AVNRT pathophysiology
|
AVNRT Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
AVNRT pathophysiology On the Web |
|
American Roentgen Ray Society Images of AVNRT pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]
Overview
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. In the usual form of AVNRT, the conduction from the atrium to the ventricle is down the slow pathway, and the retrograde conduction from the ventricle to the atrium is up the fast pathway.
Pathophysiology
Electrophysiologic Triggers
Premature Atrial Complex
The most common trigger for an episode of AVNRT is when an atrial premature complex (APC) approaches the fast pathway, and is blocked due to the longer refractory period of this pathway, and instead conducts down the slow pathway. As the impulse goes down the slow pathway, the fast pathway recovers, and allows the impulse to conduct backward or retrograde toward the atrium. It then re-enters the atrial entrance of the slow pathway and the cycle repeats itself.[1]
Premature Ventricular Complex
The second most common mechanism whereby AVNRT is triggered is via the entry of a premature ventricular complex down either the slow conducting pathway (similar to a premature atrial complex above) or down the rapidly conducting pathway.
Genetics
- There are certain types of cardiac arrhythmia that are shown to have a genetic basis.
- Wolff-Parkinson-White syndrome has an autosomal dominant inheritance model.[2]
- familial lone atrial fibrillation which is classified as "channelopathies" and is characterized by autosomal dominant inheritance, corresponding to a locus on chromosome 10.[3]
- However, whether a genetic mechanism also contributes to the development of AVNRT has not been well known, but it is shown that offspring of affected patient is at 3.4% increased risk to develop the disease.
References
- ↑ Mani, Bhalaghuru Chokkalingam; Pavri, Behzad B. (2014). "Dual Atrioventricular Nodal Pathways Physiology: A Review of Relevant Anatomy, Electrophysiology, and Electrocardiographic Manifestations". Indian Pacing and Electrophysiology Journal. 14 (1): 12–25. doi:10.1016/S0972-6292(16)30711-2. ISSN 0972-6292.
- ↑ Vidaillet, Humberto J.; Pressley, Joyce C.; Henke, Elizabeth; Harrell, Frank E.; German, Lawrence D. (1987). "Familial Occurrence of Accessory Atrioventricular Pathways (Preexcitation Syndrome)". New England Journal of Medicine. 317 (2): 65–69. doi:10.1056/NEJM198707093170201. ISSN 0028-4793.
- ↑ Brugada, Ramon; Tapscott, Terry; Czernuszewicz, Grazyna Z.; Marian, A.J.; Iglesias, Anna; Mont, Lluis; Brugada, Josep; Girona, Josep; Domingo, Anna; Bachinski, Linda L.; Roberts, Robert (1997). "Identification of a Genetic Locus for Familial Atrial Fibrillation". New England Journal of Medicine. 336 (13): 905–911. doi:10.1056/NEJM199703273361302. ISSN 0028-4793.