Catheter ablation is a procedure used to remove or terminate a faulty electrical pathway from sections of the hearts of those who are prone to developing cardiac arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardias (SVT) and Wolff-Parkinson-White syndrome (WPW syndrome). If not controlled, such arrhythmias increase the risk of ventricular fibrillation and sudden cardiac arrest. The ablation procedure can be classified by energy source: radiofrequency ablation and cryoablation.
Ablation is the removal of material from the surface of an object by vaporization, chipping, or other erosive processes. Examples of ablative materials are described below and include spacecraft material for ascent and atmospheric reentry, ice and snow in glaciology, biological tissues in medicine and passive fire protection materials.
Sudden cardiac death (SCD) is a vital public health issue, accountable for almost 50% of all cardiovascular deaths[1]. In the last three decades, SCD was the leading cause of almost 230000 to 350000 deaths per annum in the United States[1]. Ventricular arrhythmias account for 25% to 36% of witnessed sudden cardiac arrests (SCA) at home and 38% to 79% of witnessed SCA in public[rx].
Ischemic heart disease, structural disorders, various forms of cardiomyopathy associated with myocardial fibrosis, cardiac channelopathies, myocarditis, congenital heart diseases, and other genetic rare disorders are associated with ventricular arrhythmias[rx].
Even though treatment for heart failure lowers mortality and SCD, it was unsuccessful in lessening ventricular tachycardia (VT) recurrences[rx]. Implantable cardioverter defibrillators (ICD) are very effective in eliminating VT episodes and in lowering the possibility of SCD, but they are not useful for arrhythmia prevention[rx]. When the VT substrate manifests, anti-arrhythmic drug treatment or catheter ablation are the current choices to reduce VT episodes[rx]. Catheter ablation and antiarrhythmic drug therapy though, are also limited by incomplete efficacy, unfavorable side effects, and procedural risk[rx]. In this review, we outline the current advances in VT treatment options and describe the imaging modalities, progress, and novel strategies.
Epicardial catheter ablation
Endocardial catheter ablation and antiarrhythmic drug treatment are currently the mainstays of VT treatment[rx,rx]. However, the procedural success rates of VT are quite variable due to the heterogeneous substrates that reflect the variety of pathophysiological processes[rx,rx]. The success rate of endocardial ablation in patients with outflow tract VT is 84%, in patients with papillary muscle VT is 60%, and in patients with idiopathic left ventricular VT is 70%[rx]. Moreover, the VT recurrence rates of endocardial ablation in ischemic cardiomyopathy patients are between 23% and 49% and in dilated cardiomyopathy patients between 46% and 61%[rx]. Non-ischemic cardiomyopathy patients have worse outcomes than ischemic cardiomyopathy patients due to scar patterns with epicardial and intramural sites[rx].
Epicardial ablation has emerged as a potential alternative ablation strategy in order to increase the success rate in complex substrates and to eliminate VT in patients with different cardiomyopathies and more recently in patients with Brugada syndrome[rx–rx]. Percutaneous approach to the pericardial area facilitates epicardial ablation when the VT substrate is situated in the subepicardium[rx] (Figure [rx]. Adjacency to coronary circulation and the phrenic nerve may hinder the procedure in certain situations[rx]. In patients with previous heart surgery or previous epicardial ablation attempts, percutaneous access may not be possible and as such, video-assisted thoracoscopy may be a good and minimally invasive alternative to open surgery[rx].
Epicardial ablation is a safe procedure with low complication rates[rx]. Pericardial effusion is the most common complication[rx]. Damage to subdiaphragmatic organs and hemorrhage from diaphragmatic vessels have also been reported[rx].
Della Bella et al[rx] evaluated the possible benefit of endo-epicardial catheter ablation for the management of VT in 528 patients with any form of the structural cardiac disorder (Figure [rx]. Endo-epicardial catheter ablation resulted in a VT recurrence rate of 34.1%, in comparison to a rate of up to 50% with the standard endocardial approach[rx].
Intramyocardial infusion-needle catheter ablation
Transcoronary alcohol ablation has emerged to approach deep intramyocardial substrate in patients not amenable to endo-epicardial catheter ablation (mechanical valve, thrombus, significant comorbidities)[rx,rx]. Transcoronary alcohol ablation requires the injected dose of sterile pure ethanol with proximal balloon expansion to a culprit vessel with a target of abolishing perfusion[rx,rx] . This method can prevent recurrent VT, VT storm and can control incessant VT[rx,rx]. The exact recognition of the target vessel and the existence of collaterals may hinder the adoption of the method[rx–rx].
Kim et al[rx] introduced the novel use of cardioplegia as a mapping technique in order to identify the critical VT isthmus to facilitate effective transcoronary ethanol ablation and avoid irreversible myocardial injury. Furthermore, Sapp et al[rx] showed that intramyocardial needle mapping and ablation with saline infusion could create deep injuries and is a practical and efficient method. Intracoronary wire mapping and coil embolization have also been utilized just as alcohol ablation to target VT arising from intraventricular septum[rx]. After intracoronary wire mapping and recognition of a culprit’s vessel, coils are directed to embolize the branch, eliminating the desired target perfusion[rx].
Bipolar ablation
Bipolar ablation between two ablation catheters located on either position of the septum from both ventricles improves lesion transmurality because it depends less on catheter contact and alignment[rx,rx]. Bipolar ablation has the theoretical benefit of producing more powerful energy and providing deeper lesions, in comparison to two separate unipolar catheters[rx,rx]. Sakamoto et al[rx] recently successfully eliminated the critical VT circuit in a patient with an arrhythmogenic substrate (cardiac sarcoidosis), utilizing bipolar ablation.
Cardiac sympathetic denervation
Accumulated evidence strongly suggests the role of sympathetic neuromodulation in controlling refractory VT[rx–rx]. Cardiac sympathetic denervation surgery has been proven to be useful for the management of congenital long QT syndrome and catecholaminergic polymorphic VT[rx]. The procedure requires extraction of the lower fraction of the stellate ganglion and T2-T4 sympathetic thoracic ganglia[rx]. Complications regarding the procedure were infrequent, with 4% developing acute ptosis or Horner syndrome[rx]. Vaseghi et al[rx] showed that cardiac sympathetic denervation has greater shock-free survival as well as a considerable decline in shock burden in patients with recurrent VT or VT storm, regardless of antiarrhythmic drug therapy and catheter ablation. In addition, bilateral cardiac sympathetic denervation appeared to be more efficacious than left-sided denervation[rx,rx].
Augmented sympathetic activity leads to early and delayed afterdepolarization, enhances diffuse repolarization, leading to ventricular electrical susceptibility and increases the possibility of malignant VT[rx]. Stellate ganglionectomy lengthens the ventricular refractory period and raises the VF threshold, decreasing VT or VF inducibility in the context of myocardial infarction[rx,rx]. Locally invasive sympathetic ganglion block could select individuals with greater possibilities of long-term clinical benefits prior to sympathetic denervation[rx,rx].
Renal sympathetic denervation
Enhanced sympathetic tone shortens the ventricular effective refractory period, enhances automaticity, and lowers the threshold for ventricular arrhythmias[rx–rx]. Feyz et al[rx] performed bilateral renal denervation in a patient with polymorphic VT with excellent results. Aksu et al[rx] also showed that catheter-based renal denervation was successful in a patient with an electrical storm due to catecholaminergic polymorphic VT. However, the microanatomy of human renal vessels has great variability. Accessory renal vessels that bifurcated early can also influence the result negatively, and there is still the absence of procedural endpoint during the technique[rx].
As a result, renal sympathetic denervation is not currently recognized as an ideal or approved VT treatment method[rx–rx]. However, certain ventricular arrhythmias do not terminate after catheter ablation, thus making renal sympathetic denervation a possible option for patients in whom other ablative approaches were ineffective[rx,rx].
Stereotactic radioactive therapies
Despite catheter-oriented ablation, which applies radiofrequency or freezing to damaged tissues, radiotherapy is based on photons from X-rays or gamma rays to injure the desired target, mainly cancer. Through novel distribution methods such as intensity-modulated radiotherapy, a dosage of radiotherapy can be precisely and accurately directed to the desired size, while diminishing dosage to adjoining healthy tissues[rx,rx].
Ablative radiotherapy is generally a noninvasive, outpatient method, which does not involve anesthesia[rx,rx]. Potential risks consist of damage to tissue next to the ablated site, such as brain edema for intracranial lesions, pneumonitis for chest therapies, myelopathy for spinal carcinomas, or bowel perforation for abdominal locations[rx,rx]. In comparison to radiofrequency or cryo energy, the damage from ablative radiotherapy progresses over days to months, needing time for the total tissue damage to be shown[rx,rx].
The first patient was treated on a robotic radiosurgery system (CyberKnife®, Accuray, Sunnyvale, CA, United States) in 2012[rx]. The follow-up revealed no definite acute or late adverse effects, and a seven-month reduction burden in VT on standard antiarrhythmic drug therapy, suggesting a potential transient benefit of this method[rx].
Cuculich et al[rx] investigated five patients with increased-risk, refractory VT. The authors focused on arrhythmogenic scar sites by merging anatomical imaging with noninvasive electrocardiographic imaging during VT that was produced using an ICD[rx]. Patients were treated with a single dose of 25 Gy while awake, using a noninvasive distribution of accurate ablative radiation with stereotactic body radiation treatment[rx]. Cuculich et al[rx] reported a reduction in events of VT in all five patients.
Cryoablation
Catheter radiofrequency ablation of VT originating from the left ventricle’s papillary muscles has been linked to conflicting outcomes[rx,rx]. Rivera et al[rx] investigated twenty-one patients with drug-refractory VT, who underwent catheter cryoablation or radiofrequency ablation. Cryoablation was correlated with greater success rates and smaller recurrence rates than radiofrequency procedures, superior catheter support, and smaller frequency of polymorphic arrhythmias[rx]. Marai et al[rx] recently used cryoablation guided by intracardiac echocardiography, 3-dimensional mapping system, and image integration to treat a patient with refractory VT originating from papillary muscle with excellent results.
Surgical therapy for VT
Catheter ablation provides efficient outcomes for sustained monomorphic VT, but certain situations, such as the existence of mural thrombus and heavy calcification, can lead to adverse results[rx,rx]. Higuchi et al[rx] successfully treated a 67-year-old patient with sustained monomorphic VT due to ventricular scar and resistant to endocardial radiofrequency ablation, by left ventricular reconstruction with cryoablation. Li et al[34] conducted a retrospective investigation of 38 consecutive surgical epicardial VT ablation procedures and compared the results with those of a propensity-matched percutaneous epicardial access control group. Surgical epicardial access after heart surgery for VT ablation showed no statistical difference in long-term results in comparison to the percutaneous epicardial group[rx].
Recently, Berte et al[rx] presented the first animal survey utilizing a more potent cryoablation system that can generate larger, transmural ventricular lesions from both the endocardium and the epicardium. Surgical cryoablation in sheep had no acute macroscopic vascular or extracardiac damage and resulted in 100% successful lesions at necropsy[rx].
In some patients with non-ischemic cardiomyopathy and VT refractory to standard therapy or undergoing cardiac surgery, surgical ablation may be an alternative option for potentially reducing the burden of ICD shocks during long-term follow-up[rx]. Liang et al[rx] showed that detailed arrhythmogenic substrate in the electrophysiology lab before surgery, in conjunction with a direct scar and radiofrequency ablation lesions visualization in the operating room, is crucial for guiding surgical ablation.
Extracorporeal life support for refractory VT
Extracorporeal life support is a highly efficient bridging treatment in patients with refractory VT associated with cardiogenic shock[rx]. Extracorporeal life support allows the usage of negative inotropic antiarrhythmic drug therapy, leads to the weaning of catecholamine delivery, thus resolving the dangerous period of the catecholamine driven electrical storm[rx]. The utilization of extracorporeal life support maintains hemodynamic support during an ablation procedure, while mapping and induction of VT are commenced and provides sufficient vital organ perfusion in patients with refractory VT[rx]. Current literature suggests the usage of extracorporeal life support, as it has proven to be a safe, practical and efficient therapeutic solution when traditional treatments have failed[rx].
Steroid pulse therapy
Okabe et al[rx] successfully treated a patient with cardiac sarcoidosis associated with VT using steroid pulse therapy.
Gene therapy
Catecholaminergic polymorphic VT (CPVT) is a rare cardiac ion channelopathy induced by anomalies in proteins that regulate Ca2+ transport in heart cells that can lead to SCD[rx,rx]. CPVT is associated with mutations in the gene encoding the cardiac RyR2, a cardiac ryanodine receptor protein which is involved in calcium homeostasis and mutations in the gene that encodes calsequestrin (CASQ2), a protein that interacts with RyR2[rx–rx].
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