1. Definition and three-dimensional boundaries

The left ventricular summit is the superior epicardial region of the left ventricle situated beneath the bifurcation of the left coronary artery. Its two arterial borders are formed by the proximal anterior interventricular artery and the proximal circumflex artery. These vessels diverge from the left main stem and enclose a roughly triangular territory whose apex points superiorly. This geometric description is useful, but it must not convert the summit into a flat triangle or a single ablation point. The myocardium curves around the left ventricular outflow tract, varies in thickness, and is covered by a variable layer of epicardial fat containing coronary arteries, veins, autonomic nerves, and lymphatics [1–4,10].

In attitudinal orientation, the summit lies superiorly and leftward, behind the anteriorly placed right ventricular outflow tract and close to the pulmonary root. Its deeper and inferior relations include the subaortic left ventricular outflow tract, the left coronary aortic sinus, the right–left interleaflet region, and the superior aspect of the left ventricular septum. The anterosuperior mitral vestibule and aortic–mitral continuity are nearby but are not components of the epicardial summit. The left atrial appendage can overlie part of the region. Consequently, a focus within or beneath the summit may be recorded from several anatomically opposed surfaces [2–5].

2. Coronary arteries, veins, and the accessible–inaccessible concept

The great cardiac vein reaches the summit from the left atrioventricular groove and turns to continue as the anterior interventricular vein. This venous transition is commonly used to divide the summit into two procedural regions. The portion superior to the vein has been termed inaccessible because major coronary arteries and abundant epicardial fat frequently prevent safe or effective direct energy delivery. The portion inferior to the vein may be approachable from the venous system or the epicardial space. These labels are relative rather than absolute anatomical compartments: venous calibre, coronary course, fat thickness, and the distance from the arrhythmic source vary between individuals [4–6].

The coronary venous anatomy is also variable. The distal great cardiac vein and anterior interventricular vein may be joined by small communicating veins that cross the summit and occasionally provide unusually close access to an arrhythmic source. A very early signal in a vein establishes proximity to an activation pathway, not necessarily contact with the focus. The venous wall, epicardial fat, a coronary artery, and a layer of viable myocardium can intervene between the electrode and the source. Coronary venography defines the available venous routes, while coronary angiography is required before contemplated radiofrequency delivery at a venous or epicardial site where arterial proximity is possible [4,6,7].

3. Arrhythmic substrate and patterns of activation

Summit ventricular arrhythmias may arise from superficial epicardial myocardium, from myocardium adjacent to a coronary vein, or from a deep intramural source between epicardial and endocardial surfaces. The last category is particularly important. Cardiomyocytes with a shared predominant orientation form continuous three-dimensional pathways through the outflow myocardium; activation can therefore reach more than one breakout. Preferential conduction may produce an early venous electrogram, an early signal in the left coronary sinus or subaortic outflow, and a relatively early septal right ventricular outflow signal even though none of these electrodes lies directly on the source [3–5].

An intramural origin should be considered when activation is only modestly early over a broad area, when similarly early signals are found on opposing surfaces, when the unipolar electrogram is not convincingly QS, or when an apparently appropriate first ablation site fails. Partial injury can alter the preferential exit and change QRS morphology without eliminating the source. Pace mapping may reproduce an exit rather than the site of origin and is limited by epicardial fat, capture of adjacent structures, and the distance between the pacing electrode and deep myocardium. Surface ECG patterns can suggest a summit origin, but they cannot replace reconstruction of the individual three-dimensional anatomy [4,5].

4. Mapping the summit from multiple surfaces

Mapping should begin by defining the relation of the outflow tracts, aortic root, coronary arteries, and coronary venous system in a common coordinate system. Relevant sites include the distal great cardiac and anterior interventricular veins, the subaortic left ventricular outflow tract, the left coronary sinus and right–left commissural region, the adjacent septal right ventricular outflow tract, and the pulmonary root. Intracardiac echocardiography and pre-procedural computed tomography can show tissue contact and measure distances that fluoroscopy alone cannot resolve. The earliest epicardial venous signal, the endocardial earliest activation site, and the endocardial site geometrically closest to the epicardial target should be recorded as separate observations [4,5,8].

This distinction is clinically relevant because the closest endocardial site and the electrically earliest endocardial site may be several millimetres apart. The closest site offers the shortest potential lesion path to an epicardial or intramural source, whereas the earliest site may identify a preferential exit. Neither strategy is universally superior. Local activation timing, unipolar morphology, tissue thickness, catheter contact, and the measured relation to the epicardial earliest site should be integrated. The term “summit origin” should therefore describe a regional diagnosis supported by comparative mapping, not be assigned solely from an inferior-axis QRS or an early signal in one chamber [5,8].

5. Ablation strategy and anatomical limits

Direct ablation within the coronary venous system is limited by narrow calibre, catheter instability, high impedance, venous injury, and—most importantly—proximity to a major coronary artery. Percutaneous epicardial access does not automatically solve these constraints because the superior region can remain shielded by coronary vessels and thick fat. When direct treatment is unsafe, the source may be reached from the nearest endocardial or arterial-root surface. Sequential unipolar applications from anatomically opposed sites can be considered when imaging supports a sufficiently short and safe tissue path. Energy should never be delivered merely because a venous electrogram is the earliest recorded signal [4,5,7].

Refractory deep intramural arrhythmias have prompted specialised techniques such as bipolar radiofrequency, coronary venous ethanol, guidewire-based venous radiofrequency, or needle ablation. These are rescue strategies for experienced centres, not routine substitutes for anatomical mapping. Each changes the geometry and risk of lesion creation and requires detailed coronary and venous imaging. The procedural objective is to select the safest surface capable of reaching the source while preserving the left main, anterior interventricular and circumflex arteries, the coronary veins, semilunar valves, and adjacent conduction tissues. Failure from one surface should prompt anatomical reassessment rather than repeated empirical applications [5,7–9].