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Case Report
Transvenous Pacing Causing Tamponade in Patients Receiving Glycoprotein IIb/IIIa Inhibitors for Percutaneous Coronary Interventi
February 2007
A backup temporary pacing wire is often used in patients with heart block undergoing cardiac catheterization and percutaneous coronary intervention (PCI). It is particularly recommended for any patient undergoing rotational atherectomy or rheolytic thrombectomy when the vessel involved is the right coronary artery (RCA) or a dominant left circumflex artery (LCx).1,2
In recent years, there has been a marked increase in the use of glycoprotein IIb/IIIa inhibitors in patients with acute coronary syndromes prior to planned coronary intervention and also in patients undergoing elective but complex coronary intervention in line with evidence-based practice. We present four cases in which cardiac tamponade occurred following temporary pacing in patients who had received glycoprotein IIb/IIIa inhibitors during invasive cardiac procedures.
Case 1. A 52-year-old female with a history of hypertension and a positive exercise tolerance test underwent successful two-vessel angioplasty to the left anterior descending artery (LAD) and RCA. A heparin bolus (70 U/kg), aspirin 300 mg and clopidogrel 300 mg were given electively. The lesion in the RCA was complex and required the use of a rotational atherectomy system (Rotablator®, Boston Scientific Corp., Natick, Massachusetts). A 5 Fr temporary pacing wire was placed in the right ventricular (RV) apex via the right femoral vein (RFV), as is currently recommended. Abciximab (Reopro®, Eli Lilly & Company, Indianapolis, Indiana) was used electively during the procedure as recommended with rotational atherectomy.
Soon after the procedure, the patient suffered acute hemodynamic collapse. A transthoracic echocardiogram (TTE) demonstrated a pericardial effusion with tamponade, and a pericardial drain was inserted. Repeat coronary angiography showed no signs of coronary artery perforation at the treated sites. Abciximab was discontinued, and the patient made a full recovery.
Case 2. An 80-year-old female underwent elective PCI to the LAD and RCA. She was pretreated with aspirin 300 mg and clopidogrel 300 mg. A heparin bolus (70 U/kg) was given intravenously. The RCA angioplasty was complex (Figure 1) and required the use of the Rotablator. A temporary pacing wire was inserted to cover the risk of bradycardia. Abciximab (Reopro) was used electively during the procedure. Two stents were deployed in the RCA without incident. The temporary wire was removed after the procedure. Shortly afterwards, the patient suffered acute hemodynamic collapse, and TTE demonstrated a moderate pericardial effusion with signs of tamponade. Attempts at percutaneous drainage via a subcostal window were unsuccessful and complicated by intra-abdominal hemorrhage. Urgent pericardiotomy was performed and a bloody pericardial effusion drained. There were no external signs of coronary trauma. Review of the angiography films revealed no evidence of coronary perforation at the treated site. The patient made a good recovery.
Case 3. A 63-year-old male admitted with acute chest pain and presyncope was found to have electrocardiographic evidence of 2:1 atrioventricular (AV) block in association with ST-elevation in leads II, III and AvF. Aspirin (300 mg) and clopidogrel (300 mg) were administered. The electrocardiographic (ECG) findings were transient, resolving spontaneously. Following recurrent chest pain associated with further ECG changes, tirofiban with heparin (5,000 U bolus, followed by maintenance infusion of 1,000 U/hour titrated to maintain an aPTT of 2 times control) was prescribed, and the patient was transferred to the catheterization laboratory promptly for PCI. A 5 Fr temporary pacing wire was placed in the RV apex via the RFV without incident. Coronary angiography performed via the right femoral artery revealed only minor disease in the LAD and RCA, and there was no abnormality in the LCx. There was no obvious target lesion for coronary intervention. It was felt likely that the patient had suffered a thrombotic event, thus his antiplatelet therapy was continued. He remained in 2:1 AV block, therefore the temporary pacing wire was left in situ.
After 8 hours, the temporary pacing wire required repositioning; this was required again 12 hours later. Twenty minutes after repositioning, the patient experienced hemodynamic collapse and cardiac arrest. TTE revealed a small pericardial effusion but with evidence of RV collapse. Emergency pericardiocentesis was performed and there was rapid return of hemodynamic stability. The temporary pacing wire was removed and tirofiban was stopped. The patient made a full recovery.
Case 4. A 72-year-old male with a history of atrial fibrillation underwent elective PCI to a proximal stenosis in the RCA. The patient was pretreated with aspirin 300 mg and clopidogrel 300 mg. Intravenous heparin (100 U/kg) was administered. It proved difficult to cross the lesion and the procedure was complicated by proximal dissection associated with bradycardia and transient loss of cardiac output. A 5 Fr temporary pacing wire was inserted into the RV apex via the RFV. A stent was then deployed in the proximal RCA to achieve a good angiographic result.
Immediately following the procedure, the patient suffered ventricular fibrillation and was cardioverted to sinus rhythm with a single DC shock. Repeat angiography demonstrated evidence of possible emboli in the distal vessel. There was no suggestion of coronary rupture. Reopro was given to cover the risk of thrombosis and the temporary wire was left in situ.
The patient’s condition stabilized and the temporary pacing wire was removed the following day. Fifteen minutes following removal of the temporary pacing wire and venous sheath, the patient became unwell, drowsy and vomited. He was hypotensive but did not have bradycardia or ECG evidence of heart block. An immediate TTE revealed a small pericardial effusion with some right atrial collapse, but no other convincing evidence of tamponade. After a period of fluid resuscitation, the TTE was repeated and showed an increase in the size of the pericardial effusion and features consistent with tamponade physiology. Pericardiocentesis was performed urgently with rapid return of hemodynamic stability.
Over the next few days, the patient experienced respiratory difficulties and respiratory failure due to aspiration pneumonia. He died. having failed to respond to aggressive therapy with antibiotics and mechanical ventilation.
In each of these cases, it was felt that tamponade had occurred because of perforation of the RV by a pacing wire.
Discussion. We have presented four cases of cardiac tamponade in patients receiving glycoprotein IIb/IIIa inhibitors during cardiac catheterization. During the timeframe of these cases (25 months), we performed 2,596 PCIs in our institution, using glycoprotein IIb/IIIa inhibitors in 1,077 of these. There were no cases of tamponade when a temporary pacing wire was not used.
The use of rotational atherectomy is uncommon: during this timeframe, we used rotational atherectomy in 36 cases (in keeping with current recommendations, glycoprotein IIb/IIIa inhibitors have been used in all of these cases). Since we stopped routinely pacing in our rotational atherectomy cases, we have encountered no further cases of tamponade (37 subsequent cases).
We believe tamponade was caused by RV perforation by a temporary pacing wire. Although RV myocardial perforation may complicate up to 20% of temporary transvenous pacemaker insertions,3 this is usually subclinical, and progression to cardiac tamponade is uncommon.4 Perforation is more common with rigid and large-bore catheters, and the use of smaller pacing wires and balloon-tipped wires has reduced this complication rate.5 Even so, most pacing lead perforations are mitigated by the “self-sealing” properties of the RV myocardium6 which rely to a large extent on active coagulation.
Patients undergoing cardiac catheterization have a reported incidence of cardiac tamponade of between 1 and 5 per 1,000.7–11 In one series taken from a retrospectively evaluated series of 6,999 consecutive PCIs, there were 15 cases of tamponade, giving an overall incidence of 0.2%.7 In that series, 7 cases were “definitely or probably related to a temporary pacemaker”. Of note, 5 of the 15 cases of tamponade were associated with the use of abciximab, although it is not clear whether temporary pacing was used in any of these.
Previously, there has been 1 reported case of RV perforation leading to cardiac tamponade during coronary angioplasty in which abciximab and temporary pacing were used.12 Hemodynamic collapse occurred in this case following removal of the temporary wire. The authors concluded that the “profound platelet inhibition produced with the use of abciximab might be expected to lead to a clinically silent and minor perforation becoming clinically significant”.
In 3 of our patients, it would appear that tamponade occurred after removal or manipulation of the temporary wire had exposed the perforation site. This would indicate the need for a high degree of monitoring for such problems when removing temporary wires. In particular, in 2 of our cases, there was evidence of pacing malfunction with no evidence of macrodisplacement, and this may have been a clue that a perforation had occurred. Other indicators of RV perforation including pleuritic chest pain and diaphragmatic irritation were not noted in any of our cases, but these should alert a clinician to this possibility.
A high clinical suspicion of tamponade is warranted in this group of patients if hemodynamic collapse occurs: TTE facilities should be immediately available in order to promptly exclude or confirm the diagnosis. If they are not and there is good clinical suspicion, then pericardiocentesis should be attempted.
This problem may become more prevalent with the increasing use of glycoprotein IIb/IIIa inhibitors in acute coronary syndrome patients awaiting coronary intervention (a proportion of whom will have symptomatic bradycardia and need temporary pacing). In addition, operators using supportive technology during PCI such as rotational atherectomy (Rotablator) and rheolytic thrombectomy (AngioJet®, Possis Medical, Inc., Minneapolis, Minnesota) — in which the use of glycoprotein IIb/IIIa inhibitors and temporary pacing is recommended for lesions involving the RCA or LCx1,2 — will encounter this problem with increasing frequency.
The alternative use of direct thrombin inhibitors (such as bivalirudin) which has demonstrated a lower incidence of bleeding complications13 in coronary intervention may provide a potentially safer alternative, although this has not been investigated in terms of tamponade and remains unproven.
Alternatively, placing the temporary wire in a septal wall position may reduce the risk of extracardiac perforation and hence of tamponade.14 However, most PCIs are performed via the femoral route, and finding a stable position in the RV septum for a passive pacing lead via the femoral vein can be quite challenging. This lower risk of initial perforation must therefore be considered in the context of a higher risk of lead displacement for which the pacing lead may require repositioning. Frequent lead repositioning is an established risk factor for perforation.
Recently, temporary cardiac pacing using a coronary guidewire in PCI has been shown to be effective,15 and may emerge as an alternative that obviates the need for transvenous pacing, as technology improves.
These cases highlight the importance of careful management of patients with temporary transvenous pacing wires, particularly where glycoprotein IIb/IIIa inhibitors are used in coronary intervention. In this group of patients, one should first consider whether temporary pacing is necessary, and if so, one should be aware of the risk of tamponade and have some knowledge of potential indicators of perforation.
For patients undergoing rotational atherectomy and other device procedures involving the RCA or a dominant LCx, it is becoming more acceptable to place a sheath in the femoral vein and to have a temporary pacing wire available rather than to place a wire in the RV apex of all patients. Furthermore, it is important to be careful when inserting and removing temporary pacing wires that there are resources in place to identify and address tamponade promptly.
Following these cases, we have reviewed our practice in line with this. We are careful where possible to avoid using temporary pacing in coronary intervention where we plan to use rotational atherectomy or thrombectomy and are more selective about temporary pacing in patients receiving glycoprotein IIb/IIIa inhibitors. Instead, we insert a sheath in the femoral vein and intervene with pacing only if heart block becomes a problem.
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