1 Structural heart disease and the arrhythmic substrate

Sustained monomorphic ventricular tachycardia in structural heart disease is usually maintained by reentry through diseased ventricular myocardium. The substrate is not the fibrous scar alone. Dense collagen does not propagate activation; the critical anatomical element is viable myocardium that persists within, beside or between fibrotic regions. Aggregates of surviving cardiomyocytes may be separated by collagen, adipose tissue or areas of myocyte loss, yet remain connected through narrow and tortuous paths. Activation along these paths can be slow, discontinuous and direction dependent, allowing unidirectional block and reentry when conduction time exceeds local refractoriness [1–4].

The word scar therefore describes a heterogeneous three dimensional volume rather than a uniform sheet. Its components include dense replacement fibrosis, a border zone with mixed viable myocardium and collagen, interstitial fibrosis between cardiomyocytes, vascular structures and, in some diseases, adipose replacement. The arrangement of surviving cardiomyocytes is as important as their total mass. Branching and merging myocardial corridors can force activation to follow a zigzag route, producing long conduction delay across a short geometric distance. A protected isthmus is the functionally critical portion of such a route, bounded by fixed fibrosis, anatomical discontinuities or functional lines of block [3–6].

2 Postinfarction ventricular tachycardia

After coronary occlusion, irreversible injury usually begins in the subendocardium and may extend towards the epicardium according to the duration, location and completeness of ischaemia. The healed infarct follows a coronary distribution but is rarely homogeneous. Endocardial replacement fibrosis may coexist with surviving subendocardial myocardium, intramural channels, preserved epicardial layers and variable transmural extension. Infarct thinning, ventricular dilatation and aneurysm formation further alter the geometry. The border of an aneurysm and the junction between thinned scar and thicker myocardium can provide abrupt changes in thickness and cardiomyocyte orientation that influence conduction [3–6].

Classic pathological studies showed that continuous or branching tracts of surviving cardiomyocytes can cross an infarct and account for diastolic activation during ventricular tachycardia. Modern high density mapping has refined this model: the central isthmus may be narrow, but entrance, exit, outer loops and bystander pathways form a larger network. Some boundaries are anatomically fixed, while others appear only for a particular wavefront. A channel detected during sinus rhythm may therefore change when activation approaches from another direction. Conversely, a critical pathway may remain concealed when it lies intramurally or when surface activation bypasses it [4–7].

The papillary muscles, muscular ventricular septum and periannular myocardium require special attention. Infarction can leave viable cardiomyocytes within a papillary muscle or at its base, where abrupt changes in three dimensional architecture and Purkinje insertions permit multiple exits. Septal infarction may contain deep channels between the right and left ventricular endocardial surfaces. A normal voltage map on one surface does not exclude an intramural or opposite surface substrate.

3 Nonischaemic patterns of fibrosis

Nonischaemic cardiomyopathy usually produces a more patchy and less predictable substrate than healed myocardial infarction. In dilated cardiomyopathy, fibrosis may be predominantly basal anteroseptal and midmyocardial or inferolateral and subepicardial. Basal septal disease can extend around the aortic root, the superior ventricular septum and the region of the conduction axis. Its intramural position may leave relatively preserved bipolar voltage on both endocardial surfaces. Inferolateral disease is more often accessible from the epicardium, but epicardial fat, coronary arteries and the phrenic nerve may restrict the safe treatment surface [8–10].

Arrhythmogenic cardiomyopathy characteristically begins in the outer ventricular wall and can progress inward, with replacement by fibrous and adipose tissue. The right ventricular subtricuspid region, outflow tract and inferior wall are frequent components, but biventricular and left dominant patterns are well recognised. The thin right ventricular wall means that epicardial disease can influence endocardial electrograms, yet the full extent is often greater on the epicardial surface. Myocarditis commonly leaves patchy subepicardial or midwall fibrosis, often inferolateral, while cardiac sarcoidosis may create multifocal, transmural or septal lesions separated by apparently normal myocardium. Active inflammation and healed fibrosis can coexist in the same patient.

Hypertrophic cardiomyopathy produces replacement fibrosis and interstitial expansion within hypertrophied myocardium, particularly at regions of mechanical stress and ventricular insertion. An apical aneurysm can add a discrete thin walled scar with a border zone capable of supporting reentry. Other diseases have distinctive distributions: Chagas cardiomyopathy frequently involves the inferolateral wall and apex; prior cardiac surgery creates incision, patch and cannulation scars; and corrected congenital heart disease combines surgical boundaries with pressure or volume related remodelling. These patterns are guides, not substitutes for patient specific reconstruction.

4 The ventricular tachycardia circuit as a three dimensional structure

A reentrant circuit should not be represented automatically as a flat loop on the endocardium. The protected pathway may curve through the wall, connect endocardial and subepicardial surfaces, or form a predominantly intramural circuit. Recent human mapping supports circuits bounded in three dimensions, including hyperboloid configurations in which the apparent surface entrance and exit are only windows onto a deeper pathway [6,7]. The same substrate can support several tachycardias because different entrances, exits or functional boundaries recruit different portions of the surviving myocardial network.

The circuit is also dynamic. Conduction velocity and block depend on wavefront direction, cycle length, autonomic state, drugs and tissue excitability. A region that conducts during sinus rhythm can block during tachycardia, while a pathway invisible during one paced rhythm can become evident from another direction. The anatomical substrate is fixed only in part; the expressed circuit results from the interaction between tissue architecture and the activating wavefront. This explains why a complete anatomical map requires sampling from more than one rhythm or pacing direction whenever feasible [5–7].

5 From tissue anatomy to electroanatomical mapping

Low bipolar voltage is a practical marker of reduced local viable myocardium, not a direct image of collagen. Its amplitude depends on electrode size and spacing, wavefront direction, contact, wall thickness, filtering and intervening blood or fat. Unipolar recordings sample a larger tissue volume and can suggest deeper or opposite surface disease, especially when bipolar voltage appears preserved. Neither recording alone defines the transmural extent of fibrosis. Thresholds used to label dense scar and border zone are operational settings and should not be mistaken for histological boundaries [9–11].

Fractionated, prolonged or late electrograms and local abnormal ventricular activities arise from delayed activation of surviving myocardium isolated from the main wavefront. They identify electrically abnormal viable tissue rather than inert scar. Their timing changes with activation direction, and far field signals can obscure small near field components. Entrainment and activation mapping during tolerated tachycardia provide direct functional information, whereas substrate mapping during sinus rhythm or pacing infers potential circuit components. Both approaches require anatomical interpretation.

Late gadolinium enhancement cardiac magnetic resonance displays the location and transmural distribution of replacement fibrosis, while computed tomography can define wall thinning, fat, calcification, coronary arteries and surgical material. Intracardiac echocardiography confirms wall morphology, aneurysms, papillary muscles, catheter contact and pericardial relations. Positron emission tomography is particularly useful when active inflammatory disease is suspected. Image resolution, partial volume effects, device artefact and registration error prevent any modality from showing every narrow surviving corridor. Imaging and electrograms are complementary measurements of the same three dimensional substrate [8,10,12].

6 Anatomical implications for ablation

The anatomical objective of substrate ablation is to interrupt the myocardial tissue required for maintenance of the clinical circuit while preserving neighbouring structures. Endocardial failure may reflect inadequate lesion depth, an intramural isthmus, a subepicardial substrate or an incorrect exit rather than insufficient energy at the same point. Mapping of opposed surfaces, integration of imaging and measurement of wall thickness can identify the shortest safe path. The conduction axis, coronary arteries and veins, papillary apparatus, valves, phrenic nerves and oesophagus impose regional limits.

Scar homogenisation, channel interruption and elimination of abnormal electrograms are procedural strategies, but none should obscure the underlying anatomy. Extensive ablation of electrically abnormal tissue may be appropriate in selected patients, yet low voltage can include noncritical bystander regions and electrically silent tissue may conceal deep substrate. A failed lesion should prompt reconsideration of circuit depth and direction rather than automatic repetition. The most informative procedural report states the disease pattern, ventricular component, wall layer, mapped surface, imaging correlate and structures at risk.