34 Ventricular arrhythmias originating from the papillary muscle represent approximately 7% of idiopathic ventricular arrhythmias.1 Papillary muscle arrhythmias occur in a wide variety of patients, both with and without underlying cardiomyopathy. While presentation with isolated premature ventricular contractions (PVCs) is more common, patients may also present with ventricular tachycardia (VT) from the papillary muscle. Perhaps due to this variable presentation, no unifying mechanism of ectopy has been identified. In fact, many would argue that papillary muscle arrhythmias are multifactorial.2 One prevailing theory is that Purkinje fibers play a central role in triggering and maintaining papillary muscle arrhythmias. Numerous reports demonstrating the presence of Purkinje potentials at effective ablation sites have given some validity to this theory.3 The complex structure and shape of a papillary muscle (composed of interwoven layers of Purkinje fibers, myocardium, and endocardium) are also thought to contribute to the maintenance of ventricular arrhythmia through microreentrant circuitry. In either case, it remains controversial whether papillary muscle ventricular arrhythmias are sustained by a reentrant or a focal mechanism. In our experience, however, ablation targeting the discrete myocardial exit for these arrhythmias is highly effective in eliminating them. Prior to presentation to the laboratory for a papillary muscle arrhythmia ablation, standard clinical evaluation includes a screening history and physical, a surface electrocardiogram (ECG), a Holter study, a transthoracic echocardiogram, and an evaluation for ischemia. Cardiac magnetic resonance imaging (MRI) with gadolinium is often used to evaluate for the presence of scar in or around the papillary muscle. The surface ECG and Holter study play an essential role in the preprocedural planning for a papillary muscle arrhythmia procedure. A Holter study with binning can confirm a unifocal origin for a ventricular arrhythmia, but it is also necessary to capture the ventricular arrhythmia of interest on a 12-lead ECG. This allows adequate localization of the origin of the PVC or VT. Papillary muscle PVCs can be broken down into three general categories: anterolateral papillary muscle (ALPM), posteromedial papillary muscle (PMPM), and right ventricular papillary muscle (RVPM). While PVCs coming from each of these structures can vary in morphology, Figure 34.1 shows a general example of each type of papillary muscle PVC. ALPM and PMPM PVCs have a right bundle branch pattern with a QRS that transitions to negative usually by V3–V5, with an rS pattern in V6. The PMPM is often distinguished from the ALPM by a superior axis.4 This pattern can also be found in posterior fascicular ventricular arrhythmias; however, fascicular arrhythmias typically will have a small q wave in either lead I or aVL, whereas papillary muscle PVCs usually have a monophasic R-wave.2 ALPM PVCs are often characterized by a rightward axis with some negativity in lead II, but mainly positivity in lead III. RVPM PVCs are characterized by a left bundle branch block pattern with a transition at V4–V6, positive in lead I, usually somewhat positive in lead II, and negative in lead III.5,6 The above guidelines for ECG diagnosis are intended for patients with structurally normal hearts, and patients with nonischemic scar will not necessarily follow these general rules. Furthermore, individual variation in heart position, papillary muscle location, and PVC exit site on the papillary muscle can result in significant variation to these ECG guidelines. Nonetheless, a ventricular arrhythmia morphology that is close to these guidelines should prepare the physician for the likelihood of needing to target the papillary muscle during an ablation. Cardiac MRI and echocardiography are useful for anatomic characterization of the papillary muscle, as seen in Figure 34.2. Delayed enhancement on MRI can sometimes be seen in the tip or base of the papillary muscle and can suggest a location for the arrhythmogenic focus. This may be more common in patients with valves that prolapse or have redundant tissue that can lead to mechanical injury, or in patients with a history of rheumatic heart disease. The converse is not true, however, as absence of delayed enhancement does not exclude a papillary muscle from being the idiopathic arrhythmogenic focus.3 Echocardiography and MRI are also important for excluding scar in the left ventricular (LV) wall (nonischemic or ischemic) that may be the true origin of the ventricular ectopy with the above characteristics. It is our experience that PVCs originating from a LV papillary muscle can be difficult to distinguish from a scar-based PVC in the same area. Figure 34.3 highlights the similarity between a PVC originating from a LV papillary muscle and a PVC originating from an area of inferolateral scar in a patient with a nonischemic cardiomyopathy. Finally, imaging of the ascending aorta and aortic valve can be useful in determining whether a retro-aortic approach to ablation will be technically feasible and safe. The patient is brought to electrophysiology lab in a fasting, postabsorptive state and prepped and draped in a sterile fashion. It is preferable that conscious sedation or monitored anesthetic care is used during the procedure, though comorbidities such as severe lung disease or cardiomyopathy may necessitate general anesthesia. Similarly, agents with inherent arrhythmia suppression, like propofol, should be avoided when possible, as some papillary muscle arrhythmias are exquisitely catecholamine sensitive. We typically use remifentanil for our procedures, as it has rapid onset and offset. Once the patient is adequately sedated, vascular access is obtained utilizing a modified Seldinger technique under ultrasound guidance.7 Initial sheath placement includes a 4-Fr sheath in the right common femoral artery, an 8-Fr sheath in the right femoral vein, a 9-Fr sheath in the left femoral vein, and a 7-Fr sheath in the left femoral vein. Once vascular access has been obtained, intravenous heparin is given with a goal activated clotting time of 250–350 seconds. A quadripolar catheter is advanced into the right ventricular apex through the 7-Fr sheath and an ICE catheter is advanced into the right atrium through the 9-Fr sheath. We commonly use the CARTO SOUNDSTAR catheter (Biosense Webster, Diamond Bar, CA), as this allows for creation of anatomic maps based on the echocardiogram images with CARTOSOUND, which can then be integrated with subsequent electroanatomic maps (EAMs). ICE imaging may identify increased echogenicity in the papillary muscles in cases where there is a structural abnormality of the papillary muscle, focusing attention on the potential site of origin of the arrhythmia being targeted. If a retro-aortic approach is planned, a brief ICE survey is made of the aortic valve and ascending aorta to ensure that there is no significant atheroma or valvular pathology that would preclude the safety of this technique. If no atheroma is seen, then the 4-Fr arterial sheath is exchanged for a longer 8-Fr sheath that extends into the aorta. If catheter stability becomes challenging at a later point, this 8-Fr sheath can be exchanged for a long SL0 or SL1 sheath over a guidewire with the tip of the sheath placed through the aortic valve into the left ventricle. If a transseptal approach is planned, the 8-Fr femoral venous sheath is exchanged and transseptal puncture is performed under ICE guidance with a large-curl Agilis sheath, which is placed with the tip near the mitral valve ostium. Prior to induction, a detailed model of the papillary muscles is created using an EAM system paired with intracardiac ultrasound. The CARTO SOUNDSTAR ICE catheter allows for the reconstruction of the papillary muscles within the CARTO EAM system.8 Papillary muscle contours can be reproduced with a resolution that is sufficient to identify variable papillary muscle anatomy. Papillary muscles are pleomorphic in shape and more than one papillary muscle head may be present. Identifying these anatomic features and recreating them within the EAM system can be helpful to a procedure’s success. We find that if there are 2 or 3 distinct heads to a papillary muscle, it is helpful to construct separate CARTO maps of each head, which may improve localization. Despite these efforts, it may still be difficult to faithfully delineate all of the intricacies of the papillary muscle structure on an EAM, and it is still challenging to have the ICE-based anatomic map—which is typically generated during sinus rhythm beats—correlate exactly with location points taken during activation mapping of a PVC. Nonetheless, these maps serve as a necessary framework on which activation points can be built. A second advantage of CARTO and the CARTO SOUNDSTAR catheter is the green glow-tip visualization of the ablation catheter that is superimposed on the ICE image. The ready identification of the ablation catheter in the ICE image can assist in localization during manipulation and positioning of the ablation catheter (Figure 34.4).
How to Diagnose and Ablate Ventricular Tachycardia from the Papillary Muscles
Matthew C. Hyman, MD, PhD; Jeffrey P. Gordon, MD; Gregory E. Supple, MD
Introduction
Preprocedural Planning
Procedure
Setup