Vascular and Phrenic Nerve Injury and Protection

 












CHAPTER   
45
Vascular and Phrenic Nerve Injury and Protection


Domenico G. Della Rocca, MD; Michela Faggioni, MD; Ugur Canpolat, MD; Huseyin Ayhan, MD; Sanghamitra Mohanty, MD; Chintan Trivedi, MD; Carola Gianni, MD; Mohamed Bassiouny, MD; Amin Al-Ahmad, MD; J. David Burkhardt, MD; Javier E. Sanchez, MD; G. Joseph Gallinghouse, MD; Rodney P. Horton, MD; Kudret Aytemir, MD; Luigi Di Biase, MD, PhD; Andrea Natale, MD, PhD

INTRODUCTION


In 1996, the first description of a percutaneous approach to access the pericardial space in patients with Chagasic cardiomyopathy by Sosa et al.1 opened a new frontier in mapping and ablation of complex arrhythmias. Since then, our understanding of the arrhythmogenic substrate of several complex arrhythmias has steadily grown, as well as the outcomes of some ablation procedures (e.g., scarmediated ventricular tachycardia ablation) that were known to have a very low success rate.


Historically, procedures potentially requiring an epicardial access included catheter ablation of ventricular arrhythmias and accessory pathways. Over the years, indications have been expanded to include implantation of epicardial pacing leads, left atrial appendage (LAA) occlusion, mapping and ablation of several atrial tachyarrhythmias, and procedures requiring phrenic nerve displacement.


Nevertheless, compared with the endocardial approach, epicardial ablation procedures may be burdened with a higher risk of complications during subxiphoid pericardial puncture, catheter manipulation, or ablation. Lack of intervening myocardium between the ablating catheter and vulnerable structures, such as epicardial vessels and phrenic nerves, is thought to favor these complications. Although rarely fatal, both vascular and nerve injuries are associated with significant morbidity, prolonged hospital stay, and higher healthcare costs. As such, it is of utmost importance to have a thorough knowledge of the anatomy of the epicardial space in order to safely perform epicardial procedures.


Implementation of advanced imaging modalities and distancing techniques to separate the pericardial structures from epicardial ablation sites has progressively reduced the rate of complications.


Hereby, we aimed at reviewing the incidence of vascular and phrenic nerve injury during epicardial interventions, as well as providing some preventive measures to minimize the risk of complications.


EPIDEMIOLOGY


The reported rates of vascular and phrenic nerve injury vary greatly based on center experience. However, even in experienced centers where epicardial procedures have been performed for many years, the incidence of complications is “relatively” low.2 Acute complications related to the epicardial approach have been reported in up to 9% of patients and can occur at any stage of the epicardial intervention (e.g., pericardial access, catheter manipulation, ablation). It is also worth noting that the risk of complications has progressively declined owing to constant improvements in the technique. In general, the prevalence of vascular complications is reported to be around 4% in experienced centers.2 This includes peripheral vessel damage, abdominal/phrenic vessel damage, and epicardial bleeding due to myocardial wall or coronary injury. Right ventricular (RV) injury is relatively common during subxiphoid pericardial access. In around 4.5% of cases a dry RV puncture (entry of the RV without subsequent pericardial blood effusion) is observed, whereas the prevalence of significant pericardial bleeding with cardiac tamponade in large studies is reported in between 3% to 5%.3,4 The rate of coronary artery injury is estimated around 1.5% with the epicardial approach.5


Overall, the incidence of phrenic nerve injury in epicardial ablations appears to be lower than what was reported with the endocardial approach.6 The reason for this can be twofold.


So far, only small, single-center experiences have been reported on epicardial ablation. Since phrenic nerve injury can often remain undiagnosed, large case series in experienced centers are necessary to reliably estimate the risk of this complication.


Given the higher risk of direct contact and injury of the phrenic nerve with epicardial radiofrequency (RF) ablation, more frequently than in endocardial ablations, efforts have been made to map and, if necessary, protect the phrenic nerve during epicardial procedures.


So far, few studies on epicardial procedures have reported phrenic nerve injury.6,7 Interestingly, on an overall population of 25 patients, Okubo et al.7 recently reported 3 instances of phrenic nerve transient palsy in a cohort of patients treated with RF ablation in the absence of phrenic nerve distancing techniques, whereas in the remaining 13 patients, for whom intraprocedural phrenic nerve distancing with a vascular balloon was obtained, no phrenic nerve injury was reported.


Table 45.1 summarizes the studies reporting vascular and/or neurological complications with the epicardial approach.


VASCULAR INJURY: PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS


Vascular injuries can occur at the time of the subxiphoid puncture, during catheter manipulation and ablations, or postprocedurally. Based on the approach chosen for the pericardial puncture, different vascular structures are at risk of injury. For instance, an anterior puncture can result in epigastric artery injury, a septal puncture can damage the posterior descending artery, and a lateral approach increases the risk of RV puncture.8 Once the epicardial access is obtained, any coronary vessel can potentially be damaged depending on the anatomical area requiring ablation. However, vascular injury is most likely to occur in proximity to the anterior and posterior septal and basal ventricular areas, where coronary arteries and veins are known to traverse.


Manifestations of coronary artery damage can be acute, delayed, or chronic. Acute injuries comprise vasospasm, intimal damage with intravascular thrombus formation, compression, puncture, or laceration. Acute manifestations of vascular injury include acute ST-T segment changes with chest discomfort (if the patient is not anesthetized) in case of vasospasm (Figure 45.1), compression, or thrombosis and pericardial bleeding in case of laceration. Coronary compression can also result from ablation-induced edema of myocardial tissue close to the artery. Puncture or laceration of an epicardial coronary artery can be recognized via aspiration of arterial blood from the pericardial space. Laceration might require coronary stenting or surgical repair.



Figure 45.1 Left circumflex coronary artery spasm (Panel B) after left atrial appendage cryoballoon (Panel A) ablation with complete resolution after intracoronary nitrate administration (Panel C). Abbreviations: LAD, left anterior descending coronary artery; LCx, left circumflex coronary artery; LMCA, left main coronary artery.


Table 45.1 Reported Vascular and Neurological Complications in Epicardial Ablation Procedures



Delayed and chronic effects include fibrosis and coronary artery stenosis with subsequent possible ischemia.9,10 While coronary spasm can be reversible (Figure 45.1) and is usually attributed to RF-induced increases in local autonomic activity, ablation can also cause morphological damage to any layer of the coronary vessel.9 Chronic coronary injury should be suspected in patients with new-onset ischemic symptoms following a recent epicardial ablation, even if no acute manifestations were documented during ablation.


In a canine model, replacement of the coronary arterial media with extracellular matrix proliferation was reported in a few cases. Vessel hyperplasia and stenosis have also been reported both in experimental models and patients.9,10 The artery damage is thought to be inversely proportional to vessel size and interposed fat:11 larger vessels have higher volumes of blood flow/second that can partially dissipate the heat of the RF ablation. In addition, a functionally significant stenosis due to wall thickening is less likely with bigger vessel diameter. Structural damage is usually observed even when ablation does not directly involve a vessel.9,10 There is no definite safe distance between the ablation site and the coronary artery, since this distance may vary based on the RF energy applied, the presence and amount of overlying fat tissue, and the diameter and flow of the epicardial vessel. In general, a distance of at least 5 mm between the electrode and the coronary artery is considered safe.


Animal studies have shown histological evidence of coronary arterial injury when RF was delivered directly over the artery even with low contact force (10 × g). When ablation occurred in proximity to the artery, the likelihood of damage was proportional to the force used.12 Additionally, the effects of RF ablation were limited to the media when energy was delivered adjacent to the coronary artery, whereas severe intimal hyperplasia and intravascular thrombosis occurred when energy was delivered above the artery.11


PHRENIC NERVE INJURY: PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS


The phrenic is the nerve most frequently injured during ablation procedures. The left phrenic nerve descends behind the left innominate vein, crosses the aortic arch and the left lung root, and courses along the pericardium over the LAA. From there, it passes over the pericardium of the left ventricle (LV), either anteriorly or anterolaterally, and then pierces and innervates the diaphragm behind the cardiac apex. If the course is lateral (~80% of cases), the left phrenic nerve passes over the obtuse margin of the LV between the parietal pericardium and the mediastinal pleural layers, in proximity to the lateral vein and the left marginal artery.13 If the course is more anterior (~20% of cases), it can pass close to the left main coronary artery and the great cardiac vein.13


The right phrenic nerve descends anteriorly over the lateral part of the right subclavian artery, runs close to the superior vena cava (SVC) and the right superior pulmonary artery, and descends along the right atrium and the lateral wall of the RV (Figure 45.2).14 In a gross anatomical study performed in 19 cadavers,13 the minimal distance between the right phrenic nerve and the SVC was 0.3 ± 0.5 mm, and that between the right phrenic nerve and the right superior pulmonary vein (PV) was 2.1 ± 0.4 mm. Of note, the anterior wall of the right superior PV was < 2 mm from the right phrenic nerve in 32% of specimens.



Figure 45.2 Right anterior (Panel A) and posterior (Panel B) oblique views of the right atrium showing various sites of right phrenic nerve capture (white dots) assessed via high-output pacing.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Dec 13, 2021 | Posted by in CARDIOLOGY | Comments Off on Vascular and Phrenic Nerve Injury and Protection

Full access? Get Clinical Tree

Get Clinical Tree app for offline access