Pulmonary Thromboembolism after Catheter Ablation of Cardiac Arrhythmias

In-Hospital Pulmonary Arterial Embolism after Catheter Ablation of Over 45,000 Cardiac Arrhythmias: Individualized Case Analysis of Multicentric Data

Invasive electrophysiology (EP) and catheter-ablation (CA) have made a revolutionary progress in the treatment of various cardiac arrhythmias, and the annual number of these procedures is exponentially increasing worldwide.[1] Although development of different technologies for arrhythmia mapping and ablation has improved the feasibility and success of CA procedures, life-threatening complications may still occur.

Presently, the overall CA complication rate is 1 to 5%, depending on the procedure complexity.[1] The most common serious procedure-related complications are cardiac perforation, stroke, vascular injury at the puncture site, and high-degree atrio-ventricular block. Although several factors associated with right heart catheterization and endocardial ablation predispose to deep venous thrombosis (DVT), clinically relevant pulmonary embolism (PE) is surprisingly a rare and underreported complication of CA.[2] However, in the recent European Heart Rhythm Association (EHRA) survey, almost 10% of participants observed at least one PE related to CA procedure within the last year in their hospital.[3]

In this issue of the Thrombosis and Haemostasis, Doldi et al reported the low incidence of CA-related PE (0.03%), analyzing more than 47,000 CA procedures for cardiac arrhythmias (i.e., supraventricular tachycardia [SVT], atrial flutter, atrial fibrillation [AF], and ventricular tachycardia) that were performed in three German tertiary centers over the 15-year period.[4] The patients who have suffered PE were predominantly female; however, there were no differences in other main clinical characteristics between those with and without PE. The authors reported fatal outcome in 2 out of 14 patients due to massive PE. Two-thirds of patients with PE after CA had a prior indication for oral anticoagulation. DVT and coagulopathy were revealed in a third and a half of the patients who were tested after PE, respectively. Although intravenous heparin was administered in all procedures, there are no data on the level of procedural anticoagulation (i.e., activated clotting time).

Over 60 years ago, symptomatic acute PE was reported as a seldom complication in only 11 out of 12,367 after routine right heart catheterizations, but in none of patients undergoing coronary arteriography solely.[5] However, ventilation/perfusion scans obtained before and the day after the procedure showed that up to 12% of patients had new and asymptomatic postcatheterization perfusion lung defects, consistent with pulmonary infarction.[5] Moreover, these perfusion lung defects were twice as common when the groin puncture was used compared to antecubital access (16 vs. 8%, respectively).[5] It is therefore evident that (1) the right heart catheterization predisposes to PE, (2) PE is more specific for the procedures performed by the inguinal (femoral) venous approach, and (3) asymptomatic (“small”) PE is far more common than symptomatic (“moderate to massive”) PE, but these “subclinical” postprocedural PEs are commonly missed in routine practice.

Similarly, electrophysiologists reported very low incidence of clinically manifested PE complicating CA. In a systematic review of eight studies, the incidence of symptomatic PE was only 0.12 to 0.29%.[2] The present study from Germany confirmed these findings.[4] Again, the incidence of clinically inapparent PE after CA seems to be much higher than occurrence of manifest PE. For example, among 71 consecutive patients undergoing CA of AF, asymptomatic PE was demonstrated by routine computed tomography after ablation in 6 patients (8%).[6]

There are several presumed sources of procedure-related PE, such as DVT (usually at femoral vein puncture site), preexisting thrombus in the inferior caval vein or at the right atrial/ventricular wall, and thrombus formed at the catheter tip or within the (long) sheaths.[3] [6] [7] [8] [9] Importantly, duplex ultrasonography assessment before and after CA demonstrated occurrence of new nonocclusive (asymptomatic) DVT on the day following the procedure in 17.6% of the femoral veins that were used for the catheter access.[7] This thrombosis regressed spontaneously within the first week in majority of the veins. All DVTs were seen in the femoral vein(s) of the intervention leg and no thrombus was detected in the contralateral limb. Moreover, frequency of DVT was twice as high in the femoral veins with multiple (up to three) sheaths than in those in which only single introducer was inserted.[7]

The Virchow's triad implies three categories of factors that contribute to DVT—endothelial injury, stasis of blood flow, and hypercoagulability.[3] If the triad is fulfilled, a thrombus can be formed—before, during, or after the CA procedure. However, PE usually occurs 8 hours to 2 weeks after sheath withdrawal.[6] The most important patient-related and the procedure-related factors for PE occurrence after ablation are summarized in [Fig. 1]. Many cardiovascular conditions (e.g., heart failure, hypertension, AF, peripheral vascular disease, etc.) are associated with endothelial dysfunction, hypercoagulability, and/or impaired blood flow, thus predisposing to DVT and PE.[10] At least some of the patients undergoing their CA procedure could be unrecognized carriers of an inherited or acquired thrombophilia. For example, the prevalence of the most common genetic thrombophilia, e.g., factor V Leiden heterozygosity, is 3 to 8% in the general Caucasian population.[11] In addition, obesity, oral contraceptive use, autoantibody antiphospholipid syndrome, and occult neoplasm all are associated with an acquired thrombophilia and higher risk of DVT/PE.[12] [13] [14] Finally, the patients with postablation PE are reported to be older and “sicker”—more frequently had diabetes, higher CHA₂DS₂VASc score, dilated pulmonary artery, and elevated D-dimer prior to the CA.[6] [9] Many procedure-related factors have a strong impact on development of DVT and PE. Puncture of the vein disrupts endothelial surface and function.[10] Insertion of “foreign materials,” such as sheaths and mapping catheters, into the blood flow strongly activates the coagulation cascade. Obstruction of venous lumen by multiple sheath/catheters inserted via single femoral vein, the use of inguinal compressive bandages or sandbag for hemostasis, and bedrest lead to venous stasis.[5] [6] [7] [8] [9] Endocardial ablation of arrhythmic substrate by thermally mediated myocardial necrosis and surrounding tissue inflammation favors cardiac thrombosis.[15] In this regard, radiofrequency (RF) energy is significantly more thrombogenic than cryo-energy.[15] RF current directly initiates activation of coagulation system and platelets, which returns spontaneously to basal levels within 24 hours following the procedure.[16] Finally, while high power ablation with conventional RF catheters increases the risk of the catheter tip charring, denaturation of blood proteins, and thrombosis, the irrigated-tip catheter use decreases the likelihood of clot formation.[15]

Fig. 1 The patient-related and the procedure-related risk factors for pulmonary thromboembolism following catheter-ablation procedure. ACT, activated clotting time; AF, atrial fibrillation; APS, antiphospholipid syndrome; CA, catheter-ablation; DM diabetes mellitus; DVT, deep vein thrombosis; HF, heart failure; HTA, hypertension; LMWH, low-molecular-weight heparin; NOAC, non-vitamin K oral anticoagulants; OAC, oral anticoagulation; PE, pulmonary embolism; PVD, peripheral vascular disease; RF, radiofrequency.

Since the PE incidence was lower after AF (0.02–0.29%%) than after SVT ablation (0.05–1.67%),[2] [4] it seems that preprocedural anticoagulation may prevent postprocedure PE. However, although the anticoagulation strategy for AF (left-sided) ablation is well standardized, there is no consistent guidelines for routine anticoagulation in patients undergoing right-sided CA procedures.[17] The EHRA survey showed that 68% of electrophysiologists do not administer intravenous heparin during right-sided SVT ablations and 31% of them do not irrigate long sheaths during the procedure.[3] Only 24% of operators prescribe the 1-month thromboprophylaxis at discharge and most often (71%) it is only aspirin. Interestingly, two-thirds of physicians keep their routine antithrombotic strategy even in the patients with significant risk factors for thromboembolism.[3] However, prophylactic administration of dalteparin immediately before venous puncture for EP study significantly decreased the risk of the following DVT, from 62.5 to 18%.[18] In addition, postablation rivaroxaban 10 mg/d for 2 weeks was superior to aspirin 100 mg in prevention of DVT (DVT incidence rate was 5.5 vs. 16.7%, respectively).[19]

Bearing in mind the unpredictability of PE occurrence after CA and significant mortality due to acute PE of 10 to 15%,[20] an improvement in routine thromboprophylaxis for CA procedures is needed, along with further prospective large studies to inform guidance on the optimal anticoagulation for all CA procedures, while carefully weighting the risks of potential periprocedural bleeding. Indeed, bleeding risk is multifactorial, and careful assessment of patients would be needed to improve clinical outcomes peri-CA, especially in high-risk groups.[21] [22] [23]

Publication History

Received: 15 July 2024

Accepted: 15 July 2024

Accepted Manuscript online:
16 July 2024

Article published online:
26 July 2024

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