General description of procedure, equipment, technique
Angiographic complications during percutaneous coronary intervention
With the availability of improved anticoagulation methods and coronary stents, the major complication rates after percutaneous coronary intervention (PCI) have been reduced to fewer than 2% in most clinical centers. Emergency coronary bypass surgery is required in fewer than 1% of cases, generally performed for the inability to recanalize an abruptly occluded vessel or for coronary perforation that cannot be controlled with conservative measures. Despite these improvements in overall clinical outcome, a number of major and minor angiographic complications may develop that require prompt recognition and management.
Coronary dissections occur as a result of balloon induced barotrauma to the vessel wall during expansion. Controlled dissection and remodeling are important components of the “angioplasty” effect to improve the coronary lumen diameter. In the majority of cases, the dissections are benign (and therapeutic), but when the coronary dissection expands beyond the target site or results in lumen compromise, corrective treatment with a coronary stent is indicated.
Coronary dissections occur more frequently in longer and more complex lesions, particularly those with calcification. Iatrogenic guide catheter dissections also may occur in the right coronary artery and left main coronary artery, resulting from noncoaxial alignment of the guiding catheter or too vigorous contrast injection with the tip of the catheter in the subintimal space. More problematic are those iatrogenic dissections that occur distal to the treatment sites, often from the coronary guidewire.
National Heart Lung and Blood Institute (NHLBI) classification of coronary dissection
Type A: Intraluminal haziness
Type B: Linear opacification within the vessel lumen
Type C: Cap dissection associated with contrast staining
Type D: Spiral Dissection
Type E: Dissection with reduced anterograde flow
Type F: Dissection with cessation of anterograde flow
Treatment of coronary dissection depends on its physiologic importance. Non pathologic coronary dissections often heal spontaneously. The prognosis associated with coronary dissections relate to its length (>10 mm length), significant lumen compromise (>40% diameter stenosis), and dissection at the edge of coronary stents; these findings are associated with a higher risk of abrupt occlusion. Coronary stent placement is corrective in the vast majority of cases. If a dissection cannot be treated with stent placement, prolonged intravenous heparin and intravenous glycoprotein IIb-IIIa inhibitors may be useful in the acute phase to prevent thrombus formation at the treatment site. Often, dissections heal spontaneously and distal perfusion is preserved.
The incidence of coronary perforations is approximately 0.2% to 0.5% in patients undergoing PCI, and is higher in patients undergoing atheroablative procedures (e.g., rotational and directional atherectomy, excimer laser angioplasty) or treatment for chronic total occlusions. Oversized, high-pressure balloon inflation after coronary stent placement may also result in significant perforations. More recently, guidewire perforations, particularly those with hydrophilic coatings, have been a more common cause of perforation. Guidewire perforations are particularly problematic, as they can present later after the patient has left the cardiac catheterization laboratory.
Predictors of coronary perforation include female gender, increasing age, vessel calcification, use of a cutting balloon, use of an atheroablative device or treatment of a total coronary occlusion.
Coronary perforations can present in one of several ways. Free flowing coronary rupture into the pericardial space can cause immediate cardiac tamponade and cardiovascular collapse. This can be recognized with coronary injection and free flow of contrast into the pericardium. Ellis and colleagues have classified these perforations into:
Type I: crater extending outside the lumen only and in the absence of linear staining angiographically suggestive of a dissection (approximately 20%).
Type II: pericardial or myocardial blush without a greater than 1 mm exit hole (approximately 40%).
Type III: frank streaming of contrast through a greater than 1 mm exit hole (approximately 40%).
A more ominous coronary perforation is the formation of an intramural hematoma with extension into the myocardial bed. This is an uncommon manifestation of coronary perforation but can result in progressive hemodynamic collapse.
Finally, the coronary perforation can extend into a ventricular cavity (Type III CS) resulting in minor intracardiac shunts. These are most commonly seen with retrograde recanalization techniques for total coronary occlusions through the septal branches.
Treatment strategies for coronary perforation begin with prompt recognition of the complication. In patients at risk for perforation – such as a heavily calcified stenosis that suddenly yields with high pressure balloon inflation – a test injection of the coronary while the balloon is still within the vessel will allow immediate balloon inflation and cessation of extravasation.
Prolonged (longer than 10 minute) balloon inflations are often successful in sealing the perforations. Reversal of anticoagulation (1 mg protamine for every 100 U unfractionated heparin) or platelet transfusion in the event that abciximab has been used may also reduce the flow into the pericardial space. Reversal of antithrombotic effect is more problematic for agents such as bivalirudin or eptifibatide.
Placement of a pericardial drain can be life-saving in patients who develop hemodynamic compromise resulting from the tamponade.
For coronary perforations that continue despite conservative measures, use of polytetrafluoroethylene (PTFE)-covered stents may be lifesaving; however, these stents require high-pressure balloon inflation for maximum expansion. Coil embolization may be used to treat branch vessel or distal perforations.
The adverse prognosis of coronary perforation is high (2.6-15.9%) and often relates to the speed of recognition of the complication.
Microvascular obstruction (no reflow, slow flow, and no flow)
Microvascular obstruction (MVO) after PCI has been termed “no reflow” and is used to describe the development of reduced anterograde flow as “slow flow” (TIMI Grade = 2) or “no flow” (TIMI Grade 0 or 1). MVO is defined as a reduced myocardial perfusion in the absence of epicardial stenoses. In the setting of an acute coronary thrombosis, as seen with an ST segment elevation myocardial infarction (STEMI), the etiology of MVO is most often related to embolization of thrombus into the distal coronary bed. In contrast, for elective PCI, particularly in patients undergoing saphenous vein graft intervention (SVG), the MVO may related to particulate atheroembolism into the distal myocardial bed. Microvascular spasm, in situ thrombosis, release of mediators and reperfusion injury may be contributing to the development of MVO.
The most effective method to reduce the occurrence of MVO during primary PCI is the use of manual thrombectomy prior to balloon inflation. In contrast, embolic protection appears to have no effect on MVO or mortality, and mechanical thrombectomy seems to have a worsened outcome in STEMI patients in one randomized study.
A number of pharmacologic strategies have been tried to reduce the occurrence of MVO during primary PCI. Vasodilators, including nitroprusside, verapamil and adenosine, have been administered through a distal perfusion catheter prior to PCI and seem to reduce MVO, although the clinical impact of these agents is less clear.
Antiplatelet agents, such as abciximab and tirofiban, appear to improve ST segment resolution and reduce no reflow, particularly when these agents are administered into the thrombus. Cardioprotectants, such as super-saturated oxygen, cyclosporin, ischemic preconditioning and nicorandil, have been shown to reduce infarct size in smaller subsets of patients.
In patients undergoing non-STEMI PCI, preprocedural administration of glycoprotein IIb-IIIa inhibitors, such as abciximab and eptifibatide, reduced the frequency of peri-procedural MI in native coronary arteries, although these agents had limited effect in patients undergoing SVG PCI. Proximal and distal embolic protection devices have been shown to reduce MVO in patients undergoing SVG intervention, although embolic protection devices are used in fewer than 25% of cases of SVG PCI in the United States.
Once no reflow develops, it has been associated with a five-fold increase in myocardial infarction and a three-fold increase in the risk for peri-procedural mortality. Many of the episodes of MVO resolve with time. For sustained episodes of MVO, the treatment of no reflow is best performed using a distal injection of vasoactive drug through a balloon catheter that is placed at the site of reduced flow. Agents that have used to treat no reflow include:
Nitroprusside (50-200 mcg)
Adenosine (100 mcg)
Verapamil (50-1000 mcg)
Inadvertent injection of air may occur during diagnostic intervention and PCI, and its frequency (0.1-0.3%) can be reduced with meticulous flushing of the catheter. Air also can be entrained within the guiding catheter by movement of equipment into the guide catheter through the Tuohy-Borst Y connector. Air embolization also can occur with rupture of a balloon catheter during inflation.
Trapping of air within the distal microcirculation can result in “air lock” into the distal capillary bed. High intracoronary pressure is required to force tiny bubbles through the microcirculation. Signs and symptoms of air embolization include chest pain, ST segment elevation, and potentially hypotension. Ventricular arrhythmias including ventricular fibrillation can occur as a result of air embolization. These can be treated with direct cardioversion and lidocaine.
Should air embolization and air lock occur, 100% oxygen should be immediately administered to permit resorption over the ensuring 2-5 minutes. Forceful injection of blood or contrast may be useful in forcing the air through the capillary bed. Manual aspiration of air using an Export or Pronto catheter can be performed with large emboli. Vasospasm is also common with air embolization and can be treated with adenosine and other vasodilators, such as nitroprusside.
Detached and retained stents
With the availability of lower profile stents and balloons, retained fragments within the coronary circulation are much less common (0.3-0.5%) than in prior years. Stent dislodgement and embolization occur more often with angulated and calcified lesions. Stent dislodgement also may occur when the stent is withdrawn into a guiding catheter that is deeply seated or at an angle relative to the stent, resulting in the stent being “stripped’ off the balloon catheter.
When dislodgement occurs, the first step is to determine whether the coronary guidewire is still through the center of the stent. If so, a small diameter balloon catheter can be advanced through the stent and inflated distal to the stent. This will allow the stent to be retrieved within the guiding catheter. In the event that the stent cannot be retrieved, progressive balloon dilatations can be performed and the stent can be deployed within the coronary vessel. If the wire is no longer within the stent, the stent can be snared and removed, or a guidewire can be passed along side the stent, and an additional stent can be placed to “exteriorize” the stent.
Procedural complications during percutaneous coronary intervention
Peri-procedural myocardial infarction
Varying degrees of myocardial necrosis may occur after PCI. There have been two general classification systems for myocardial infarction (MI) after PCI. The World Health Organization (WHO) defines MI as a total creatine kinase (CK) elevation more than two times normal in association with elevation of the CK-MB isoform. More recently, the Third Universal Definition of MI has defined a peri-procedural MI as an increase of the troponin level more than five times the 99th percentile upper normal limit with clinical evidence of ischemia. Clinical evidence of post-procedural MI includes:
Evidence of prolonged ischemia (20 minutes or more) as demonstrated by prolonged chest pain.
Ischemic ST changes or new pathologic Q waves.
Angiographic evidence of flow limiting complication, such as loss of patency of a side branch, persistent slow flow or no reflow, or embolization.
Imaging evidence of new loss of viable myocardium or new wall motion abnormality.
In patients with troponin levels that are elevated and are stable and falling, a greater than 20% re-elevation is required for the diagnosis of peri-procedural MI. Accordingly, troponin measurement prior to PCI is recommended in many laboratories.
Asymptomatic elevation of cardiac biomarkers may occur in up to 10% of patients after PCI. Larger MIs (more than 5-10 x normal) appear to have prognostic importance. The effect of peri-procedural MI on late mortality may be confounded by the degree of atherosclerosis within the coronary bed.
Reactions to iodinated contrast agents are manifest in two ways: side effects and true anaphylactoid reactions. The majority of side effects to contrast agents relate to their hyperosmolality. Reactions include nausea and vomiting, arrhythmias and a flushing feeling. Allergic radiocontrast reactions are graded as mild (grade I: single episode of emesis, nausea, sneezing or vertigo), moderate (grade II: hives; multiple episodes of emesis, fevers or chills), or severe (grade III: clinical shock, bronchospasm, laryngospasm or edema, loss of consciousness, hypotension, hypertension, cardiac arrhythmias, angioedema or pulmonary edema).
Severe reactions are uncommon (0.2-1.6%), and may be more difficult to manage in patients receiving beta blocker therapy. Due to a recurrence rate that may be up to 50% on reexposure, prophylactic H1 and H2 histamine-blocking agents, aspirin, and corticosteroids have been used to reduce the frequency of the episodes. Patients with a suspected severe prior reaction to a contrast agent may be treated with two doses of prednisone, 60 mg (or its equivalent), the night before and again at 2 hours before the procedure. Diphenhydramine 50 mg and cimetidine 300 mg may also be given before the procedure.
Contrast induced nephropathy has been defined as a 0.5 mg/dL rise in the serum creatinine or a 25% increase in the creatinine from baseline. The former criterion has been more predictive of outcomes in one large administrative database with a higher mortality rate (16.7% v. 1.7%) and requirement for dialysis (9.8% v. 0%).
Contrast nephropathy may develop in up to 20% of patients, particularly those with prior renal insufficiency, diabetes mellitus, dehydration before the procedure, congestive heart failure, larger volumes of contrast material and recent (less than 48 hours) exposure to contrast material.
Fluid administration and limitation of contrast load are the most effective measures for preventing contrast nephropathy. There have been no medications shown in large randomized studies to prevent contrast nephropathy, and recent studies evaluating the use of sodium bicarbonate infusions have been inconclusive.
The peak creatinine generally occurs 48-72 hours after the procedure, a time at which the kidneys are particularly vulnerable to repeated contrast administration. The duration of the nephropathy may last 1 week, and in most cases, renal function returns towards normal if there was no severe renal impairment at baseline.
Neurologic events after PCI
Stroke is an uncommon event after PCI (0.22-0.34%) and may relate to the embolization of atherosclerotic debris by abrasion of the injection catheters in the setting of an atherosclerotic and friable aorta. In patients with multivessel coronary artery disease, a meta-analysis by Palmerini and colleagues has shown that the risk for 30-day stroke was higher for patients undergoing coronary artery bypass surgery (1.2%) compared with PCI (0.34%) (P < 0.001).
Clinical factors predictive of stroke after PCI include acute coronary syndromes, cerebrovascular disease, age, patients with lower ejection fractions, and those with diabetes. Technical risk factors for stroke after PCI include the use of more catheters, greater contrast volumes, larger guiding catheter sizes, and use of rotational atherectomy and an intra-aortic balloon pump. Careful pre-procedural planning may permit less manipulation of the aorta during the procedure and reduce the frequency of stroke.
In-hospital mortality may approach 30% in patients who develop a stroke after PCI, whereas it is 1% if there is no stroke during the procedure. Neurovascular intervention may be used for acute embolization after PCI if recognized early and the occlusion is located in a large intracerebral vessel.
What’s the evidence?
Biondi-Zoccai, GG, Agostoni, P, Sangiorgi, GM. “Incidence, predictor, and outcomes of coronary dissections left untreated after drug-eluting stent implantation”. Eur Heart J. vol. 27. 2006. pp. 540-6. (In a consecutive case series from four Italian centers that included 2,418 patients, significant residual dissections were noted in 1.7% of lesions and 2.8% of patients. Dissections were found more often in longer and complex lesions and in the left anterior descending artery. Dissections were associated with a significant increase in in-hospital and 1-month major adverse clinical events.)
Ellis, SG, Aijuli, S, Arnold, AZ. “Increased coronary perforation in the new device era. Incidence, classification, management, and outcome”. Circulation. vol. 90. 1994. pp. 2725-30. (Coronary perforations were reviewed from 11 clinical centers and compared with a sample of patients who did not develop a perforation. A classification scheme was developed with Type III coronary perforations having the worst prognosis.)
Fasseas, P, Orford, JL, Panetta, CJ. “Incidence, correlates, and clinical outcome of coronary perforation: analysis of 16,298 procedures”. Am Heart J. vol. 147. 2004. pp. 140-5. (A comprehensive analysis of 16,298 PCI procedures that identified 95 perforations. Perforations were more common with the use of atheroablative devices and in women and were associated with substantial morbidity and mortality.)
Hendry, C, Fraser, D, Eichhofer, J. “Coronary perforation in the drug eluting stent era: incidence, risk factors, management, and outcome: the UK experience”. Eurointervention. vol. 8. 2012. pp. 79-86. (A total of 12,729 PCI were reviewed with a total of 44 [0.56%] perforations. The in-patient mortality rate was 15.9%. The occurrence of perforation was associated with female gender, age, coronary calcification, use of a cutting balloon, atheroablation treatment and treatment of a chronic total occlusion.
Dib, J, Boyle, AJ, Chan, M. “Coronary air embolism: A case report and review of the literature”. Catheter Cardiovasc Interv. vol. 68. 2006. pp. 897-900. (A review of the diagnosis and treatment of air embolism.)
Jaffe, R, Dick, A, Strauss, BH. “Prevention and treatment of microvascular obstruction-related myocardial injury and coronary no reflow following percutaneous coronary intervention”. JACC CV Intervent. vol. 3. 2010. pp. 695-704. (A systematic review of the etiology and treatment pathways for microvascular obstruction after PCI.)
Rezkalla, SH, Kloner, RA. “Coronary no-reflow phenomenon: from the experimental laboratory to the cardiac catheterization laboratory”. Catheter Cardiovasc Interv. vol. 72. 2008. pp. 950-7. (A systematic review of the etiology and treatment pathways coronary re-flow after PCI.)
Colkesen, AY, Baltali, M, Acil, T. “Coronary and systemic stent embolization during percutaneous coronary interventions. A single center experience”. Int Heart J. vol. 48. 2007. pp. 129-36. (A review of the frequency and etiology of coronary stent embolization.)
Thygesen, K, Alpert, JS, Jaffe, AS. “Third Universal Definition of Myocardial Infarction”. Circulation. vol. 126. 2012. pp. 2020-35. (A consensus document that provides contemporary definitions for myocardial infarction after PCI.)
Slocum, NK, Grossman, PM, Moscucci, M. “The changing definition of contrast-induced nephropathy and its clinical implications: insights from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium BCM2”. Am Heart J. vol. 163. 2012. pp. 829-34. (A systematic review of 58,957 cases of PCI that compared two definitions of contrast nephropathy and demonstrated that the definition of a 0.5 mg/dl increase in serum creatinine was superior to a definition of an 25% increase in serum creatinine in correlating with a worse outcome after PCI.)
Fuchs, S, Stabile, E, Kinnaird, TD. “Stroke complicating percutaneous coronary intervention: incidence, predictors, and prognostic implications”. Circulation. vol. 106. 2002. pp. 86-91. (A series of 9,662 patients undergoing 12,407 PCIs found that stroke occurred in 43 patients [0.38% of procedures]. Stroke occurred more often in elderly patients, those with lower left ventricular ejection fraction, diabetes, and use of an intra-aortic balloon pumps. Stroke was associated with higher in-hospital mortality and morbidity.)
Palmerini, T, Biondi-Zoccai, G, Reggiani, LB. “Risk of stroke with coronary artery bypass surgery compared with percutaneous coronary intervention”. J Am Coll Cardiol. vol. 60. 2012. pp. 798-805. (A meta-analysis of randomized PCI versus CABG studies showed a higher incidence of stroke in patients undergoing CABG [1.2%] versus PCI [0.34%].)
Hoffman, SJ, Routledge, HC, Lennon, RJ. “Procedural factors associated with percutaneous coronary intervention-related ischemic stroke”. JACC Cardiovasc Interv. vol. 5. 2012. pp. 200-6. (In a comparative analysis of 21,497 PCI procedures, the use of more catheters, more contrast use and large guiding catheter diameters were associated with a higher stroke risk. There was no difference in stroke with radial versus femoral approaches.)
Aggarwal, A, Dai, D, Rumsfeld, JS. “Incidence and predictors of stroke associated with percutaneous coronary intervention”. Am J Cardiol. vol. 104. 2009. pp. 349-53. (In a review of the NCDR registry, the incidence of peri-procedural stroke was 0.22%. Multivariable predictors of stroke included known cerebrovascular disease, older age, acute coronary syndrome and use of an intra-aortic balloon pump.)
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- General description of procedure, equipment, technique
- Angiographic complications during percutaneous coronary intervention
- Coronary dissections
- Coronary perforation
- Microvascular obstruction (no reflow, slow flow, and no flow)
- Air embolization
- Detached and retained stents
- Procedural complications during percutaneous coronary intervention
- Peri-procedural myocardial infarction
- Contrast reactions
- Contrast nephropathy
- Neurologic events after PCI
- What’s the evidence?