Complications of diagnostic cardiac catheterization

INTRODUCTION — Throughout the 1960s and 1970s, cardiac catheterization was primarily a diagnostic procedure that was used to evaluate hemodynamics, ventricular function, and coronary anatomy. However, the introduction of improved angioplasty equipment and new interventional devices in the 1980s made catheterization an important tool in the treatment of ischemic and other cardiovascular disease.

Although diagnostic catheterization and percutaneous coronary intervention (PCI) are done by percutaneous puncture rather than incision, and under local rather than general anesthesia, they can cause a variety of adverse events, ranging from minor problems without long-term sequelae to major complications requiring immediate corrective action. Furthermore, newer interventional procedures may be associated with different and, in some cases, more frequent complications.

The most common complications associated with diagnostic cardiac catheterization will be reviewed here. The complications associated with cardiac catheterization involving PCI are discussed separately. (See "Periprocedural complications of percutaneous coronary intervention".)

MAJOR COMPLICATIONS — The risk of producing a major complication (death, myocardial infarction, or major embolization) during diagnostic cardiac catheterization is generally well below 1 percent (table 1). As a result, the risk-to-benefit ratio still favors performing this procedure as a part of the evaluation of potentially fatal or lifestyle-limiting cardiac disease.

For the individual patient, the risk of an adverse event is dependent upon demographics, cardiovascular anatomy, clinical circumstances including comorbidities, the experience of the operator, and the type of procedure being performed (table 2 and table 3) [1]. Severe peripheral artery disease is a risk factor for all of the major complications.

Death — Death following diagnostic cardiac catheterization is now rare. Compared with the 1 percent mortality rate seen in the 1960s, the second registry of the Society for Cardiac Angiography revealed that the procedural mortality had fallen to 0.1 percent in the more than 200,000 patients catheterized between 1984 and 1987 [2].

High-risk subgroups have been identified in multiple large series [1-9]:

●Age above 60 years and below one year and women have an increased mortality rate after catheterization.

●New York Heart Association functional class IV is associated with an almost tenfold increase in mortality compared with classes I and II (table 4).

●A similar increase in risk is seen with severe disease of the left main coronary artery (compared to single vessel disease) and with a left ventricular ejection fraction (LVEF) below 30 percent (compared to an LVEF above 50 percent).

●Patients with valvular heart disease, chronic kidney disease, diabetes mellitus requiring insulin therapy, peripheral artery disease, cerebrovascular disease, and pulmonary insufficiency all appear to have an increased incidence of death and major complications from cardiac catheterization. Mortality is especially high in those with preexisting renal insufficiency who have further deterioration of renal function within 48 hours after the procedure, particularly when dialysis is required [10]. (See 'Acute renal failure' below.)

Myocardial infarction — Although periprocedural myocardial ischemia is fairly common, infarction is rare. The general risk of myocardial infarction (MI) in most series is less than 0.1 percent [2-7]. However, the risk of precipitating an MI in an individual patient is influenced by patient-related and technique-related factors. Risk factors that predispose patients to MI during the procedure include:

●The extent of disease (0.17 percent with left main coronary disease versus 0.06 percent in single vessel disease) [2].

●Recent non-ST elevation acute coronary syndrome.

●Diabetes mellitus requiring insulin therapy [1].

Stroke — The discussion of stroke consequent to cardiac catheterization is presented separately. (See "Stroke after cardiac catheterization".)

LOCAL VASCULAR COMPLICATIONS — Local complications at the site of catheter insertion are among the most common problems seen after cardiac catheterization (table 1). These problems may include acute thrombosis, distal embolization (image 1), dissection or poorly controlled bleeding (which may be manifested as free hemorrhage or contained hematoma in the femoral or retroperitoneal areas), pseudoaneurysm, or arteriovenous fistula. Hemorrhage and hematoma are usually evident within 12 hours after the procedure by virtue of local discomfort, hypotension, or falling hematocrit, which lead to confirmatory noninvasive testing (ultrasound or computed tomography [CT]). In contrast, other complications such as pseudoaneurysm and arteriovenous fistula may not become apparent for days to weeks afterward.

Ultrasound-guided access of the femoral artery may improve efficacy and reduce vascular complications. A meta-analysis from 2020 reported a higher initial success rate (RR = 1.36; 95% CI 1.17-1.57) and a reduction in vascular complications (RR = 0.48; 95% CI 0.25-0.91) [11].

The vascular complications associated with percutaneous coronary intervention are discussed separately. (See "Periprocedural complications of percutaneous coronary intervention".)

Hemostasis at the femoral access site — The traditional approach to catheter removal at the conclusion of cardiac catheterization was local hand-applied pressure for 15 to 30 minutes. Two alternative approaches are available: mechanical clamp compression and, more importantly, arterial puncture closing devices.

Mechanical clamp — Mechanical clamp compression reduces the amount of staff time and effort required to assure hemostasis, and may reduce the rate of vascular complications. One trial randomly assigned 778 patients to hand applied pressure or mechanical clamp pressure; the latter reduced the frequency of ultrasound-defined femoral vascular complications (femoral artery thrombosis, echogenic hematoma, pseudoaneurysm, or arteriovenous fistulae formation) by 63 percent [12]. However, clamping does not decrease the importance of having staff in attendance to ensure that the device is placed and remains in the correct position.

The circumstances which may make mechanical clamps the preferred method of achieving hemostasis include procedures where longer hemostasis time is anticipated: larger sheaths, excessively anticoagulated patients, recognized hematoma, and dual antiplatelet therapy.

Closure devices — Arterial puncture closing devices (APCDs) eliminate the need for prolonged arterial compression and reduce the subsequent interval of bed rest that is otherwise required. Two types of APCDs in clinical use include collagen hemostatic puncture closure devices (figure 1) [13-16] and suture-mediated devices [17].

APCDs may increase the risk of local vascular complications. In a meta-analysis of 30 trials including 4000 patients who underwent coronary angiography or percutaneous coronary intervention (PCI), nonsignificant increases in the incidence of groin hematoma, bleeding, and pseudoaneurysm formation were associated with use of these devices compared to manual compression [18]. When only those trials with an intention-to-treat analysis were included, the relative risks of groin hematoma and pseudoaneurysm formation were significantly increased (1.89 and 5.40, respectively).

A larger meta-analysis that included 30 studies involving 37,066 patients concluded that the risk of complications depended upon the specific device used and whether the procedure was a diagnostic catheterization or a PCI [19]. In the overall analysis, there was a significant increase in risk with an APCD (odds ratio [OR] 1.34, 95% CI 1.01-1.79).

For reports limited to diagnostic studies, there were no significant differences between APCDs and mechanical compression, although there were trends toward fewer complications with the AngioSeal device (OR 0.71) and toward more complications with the VasoSeal and Perclose devices (OR 1.85 and 1.51, respectively).

For reports limited to PCI, there were no significant differences between APCDs and mechanical compression overall. However, there was a significant increase in vascular complications with the VasoSeal device (OR 2.52).

Closure devices also increase the risk of local infection or endarteritis [20,21]. Although this complication is infrequent (0.3 percent in one series) [21], it can be serious when it occurs. Consideration should be given to periprocedural antibiotics in immunocompromised patients following prolonged arterial access or when sterility has been breached when a closure device is used. It may also be prudent for the operator to change gloves prior to using an arterial closure device (see 'Infection' below). An angiogram of the femoral artery should be performed prior to use of an APCD. Use of closure devices should be avoided if a hematoma has formed during the procedure, or in the presence of severe iliofemoral vascular disease, and when the access site is below the bifurcation of the superficial and profunda femoral arteries.

Chronic warfarin anticoagulation — In patients receiving chronic anticoagulation with warfarin, the risk of excess bleeding (without warfarin discontinuation) needs to be balanced against the risk of thrombus formation and embolization (with short-term discontinuation). In most cases, we withhold warfarin and wait until the International Normalized Ratio (INR) reaches 1.5 before proceeding with catheterization. The following additional comments may help guide the periprocedural use of warfarin:

●When the procedure cannot be delayed or for patients at particularly high risk of periprocedural embolic events with temporary warfarin therapy discontinuation, such as those with prior embolization off warfarin therapy, a transradial approach may allow for reduced risk of major access-related bleeding in patients with an INR of 1.5 to 3 [22]. If a transradial approach is not an option, then careful management of femoral artery hemostasis with manual compression or a closure device may also allow the procedure to be completed safely for INR of 1.5 to 3.

●In patients with an INR >3, administration of fresh frozen plasma prior to arterial sheath removal may be warranted.

●The risk of local bleeding in warfarin-treated patients is likely to be greater in those undergoing PCI who are often treated with heparin, clopidogrel, and a glycoprotein IIb/IIIa inhibitor. These patients typically have longer intraarterial times and more manipulation of the arterial access site. (See "Antithrombotic therapy for elective percutaneous coronary intervention: General use".)

Hematoma formation — Hematoma formation is not uncommon in the soft tissue of the upper thigh and the patient should be advised that the development of a large area of ecchymosis is likely. Although most resolve over a period of days, femoral nerve compression can occur, which may take weeks to months to resolve. Patients should be advised to avoid strenuous activity or lifting heavy objects within the first week following arterial catheterization. Surgical repair for a hematoma is generally not required.

Retroperitoneal extension — If the arterial puncture occurs above the inguinal ligament, a hematoma may extend into the retroperitoneal space, causing hypotension and ipsilateral flank pain. CT scanning or abdominal ultrasonography can help to establish the diagnosis. Treatment is usually conservative, consisting of bed rest and blood transfusion rather than surgical correction. Reversal of systemic anticoagulation may be indicated if bleeding persists or is associated with hemodynamic compromise. If the puncture site is above the inguinal ligament and there is significant retroperitoneal hemorrhage, temporary balloon occlusion or placement of a covered stent may promote hemostasis.

Arteriovenous fistula — Ongoing bleeding from the arterial puncture site may decompress into the adjacent venous puncture site, leading to the formation of an arteriovenous fistula. This complication may be recognized by the presence of a thrill or continuous bruit at the site of catheter insertion.

Surgical repair is usually necessary, since fistulae tend to enlarge over time. The most common finding at surgery is a puncture site below the common femoral artery, which illustrates the importance of careful technique in avoiding this complication [1].

Pseudoaneurysm — If a hematoma remains in continuity with the arterial lumen, a pseudoaneurysm may develop with blood flow into and out of the hematoma cavity during systole and diastole. A pseudoaneurysm is most often recognized by the presence of a pulsatile mass with a systolic bruit over the catheter insertion site; it can be confirmed by duplex ultrasonography. Almost all pseudoaneurysms occur within the first three days after removal of the arterial sheath, and most of the remaining cases by seven days after sheath removal [23].

The main risk factor for pseudoaneurysm formation is an inadequate period of manual compression. This was illustrated in a series of 581 angiographic procedures involving transfemoral arterial catheterization [24]. A pseudoaneurysm occurred in 14 percent of the first 300 procedures in which standard manual compression was performed, compared to 1.1 percent of the next 281 procedures when manual compression was continued for at least five minutes after local bleeding had stopped.

Other risk factors include large bore sheaths, postprocedural anticoagulation, antiplatelet therapy during the intervention, age >65 years, obesity, hypertension, peripheral artery disease, hemodialysis, cannulation of the superficial rather than common femoral artery, and complex interventions [23-25].

Surgical management should be performed when a pseudoaneurysm occurs at the site of a vascular anastomosis, becomes very large and threatens or causes skin necrosis, is expanding rapidly, occurs spontaneously, as it may be infected, or there is a failure of a minimally invasive procedure [25]. Expanding hematomas have a propensity towards eventual rupture, especially if the patient is maintained on anticoagulation [1,7,26,27].

Treatment of smaller pseudoaneurysms may be accomplished with either direct ultrasound-guided compression or with ultrasound-guided local injection of thrombin or collagen into the pseudoaneurysm cavity, which has a higher success rate [23,28-30]. Although an effective approach, ultrasound-guided compression is uncomfortable for both the patient and the person applying compression.

The success rate of ultrasound-guided injection of bovine thrombin was illustrated in a series of 240 patients with simple or complex pseudoaneurysms [23]. The primary success rate was 96 percent with simple pseudoaneurysms and 89 percent with complex pseudoaneurysms. The secondary success rate was 99.6 percent (all but one patient). The authors also reviewed 34 studies with 1388 patients; the overall success rate was 97.2 percent.

The high success rate of ultrasound-guided injection has made it the treatment of choice for most postcatheterization pseudoaneurysms [25]. However, the procedure should not be performed when, as defined above, there is an indication for surgical management.

In rare cases, pseudoaneurysms less than 2 cm can be managed conservatively and monitored by serial imaging to confirm spontaneous resolution.

Arterial thrombosis — Arterial thrombosis is rare and occurs slightly more often when the brachial approach is used [3,4]. Predisposing factors to femoral artery thrombosis include small vessel lumen, peripheral artery disease, diabetes mellitus, female sex, placement of a large diameter catheter or sheath (eg, intraaortic balloon pump), or a long catheter dwell time [2-7,26,27].

Patients with lower extremity pain or paresthesia, plus reduced or absent distal pulses not responding to catheter removal, should be evaluated for possible flow obstructing thrombus or dissection. Urgent vascular surgery or thrombectomy may be required for preservation of the limb.

Radial artery access — Local vascular complications appear to occur less frequently with radial artery access. This issue is discussed in detail elsewhere (see "Periprocedural complications of percutaneous coronary intervention", section on 'Vascular complications' and "Access-related complications of percutaneous access for diagnostic or interventional procedures"). The SAFARI-STEMI Trial presented at the American College of Cardiology Conference in March 2019 found that in a contemporary practice, there was no significant difference in mortality or access site complications in patients randomized to femoral versus radial artery intervention. This was driven by improvements in outcomes with femoral access, possibly from use of ultrasound guidance, fluoroscopic landmark assessments, and use of micropuncture techniques.

Is the palmar arch intact? — Radial artery cannulation is associated with a 5 to 19 percent chance of radial artery occlusion [31]. This complication is not clinically important in most patients because the hand is perfused by both the radial and ulnar arteries with extensive collateral flow between the two. However, some patients have incomplete palmar arches, which may diminish collateral perfusion, possibly leading to hand ischemia in the presence of radial artery occlusion (figure 2).

The modified Allen test has traditionally been used to identify patients at increased risk from radial artery catheterization. However, many centers now use pulse oximetry and plethysmography. (See "Arterial blood gases", section on 'Ensure collateral circulation'.)

The modified Allen test, originally developed to evaluate patients with thromboangiitis obliterans, assesses the adequacy of collateral blood supply from the ulnar artery to the hand via the palmar arches (figure 2). The test consists of the following steps (figure 3):

●The patient's hand is initially held high while the fist is clenched and both radial and ulnar arteries are compressed; this allows the blood to drain from the hand.

●The hand is then lowered and the fist is opened.

●After pressure is released over the ulnar artery, color should return to the hand within six seconds, indicating a patent ulnar artery and an intact superficial palmar arch. The test is considered abnormal if 10 seconds or more is required for color to return.

In two large series of patients undergoing cardiac catheterization, an abnormal Allen test result was obtained in 6 and 27 percent [32,33]. The importance of an abnormal test was evaluated in a study of 55 patients undergoing coronary angiography, 20 of whom had an abnormal test [31]. After 30 minutes of subsequent radial artery occlusion, the patients with an abnormal test had significantly reduced blood flow to the thumb and an elevated thumb capillary lactate.

Based upon such observations, radial artery catheterization is usually not performed in patients with an abnormal modified Allen test. A possible exception occurs in patients with an excessive estimated risk from a femoral approach (eg, severe peripheral artery disease, large abdominal aortic aneurysm, morbid obesity) [31].

The results of the modified Allen test can be altered by a number of factors, including overextension of the wrist, skin tension over the ulnar artery, and operator error. As a result, an appreciable number of false positive and false negative results have been reported [32]. As an alternative, many centers use a more direct assessment of blood flow to the thumb during radial artery occlusion, which can be accomplished with pulse oximetry and plethysmography [32,34].

The traditional modified Allen test was compared to pulse oximetry and plethysmography in a consecutive series of 1010 patients referred for diagnostic cardiac catheterization [32]. The modified Allen test was considered abnormal if palmar blanching persisted for ≥10 seconds after release of ulnar compression. Plethysmography was observed for two minutes during radial artery compression. Plethysmography was characterized as follows:

●A – No change in the amplitude of the pulse tracing during compression

●B – Reduction in amplitude with compression

●C – Loss of pulse tracing with initial compression, but recovery of flow during two minutes of compression (signifying development of collateral flow)

●D – Loss of pulse tracing with no recovery

Patients in categories A, B, and C were considered to have a patent ulnopalmar arch, and therefore eligible for radial catheterization.

The modified Allen test was abnormal in significantly more patients than plethysmography (6.3 versus 1.5 percent). The authors concluded that plethysmography more accurately demonstrates the adequacy of the ulnopalmar arch, and that the modified Allen test may unnecessarily exclude some patients from radial artery catheterization. However, the number of patients who underwent radial artery catheterization was not reported, and the value of either test for predicting ischemic complications following radial artery catheterization was not assessed.

Radial artery occlusion has been reported in 1 to 10 percent of patients [35]. Systemic anticoagulation and use of smaller sheaths may reduce the risk. Also, sheath removal using a technique termed “non-occlusive hemostasis” may improve arterial patency. This technique involves using the minimal amount of compression to achieve hemostasis while still maintaining flow through the radial artery. This can be confirmed by using plethysmography to assess pulse amplitude when the ulnar artery is compressed simultaneously with non-occlusive compression of the radial artery. In the PROPHET study, patients were randomly assigned to standard compression versus plethysmography guided hemostasis [36]. At one month, the incidence of radial artery occlusion was reduced from 7 to 1.8 percent with guided hemostasis. Similarly, the RACOMAP study demonstrated a 10-fold reduction in radial artery occlusion with arterial pressure guided versus occlusive hemostasis [37].

ARRHYTHMIAS — A variety of arrhythmias and conduction disturbances can occur during catheterization. The most common, ventricular premature beats, may be induced by catheter introduction into the right or left ventricle, and are generally without clinical importance or impact.

Ventricular tachycardia or fibrillation — Ventricular tachycardia or fibrillation is rare complications of catheterization, occurring in 0.4 percent of cases in the second registry of the Society for Cardiac Angiography [2]. These arrhythmias may result from excess catheter manipulation or, more commonly, from intracoronary contrast injection. This complication occurs more commonly when ionic and hyperosmolar contrast agents are used. (See "Therapies of uncertain benefit in basic and advanced cardiac life support", section on 'Mechanical compression devices'.)

Atrial arrhythmias — Atrial arrhythmias can be induced by cardiac catheterization, especially in response to catheter placement into or out of the right atrium during right heart catheterization. These arrhythmias usually do not require immediate treatment unless they produce ischemia or hemodynamic instability.

Atrial flutter is generally well tolerated and can be treated with burst atrial pacing, or electrical or pharmacologic cardioversion. Atrial fibrillation, on the other hand, can cause clinical sequelae in the setting of a rapid ventricular response or if the loss of atrial systole results in hypotension, as in a patient with mitral stenosis or diastolic ventricular dysfunction. Synchronized cardioversion should be performed immediately in patients who are hemodynamically unstable. (See "Atrial fibrillation: Cardioversion", section on 'Electrical cardioversion'.)

Bradycardia — Bradycardia commonly occurs during coronary angiography, most often at the end of the injection of ionic contrast into the right coronary artery. Forceful coughing helps to clear the contrast, support perfusion, and restore normal cardiac rhythm.

Vasovagal reactions, which can include bradycardia, hypotension, yawning, and/or sweating, are seen in up to 3 percent of patients, particularly if they have pain or are anxious [2]. These reactions may occur with palpation or compression of the artery prior to needle access.

Treatment usually consists of volume administration, atropine (0.5 to 1.0 mg intravenously), and removal of the painful stimulus. Patients with critical coronary or valvular disease may undergo irreversible decompensation from vagally-mediated hypotension. As a result, rapid reversal of hypotension is crucial in this setting.

Conduction disturbances — Conduction disturbances are a rare cause of bradycardia in the catheterization laboratory. Patients with pre-existing left bundle branch block may develop asystole with right heart catheterization. Patients with pre-existing right bundle branch block may develop asystole during left heart catheterization. Atropine is rarely helpful in patients who develop complete heart block, but its administration is still recommended. Coughing may help support the circulation while the right heart catheter is exchanged for a temporary pacing wire. Prophylactic placement of a temporary pacemaker is not necessary, even in patients with bundle branch block or intervention in the right coronary artery.

Frank asystole is rare and there is generally sufficient time for insertion of a pacing wire through a venous sheath [38].

PERFORATION OF THE HEART OR GREAT VESSELS — Perforation is an extremely rare complication of cardiac catheterization. Higher risk procedures are those that involve stiffer catheters, including transseptal catheterization, endomyocardial biopsy, balloon valvuloplasty, needle pericardiocentesis, and placement of a pacing catheter. Older adult women appear to be at particular risk.

Cardiac perforation is generally heralded by bradycardia and hypotension due to vagal stimulation induced by blood in the pericardium. If the patient is hemodynamically stable, echocardiography is suggested to document the presence of blood in the pericardial space. However, emergent pericardiocentesis should be performed via the subxiphoid approach in the presence of hemodynamic instability.

Since pericardiocentesis is itself associated with complications, it is best performed under echocardiographic guidance or with pressure monitoring. In a study of 91 cases of acute tamponade during catheterization, pericardiocentesis was the only therapy necessary in 82 percent [39].

Reversal of anticoagulation may cause blood in the pericardial space to "gel." As a result, we generally try to aspirate the majority of the blood in the pericardial space prior to the administration of protamine [1].

ALLERGIC REACTIONS — Allergic reactions during catheterization may be precipitated by the local anesthetic, the contrast agent, protamine sulfate, or rarely heparin.

Local anesthetic — In patients reporting a reaction to all previous local anesthetics, a preservative-free agent may be a safe alternative [1]. In patients reporting a previous reaction to a specific local anesthetic, a different local anesthetic can be chosen. If the causative drug is not known or a preservative-free agent is not readily available, then lidocaine may be considered because it is a commonly used agent to which very few immediate reactions have been documented. (See "An approach to the patient with drug allergy".)

Iodinated contrast agents — Reaction to the contrast agent occurs in up to 1 percent of patients [2-7]. The risk of such a reaction is highest in patients with a history of prior contrast reactions. Other conditions, such as asthma and other atopic diseases, also confer some risk. Immediate hypersensitivity reactions to radiocontrast media are discussed in detail elsewhere. (See "Diagnosis and treatment of an acute reaction to a radiologic contrast agent".)

There are several steps that can reduce the incidence of a reaction in a high-risk patient:

●Premedication with corticosteroids and H1 antihistamines can reduce the incidence of a severe reaction (eg, bronchospasm or shock) to below 1 percent (table 5).

●The patient should receive a nonionic contrast agent. The incidence of crossreactivity in patients who have had previous reactions to older agents is low, although all patients with previous reactions should be premedicated [1]. In the past, nonionic contrast agents were used selectively, given their higher cost. However, the cost of nonionic contrast has fallen significantly. Thus, we recommend using nonionic contrast in all patients undergoing coronary angiography.

If a severe reaction does occur, it should be treated in the same manner as anaphylaxis. This issue is discussed separately. (See "Anaphylaxis: Emergency treatment", section on 'Pharmacologic treatments'.) .

Contrast-induced acute renal failure represents another complication that is discussed below. (See 'Contrast nephropathy' below.)

Protamine — Allergic reactions to protamine sulfate occur occasionally, more often in insulin-dependent diabetic patients who have received NPH insulin (which contains protamine) in the past [1]. The rapid administration of protamine sulfate can also provoke back pain of unknown etiology.

Protamine is rarely administered. Most diagnostic catheterizations with femoral access are done without heparin anticoagulation and protamine is rarely needed after heparin administration for radial access. In most interventional procedures, the heparin is either allowed to wear off over the next two to three hours prior to sheath removal, or the sheath is removed in the fully anticoagulated state using an arterial closure device.

Heparin — Allergic or anaphylactic reactions to heparin have been reported. If these occur, the reaction might be an early sign of heparin-induced thrombocytopenia (HIT). The evaluation for possible HIT is discussed separately. (See "Clinical presentation and diagnosis of heparin-induced thrombocytopenia", section on 'Suspecting HIT'.)

ATHEROEMBOLISM — During the process of cardiac catheterization, atheromatous debris is often scraped from the aortic wall. This debris can cause systemic embolization, including cutaneous, renal, retinal, cerebral, and gastrointestinal emboli (picture 1A-D). To minimize the risk of stroke or visual impairment, arterial catheter exchanges are best performed over a wire in the descending aorta at the level of the diaphragm (for closed loop catheters) and in the ascending aorta for angiographic catheters. Once arterial access has been obtained, the practice of readvancing the guidewire through the infrarenal aorta rather than exchanging it through a catheter should be avoided.

The high rate of release of atheromatous debris was illustrated in a series of 1000 patients undergoing percutaneous coronary intervention: 51 percent had aortic atheromatous material retrieved from the catheter after back flow of blood [40]. There were no associated in-hospital ischemic complications, probably due to sufficient withdrawal of blood containing the debris prior to the injection of contrast.

The reported incidence of atheroembolic events varies from 0.6 to 0.9 percent in retrospective studies to 1.4 to 1.9 percent in prospective series [41]. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

The clinical features of atheroembolism after diagnostic cardiac catheterization were examined in a prospective evaluation of 1786 patients ≥40 years of age [42]. The following observations were made:

●25 patients (1.4 percent) were diagnosed with atheroembolism; 12 had cutaneous signs (eg, "blue toes" syndrome, livedo reticularis) (picture 1A-C) and 16 had acute renal failure that was considered to be atheroembolic in origin because it persisted for at least two weeks (while contrast nephropathy typically reverses within the first week). (See 'Acute renal failure' below.)

●Eosinophil counts were significantly higher in patients suffering from atheroembolism both before and after catheterization.

●Four patients with atheroembolism died in hospital (16 percent); all had progressive renal dysfunction. The mortality rate was much lower (0.5 percent) in the patients without atheroembolism.

Treatment of atheroembolism is largely supportive. Therapies that have been evaluated are discussed separately. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on 'Treatment'.)

ACUTE RENAL FAILURE — There are three major causes of renal dysfunction related to cardiac catheterization: contrast-induced acute renal failure, renal atheroemboli, and hemodynamic instability with renal hypoperfusion.

Contrast nephropathy — At least 5 percent of patients who undergo cardiac catheterization experience a transient rise in the plasma creatinine concentration of more than 1.0 mg/dL (88 micromol/L) due to contrast-induced renal dysfunction [43]. However, there is substantial variability in risk among patients, some of whom have a risk that exceeds 50 percent. The risk is greatest in patients with moderate to severe renal insufficiency and diabetes. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

The plasma creatinine concentration usually returns to baseline within seven days, and less than 1 percent of patients, usually diabetic patients with underlying severe chronic kidney disease, go on to require chronic hemodialysis.

Nonionic low osmolal contrast agents are now administered for the majority of radiologic procedures using intravascular contrast media, as a result of increased patient tolerability and decreased hypersensitivity reactions. However, in patients at risk for contrast nephropathy, we prefer the use of iso-osmolal agents (approximately 290 mosmol/kg) rather than low osmolal agents (500 to 850 mosmol/kg) because of a lower risk of contrast nephropathy. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

Renal atheroemboli — The kidney is one of the principal end organs that may be affected by atheroembolic events. (See 'Atheroembolism' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures", section on 'Atheroembolism'.) There are three main findings that suggest that atheroemboli rather than contrast nephropathy is responsible for the development of acute renal failure after catheterization:

●The presence of other signs of embolization such as blue toes (picture 1A), livedo reticularis (picture 1B-C), Hollenhorst plaques in the retina (picture 1D), and/or abdominal pain.

●Transient eosinophilia and hypocomplementemia.

●Persistent renal failure after seven days.

(See "Clinical presentation, evaluation, and treatment of renal atheroemboli" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

In a review of 1786 consecutive patients undergoing cardiac catheterization, acute renal failure developed in 0.9 percent overall and in 64 percent of those with evidence of any atheroembolism [42]. In this report, acute renal failure was considered to be due to renal atheroembolism if it had persisted for at least two weeks, well beyond the time at which contrast nephropathy should have resolved.

Treatment for this condition is largely supportive. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on 'Treatment'.)

INFECTION — Cardiac catheterization procedures are performed using sterile technique. Thus, both local infection and bacteremia are rare and endocarditis prophylaxis during cardiac catheterization is not recommended for patients with valvular disease. Infection is approximately 10 times more common with the brachial approach compared to the femoral approach (0.6 versus 0.06 percent) [2-7].

RADIATION EXPOSURE — Patients undergoing diagnostic and interventional cardiac catheterization 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".)

ENDOMYOCARDIAL BIOPSY — Endomyocardial biopsy of right ventricular tissue is made using a relatively stiff catheter. Complications such as perforation of the heart or great vessels, life threatening arrhythmias, or heart block requiring permanent pacing occur uncommonly. This issue is discussed in detail elsewhere. (See "Endomyocardial biopsy", section on 'Complications'.)

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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.)

●Basics topic (see "Patient education: Cardiac catheterization (The Basics)")

SUMMARY

●The risk of a major complication (death, myocardial infarction, or major embolization) during or after diagnostic cardiac catheterization is well below 1 percent (table 1). As a result, the risk-to-benefit ratio still favors performing this procedure as a part of the evaluation of potentially fatal or lifestyle-limiting cardiac disease.

●Mortality is under 0.1 percent. Risk factors for death include advancing age, higher New York Heart Association heart failure class, left main coronary artery disease, severe left ventricular dysfunction, as well as the presence of valvular heart disease, chronic kidney disease, diabetes mellitus requiring insulin therapy, peripheral artery disease, cerebrovascular disease, and pulmonary insufficiency. (See 'Death' above.)

●The risk of myocardial infarction is under 0.1 percent. Risk factors include the extent of disease, the presence of insulin dependent diabetes mellitus, and recent non-ST elevation myocardial infarction. (See 'Myocardial infarction' above.)

●The risk of stroke has been reported to be as high as 0.2 to 0.4 percent. Risk factors for stroke include the severity of coronary artery disease, the length of fluoroscopy time, diabetes, hypertension, prior stroke, or renal failure. (See 'Stroke' above.)

●Local complications at the site of catheter insertion are among the most common problems seen after cardiac catheterization. These problems may include acute thrombosis, distal embolization, dissection, poorly controlled bleeding, hematoma, retroperitoneal hemorrhage, pseudoaneurysm, or arteriovenous fistula. (See 'Local vascular complications' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures".)

●Other potentially serious complications include: ventricular tachyarrhythmias, severe bradycardia, allergic reactions, atheroembolism, and acute kidney injury (contrast nephropathy). (See 'Arrhythmias' above and 'Allergic reactions' above and 'Atheroembolism' above and 'Acute renal failure' above and "Access-related complications of percutaneous access for diagnostic or interventional procedures", section on 'Atheroembolism'.)