Abstract:
Complications can occur during or after diagnostic angiography and percutaneous coronary intervention. Acute complications can be classified into (a) coronary, including acute vessel closure, perforation, and equipment loss or entrapment; (b) cardiac non-coronary, including hypotension, myocardial infarction, arrhythmias and tamponade ; and (c) non-cardiac, such as vascular access complications, thromboembolic complications, contrast-related complications, radiation injury, and side effects of medications. Chronic complications include restenosis and stent thrombosis. Awareness of potential complications can facilitate prevention and early diagnosis and treatment.
Keywords:
high-risk percutaneous coronary intervention, complications, prevention
Diagnostic coronary angiography and percutaneous coronary intervention (PCI) may lead to complications, both acute (during the procedure or during the hospital stay) ( Fig. 8.1 ) and long-term (such as restenosis or stent thrombosis). Acute complications include death, myocardial infarction, stroke or other thromboembolism, vascular complications, bleeding, need for emergency surgery, contrast reactions, radiation injury, and arrhythmias ( Table 8.1 ). An in-hospital complication is expected to occur in approximately 1 of 74 patients undergoing diagnostic catheterization, 1 of 22 patients without ST-segment elevation acute myocardial infarction (STEMI), and 1 of 8 patients undergoing PCI for STEMI (primary PCI).
| Diagnostic Catheterization Only Patients Without STEMI ( n = 1,091,557) | PCI Patients Without STEMI ( n = 787,980) | PCI Patients With STEMI ( n = 153,268) | |
|---|---|---|---|
| Complications (%) | |||
| Any adverse event | 1.35 | 4.53 | 12.4 |
| Cardiogenic shock | 0.24 | 0.47 | 3.87 |
| Heart failure | 0.38 | 0.59 | 3.46 |
| Pericardial tamponade | 0.03 | 0.07 | 0.15 |
| CVA/stroke | 0.17 | 0.17 | 0.56 |
| % of total strokes that were hemorrhagic | 9.16 | 15.6 | 19.7 |
| New requirement for dialysis | 0.14 | 0.19 | 0.63 |
| In-hospital mortality | |||
| Non–risk-adjusted | 0.72 | 0.65 | 5.2 |
| Non–risk-adjusted excluding CABG patients | 0.60 | 0.62 | |
| CABG performed during admission | 7.47 | 0.81 | |
| CABG Status | |||
| Salvage/emergency | 0.01/0.27 | 0.01/0.17 | 0.05/0.87 |
| Urgent/elective | 5.27/1.92 | 0.47/0.16 | 2.08/0.43 |
| CABG Indication | |||
| PCI failure without clinical deterioration | 0.26 | 0.58 | |
| PCI complication | 0.14 | 0.22 | |
| Bleeding Complications (%) | |||
| Any bleeding event within 72 h of procedure | 0.49 | 1.40 | 3.85 |
| Any other vascular complication requiring treatment | 0.15 | 0.44 | 0.62 |
| RBC/whole-blood transfusion | N/R | 2.07 | 5.61 |
High-risk patient: Definition
Patients classified as high risk are more likely to die or have complications during cardiac catheterization than are other patients. Numerous studies have summarized the clinical and anatomic characteristics of patients at high risk ( Table 8.2 ). Increased patient risk may be immediately obvious (for example in the acute myocardial infarction patient in cardiogenic shock) or less obvious (such as patients with high international normalized ratio [INR]).
| Demographics |
| Age >60 years or <1 year |
| Female sex |
| Comorbidities: Non-cardiac |
| Poorly controlled hypertension |
| Diabetes mellitus |
| Renal insufficiency, including dialysis |
| Pulmonary disease (COPD, asthma, OSA) |
| Anemia ± bleeding diathesis, active bleeding, elevated INR, thrombocytopenia |
| Cerebrovascular disease |
| Severe peripheral vascular disease (vascular access difficulty is also included) |
| Very small or very large body habitus |
| High and low BMI |
| Frailty |
| Comorbidities: Cardiac |
| Severe left ventricular dysfunction (EF<30%) |
| Decompensated heart failure (especially NYHA class IV) |
| Pulmonary hypertension |
| Atrial/ventricular arrhythmias |
| Severe valvular disease |
| Prior PCI |
| Prior CABG |
| Medications |
| Erectile dysfunction drugs |
| Oral anticoagulants |
| Metformin |
| Insulin |
| Diuretics |
| IV contrast allergy |
| Presentation |
| Cardiac arrest |
| Cardiogenic shock |
| Acute myocardial infarction |
| Emergent procedure |
| Coronary Anatomy |
| Left main disease |
| Multivessel disease |
| Severe calcification |
| Tortuosity |
| Saphenous vein graft lesion |
| Small vessel size |
| Chronic total occlusions |
| Bifurcations |
| TortuositySpontaneous coronary dissection |
| Technique |
| Femoral access |
| Use of radiation |
High risk may be a function of the patient demographics (age, gender), cardiac and noncardial comorbidities, presentation, coronary anatomy, urgency of the procedure, and technique ( Table 8.2 ). Several scores have been developed to predict the risk of acute and chronic complications during catheterization and PCI and have been implemented in online calculators, such as the SCAI online calculator ( http://www.scai.org/PCIRisk AssessmentTools/default.aspx ).
Prevention of complications
Meticulous attention to the precatheterization patient assessment and recognition of potential risks decreases procedure-related complications.
The best complications are those that never occur.
Anonymous
Acute vessel closure
Several mechanisms can lead to acute vessel closure ( Fig. 8.1 ), highlighting potential prevention strategies. Meticulous attention to pressure waveform (to avoid dampening) can minimize the risk for creating (and extending) an aortocoronary dissection. Protection of side branches (by inserting and jailing a guidewire) can reduce the risk of occlusion during bifurcation stenting. Careful wire manipulation may decrease the risk of subintimal entry and dissection. Careful preparation of the manifold and back-bleeding of the catheter after wire removal, equipment exchanges, and use of the trapping technique may minimize the risk of air embolization. A small air embolus usually resolves and does not often result in permanent damage. Significant air embolus to the coronary circulation can cause myocardial ischemia and circulatory collapse. Air aspiration should be promptly performed in such cases, together with administration of 100% oxygen (to help dissolve the air bubbles) and possibly use of intracoronary epinephrine and cardiopulmonary support.
Perforation
Coronary perforation can be classified according to location (large vessel, small vessel, septal and epiocardial collateral perforation, Fig. 8.2 ) and according to severity (Ellis classification, Box 8.1 ). The risk of perforation may be minimized by avoiding use of oversized balloons and stents, careful use of atherectomy devices, and meticulous attention to distal guidewire position.
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Class 1: a crater extending outside the lumen only in the absence of linear staining angiographically suggestive of dissection.
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Class 2: Pericardial or myocardial blush without a ≥1 mm exit hole
- •
Class 3: Frank streaming of contrast through a ≥1 mm exit hole.
- •
Class 3-cavity spilling: Perforation into an anatomic cavity chamber, such as the coronary sinus, the right ventricle, etc.
The first step in the management of coronary perforation is to inflate a balloon rapidly to minimize blood extravasation into the pericardium ( Fig. 8.3 ). In case of tamponade, emergency pericardiocentesis is performed. If pericardial bleeding continues after balloon inflation, use of a covered stent and fat or coil embolization are usually used to achieve hemostasis ( Fig. 8.3 ). Anticoagulation should not be reversed until all equipment is removed from the coronary artery.
Equipment loss and entrapment
Equipment loss or entrapment in the intravascular or intracoronary space may lead to emergency surgery for removal. Adequate lesion preparation is key for reducing the risk of stent loss or entrapment. In many cases, lost devices may not need to be retrieved: for example, lost stents can sometimes be deployed or crushed using another stent.
Hypotension
Hypotension may occur before, during, and after cardiac catheterization from a variety of conditions. Hypotension should be distinguished from pseudohypotension, for example when there is dampening of the pressure waveform because of deep catheter engagement or obstruction from thrombus/plaque. Correlation with noninvasive pressure can help make the diagnosis. If catheter obstruction is suspected, the catheter should be withdrawn without injection contrast or attempting to advance a guidewire through it (to minimize the risk for systemic thromboembolism).
Hypotension during any stage of the procedure may be caused by myocardial ischemia or cardiogenic shock that may require treatment with inotropic and vasopressor agents and with hemodynamic support devices.
Before cardiac catheterization , hypotension may be caused by hypovolemia induced by fasting before the procedure or diuretics.
During the procedure , hypotension may be caused by vasovagal reaction. Untreated vasovagal reactions with hypotension can lead to irreversible shock. Vasovagal reactions are often the result of pain at the vascular access site. In some elderly patients, a vagal reaction may occur without bradycardia and appear as unexplained hypotension. Hypotension that develops after coronary angiography or left ventriculography is generally transient, self-limited, and responds to IV fluids. Other considerations during the procedure include oversedation, IV contrast allergy, or vagal reaction from a full bladder. Nitroglycerin administration can also lead to hypotension.
During and after the procedure , hypotension may be caused by hypovolemia, myocardial ischemia, bleeding from the arterial access site, cardiac tamponade, or retroperitoneal hemorrhage. Any of these can present with bradycardia and hypotension and initially appear to be a vagal response.
Hypotension resulting from hypovolemia is treated with IV saline infusion. Patients often respond acutely to elevation (>30 degrees) of the legs (increased venous inflow, internal transfusion). Generally, several hundred milliliters of saline is required to restore adequate blood pressure in patients who have hypotension caused by hypovolemia. Preprocedure prevention of hypovolemia can be avoided by IV saline (>500 mL) for 4 to 6 hours before the start of the procedure.
For patients who have hypovolemia caused by hemorrhage, administration of blood products is necessary and hemostasis must be achieved as soon as possible. Care should be taken to prevent volume overload in patients with congestive heart failure. If a patient’s volume status cannot be determined clinically, a pulmonary artery catheter and pulmonary capillary wedge pressure measurement may be necessary.
For patients with hypotension resulting from vasovagal or ischemia reaction, pharmacologic therapy may be necessary to restore adequate blood pressure. Atropine for vasovagal hypotension (0.5 mg IV every 3 minutes as needed) is used first. IV phenylephrine (0.1 to 0.3 mg) or an epinephrine bolus (1 mL of 1:10,000-U dilution) temporarily increases blood pressure to normal range while the staff member continues to assess the patient and prepare other vasopressors. For patients with prolonged hypotension or hypotension without hypovolemia, IV infusions of pressors may be initiated and can be titrated as needed. Dopamine starting at 5 mcg/kg/min or norepinephrine at 10 mcg/min can be titrated according to response.
Drug-induced hypotension should be addressed with agents that antagonize, ameliorate, or minimize the actions of the offending agent. Narcotic-induced hypotension can be treated with administration of naloxone (Narcan). The initial dose is 0.4 mg (1-mL ampule), which may be repeated every 2 to 3 minutes as needed. Hypotension (or hypoventilation) resulting from benzodiazepine administration can be treated with flumazenil (Romazicon). The initial dose is 0.2 mg (2 mL) administered over 30 seconds; additional doses of 0.2 mg (up to 1 mg) can be administered every 1 minute. Because of the sedatives’ longer half-life than that of reversal agents, resedation can occur, and repeat doses can be given every 20 minutes, with a maximum dose of 3 mg/h.
Hypotension can result from negative inotropic, negative chronotropic, and vasodilator actions of calcium channel blockers. Vasodilator actions can be at least partially reversed by administration of calcium chloride (1 ampule, 13.6 mEq). Administration of glucagon (1 mg) may partially ameliorate the effects of β-blockers. If nitroglycerin-induced hypotension develops, IV infusion should be stopped or the nitropaste wiped off.
Hypotension resulting from cardiac tamponade is an emergency condition that requires immediate pericardiocentesis.
Management of refractory myocardial ischemia and hemodynamic instability
Transient ischemia and coronary artery occlusion can be caused by catheter-induced spasm, cannulation of a severely diseased coronary artery, or a severe ostial lesion. Initial intervention is removal of the catheter from the coronary ostium. Continued myocardial ischemia should initially be treated with pharmacologic therapy beginning with nitrates, either sublingual nitroglycerin (0.4 mg every 5 minutes), or IV or intracoronary nitroglycerin (100-mcg boluses repeated every 5 minutes as necessary). Nitroglycerin can be used, provided that the patient does not have hypotension. For patients with tachycardia, negative inotropic therapy with a β-blocker, such as metoprolol (5 mg IV every 5 minutes), or a calcium channel blocker, such as verapamil (2.5 to 5 mg IV every 5 minutes), should be considered if the patient is otherwise hemodynamically stable.
When ischemia persists after optimal medical treatment, or when it is associated with significant hemodynamic instability including pulmonary edema or hypotension or both, mechanical circulatory support should be considered.
Circulatory support devices
Circulatory support devices can be used either prophylactically or after occurrence of a complication during CTO PCI. Four devices are currently available in the United States for providing percutaneous left ventricular hemodynamic support: the intraaortic balloon pump (IABP), the Impella (2.5, CP, and 5.0, Abiomed Inc., Danvers, MA), the TandemHeart (Cardiac Assist Inc., Pittsburgh, PA), and venoarterial extracorporeal membrane oxygenator (VA ECMO) ( Fig. 8.4 , Table 8.3 ).
| IABP | Impella | TandemHeart | VA ECMO | |
|---|---|---|---|---|
| Feasibility | ||||
| Availability | +++ | ++ | + | + |
| Arterial access size required | 7–8 F | 12 F (Impella 2.5) 14 F (Impella CP) 21 F (Impella 5.0) | 15–17 F arterial 21 F venous | 14–17 F arterial 18–21 F venous |
| Contraindications |
|
|
|
|
| Efficacy | ||||
| Cardiac output increase (L/min) | 0.3–0.5 | ≈2.5 (Impella 2.5) ≈4.0 (Impella CP) ≈5.0 (Impella 5.0) | 4–5 b | 4–5 b |
| Affected by arrhythmias | Yes | No | No | No |
| Requires adequate right ventricular function | Yes | Yes | Yes | No |
| Can correct respiratory failure | No | No | Yes c | Yes |
| Complications | ||||
| Risk for lower limb ischemia | + | ++ | +++ | +++ |
| Transseptal puncture required | No | No | Yes | No |
| Risk for bleeding | + | ++ | ++ | ++ |
| Risk for hemolysis | + | ++ | ++ | ++ |
a Transcaval access can be used for placing the arterial cannula in case of severe peripheral arterial disease
b Depending on arterial cannula size
Determining the need for prophylactic or urgent insertion of a hemodynamic support device depends on the patient’s clinical condition (hemodynamic status, left ventricular systolic function and end-diastolic pressure), procedural risk (for example retrograde chronic total occlusion [CTO] PCI through the last remaining vessel), and local device availability and expertise.
Intraaortic balloon pump
The IABP is the smallest circulatory support device, but it also provides the least hemodynamic support (0.5 L/min of blood flow). The IABP is usually inserted percutaneously through a 7-F or 8-F femoral arterial sheath. The IABP mechanism of action is inflation of a balloon with helium in the aorta during diastole, displacing blood peripherally and increasing cardiac output, while reducing left ventricular end diastolic pressure. Indications and contraindications for IABP use are summarized in Box 8.2 .
Indications
Refractory unstable angina
Cardiogenic shock
Postoperative hemodynamic compromise
Acute myocardial infarction with mechanical impairment as a result of mitral regurgitation or ventricular septal defect
Intractable ventricular tachycardia as a result of myocardial ischemia
Patients with left main coronary stenosis or severe three-vessel disease undergoing anesthesia for cardiac surgery
High-risk PCI
Maintenance of vessel patency after PCI with slow flow
Contraindications
Anatomic abnormality of femoral-iliac artery
Iliac or aortic atherosclerotic disease impairing blood flow runoff
Moderate or severe aortic regurgitation
Aortic dissection or aneurysm
Patent ductus (counterpulsation may augment the abnormal pathway of aortic-to-pulmonary artery shunting)
Bypass grafting to femoral artery
Bleeding diathesis
Sepsis
PCI, Percutaneous coronary intervention; PTCA, percutaneous transluminal coronary angioplasty.
IABP counterpulsation increases diastolic pressure and coronary blood flow and decreases myocardial oxygen demand (i.e., reduces afterload). Balloon inflation in diastole (at the dicrotic notch on the central arterial pressure tracing) increases diastolic pressure, which increases coronary artery pressure and coronary flow. Deflation of the balloon just before systole (at end diastole, at the upstroke of arterial pressure tracing) results in decreased ventricular afterload, which decreases myocardial oxygen consumption and increases cardiac output ( Fig. 8.5 ).
Technique
Before percutaneous insertion of an intraaortic balloon (IAB), the operator assesses the iliofemoral arteries and aorta for vascular disease. Significant peripheral vascular disease is a relative contraindication. An abdominal aortogram helps identify the course and disease of iliac and femoral vessels before IABP insertion.
Complications of IAB placement most commonly result from a puncture site that is too low, perforation of the superficial femoral artery, or forceful artery dissection caused by advancement of the guidewire. The puncture site should be located similar to or slightly more cranial than a standard femoral puncture for diagnostic catheterization. A low puncture may involve the superficial femoral artery, which is often too small to accept the IABP, and this may result in subsequent leg ischemia.
The IABP balloon sheath (or sheathless IABP catheter) is inserted into either groin using the modified Seldinger technique. Before IABP catheter insertion, a negative vacuum to the balloon is applied using a large syringe and the one-way valve provided in the IABP insertion kit. The catheter is loaded with the 0.018-inch or 0.025-inch guidewire provided in the IABP kit. The assembly is inserted through the sheath with the guidewire leading. The marker at the tip of the IABP catheter should be 1 to 2 cm below the top of the aortic arch at the level of the carina of the trachea. The guidewire is then removed. The central lumen is carefully flushed and connected to a pressure transducer. Fluoroscopic observation of the balloon inflation above the renal arteries confirms optimal placement.
After the catheter is positioned, the IABP tubing is connected to the IABP console and counterpulsation is initiated. In short patients, pumping may not begin if the distal end of the balloon catheter remains in the sheath. Partial withdrawal of the sheath from the femoral artery may remedy this problem. The balloon catheter is secured with sutures. The position of the balloon is rechecked before the patient is moved. After the patient has been returned to the intensive care unit, the position of the IABP is checked again with a chest radiograph.
The timing cycle of IABP inflation should begin at 1:2 pumping (one inflation for every two beats). Balloon inflation timing is adjusted to optimize the augmented diastolic pressure waveform ( Fig. 8.6 ). The rate of central aortic pressure through the IABP lumen is used to assess hemodynamic effects.
