cTn was associated with a twofold increase in the rate of death or MI at one year, including an increase in the rate of death from 0.4 to 2.4 percent [18]. (See "Periprocedural myonecrosis following percutaneous coronary intervention".)

The issue of whether either bleeding or urgent revascularization (both within 30 days) are also associated with late mortality was evaluated in an analysis of 5384 patients from four trials of patients referred for PCI [19]. Mortality at one year was 3.6 percent in all patients and was significantly higher in those with either bleeding or urgent revascularization at 30 days (14.1 versus 3.3 and 15.4 versus 3.6 percent, respectively). Both major and minor bleeding were associated with late mortality.

There is no definitive explanation for the association between bleeding and late mortality, but the analysis controlled for factors such as age, risk factors, left ventricular ejection fraction, creatinine level, and presence of multivessel coronary artery disease. The presence of other potential confounders that may be associated with a sicker population cannot be excluded.

Mortality at five years — There is a prevalent opinion, supported in part by evidence from randomized trials, that the primary cause of death in patients who undergo PCI is a complication of coronary heart disease [20-22]. However, a 2014 single center (Mayo Clinic, MN, United States) study found a temporal trend toward a higher frequency of noncardiac deaths [23]. Among 19,000 patients who underwent the procedure during three time periods (1991 to 1996, 1997 to 2002, and 2003 to 2008), the following findings were noted:

Overall mortality was 37 percent (4.48 per 100 person-years). The unadjusted rate of five-year mortality was slightly higher in the most recent era (17.0, 15.9, and 18.2 percent, respectively).

The incidence of cardiac death at five years fell across the three time periods (9.8, 7.4, and 6.6 percent, respectively), while the incidence of noncardiac death rose (7.1, 8.5, and 11.2 percent). Only 36.8 percent of deaths in the latter era were cardiac. The former was driven by a decline in fatal MI or sudden cardiac death, while the latter was associated with increased noncardiac comorbidities at baseline.

After adjustment, there was a 50 percent temporal decline in cardiac mortality but no change in noncardiac mortality.

We agree with the authors’ interpretation that increased use of secondary preventive strategies is the principal explanation for the fall in long-term cardiac mortality. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

CORONARY ARTERY COMPLICATIONS — The use of larger guiding catheters and sheaths makes damage to the proximal coronary artery more likely compared with diagnostic coronary arteriography. In addition, the advancement of guidewires and catheters into diseased coronary arteries may lead to vessel injury. Complications include coronary artery dissection, intramural hematoma, coronary artery perforation, and occlusion of branch vessels.

Intramural hematoma — Coronary artery intramural hematoma is defined as an accumulation of blood within the medial space displacing the internal elastic membrane inward and the external elastic membrane outward, with or without identifiable entry and exit points. The following findings were noted in a study of 905 patients undergoing PCI [24]:

IVUS identified an intramural hematoma in 6.7 percent of procedures; the incidence was higher with angioplasty compared to stenting.

The location was proximal to the lesion in 36 percent, confined to the lesion in 18 percent, and distal to the lesion in 46 percent.

On angiography, the hematoma had the appearance of a dissection or a new lesion in 60 and 11 percent of cases; no significant abnormality was seen in 29 percent, in whom the diagnosis could only be made by IVUS.

Patients with a hematoma had the same incidence of post-percutaneous coronary intervention (PCI) non-ST-elevation MI as those without a hematoma (26 percent), but a higher incidence of repeat revascularization within one month (6.3 versus 2 percent). Patients undergoing PCI for spontaneous coronary dissection have a higher incidence of intramural hematoma. (See "Spontaneous coronary artery dissection", section on 'Pathophysiology'.)

Perforation — Coronary artery perforation in the stent era is a rare but potentially catastrophic complication. In a series of over 10,000 PCIs (6836 with stenting) from 1993 to 2001, the risk of perforation was 0.84 percent [25]. Perforation occurred more often when an atheroablative device or IVUS was used. However, perforation can also occur during stent placement, particularly when the stent is oversized and high deployment or post-dilation pressures are used. Significant cardiac events occurred in 29 of 84 patients with a perforation (35 percent) and included MI in 15, repeat PCI in four, CABG in 11, and death in seven.

The degree of perforation varies from barely perceptible to severe and a classification scheme based upon angiographic appearance of the perforation has been proposed [26]:

Class I – Intramural crater without extravasation

Class II – pericardial or myocardial blushing (staining)

Class III – perforation ≥1 mm in diameter with contrast streaming or cavity spilling

The incidence of complications varies with the severity of the perforation. For class I, II, and III lesions, the respective values were 0, 14, and 50 percent for MI and 8, 13, and 63 percent for tamponade.

Overall mortality with coronary perforation is about 5 to 10 percent, with the main risk factors being tamponade, requirement for emergency surgery, and the severity of the perforation [26,27]. In the above report of 62 patients, for example, deaths occurred only in patients with class III perforations (19 percent mortality) [26].

The use of newer hydrophilic guidewires in conjunction with aggressive antiplatelet therapy is anecdotally linked to an increased risk of distal wire perforation.

Serious perforations require immediate treatment within the cath lab. The first measure is inflation of either a PTCA balloon or perfusion balloon catheter at the site of perforation to stop the flow of blood into the pericardium (giving time for pericardiocentesis, hemodynamic stabilization, and preparation of subsequent therapies), and may also be sufficient to seal off small perforations following a 15-minute inflation. If the perforation has not sealed, and evidence of hemodynamic compromise is seen (eg, hypotension), emergency pericardiocentesis with placement of a pericardial drain should be performed. Reversal of anticoagulation should occur only after access to the pericardial space is secured as blood in the pericardium may clot, making pericardiocentesis difficult.

Significant distal perforations of small branches by guidewires can be managed by placement of embolization coils or other materials. This maneuver will result in total occlusion of that arterial segment and periprocedural MI.

The covered stent, produced by attaching a polytetrafluoroethylene (PTFE) membrane to one stent or sandwiching such a layer between two stents, may be the stent of choice for treating coronary artery perforation [28]. One report evaluated 11 patients with a coronary rupture that was not treated successfully with prolonged balloon inflation [29]. Emergency insertion of a covered stent effectively sealed the perforation in all patients. Other patients who received a non-covered stent had a lower success rate and a higher incidence of tamponade and early surgery. During a 14-month follow-up, there were no major cardiac adverse events in the patients receiving a covered stent.

These stents are available for treatment of perforations that cannot be managed by more conservative measures. The United States Food and Drug Administration has approved the Graftmaster PTFE-covered stent and the Papyrus PTFE-covered stent under a Humanitarian Device Exemption for the treatment of coronary perforation. When bleeding from the perforation site continues, emergent coronary bypass may be required [26,27]. The indications for emergency surgery are continued bleeding or hemodynamic compromise unrelieved by pericardiocentesis (table 4). (See 'Emergency CABG for failed PCI' below.)

Distal embolization — Downstream embolization of thrombus or plaque contents (atheroma) with microvascular obstruction is common after PCI [30]. Slow antegrade flow from embolization is correlated to creatine kinase MB fraction rise, supporting an association between microembolization and periprocedural necrosis [31]. (See "Periprocedural myonecrosis following percutaneous coronary intervention" and "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'No reflow' and "Coronary artery bypass graft surgery: Prevention and management of vein graft stenosis", section on 'Embolic protection devices'.)

Side branch occlusion — Occlusion of side branches has been reported in up to 19 percent of cases in which a stent was placed across a major (>1 mm) side branch (figure 1) [32,33]. In most cases, a greater than 50 percent stenosis has been present at the ostium of the side branch, and most occlusions occur after post-stent dilation performed with high-pressure inflations [32]. By six to nine months, all branches in these reports, including those previously occluded, were patent [32-34]. The low morbidity in these series may have reflected a tendency to avoid stent placement across large or diseased side branches.

In a study of the mechanisms of myocardial injury after complex PCI, side branch occlusion at or adjacent to the site of stent placement was associated with myonecrosis in 12 percent of cases [35]. In the TAXUS V study, overlapping paclitaxel eluting stents had a higher incidence of periprocedural MI, possibly related to increased coverage of side branches [36]. (See "Periprocedural myonecrosis following percutaneous coronary intervention".)

Complications seen with stenting — Improved stent design and technique have led to a decreasing risk of acute complications of PCI despite the increasing complexity of cases [37,38].

Two complications specific to stenting, failure of stent deployment and stent thrombosis, will be reviewed here. Complications of stenting that can also be seen with PTCA are discussed above. These include intramural hematoma, coronary artery perforation, distal embolization, and side branch occlusion.

Stent jail — Stent coverage of a branch leaves the affected branch in "stent jail" [39,40]. If needed, a guidewire can often be placed into this jailed branch and the ostium dilated through the stent struts [39]. This is possible with all new second-generation stents, but many jailed side branches do not need further "rescue" maneuvers, especially if TIMI III flow is present and there is no evidence of ischemia.

Failure of stent deployment — With first generation stents, failed deployment due to an inability to deliver the stent to or expand it within the target lesion occurred in 2.0 to as many as 8.3 percent of procedures [41-44].

Current second- and third-generation stents appear to have a higher rate of delivery success (>98 percent) [45], even in challenging anatomic situations, and are much less likely (<0.5 percent) to strip off the delivery balloon during attempted placement or retrieval if the stent cannot cross the target lesion. In a large review, the incidence of stent loss with newer stents, which are premounted and have a low profile, ranged from 0.4 to 2 percent [46].

Stent thrombosis — Stent thrombosis is a potentially catastrophic complication that usually leads to death or MI. The patient often presents with symptoms and signs of acute MI, and the electrocardiogram may show ST-segment elevation. This is a medical emergency and should be managed as such. The event can occur acutely (during or soon after the PCI), subacutely (within 30 days after stent placement), or as late as one year or more. (See "Coronary artery stent thrombosis: Incidence and risk factors" and "Long-term antiplatelet therapy after coronary artery stenting in stable patients".)

Stent infection — Infection of a coronary artery stent is a rare but potentially life threatening complication [47,48]. It has been associated with formation of mycotic aneurysms and spontaneous coronary artery perforation. However, prophylactic antibiotics in the immediate post-procedure period or before dental or other procedures are not recommended.

Coronary artery aneurysms — Coronary artery aneurysms (CAAs) have been rarely reported after placement of drug-eluting stents (DES) [49-51]. In a retrospective study of 1197 patients who underwent stenting with DES, CAAs were found at follow-up angiography in 15 (1.25 percent); the mean time between placement and CAA diagnosis was 313 days [49]. Risk factors for the development of CAA included DES placement during acute MI or in an occluded vessel, longer or multiple DES, and residual dissection. These reports have also been confined largely to first generation DES.

Other causes of CAA include congenital and Kawasaki disease-related aneurysms. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation", section on 'Coronary artery abnormalities' and "Congenital and pediatric coronary artery abnormalities", section on 'Abnormalities in the caliber of the coronary arteries'.)

MYOCARDIAL ISCHEMIA AND INFARCTION

Myocardial ischemia — Myocardial ischemia can result from any of the coronary artery complications discussed above and can lead to variety of complications either during or after percutaneous coronary intervention (PCI), including chest pain, ST-elevation MI, troponin elevation, and myocardial stunning.

Patients may develop chest pain after coronary stenting for one of two reasons: ischemic chest pain (for which there is usually an apparent angiographic cause) and chest pain without an apparent angiographically identifiable cause [52]. Chest pain without an apparent cause may be associated with a small troponin elevation.

Ischemic chest pain within 48 hours after stenting usually results from procedure-related events such as transient or persistent acute vessel closure (usually due to stent thrombosis or progression of an untreated dissection), transient coronary spasm, side branch occlusion of greater than 1.0 mm size, coronary dissection type C (as defined above), slow-flow or no flow, coronary perforation, prolonged hypotension, or distal embolization of atherosclerotic or thrombotic debris or air.

In the EPISTENT trial, for example, ischemic chest pain after PCI occurred in 11 percent of patients, 12 percent of whom had associated electrocardiographic (ECG) changes [53]. When ECG changes were present, there was a significantly increased risk of a cardiac event (death, all MI, repeat revascularization) compared to an intermediate risk when chest pain without ECG changes was present and low risk in the absence of chest pain (42 versus 12 and 5 percent, respectively).

Chest pain without an apparent cause is chest pain that is often atypical in quality and occurs within the first 24 hours after PCI in the absence of ECG changes or elevation in cardiac enzymes. It appears to occur more often after stenting compared to percutaneous transluminal coronary angioplasty (PTCA) alone. Most patients describe the pain characteristics as being different from their typical angina (more localized and frequently pleuritic). This discomfort lasts for less than 72 hours in about 80 percent of patients, and less than two weeks in the remainder [52].

This issue was addressed in an analysis of 1362 consecutive nonacute MI patients undergoing stenting [52]. After exclusion of 312 patients who were identified as having postprocedural chest pain and procedural events, 176 (13 percent) patients with postprocedural chest pain and no procedural events were compared to 874 patients without chest pain. Minor elevations in serum troponin I (56 versus 14 percent) and creatine kinase MB fraction (CK-MB) (26 versus 10 percent) were found more often in the group with post-procedural chest pain suggesting that, even in patients with atypical chest pain and no ECG changes, myocardial ischemia may exist (subclinical micromyonecrosis). (See "Periprocedural myonecrosis following percutaneous coronary intervention".)

In addition, the following observations were made in the patients with presumed nonischemic chest pain [52]:

They had significant increase in post-procedural minimum lumen diameter (2.73 versus 2.45 mm), stent-to-vessel ratio, and inflation pressure (16 versus 13 mmHg) compared to patients without chest pain.

Multivariate predictors of CK-MB elevation included a diagnosis of acute coronary syndrome, stent-to-vessel ratio >1.1, inflation pressure >16 atmospheres, thrombotic lesion, age, and American College of Cardiology/American Heart Association type C lesion.

The patients with presumed nonischemic chest pain also had more frequent cardiac events at follow-up:

At 30 days, a higher frequency of emergency room visits, readmissions, and repeat angiography (16 versus 3 percent) but no increase in repeat intervention, subacute thrombosis, death, or repeat MI.

At six to nine months, a significantly higher rate of target vessel revascularization (30 versus 17 percent).

Myocardial infarction — MI, when defined as a rise in troponin level after PCI, occurs frequently. This topic is discussed in detail separately. (See "Periprocedural myonecrosis following percutaneous coronary intervention".)

Emergency CABG for failed PCI — The major indications for emergency coronary artery bypass graft surgery (CABG) for patients who undergo PCI are hemodynamic compromise, ongoing ischemia or threatened occlusion (eg, acute vessel closure with PTCA alone) with significant myocardium at risk, and coronary rupture (table 4) [54]. These complications may result from extensive dissection, perforation/tamponade, or recurrent acute closure [55]. Patients who have had an MI tend to require emergency CABG more often than those who have not [55,56].

The most common indication for emergency CABG in patients who undergo PCI with stenting is failed stent deployment, which is identified in the catheterization laboratory. The magnitude of decline in emergency CABG can be illustrated by the following observations:

In a review of almost 19,000 PCIs performed at the Cleveland Clinic, the rate of emergency CABG fell from 1.5 percent in 1992 to 0.14 percent in 2000 [55]. This improvement was associated with marked increases in the use of coronary artery stents (5 to 81 percent), which were used significantly less often in the patients who required emergency CABG. From 1996 onward, emergency CABG was less likely in patients who received a stent.

In a review of over 23,000 PCIs performed at the Mayo Clinic, the rate of emergency CABG fell from 2.9 percent in the pre-stent era (1979 to 1994) to 0.7 percent in the initial stent era (1995 to 1999) to 0.3 percent from 2000 to 2003 [57]. The improvement in outcome occurred despite an increase in high-risk patients requiring urgent or emergent PCI. In the last time period, there were fewer patients requiring CABG because of coronary artery dissection or abrupt vessel closure than in the pre-stent era.

The operative mortality in patients who required emergency CABG remained high and unchanged over time in these two series (10 to 15 percent) [55,57]. Acute MI and arrhythmia were the major causes of death.

VASCULAR COMPLICATIONS — Vascular access site complications, such as bleeding and the need for surgical repair occurring after percutaneous coronary intervention (PCI) will be reviewed here (table 4). Similar complications occurring after diagnostic cardiac catheterization are discussed separately. (See "Complications of diagnostic cardiac catheterization", section on 'Hemostasis at the femoral access site' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Hemostasis at the access site'.)

The common femoral artery was the most frequent access site until about 2005, at which time many interventional cardiologists started preferring the radial artery for reasons presented below. (See 'Radial artery access' below and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Radial artery'.) The discussion here focuses principally on vascular complications using the common femoral artery.

Vascular complications at the femoral artery access site, which occur in up to 6 percent of cases, make up a significant portion of the morbidity associated with PCI [58-60]. Minor or major hematomas and pseudoaneurysms are most common, followed by arterial laceration, retroperitoneal hematoma, arteriovenous fistula, arterial occlusion, and local infection with or without sepsis.

Risk factors for vascular complications include periprocedural use of heparin or fibrinolytic therapy, especially if there is prolonged or excessive anticoagulation, repeat procedure, atherectomy rather than percutaneous transluminal coronary angioplasty; peripheral artery disease, advanced age, obesity, duration of time that the sheath remains in place, particularly if >15 hours, use of intraaortic balloon pump, and, in some but not all series, larger arterial sheath size and cannulation of the superficial femoral artery [58-60]. (See "Complications of diagnostic cardiac catheterization".)

Access site bleeding — Access site bleeding is, in part, related to anticoagulant and antiplatelet therapy.

Women are at higher risk for bleeding and vascular complications compared with men; this difference is not fully explained by smaller vessel or body size [61].

The risk of bleeding requiring transfusion is also increased in patients 80 years of age or older undergoing PCI, with a rate of 9 percent noted in one series [62].

Prevention of access site bleeding may be possible by reducing the intensity of anticoagulation. (See 'Anticoagulation-associated bleeding' below.)

Heparin is almost always used during PCI to reduce the risk of thrombosis, but continued therapy makes it more difficult to achieve hemostasis at the arterial access site. Some experts advocate that the dosing of unfractionated heparin during PCI should be guided by measurement of activated clotting times. Over-anticoagulation, especially with concomitant administration of GP IIb/IIIa receptor blockers is associated with higher risk of hemorrhage. The use of direct thrombin inhibitors such as bivalirudin rather than heparin and a GP 2b/3a receptor blocker is associated with lower risk of hemorrhagic complications [63-66]. Post-procedural heparin is no longer recommended since the majority of abrupt closures occur immediately after the procedure, and the incidence of other ischemic events has decreased with the use of stents and antiplatelet agents given during or immediately after PCI. (See "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies", section on 'Heparin'.)

Attaining hemostasis — The traditional approach to catheter removal from the femoral artery at the conclusion of PCI was local hand-applied pressure for 15 to 30 minutes. Two alternative approaches are available: mechanical clamp compression and, more important, arterial puncture closing devices, which may increase the risk of complications. These issues are discussed elsewhere. (See "Complications of diagnostic cardiac catheterization", section on 'Hemostasis at the femoral access site' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Hemostasis at the access site'.)

Retroperitoneal bleeding — Retroperitoneal bleeding represents a particularly serious type of preventable vascular complication. In our experience, it is the most common cause of unexpected mortality after diagnostic or interventional cardiac catheterization. Retroperitoneal bleeding is frequently related to artery puncture that is above the inguinal ligament and can be prevented in most cases by careful attention to anatomic landmarks and fluoroscopy of the femoral head prior to needle puncture. Retroperitoneal hemorrhage can also occur with puncture sites below the inguinal ligament, as blood can track along the vascular fascial sheath into the retroperitoneum or rectus sheath. Even with appropriate access position, back wall punctures that exit above the inguinal ligament may result in retroperitoneal bleeding and may not be sealed by manual compression or closure devices. Injudicious advancement of the guidewire or sheath by an inexperienced operator can also traumatize the iliac artery or the lateral circumflex artery and result in bleeding into the retroperitoneal space.

The event is usually recognized by hemodynamic compromise. It can sometimes be mistaken for the more common and benign "vagal" reaction, since it may also present with profound bradycardia and associated hypotension. It is distinguished by only a transient response to initial volume loading and atropine.

Successful management depends on early recognition and volume resuscitation with crystalloid and blood. The diagnosis is usually confirmed by computed tomography imaging. The vascular surgical team should be alerted, although surgical management is not commonly needed or helpful. We have used percutaneous methods including balloon inflation or placement of a covered stent to tamponade or seal the bleeding segment.

Radial artery access — For patients with acute coronary syndromes treated with PCI, we prefer access using the radial rather than the femoral artery to reduce the risk of major access site bleeding. For stable patients, the site for arterial access is individualized. We believe there is insufficient evidence to recommend routine use of the radial artery in all stable patients.

Catheterization using the radial, as opposed to the common femoral, artery has the potential to reduce the risk of major access site bleeding due to the fact that the former is smaller and readily compressible. Any intervention that reduces the risk of bleeding could potentially improve outcomes given the observations of increased mortality and ischemic events in patients who bleed at the time of PCI. This is particularly true for patients undergoing catheterization for an acute coronary syndrome. (See "Periprocedural bleeding in patients undergoing percutaneous coronary intervention", section on 'Outcomes after bleeding'.)

The best evidence supporting better outcomes with radial catheterization comes from a 2016 meta-analysis of 24 trials (n = 22,843), including the four large, contemporary trials of acute coronary syndrome patients: RIVAL [67], MATRIX [68], RIFLE-STEACS [69], and STEMI RADIAL [70,71]. Comparing radial with femoral access, the risk of following end points were significantly reduced:

Major bleeding (odds ratio [OR] 0.53, 95% CI 0.42-0.65).

All-cause mortality (OR 0.71, 95% CI 0.59-0.87).

Major adverse cardiovascular events (OR 0.84, 95% CI 0.75-0.94).

In this meta-analysis, the benefits of radial access were consistent across the spectrum of patients with coronary artery disease (ie, patients with stable or unstable disease). After publication of the meta-analysis, the one-year results of the MATRIX trial were published [72]. There was no difference between the radial and femoral access groups with regard to major adverse cardiovascular events but net adverse clinical events (a composite of non-coronary artery bypass graft-related major bleeding, or major adverse cardiovascular events) were fewer with radial access (15.2 versus 17.2 percent; rate ratio 0.87, 95% CI 0.78-0.97).

There is some evidence that the risk of stroke is lower with a radial as opposed to a femoral artery approach. In a prospective database study of 17,966 patients with stable or unstable coronary artery disease who underwent PCI between 2008 and 2016, the risk of periprocedural stroke was 0.3 percent [73]. In a propensity score matching analysis (n = 8726), the risk was lower (odds ratio 0.33, 95% CI 0.16-0.71) with radial as opposed to transfemoral catheterization.

In patients for whom a radial artery approach may be used, we assess the palmar arch circulation prior to the procedure. The adequacy of the arch should be documented in the medical record. We also assess the patient for adequate hemostasis and circulation after the procedure and document the results.

For patients who undergo PCI using radial access, radial artery occlusion is a potential complication that occurs in approximately 5 percent of cases. A potential clinical consequence is the inability to use the radial artery for future access. Perfused hemostasis with non-occlusive radial artery compression, documented with confirmed perfusion of the hand during ipsilateral ulnar compression ("reverse Allen’s test"), has been shown to decrease the risk of this complication. In a study of 3000 patients undergoing diagnostic coronary angiography (5 French sheath) who were randomly assigned to ulnar compression or standard hemostasis, the primary end point of 30-day radial artery occlusion occurred less often with ulnar compression (3 versus 0.9 percent; p = 0.0001) [74].

For patients in whom the likelihood of coronary artery bypass graft surgery is high, consideration should be given to using the radial artery from the dominant hand, as the radial artery from the non-dominant hand may be used as a conduit for bypass. Endothelial disruption from radial catheterization may increase the risk of vasospasm in the radial conduit.

Non-radial access should be considered in patients with end stage renal disease undergoing renal replacement therapy who have fistulae or in whom fistulae implantation is anticipated.

Some operators are now using the ulnar instead of the radial artery, especially if ultrasound documents a small radial artery or if prior catheterization from the radial artery was unsuccessful due to significant tortuosity.

Atheroembolism — The use of stiff, large-bore guiding catheters results in aortic trauma and the "scraping" of atheromatous debris from the aortic wall, providing a potential source of systemic embolism. In a series of 1000 patients undergoing PCI, 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 [75]. There were no associated in-hospital ischemic complications, probably due to sufficient withdrawal of blood containing the debris prior to the injection of contrast. Placement of a Y-adapter on the guiding catheter as the catheter is advanced over the guidewire should be discouraged, as this prevents backbleeding of atheromatous debris from the catheter.

Atheroembolism related to cardiac catheterization and PCI is discussed in detail separately. (See "Complications of diagnostic cardiac catheterization", section on 'Atheroembolism' and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)" and "Access-related complications of percutaneous access for diagnostic or interventional procedures", section on 'Atheroembolism'.)

OTHER

Acute kidney injury — Acute renal failure may occur after percutaneous coronary intervention (PCI). The most common causes are hemodynamic instability, radiocontrast toxicity, and atheroembolism. This subject is discussed in detail elsewhere. (See "Complications of diagnostic cardiac catheterization", section on 'Acute renal failure' and "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management" and "Clinical presentation, evaluation, and treatment of renal atheroemboli".)

Stroke — Stroke as a complication of cardiac catheterization is discussed separately (see "Stroke after cardiac catheterization"). In patients undergoing PCI, there is some evidence that radial as opposed to femoral artery catheterization is safer. (See 'Radial artery access' above and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Radial artery'.)

The relative risk of stroke, comparing PCI to coronary artery bypass graft surgery, is discussed separately. (See "Revascularization in patients with stable coronary artery disease: Coronary artery bypass graft surgery versus percutaneous coronary intervention", section on 'Multivessel disease'.)

Anticoagulation-associated bleeding — The use of antiplatelet and antithrombotic agents increases the risk of major periprocedural bleeding and the likelihood of a need for a transfusion of blood components, particularly when they are used in combination. The most common sites for bleeding requiring transfusion are the femoral access site as described above, the retroperitoneal space, and the gastrointestinal tract. Genitourinary tract bleeding is not uncommon, but usually does not require transfusion. (See 'Access site bleeding' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures", section on 'Access site bleeding'.)

Both unfractionated heparin and low molecular weight heparin are associated with an increased risk of bleeding. The relative safety of these two agents in the setting of PCI is discussed elsewhere. (See "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies", section on 'Low molecular weight heparin'.)

The use of high doses of periprocedural heparin may be associated with gastrointestinal bleeding or hematuria. As an example, gross hematuria has been reported in up to 2 percent of patients [76]. It should prompt a careful urologic evaluation since organic urinary tract disease, such as a urologic cancer, is a potential source [76]. (See "Etiology and evaluation of hematuria in adults".)

The aggressive systemic anticoagulation used in the past led to the need for blood transfusions and/or vascular repair of the arterial vascular site in up to 14 percent of patients [60]. However, the incidence of major bleeding complications has fallen with the appreciation that full stent deployment minimizes the need for systemic anticoagulation [77]. In a controlled trial, for example, aspirin and ticlopidine were associated with fewer major bleeding episodes than a regimen of aspirin, intravenous heparin, and phenprocoumon (0 versus 6.5 percent) [78].

In the ACUITY and HORIZONS-AIM trials, use of monotherapy with the direct thrombin inhibitor bivalirudin was associated with lower risk of hemorrhage compared to the combination of heparin (either unfractionated or low-molecular weight heparin) and a GP IIb/IIIa receptor inhibitor [65]. (See "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies", section on 'Bivalirudin'.)

Arrhythmia — Bradycardia is most often associated with the injection of contrast material into the coronary circulation. This issue is discussed separately. (See "Complications of diagnostic cardiac catheterization", section on 'Bradycardia'.)

Ventricular tachycardia (VT) and ventricular fibrillation (VF) appear to be uncommon after PCI, including primary PCI. In a review of almost 20,000 PCIs performed at a single hospital, VF occurred in 164 (0.8 percent) [79]. VF usually followed intracoronary contrast injection and all patients were successfully defibrillated in less than one minute with no sequelae.

The frequency of these arrhythmias occurring in the cardiac catheterization laboratory at the time of planned primary PCI for ST-elevation MI was analyzed in a review of 3065 patients from the PAMI trials, one-third of whom received a stent [80]. Ventricular arrhythmias occurred in 133 (4.3 percent). Variables independently associated with an increased risk of VT or VF included smoking, lack of preprocedural beta blockers, shorter time from symptom onset to emergency department arrival, initial TIMI flow grade 0, and right coronary artery-related infarct. Patients with VT or VF had higher rates of complications, including cardiopulmonary resuscitation and intubation in the catheterization laboratory but had similar frequencies of major adverse cardiac events in-hospital and at one year.

Ventricular arrhythmias occurring in the catheterization laboratory during primary PCI may be attributable to the procedure, the MI, or both. The discussion of ventricular arrhythmias in patients with ST-elevation MI who are referred for PCI is found elsewhere. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

Radiation exposure — Patients undergoing diagnostic and interventional cardiac catheterization (and healthcare personnel performing them) receive substantial radiation exposure. This issue is discussed in detail separately. (See "Radiation dose and risk of malignancy from cardiovascular imaging" and "Radiation-related risks of imaging".)

The use of a remote-controlled, robotic PCI system to reduce radiation exposure was evaluated in a study of 164 patients with non-complex coronary lesions [81]. The system consists of a remote interventional cockpit and a bedside disposable cassette from which the operator can advance, retract, and rotate guidewires and catheters. Clinical success, defined as <30 percent residual stenosis without major adverse cardiovascular events within 30 days, and technical success, defined as successful manipulation of the intracoronary devices using the robotic system only, was achieved in 97.6 and 98.8 percent of cases, respectively. Radiation exposure for the primary operator was 95 percent lower than levels found at the traditional table position.

It not known whether there is a clinically important increase in radiation risk for the patient or the operator with radial artery catheterization compared with the transfemoral approach. (See 'Vascular complications' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures".) In a meta-analysis of data from 24 randomized trials (n = 19,328) of PCI or diagnostic angiography, transradial artery catheterization during PCI, compared with femoral artery catheterization, was associated with a small but significant increase in fluoroscopy time (1.15 min, 95% CI 0.96-1.33; p<0.0001) and a higher kerma-area product (0.55 Gy-cm2, 95% CI 0.08-1.02; p = 0.02), which is one measure of radiation dose [82].

Peripheral artery disease — Patients with peripheral artery disease (PAD) appear to be at an increased risk for periprocedural complications after PCI.

The trend for the use of smaller vascular sheaths (ie, 6F rather than 8F) and lower doses of heparin may reduce the incidence of complications in this high-risk population. Also, use of radial artery access site in this high-risk population is recommended.

Hypersensitivity reactions — Hypersensitivity reactions have been reported after placement of drug-eluting stents (DES) and are considered as a potential mechanism for stent thrombosis. In a review of the US Food and Drug Administration database through 2004, there were 262 unique cases that included hypersensitivity symptoms after placement of first generation sirolimus or paclitaxel stents [83]. Placement of a DES was thought to be a probable or possible cause in only 10 cases. This report also identified 17 cases not in the database, including four autopsies that were probably or certainly caused by the stent; nine of these patients had symptoms that lasted more than four weeks. Intrastent eosinophilic inflammation, thrombosis, and lack of intimal healing were noted in the autopsied cases. Hypersensitivity reactions to the newer DES (everolimus- or zotarolimus-eluting stents) are suspected to be much less common; however, a case has been reported [84].

A single case of zotarolimus-eluting stent-induced hypersensitivity pneumonitis has also been reported [85]. (See "Acute interstitial pneumonia (Hamman-Rich syndrome)" and "Taxane-induced pulmonary toxicity", section on 'Interstitial pneumonitis'.)

SAME-DAY DISCHARGE — For many patients who undergo elective percutaneous coronary intervention (PCI), same-day discharge (SDD) can be considered. As most of the adverse outcomes discussed above occur within the first six hours after the procedure, we typically wait at least six hours prior to discharge.

SDD is safe in low-risk patients with the following characteristics: age <75 years, stable coronary artery disease, estimated glomerular filtration rate >60 mL/min per 1.73 m2, left ventricular ejection fraction >30 percent, no contrast allergy, adequate social support, no significant left main coronary artery disease, no complex intervention or significant complication, hemodynamic stability, and no recurrent chest pain after the procedure [86,87]. These are examples of low-risk characteristics, but other patients may also be candidates for SDD on a case-by-case basis. Many practitioners are more comfortable with SDD in patients who have undergone a radial artery procedure rather than one from a femoral artery.

Many large studies have found that SDD is not associated with an increased risk of complications compared with discharge the following day, and that the rate of SDD has increased in many locations in the last 10 years:

In a 2013 meta-analysis of data from 12,803 patients in seven randomized trials and 30 observational studies who underwent PCI for stable angina, there was no significant difference between SDD and overnight observations with regard to the co-primary end points of death, MI, target lesion revascularization and major bleeding, and vascular complications [87].

A second 2013 meta-analysis, which included a study of over 107,000 patients ≥65 years undergoing elective PCI in the United States American College of Cardiology-National Cardiovascular Disease Registry [88], came to similar conclusions [89].

A 2019 report using data from nearly 170,000 British patients undergoing elective PCI between 2007 and 2014 found that the rate of SDD increased from 23.5 to 57.2 percent [90]. This increase was accounted for in large part by the increased use of radial artery catheterization. These patients in this report were likely to be at higher risk than those in the above two meta-analyses.

The observed 30-day mortality (about 0.4 percent) was low and did not differ between SDD and overnight stay (odds ratio 1.15, 95% CI 0.29-4.48). In addition, mortality was not increased compared with mortality predicted by an accepted risk model.

READMISSION WITHIN 30 DAYS — Readmission rates at 30 days after percutaneous coronary intervention (PCI) as high as 15 percent have been reported [91]. In a single center study of over 15,000 patients who underwent (both urgent and non-urgent) PCI between 1998 and 2008, the 30-day rate was 9.4 percent [92]. After multivariable analysis, the following factors (none of which is modifiable) were associated with an increased risk of readmission: female sex, Medicare insurance, having less than a high school education, unstable angina, cerebrovascular accident or transient ischemic attack, moderate to severe renal disease, chronic obstructive pulmonary disease, peptic ulcer disease, metastatic cancer, and a length of stay of more than three days. Readmission was associated with a higher risk of one-year mortality (adjusted hazard ratio, 1.38, 95% CI 1.08-1.75).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Percutaneous coronary intervention".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Beyond the Basics topic (see "Patient education: Stenting for the heart (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Aside from comorbidities, important predictors of adverse short-term outcomes in the periprocedural period include absence of on-site cardiac surgery and lesion complexity. Risk scores are available to predict adverse outcomes. (See 'Predictors of mortality and major complications' above.)

Mortality at one year is predicted by periprocedural myocardial infarction (MI) and bleeding. (See 'Long-term mortality' above.)

Important complications include:

In-hospital death, which occurs at a rate around 1 percent. (See 'Short-term outcomes' above.)

Coronary artery complications such as perforation, distal embolization, side branch occlusion, or stent thrombosis. (See 'Coronary artery complications' above.)

Myocardial ischemia and infarction. Occasionally, this may require urgent coronary artery bypass graft surgery. (See 'Myocardial ischemia and infarction' above.)

Vascular complications including access site and retroperitoneal bleeding or atheroembolism. (See 'Vascular complications' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures".)

Stroke, which occurs at a rate of about one to four per thousand. (See 'Stroke' above.)

Other important complications include acute kidney injury and anticoagulation-associated bleeding. (See 'Other' above.)

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Topic 1562 Version 48.0

References

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