1 Right and left outflow tract ventricular tachycardia

Idiopathic outflow tract ventricular arrhythmias include premature ventricular complexes, nonsustained ventricular tachycardia, and sustained ventricular tachycardia occurring in hearts without demonstrable structural disease. Most are focal and commonly show features consistent with triggered activity. The anatomical site of origin, however, cannot be reduced to a binary choice between the right ventricular outflow tract and the left ventricular outflow tract. The outflow region also includes the pulmonary and aortic roots, myocardial extensions within the arterial sinuses, the aortic–mitral continuity, the epicardial ventricular summit, and adjacent coronary venous structures [1–4].

In attitudinal orientation, the right ventricle is the most anterior chamber. Its outlet ascends superiorly and leftward toward the pulmonary trunk, crossing in front of the left ventricular outlet. The left ventricular outflow tract is more central and posterior and is directed superiorly and rightward toward the aortic root. Consequently, most of the distal right ventricular outflow tract lies to the left of the left ventricular outflow tract. The two roots are neither parallel nor positioned side by side in a single frontal plane. This crossover explains why a focus can be recorded from several apparently different chambers and why fluoroscopic labels alone can be misleading [1–4].

The posterior wall of the right ventricular infundibulum is closely related to the anterior aspect of the left ventricular outlet and to the right and left coronary aortic sinuses. At their zone of contact, cardiomyocyte aggregates from the two ventricles can approach one another closely, although the arrangement and thickness of intervening myocardium vary. A focus located intramurally within this region may activate both surfaces. The earliest electrogram in the septal right ventricular outflow tract can therefore be a breakout from a left-sided or intramural origin rather than proof of a right ventricular source [2,5,6].

The arterial leaflet hinges add further complexity. Their crown-shaped attachments cross the anatomical ventriculoarterial junction, so crescents of ventricular myocardium are incorporated within the bases of the arterial sinuses. Cardiomyocytes can also extend for variable distances above the anatomical junction, more often in the pulmonary than the aortic root. These are focal myocardial extensions rather than a uniform sleeve surrounding the arterial trunk. They provide an anatomical explanation for ventricular arrhythmias mapped above a semilunar leaflet or within the proximal pulmonary artery or aortic root [2,5].

A left bundle branch block configuration with an inferior axis suggests an origin in the general right outflow region, whereas an earlier precordial transition favours a more posterior or leftward source. These patterns are useful guides but are not anatomical diagnoses. Cardiac rotation, chest shape, lead placement, preferential intramyocardial conduction, and closely apposed structures limit every surface electrocardiographic algorithm. The electrocardiogram should determine the initial mapping strategy, not prevent exploration of the neighbouring outflow tract when local activation is insufficiently early or ablation fails [6,7].

A rational procedure reconstructs the outflow region as one three-dimensional neighbourhood. Activation and pace mapping are interpreted together with intracardiac echocardiography, angiography, or tomographic imaging. When the earliest site is broad, only modestly premature, or associated with an imperfect pace map, the operator should consider a remote breakout, a deep intramural source, or preferential conduction. Before energy delivery, the intended target must be related to the coronary ostia and proximal arteries, the conduction axis, the semilunar leaflets, and the thickness of the intervening myocardium [3,7,8].

2 Right ventricular outflow tract tachycardia

The right ventricular outflow tract is the muscular infundibulum supporting the pulmonary root. It extends from the body of the right ventricle toward the pulmonary valve and is separated from the tricuspid inlet by the supraventricular crest. The crest is not a single cord but a complex muscular structure formed by the ventriculoinfundibular fold together with adjacent septal and parietal myocardium. The septomarginal trabeculation divides into limbs that contribute to the septoparietal trabeculations, which extend toward the free wall and form part of the endocardial architecture of the outlet [1,2].

The infundibulum is a freestanding muscular sleeve because the pulmonary valve is supported circumferentially by right ventricular myocardium. Its anterior and leftward walls are parietal; its posterior wall is related to the aortic root and left ventricular outlet. The thickness is not uniform. The posterior infundibular region adjacent to the ventricular septum and aortic root can be relatively substantial, whereas portions of the anterior, rightward, and subpulmonary walls can be thinner. Aggregates of cardiomyocytes change orientation through the wall, with longitudinal, oblique, and circumferential arrangements overlapping at different depths [2,3].

Most conventional right ventricular outflow tract arrhythmias are mapped in the superior infundibulum, commonly on its anterior or septal-facing aspects immediately below the pulmonary valve. “Septal RVOT” is a practical endocardial descriptor, but it does not imply that every target lies within the true ventricular septum. Distally, the posterior-facing wall is in close contact with the aortic root; more proximally, parietal trabeculations and the supraventricular crest can separate a catheter from a deeper focus. A single fluoroscopic projection may therefore confuse a trabecular surface, a true septal contact, and a site adjacent to an aortic sinus.

The pulmonary valve has three semilunar leaflets attached along crown-shaped hinge lines. There is no complete fibrous annulus. The hinge lines descend below and rise above the anatomical ventriculoarterial junction, placing crescents of infundibular myocardium within the bases of all three pulmonary sinuses. Additional myocardial extensions may continue above the junction within the adventitial or epicardial aspect of the pulmonary root. Their height, width, continuity, and circumferential distribution vary. Thus, an arrhythmia recorded above the valve can arise from local cardiomyocytes or represent activation from adjacent infundibular, aortic-root, or summit myocardium [2,5].

Mapping should begin below the pulmonary valve with complete reconstruction of the septal-facing and parietal surfaces. The valve plane should be identified by imaging or angiography rather than by catheter position alone. If activation becomes earlier above a leaflet, the corresponding pulmonary sinus and proximal trunk should be mapped. Discrete arterial potentials can reflect local myocardial extensions, but far-field signals from the infundibulum remain possible. Pacing can be limited by high output, poor capture, or simultaneous capture of neighbouring myocardium, so activation timing and unipolar morphology remain essential [7,8].

The posterior and leftward RVOT must always be compared with the aortic root and LVOT when activation is only modestly premature, when the earliest region is broad, or when an apparently appropriate application fails. Clinical and anatomical studies show that the longitudinal position of earliest septal RVOT activation relative to the pulmonary valve helps identify whether a left-sided origin is likely. A focus deep within the contact region can show different exits toward the RVOT and LVOT; elimination or change of one QRS morphology may unmask another exit rather than indicate a new arrhythmia [6,9].

Coronary relations constrain ablation. The left main coronary artery passes behind and leftward of the pulmonary trunk before dividing, while the proximal anterior interventricular artery descends near the anterior and leftward outlet. The right coronary artery and conus branch relate to the rightward aspect. Within the posterior pulmonary sinuses, a catheter may be close to the left or right coronary aortic sinus and its proximal artery. Coronary angiography or appropriately registered tomographic imaging is required whenever a safe separation cannot be established [1–3].

Other structures also matter. The conduction axis is situated at the rightward and proximal limit of the outflow region near the membranous septum, not at the usual distal RVOT target, but superior paraseptal mapping can approach the His bundle. Epicardially, fat and coronary vessels can separate an electrode from the focus. The left anterior descending artery may make a superficially attractive site unsafe. The aim is therefore not simply to select the earliest RVOT point, but to identify whether it represents the origin or the safest accessible exit from a three-dimensional source.

3 Left ventricular outflow tract tachycardia

The left ventricular outflow tract is shorter and more central than the right ventricular infundibulum. It lies between the ventricular septum anteromedially and the aortic leaflet of the mitral valve posteriorly. Because the aortic and mitral leaflets are in fibrous continuity, the left ventricle has no complete muscular infundibulum separating inlet from outlet. Blood entering through the mitral valve turns around the free margin of its aortic leaflet and passes superiorly and rightward toward the aortic root. This curved relation must be appreciated when interpreting catheter orientation and local electrograms [1–4].

The aortic root contains right coronary, left coronary, and non-coronary sinuses. The right and left coronary sinuses are partly supported by ventricular myocardium, whereas the non-coronary sinus is predominantly related to fibrous continuity and the interatrial region. The semilunar hinge lines cross the anatomical ventriculoarterial junction, incorporating crescents of ventricular myocardium into the bases of the right and left coronary sinuses. The deepest point of a sinus is therefore not synonymous with a fibrous arterial wall, and an aortic-root electrogram may include local or far-field ventricular activation [2,3,5].

The right coronary sinus is closely related to the upper muscular ventricular septum and posterior RVOT. The left coronary sinus faces the leftward outflow and the epicardial ventricular summit. The commissural region between them overlies the contact zone between the outflow tracts. By contrast, the non-coronary sinus is related mainly to the central fibrous body and atrial myocardium and is an unusual source of true ventricular outflow arrhythmia. Near the right–non-coronary interleaflet triangle, the penetrating atrioventricular bundle and proximal left bundle branch create an important limit to ablation [1–4].

Left-sided outflow arrhythmias may arise below the aortic valve, within myocardial crescents or extensions of the coronary sinuses, at the right–left commissural region, from the aortic–mitral continuity, or from the epicardial summit. These locations are anatomically close, and preferential conduction can produce an exit remote from the focus. An apparently excellent pace map at the aortic root can represent capture of an exit, while the true source remains intramural or epicardial. Mapping should compare the subaortic LVOT, aortic sinuses, adjacent RVOT, pulmonary root, and—when indicated—the coronary venous system [3,7,8].

The left ventricular summit is an epicardial region at the superior left ventricular surface. It is bounded by the bifurcating anterior interventricular and circumflex coronary arteries and traversed by the great cardiac vein as it continues toward the anterior interventricular vein. The vein divides the region conceptually into an inferior portion that may sometimes be approached epicardially and a superior portion rendered relatively inaccessible by the proximity of major coronary arteries and overlying epicardial fat. The summit is not a point; it is a region whose endocardial neighbours include the left coronary sinus, subaortic LVOT, anterosuperior mitral region, septal RVOT, and pulmonary root [10].

A summit focus may be mapped from the great cardiac or anterior interventricular vein, but the earliest venous signal does not guarantee that ablation is safe or that the electrode is at the origin. The venous wall, epicardial fat, and coronary artery may intervene. Coronary angiography is mandatory before energy delivery at a potentially close venous or epicardial site. When direct treatment is unsafe or ineffective, the arrhythmia may be approached from the nearest endocardial or arterial-root surface, accepting that lesion depth and the thickness of intervening myocardium determine success [10,11].

Intramural outflow arrhythmias are suggested by similarly early activation at several opposing sites, a broad early activation area, suboptimal unipolar morphology, or failure of ablation from the first surface. A deep septal or summit source can connect to more than one exit and change QRS morphology after partial injury. In such cases, repeated applications at the same endocardial point may add risk without reaching the focus. Sequential mapping from anatomically opposed surfaces, intracardiac echocardiography, and coronary imaging should define the shortest safe tissue path before considering advanced energy strategies [8,10,11].

The coronary ostia are the dominant constraint within the aortic sinuses. Their height and circumferential position vary, and catheter location cannot be judged reliably in one projection. The leaflet tissue itself may be injured by unstable contact, while the nearby central fibrous body and conduction axis limit ablation in the rightward subaortic region. At the aortic–mitral continuity, fibrous tissue can prevent effective energy transfer to a deeper focus, and the anterior mitral leaflet must be respected. Patient-specific imaging converts these relations from assumptions into measurable distances.

Successful LVOT ablation therefore depends on recognising which surface is being mapped. “Aortic cusp,” “LVOT,” and “summit” should not be used interchangeably. Reports should identify the sinus or interleaflet region, whether the catheter is above or below the hinge, the relation to coronary ostia, and the alternative sites mapped. The procedural endpoint is elimination of the clinical arrhythmia with preserved coronary, valvar, and conduction-system function, achieved from the safest surface capable of reaching the source.