What are the possible complications of percutaneous coronary intervention (PCI)?

Updated: Nov 27, 2019
  • Author: George A Stouffer, III, MD; Chief Editor: Karlheinz Peter, MD, PhD  more...
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Answer

The common complications of PCI are bleeding, hematoma, and pseudoaneurysm at the access site. To minimize the risk of these complications, extreme care must be taken in obtaining access at the beginning of the procedure.

Bleeding avoidance strategies (eg, bivalirudin and the radial approach) appear to lower the risk of post-PCI bleeding for both men and women; however, such strategies may be of particular significance in female patients, in that the absolute differences in risk are substantially greater in women. [115]

A retrospective cohort analysis of data on 2,820,874 PCI procedures from the CathPCI registry demonstrated that the use of radial access for PCI (r-PCI) was on the increase and that the procedure was associated with a lower risk of bleeding and vascular complications than traditional transfemoral PCI, even after age, sex, and clinical presentation were accounted for. [116]

Anaphylaxis caused by the contrast agent can occur; therefore, a careful preprocedural history must be obtained. Patients with a prior anaphylactoid reaction to the contrast media should receive appropriate steroid prophylaxis before repeat contrast administration. Contrast administration is one of the leading causes of hospital-acquired acute kidney injury (AKI). The only strategies that have been shown to minimize the risk of AKI are hydration and minimizing the use of contrast.

Early registries of balloon angioplasty results showed complication rates that were much higher than those typically observed today. Reductions in the complication rate have been complemented by improvements in the acute success rate. Previously, registries such as the National Heart, Lung, and Blood Institute (NHLBI) Coronary Angioplasty Registry reported primary success rates of 61%. Today, with the use of stents and adjunctive pharmacotherapy, success rates range from 95% to 99%.

The mechanism by which balloon angioplasty or stenting improves luminal diameter is associated with significant local trauma to the vessel wall, which can, in turn, lead to occlusive complications in a minority of patients. Coronary artery dissection typically results from the vessel injury secondary to balloon expansion. Animal and postmortem human studies have shown that localized dissection at the site of balloon expansion is detected angiographically in as many as 50% of patients immediately after balloon angioplasty.

Such small dissections probably are necessary to obtain adequate lumen expansion; they rarely interfere with antegrade blood flow and are usually unimportant. Angiographic follow-up typically shows no residual evidence of a dissection as early as 6 weeks after angioplasty in most of the cases studied. However, larger dissections can lead to complications.

Often, these dissections are treated with a stent to cover the dissection flap. Coronary perforation or rupture is very rare (occurring in fewer than 1% of cases) and is typically associated with the use of ablative devices or oversized balloons. It can occur from the wire tip or at the culprit lesion. Wire perforations are typically small and usually do not warrant further intervention; perforations from balloon inflation or stent implantation can occasionally necessitate treatment with a covered stent graft.

Abrupt vessel closure may occur in as many as 5% of balloon angioplasty cases, usually developing when the true lumen is compressed by a large dissection flap, thrombus formation, superimposed coronary vasospasm, or a combination of these processes. The presence of large coronary dissections immediately after balloon angioplasty is associated with a fivefold increase in the risk of abrupt closure.

Since the introduction and implementation of intracoronary stents and newer antiplatelet drugs, the incidence of abrupt closure has decreased significantly, to less than 1%. Microembolization of plaque debris or adherent thrombus may also cause acute complications during angioplasty and may contribute to postprocedural cardiac enzyme elevation and chest pain in some patients.

In fewer than 1% of angioplasty patients, microembolization of the platelet-rich thrombus may cause diffuse distal arteriolar vasospasm secondary to release of vasoactive agents, resulting in no-reflow. This complication is difficult to treat but may respond to intracoronary calcium channel antagonists, adenosine, or nitroprusside. Patients undergoing balloon angioplasty of saphenous vein graft lesions and primary angioplasty in the setting of acute MI with a large amount of adherent thrombus are at greatest risk for distal embolization.

Restenosis after balloon angioplasty necessitating a second revascularization procedure is a major limitation that occurs in about 15-30% of patients, depending on the definition of restenosis applied. With the advent of DESs, restenosis rates have fallen to less than 10%.

Some of the very rare but serious complications of PCI are stroke, MI, and death. With advances in technique, technology, and adjuvant medical therapy, PCI is now associated with mortality and emergency bypass rates lower than 1%. The rate of nonfatal MI after coronary angioplasty ranges from 5% to 15%, whereas the rate after stent placement ranges from 2% to 5%.


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