How to Map and Ablate Unstable Ventricular Tachycardia: The Brigham Approach
Usha B. Tedrow, MD, MSc; William G. Stevenson, MD
Ventricular tachycardia is an important cause of morbidity and mortality in patients with structural heart disease. In patients with ICDs, shocks to terminate the arrhythmia decrease quality of life and cause significant emotional distress. In addition, shocks are associated with increased risk for exacerbation of heart failure and mortality, and have been suggested to have a causative role. Catheter ablation for VT is an increasingly important therapeutic modality for reducing shocks and reducing the need for antiarrhythmic drugs, which have their own toxicities. Ablation can be life-saving when VT is incessant.
Of patients with ICDs who are referred to us for ablation after failing antiarrhythmic drug therapy, fewer than one-third have VT that is sufficiently stable to allow mapping during VT. The majority have a combination of stable and unstable VTs, or only unstable VT. VT can be unstable for mapping due to hemodynamic intolerance, requiring immediate termination, inability to reliably induce VT, or frequent, spontaneous shifts in QRS morphology. Catheter ablation of VT requires mapping to locate the arrhythmogenic substrate. Catheter ablation techniques for stable VT rely on activation and entrainment mapping during sustained VT, which is only possible in a limited way in patients with unstable VT. There are many mapping techniques that can be used to target the substrate for these unstable VTs in these patients.
All patients undergoing VT catheter ablation require evaluation of the underlying substrate prior to the procedure. Reentry related to ventricular scars from prior MI, cardiomyopathies, or surgical incisions is the most common cause of sustained monomorphic VT associated with structural heart disease. For this reason, when patients present with new episodes of VT, evaluation of possible new ischemic lesions with either stress testing or cardiac catheterization is essential to determine the safety of proceeding with catheter ablation, as well as the need for possible revascularization. It is important to note, however, that new ischemic lesions are rarely the sole cause of monomorphic VT.
For patients with underlying cardiomyopathic processes such as sarcoidosis, the extent of disease activity is important to consider. For those with active inflammation, immunosuppression may be a more prudent initial course than catheter ablation. Cardiac MRI (Figure 41.1) can also be helpful in patients without ICDs to identify arrhythmogenic processes such as giant cell arteritis, which may warrant other therapies and even consideration for LV assist device or transplantation rather than catheter ablation.
Approach to Ventricular Access
The ventricles can be approached from the endocardium or epicardium, and the LV endocardium can be approached via a retrograde aortic or transseptal route. Echocardio-graphy is an essential component of the preprocedural evaluation of the patient. The first priority is to assess the presence of mobile thrombus in the left ventricle ( Video 41.1). If LV thrombus is present, an epicardial approach to the LV can still be considered, but endocardial LV mapping should be avoided, due to risk of embolic stroke. In addition, echocardiography can evaluate the possible presence of aortic stenosis that might make a retrograde aortic approach difficult. A mechanical aortic valve is a contraindication to a retrograde aortic approach. A transseptal approach is preferred for these situations as well as in instances of severe peripheral vascular disease or abdominal aortic aneurysm. Mitral stenosis or a mechanical valve prosthesis in the mitral position is a contraindication to a transseptal approach. Patients who have failed an endocardial attempt are reasonable candidates for an epicardial approach, independent of QRS morphology.
Mapping and ablation may be performed with either conscious sedation or general anesthesia. An anesthesia consultation is obtained, and the majority of our patients with unstable VT undergo catheter ablation under general anesthesia. General anesthesia allows complete control of the patient during induction of arrhythmias that may require prompt cardioversion, in a patient who may require hemodynamic support with intravenous vasopressors, an IABP, or percutaneous assist device. It also ensures absence of movement during mapping, reducing the chance that patient movement invalidates an electroanatomic map. It is our impression, however, that hypotension occurs more promptly under general anesthesia as compared to conscious sedation. A urinary catheter is placed in all patients, since the volume of fluid given during the procedure with an external irrigated-tip catheter can be substantial.
Access in the RFV accommodates 2 venous sheaths, an 8-Fr to ultimately accommodate the ablation catheter if the RV is mapped endocardially, and a sheath for a custom hexapolar catheter with an intravascular electrode located 15 to 20 cm proximal to the tip. This can be positioned at the HB or in the right ventricle for pacing and recording. The LFV usually accommodates an 11-Fr sheath for the placement of a phased-array ICE catheter. An arterial line is often placed either radially or in the right femoral artery initially for hemodynamic monitoring. The 5-Fr femoral arterial sheath can be upsized to an 8-Fr sheath if a retrograde aortic approach to the LV endocardium is to be used. A long (35 cm) vascular sheath can help to negotiate tortuosities in the femoral arterial system and reduce risk of retrograde dissection.
Transseptal punctures are performed using ICE guidance. A large-curl steerable sheath (Agilis, St. Jude Medical, St. Paul, MN) is typically used to reach the mitral annulus with the ablation catheter. A view encompassing the IAS and fossa ovalis is selected on ICE. The sheath and needle are withdrawn from the SVC down the atrial septum until indentation of the fossa is seen. Blood is withdrawn from the LA and saline is flushed down the transseptal sheath, producing echocontrast that can be seen in the LA. A transeptal guidewire (SafeSept, Pressure Products Medical Supplies, Inc., San Pedro, CA) is then advanced out the transseptal needle, though the LA and out the LSPV. The position of the wire is confirmed by fluoroscopy and ICE. The needle is then covered by the dilator, and the sheath is advanced over the dilator into the LA. Needle, sheath, and angioplasty wire are then carefully withdrawn as a unit. Heparin is administered prior to transeptal access and then every 30 minutes as needed to maintain ACTs of greater than 300 to 350 seconds. The transeptal sheath is continuously irrigated.
One option for approaching unstable VTs is with the use of percutaneous LV assist, or extracorporeal membrane oxygenation to support the circulation during mapping in VT. We have generally avoided these measures as a first approach. Deployment of these devices complicates vascular access and introduces the potential for complications related to the device. These may be considered when a substrate guided approach fails, or for severely compromised patients. More often, we consider placement of an IABP to provide some degree of support during mapping in sinus rhythm, and to facilitate hemodynamic recovery from VT that causes hypotension. Adjunctive inotropic medication is also often helpful.
Once vascular access has been obtained, the next step is usually to use programmed stimulation to induce VT. This serves several purposes. We confirm that the arrhythmia induced is indeed VT and not SVT with aberrancy or an antidromic tachycardia. We assess the possibility of bundle branch reentry, which may only require ablation of the right bundle branch. Most commonly this tachycardia has a LBBB-like configuration. Entrainment from the RVA usually reveals a postpacing interval that is within 50 ms of the TCL, and the VT is often easy to pace terminate. Analysis of H–H oscillations and confirming His-to-right bundle anterograde activation during a LBBB tachycardia further support the diagnosis. If the tachycardia is not due to bundle branch reentry, the QRS morphology influences the next step. LBBB-like tachycardias generally will warrant RV mapping to assess the possibility of RV scar. This may be done in a limited fashion, focusing on identifying whether scar is present in the region where the pace map approximates the VT QRS, if one can be identified. Even in patients with coronary artery disease and prior MI, RV tachycardias occasionally occur, possibly from RV infarction. If RV mapping does not suggest a scar-related RV tachycardia, or tachycardia has an RBBB–like configuration, we promptly focus on the LV. The next decision then relates to whether to obtain epicardial access prior to endocardial LV mapping and anticoagulation.
The possibility that percutaneous epicardial access may be needed is considered in all patients who have not had prior cardiac surgery. In particular, those who have failed an endocardial ablation attempt and patients with NICM are more likely to require this approach. We avoid percutaneous epicardial access in patients with prior cardiac surgery because residual adhesions frequently prohibit access. A surgical approach to the LV epicardium can be feasible, however. In patients with NICM, VTs that originate from the basal lateral LV often require epicardial ablation and the QRS morphology can suggest an epicardial exit, but exceptions occur. In patients with prior MI, we have not been able to predict epicardial exits based on the QRS morphology of VT. If no prior ablation has been performed, limited transvenous mapping of brief, induced VT via the CS and accessible LV branches can suggest an epicardial VT circuit. Epicardial mapping can be considered as the first approach in patients with LV thrombus, if their anticoagulation can be safely interrupted for the procedure.1
Epicardial access is obtained using either a Tuohy needle (Codman Inc., Rayham, MA) with a soft-tipped wire with firm body such as a Bentson wire (Cook Co., Bloomington, IN) or a long micropuncture needle inserted through a short 18 g needle (see Chapter 42). Access is feasible in more than 90% of patients who have not had cardiac surgery.
From 2 to 3 cm below the xiphoid process the needle is directed toward the cardiac silhouette to enter the pericaridum either anteriorly over the RV or inferiorly between the diaphragm and RV as observed in biplane fluoroscopy. Injection of a small amount (1 cm3) of contrast can help assess the relation of the needle to the parietal pericardium. Once tenting of the pericardium is seen, a slight advance achieves entry into the space. Aspiration without blood indicates that the needle has not entered the RV. Injected contrast should layer in the pericardial space. The needle is directed toward the cardiac silhouette to enter the pericaridum either anteriorly over the RV or inferiorly between the diaphragm and RV as observed in biplane fluoroscopy. Injection of a small amount (< 1 cm3) of contrast can help assess the relation of the needle to the parietal pericardium. Once tenting of the pericardium is seen, a slight advance achieves entry into the space. Aspiration without blood indicates that the needle has not entered the RV. Injected contrast should layer in the pericardial space. The guidewire is then advanced generously into the pericardial space ( Video 41.2, A and B). It is essential to observe the wire in the LAO projection observing that it hugs the cardiac silhouette, crossing more than one chamber, circumferential to both the right and left heart. Monitored by ICE allows visualization of any pericardial bleeding or fluid accumulation, both during access and during the procedure ( Video 41.3). Before ablation, coronary angiography is often performed to ensure the site is performed at least 5 mm from any important coronary artery (Figure 41.2).