What is the mechanism of SCAR (Scar-related) ventricular tachycardia?

Mechanism of Scar-Related Ventricular Tachycardia

The primary mechanism of scar-related ventricular tachycardia is reentry, where electrical impulses circulate through surviving myocardial strands that traverse the scar tissue, creating a zigzag conduction pathway with areas of slow conduction that facilitate the maintenance of the arrhythmia. 1, 2

Pathophysiological Basis

Scar-related VT typically develops in patients with:

• Prior myocardial infarction
• Cardiomyopathy
• Previous cardiac surgery

Structural Substrate

The structural substrate for scar-related VT includes:

• Heterogeneous Scar Composition:

  • Islands of fibrosis create barriers that lengthen excitation pathways 1
  • Narrow strands of surviving myocardial tissue within the scar 3
  • Increased separation of myocardial bundles by fibrosis 1
  • Disruption of parallel orientation of myocardial fibers 1

• Electrophysiological Consequences:

  • Abnormal conduction velocities in and around the scar 4
  • Fragmentation of local electrograms 1
  • Heterogeneous patterns of activation 1

Reentry Circuit Components

The reentrant circuit in scar-related VT consists of several critical elements:

1. Entry Site: Where the electrical impulse enters the circuit
2. Central Isthmus: A critical protected channel of slow conduction within the scar
3. Exit Site: Where the impulse emerges from the scar to activate the ventricle 3
4. Outer Loop: The returning wavefront that completes the circuit

Characteristics of the Circuit

• Slow Conduction: Particularly evident within the isthmus, characterized by:

  • Decreased gap junction density 2
  • Impaired myocyte excitability 2
  • Crowding and zigzag pattern of activation isochrones 3

• Unidirectional Block: Required for initiation of reentry

  • May occur due to functional or anatomical barriers 1
  • Often triggered by premature ventricular contractions 1

• Excitable Gap: Separates the excitation wavefront from its tail of refractoriness 1

Electrophysiological Markers

Several electrophysiological markers identify the arrhythmogenic substrate:

• Late Potentials: Represent delayed activation of myocardium within the scar 1
• Local Abnormal Ventricular Activities (LAVAs): Found in VT isthmus and other areas 4
• Intra-Scar Conduction Corridors (ISCC): Channels of relatively preserved conduction within dense scar 4, 5
• Deceleration Zones: Areas where conduction velocity significantly slows 4

Three-Dimensional Nature of the Circuit

Importantly, scar-related VT circuits are often complex three-dimensional structures:

• Some reentry circuits involve both epicardial and endocardial layers 3
• The circuit may traverse the myocardial wall through intramural pathways 3
• Complete understanding requires simultaneous mapping of both epicardial and endocardial surfaces 3

Initiation and Maintenance Factors

Several factors contribute to the initiation and maintenance of scar-related VT:

• Triggers: Often premature ventricular contractions (PVCs)

• Autonomic Influence: Enhanced sympathetic tone can:

  • Decrease action potential duration
  • Increase sarcoplasmic reticular calcium leak
  • Promote triggered activity 2

• Functional Barriers: The location of functional barriers (deceleration zones) may differ depending on the direction of activation wavefronts 4

Clinical Implications

Understanding the mechanism of scar-related VT has important implications for management:

• Mapping Approaches: High-density mapping during different activation wavefronts can help identify the critical isthmus 4
• Ablation Targets: Include sites with late potentials, isolated potentials, and corridors of preserved voltage within dense scar 5
• Linear Lesions: Often created to transect putative isthmus sites 5

The complex nature of scar-related VT explains why these arrhythmias can be difficult to treat and why comprehensive mapping and ablation strategies targeting the specific components of the reentry circuit are essential for successful management.