Translational Approach for Percutaneous Interventions for the Treatment of Cardiac Arrhythmias

New translational concepts on cellular and tissue substrate of cardiac arrhythmias have been responsible for the development of non-pharmacological interventions, with important achievements compared to the conventional approach with antiarrhythmic drugs. In addition, the increasing knowledge of anatomical and electrophysiological studies, sophisticated mapping methods, special catheters, and controlled clinical trials have favored the progression of ablation of tachyarrhythmias, particularly of ventricular tachyarrhythmias and atrial fibrillation.

Arrhythmias, Cardiac/physiopathology; Catheter Ablation; Anti-Arrhythmia Agents; Cryosurgery/methods; Translational Medical Research; Atrioventricular Node; Echocardiography/methods; Tomography, X-Ray Computed/methods

Authorship

Angelo Amato Vincenzo de Paola

UNIFESP - Universidade Federal de São Paulo, São Paulo, SP – Brazil.Universidade Federal de São PauloBrazilSão Paulo, SP, BrazilUNIFESP - Universidade Federal de São Paulo, São Paulo, SP – Brazil.

http://orcid.org/0000-0001-9101-3170

Mailing Address: Amato Vincenzo de Paola Rua Pedro de Toledo 980 – cj 144. Postal Code 04039-002, São Paulo, SP – Brazil. E-mail: depaola@uol.com.br

Author Contributions

Conception and design of the research: De Paola AAV. Acquisition of data: De Paola AAV. Analysis and interpretation of the data: De Paola AAV. Writing of the manuscript: De Paola AAV. Critical revision of the manuscript for intellectual content: De Paola AAV.

Potential Conflict of Interest

No potential conflict of interest relevant to this article was reported.

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Figures

Figures (13)

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Figure 1
– (A) Ionic currents determining the action potential: inward currents are directed from outside to inside the cell; and outward currents come from within the cell and are directed to the extracellular environment; (B) Automatic cells, with oscillations in their action potential by early and late ionic fluxes PDP: early post-depolarizations, PDT: late post-depolarizations.

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Figure 2
– (A) Tissue with a structural or functional change in conduction without impairing passage in the stimulus under normal conditions. (B) In the presence of an ectopia, there is a bidirectional block. (C) During a precocious ectopia, there is a unidirectional anterograde block and, due to the delayed conduction, there is time to enable retrograde activation and triggering of arrhythmia.

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Figure 3
– (A and B) Anatomy of structures related to atrioventricular nodal reentry tachycardia, which follows the same principles of reentry of the electrocardiographic (C) identification of saltatory conduction through the atrioventricular node that precedes tachycardia. (D) Radiographic images of catheters used in the left anterior oblique projection and their positions. AV: atrioventricular, HRA: high right atrium, H: His, CS: coronary sinus, ABL: ablation catheter. RIE: Right inferior extension, LIE: Left inferior extension. Modified from Inoue.10

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Figure 4
– Surface lead (V6) and ablation catheter electrogram.Fragmented and late potentials in sinus rhythm of the arrythmogenic substrate in patients with sustained ventricular tachycardia, who underwent radiofrequency ablation.

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Figure 5
– (A) Sagittal and (B) transverse section of the heart. (A) Complete left bundle-branch block (LBBB) ventricular tachycardia suggests a RV (right ventricular) origin, comprising Right ventricular outflow tract tachycardia (RVOT) .The V3 and V4 leads can characterize the basal and apical left ventricular (LV) regions and, by the vectorial result in the electrocardigram, differentiate the basal (predominant R waves) from the apical (prdominant S waves) origins.

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Figure 6
– Reentry models in a scheme represented by pink areas of non-conducting fibrosis, surrounded by viable muscle that allows the passage of the stimulus in the form of "8". "Bystander" areas do not actively participate in the circuit but can communicate with the external stimulus loop that will enter a central channel called "isthmus", a channel of viable tissue, surrounded by barriers of unexcitable tissue, wich aids in the stability and perpetuation of arrhythmia. This mechanism forms the basis for "reentry", a continuous and circular process of wavefront propagation, wich returns and reactivates its place of origin.

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Figure 7
– Electroanatomic mapping of the heart in anterior and posterior views showing regions of low voltage (red), which, combined with conventional electrophysiological techniques, define the location for ablation (red points) in the left ventricular epicardium.

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Figure 8
– Electrocardiogram of a patient with sustained ventricular tachycardia with an epicardial focus, showing the pseudo-delta waves (between yellow lines in precordial leads V1 to V6) originated by the slow conduction of epicardial activation

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Figure 9
– EPatient with idiopathic ventricular fibrillation related to the His-Purkinje system. Left: Electrocardiogram showing that the morphology of the ventricular extrasystole that triggers polymorphic ventricular tachycardia (VT) is compatible to its origin in the His-Purkinje system of the posterior-inferior left ventricle. Right: Intracardiac signals, surface ECG leads I, II, III and VI, ablation proximal (LVp) and distal (LVd) indicating the potential and the probable region of slow conduction that gives rise to polymorphic VT.

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Figure 10
– Transversal and sagittal sections of the heart showing relations between the right ventricular outflow tract, aorta, left atrium, and left ventricle and the morphology of the QRS complex in lead V1, in five possibilities of the origin of ventricular tachycardia. Note the increase in R-wave amplitude when the origin of the ventricular tachycardia and ventricular extrasystoles are more posterior. Modified from Asirvatham.14

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Figure 11
– Posterior view of the left atrium (red circle) showing that the complex mesh of muscle fibers is more entrapped in the pulmonary vein ostium, allowing anisotropic conduction and arrhythmogenic phenomena. Modified from Nathan et al.,28

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Figure 12
– Images of pulmonary vein ablation for treatment of atrial fibrillation (AF). (A) Posteroanterior radiograph showing the insertion of microcatheters into pulmonary veins to detect the culprit vein. (B) Induction of AF. (C) Resolution of tachycardia and AF control after application of radiofrequency in the left superior pulmonary vein (LPSV) in another patient. (D) Electroanatomic voltage map of the left atrium in anteroposterior view, projected on a 3D model, showing the area of antral ablation and isolation of the pulmonary veins (red dots).

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Figure 13
– Electroporation - modified from Maor.43 Formation of pores driven by local electric field gradient (from A to C), followed by water penetration in the bilayer interface, creating pores (D). Leakage of ions and osmotic balance, loss of cell homeostasis entrance of calcium and release of damage-associated molecular patterns (DAMP) with alteration of function and structure of membrane proteins (E)

Figure 1 – (A) Ionic currents determining the action potential: inward currents are directed from outside to inside the cell; and outward currents come from within the cell and are directed to the extracellular environment; (B) Automatic cells, with oscillations in their action potential by early and late ionic fluxes PDP: early post-depolarizations, PDT: late post-depolarizations.

Figure 2 – (A) Tissue with a structural or functional change in conduction without impairing passage in the stimulus under normal conditions. (B) In the presence of an ectopia, there is a bidirectional block. (C) During a precocious ectopia, there is a unidirectional anterograde block and, due to the delayed conduction, there is time to enable retrograde activation and triggering of arrhythmia.

Figure 3 – (A and B) Anatomy of structures related to atrioventricular nodal reentry tachycardia, which follows the same principles of reentry of the electrocardiographic (C) identification of saltatory conduction through the atrioventricular node that precedes tachycardia. (D) Radiographic images of catheters used in the left anterior oblique projection and their positions. AV: atrioventricular, HRA: high right atrium, H: His, CS: coronary sinus, ABL: ablation catheter. RIE: Right inferior extension, LIE: Left inferior extension. Modified from Inoue.10

Figure 4 – Surface lead (V6) and ablation catheter electrogram.Fragmented and late potentials in sinus rhythm of the arrythmogenic substrate in patients with sustained ventricular tachycardia, who underwent radiofrequency ablation.

Figure 5 – (A) Sagittal and (B) transverse section of the heart. (A) Complete left bundle-branch block (LBBB) ventricular tachycardia suggests a RV (right ventricular) origin, comprising Right ventricular outflow tract tachycardia (RVOT) .The V3 and V4 leads can characterize the basal and apical left ventricular (LV) regions and, by the vectorial result in the electrocardigram, differentiate the basal (predominant R waves) from the apical (prdominant S waves) origins.

Figure 6 – Reentry models in a scheme represented by pink areas of non-conducting fibrosis, surrounded by viable muscle that allows the passage of the stimulus in the form of "8". "Bystander" areas do not actively participate in the circuit but can communicate with the external stimulus loop that will enter a central channel called "isthmus", a channel of viable tissue, surrounded by barriers of unexcitable tissue, wich aids in the stability and perpetuation of arrhythmia. This mechanism forms the basis for "reentry", a continuous and circular process of wavefront propagation, wich returns and reactivates its place of origin.

Figure 7 – Electroanatomic mapping of the heart in anterior and posterior views showing regions of low voltage (red), which, combined with conventional electrophysiological techniques, define the location for ablation (red points) in the left ventricular epicardium.

Figure 8 – Electrocardiogram of a patient with sustained ventricular tachycardia with an epicardial focus, showing the pseudo-delta waves (between yellow lines in precordial leads V1 to V6) originated by the slow conduction of epicardial activation

Figure 9 – EPatient with idiopathic ventricular fibrillation related to the His-Purkinje system. Left: Electrocardiogram showing that the morphology of the ventricular extrasystole that triggers polymorphic ventricular tachycardia (VT) is compatible to its origin in the His-Purkinje system of the posterior-inferior left ventricle. Right: Intracardiac signals, surface ECG leads I, II, III and VI, ablation proximal (LVp) and distal (LVd) indicating the potential and the probable region of slow conduction that gives rise to polymorphic VT.

Figure 10 – Transversal and sagittal sections of the heart showing relations between the right ventricular outflow tract, aorta, left atrium, and left ventricle and the morphology of the QRS complex in lead V1, in five possibilities of the origin of ventricular tachycardia. Note the increase in R-wave amplitude when the origin of the ventricular tachycardia and ventricular extrasystoles are more posterior. Modified from Asirvatham.14

Figure 11 – Posterior view of the left atrium (red circle) showing that the complex mesh of muscle fibers is more entrapped in the pulmonary vein ostium, allowing anisotropic conduction and arrhythmogenic phenomena. Modified from Nathan et al.,28

Figure 12 – Images of pulmonary vein ablation for treatment of atrial fibrillation (AF). (A) Posteroanterior radiograph showing the insertion of microcatheters into pulmonary veins to detect the culprit vein. (B) Induction of AF. (C) Resolution of tachycardia and AF control after application of radiofrequency in the left superior pulmonary vein (LPSV) in another patient. (D) Electroanatomic voltage map of the left atrium in anteroposterior view, projected on a 3D model, showing the area of antral ablation and isolation of the pulmonary veins (red dots).

Figure 13 – Electroporation - modified from Maor.43 Formation of pores driven by local electric field gradient (from A to C), followed by water penetration in the bilayer interface, creating pores (D). Leakage of ions and osmotic balance, loss of cell homeostasis entrance of calcium and release of damage-associated molecular patterns (DAMP) with alteration of function and structure of membrane proteins (E)

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[1] Mailing Address: Amato Vincenzo de Paola Rua Pedro de Toledo 980 – cj 144. Postal Code 04039-002, São Paulo, SP – Brazil. E-mail: depaola@uol.com.br