Disseminated Intravascular Coagulation after Radiofrequency Catheter Ablation of Idiopathic Ventricular Tachycardia

DOI: 10.19102/icrm.2013.040403

NAGA K. POTHINENI, MD, RAVI K. SUREDDI, MD and HAKAN PAYDAK, MD

Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AK

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ABSTRACT.  Symptomatic drug-refractory premature ventricular complexes (PVCs) and ventricular tachycardia originating from the outflow tract region in the setting of a structurally normal heart are amenable to curative radiofrequency catheter ablation therapy with a low incidence of serious complications. We describe a patient with idiopathic right ventricular outflow tract PVCs who developed disseminated intravascular coagulation (DIC) following catheter ablation. After exclusion of common causes of DIC, this unusual complication was felt to result from inflammation related to ablation and catheterization and/or pericarditis. To the best of our knowledge, this is the first reported case of a DIC following ablation of ventricular tachycardia

KEYWORDS.  disseminated intravascular coagulation, radiofrequency ablation, ventricular tachycardia.

The authors report no conflicts of interest for the published content.
Manuscript received January 30, 2013, Final version accepted February 26, 2013.

Address correspondence to: Naga K. Pothineni, MD, 4301 W Markham Street, Slot 634 Little Rock, AR 72205. E-mail: nkpothineni@uams.edu

Introduction

Symptomatic drug-refractory premature ventricular complexes (PVCs) and ventricular tachycardia originating from the outflow tract region in the setting of a structurally normal heart are amenable to curative radiofrequency catheter ablation therapy with a low incidence of serious complications.¹ We describe a patient with idiopathic right ventricular outflow tract (RVOT) PVCs who developed disseminated intravascular coagulation (DIC) following catheter ablation. After exclusion of common causes of DIC, this unusual complication was felt to result from inflammation related to ablation and catheterization and/or pericarditis.

Case report

The patient is a 48-year-old woman with highly symptomatic PVCs with morphology consistent with origin from the outflow tract region. During an initial electrophysiologic (EP) study, PVCs could not be induced. She later underwent a second procedure during which ablation lesions were delivered in the RVOT. However, PVCs recurred during follow-up and were refractory to therapy with β-blockers and sotalol. Patient was subsequently offered, and opted to undergo a third EP study.

The EP study was done in the post-absorptive state under minimal sedation. All baseline laboratory values (Table 1) prior to the procedure were normal. Bilateral femoral venous and right femoral arterial accesses were obtained. Multipolar catheters were positioned at the His bundle location and in the RVOT. Non-sustained and sustained runs of ventricular tachycardia (VT) were induced by programmed stimulation during isoproterenol infusion at 2 μg/kg/min. Because of lack of success with prior ablation in the RVOT, and because of early precordial transition of the PVCs, mapping was initially done in the left ventricular outflow tract (LVOT) using an 8 mm mapping and ablation catheter (Sapphire, St. Jude Medical, St Paul, MN) and a non-contact multielectrode catheter (Ensite Array, St. Jude Medical). However, mapping suggested PVC origin from the RVOT. The array and the mapping catheters were then positioned in the RVOT (Figure 1). A total of 50 radiofrequency ablation lesions were delivered in the RVOT, guided by activation and pace mapping. Patient was anticoagulated with unfractionated heparin, targeting an activated clotting time (ACT) of 350 s during mapping in the LVOT, and 300 s during mapping and ablation in the RVOT. Radiofrequency (RF) applications were limited to a power of 50 watts and temperature of 60°C. The post-ablation, programmed ventricular stimulation protocol with isoproterenol was repeated, and PVCs and VT could no longer be induced. At the conclusion of the procedure, no complications occurred and the patient was admitted for 24-h observation as per the routine practice at our institution.

Overnight she developed persistent nausea and chest discomfort, sinus tachycardia, and limited urine output. A transthoracic echocardiogram showed moderate pericardial effusion with no tamponade physiology. Over the next 24 h, she developed atrial fibrillation with rapid ventricular response and required amiodarone and metoprolol for rhythm control. Serial metabolic panels over the next 4 days revealed multiple abnormalities (Table 1) including acute kidney injury, elevated transaminases, elevated LDH, leukocytosis, anemia, and severe thrombocytopenia. Patient also developed intermittent fevers, and multiple painful bilateral lower extremity cyanotic lesions associated with diminished arterial pulses, consistent with thromboembolic peripheral arterial occlusions. Vascular Doppler examination revealed deep venous thromboses in the right axillary, cepahlic, and basilic veins and diminished arterial pulse wave from in the lower extremities.

The patient was diagnosed with DIC based on the concomitant presence of thrombosis and bleeding in combination with abnormal serum D-dimer and fibrinogen levels and prolonged prothrombin time and partial thromboplastin time. She underwent extensive evaluation (Table 2) to identify the etiology of the DIC. Empiric broad-spectrum antibiotic therapy with vancomycin and imipenem was initiated after multiple blood and urine cultures were obtained. However, all of the cultures remained negative. Work-up for autoimmune disorders including antiphospholipid syndrome was negative. Heparin–platelet complex antibodies were negative.

The patient received supportive care over the next few days, with platelet and fresh frozen plasma transfusion for reversal of coagulopathy, volume resuscitation for the acute kidney injury, and serial echocardiograms to assess the pericardial effusion. Although there was no overt hemorrhage, the acute anemia probably resulted from a combination of hemolysis, hemopericardium, and gastrointestinal bleeding (positive fecal occult blood test) from the DIC. Anticoagulation was not initiated due to thrombocytopenia, the presence of the pericardial effusion, and concern for ongoing gastrointestinal bleeding. Serial echocardiograms suggested development of tamponade physiology, although there were no clinical signs. An elective pericardiocentesis was performed on day 9 with drainage of 800 ml of bloody fluid. A limited echocardiogram on day 10 revealed no recurrence of the pericardial effusion. By day 10, the patient’s coagulation profile, liver enzymes, and leukocytosis normalized, and renal function significantly improved. Lower extremity perfusion also normalized with resolution of the ischemic territories. Patient was discharged home on day 10 after her catheter ablation procedure.

Since extensive work-up excluded systemic infection, autoimmune pathology, and heparin-induced thrombocytopenia; the patient was felt to have developed DIC as a result of the substantial number of radiofrequency lesions delivered in the RVOT.

Discussion

Radiofrequency catheter ablation is an effective therapeutic strategy for patients with symptomatic idiopathic ventricular arrhythmias but is not entirely without risk. Various complications including cardiac tamponade, thromboembolism, complete heart block, pulmonary embolism, valvular rupture, coronary artery injury, cardiogenic shock from repeated VT induction, and death have been reported.² However, there were no case reports of systemic complications. To the best of our knowledge, this is the first reported case of DIC occurring as a complication of VT ablation. Park et al,³ have previously described DIC occurring in a patient following catheter ablation for atrial fibrillation, with striking similarities in the clinical course to our patient.

DIC is a systemic syndrome characterized by widespread intravascular coagulation leading to multiple microthrombi. The consumption of platelets and coagulation factors leads to an increased risk of bleeding that encompasses the other end of the spectrum of DIC. It usually occurs with severe infections, major trauma, malignancies, and obstetric disorders. Cytokine-mediated systemic intravascular coagulation, impaired anticoagulant mechanisms, and defective fibrinolysis play an important role in the pathogenesis of this syndrome.⁴ The major inciting factor is the release of tissue factor that activates the extrinsic coagulation pathway, which in turn leads to consumptive coagulopathy. DIC is diagnosed by the presence of thrombocytopenia, decreased anticoagulant (antithrombin, protein C) levels, elevated fibrin degradation products, and clinical evidence of thrombosis and bleeding in an appropriate setting.⁵ The mainstay of management of DIC is treatment of the underlying disease, supportive care, aggressive monitoring for signs of organ dysfunction, and use of anticoagulants as indicated in patients with no signs of active bleeding.

The pathogenesis of DIC following VT ablation in our patient is not clear. Potential mechanisms include release of tissue factor due to thermal injury to the myocardium caused by RF application and endovascular injury from the prolonged placement and manipulation of multiple intravascular catheters. Endothelial injury can lead to rapid activation of coagulation leading to platelet consumption, although it is unclear why DIC is not a common complication in other electrophysiology procedures that involve prolonged intravascular catheter placement. We used an 8-mm-tip ablation catheter and this could have caused more extensive lesions and a greater amount of charring. Though all blood cultures were negative, DIC due to systemic infection arising during the introduction of multiple catheters cannot be completely excluded. Inflammation related to the pericardial effusion and pericarditis from the ablation lesions could also have precipitated the DIC.

References

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