Paroxysmal AV Block Extrinsic Idiopathic AV Block: Difference between revisions
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==Overview== | ==Overview== | ||
Individuals with low levels of adenosine are susceptible to sudden surges in adenosine levels which act on the AV node and cause episodes of presyncope or syncope. This would be seen on an ECG as a sudden increase in sinus rate with narrow QRS complexes just prior to the period of asystole. | Individuals with low levels of [[adenosine]] are susceptible to sudden surges in [[adenosine]] levels which act on the [[AV node]] and cause episodes of [[presyncope]] or [[syncope]]. This would be seen on an [[ECG]] as a sudden increase in [[sinus rate]] with narrow [[QRS complexes]] just prior to the period of [[asystole]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
*The pathogenesis of extrinsic idiopathic paroxysmal AV block (EI-AVB) can be correlated to ''' adenosine plasma levels (APL) and increased affinity of adenosine A1 receptors'''. | *The [[pathogenesis]] of [[extrinsic idiopathic paroxysmal AV block]] (EI-AVB) can be correlated to ''' [[adenosine]] [[Blood plasma|plasma]] levels (APL) and increased [[affinity]] of [[Adenosine A1 receptor|adenosine]] A1 receptors'''. | ||
*There is a recurrent history of unexplained syncope, absence of ECG and cardiac abnormalities and a good prognosis. | *There is a recurrent history of unexplained [[syncope]], absence of [[ECG]] and [[cardiac]] abnormalities and a good [[prognosis]]. | ||
*Due to | *Due to [[innate]]<nowiki/>ly low APL values seen in these patients, there is '''an [[upregulation]] of A1 receptors''', such that even during a mild transient surge in [[endogenous]] [[adenosine]] levels, [[AV block]] occurs. | ||
*A1 receptors, which are present more in the AV node than the SA node, impose an '''antiadrenergic action''' by antagonizing β1 receptors, the sympathetic nervous system, hyperpolarizing the SA and AV nodes through potassium channels and lowering intracellular cAMP levels. <ref name="pmid26115830">{{cite journal| author=Brignole M, Deharo JC, Guieu R| title=Syncope and Idiopathic (Paroxysmal) AV Block. | journal=Cardiol Clin | year= 2015 | volume= 33 | issue= 3 | pages= 441-7 | pmid=26115830 | doi=10.1016/j.ccl.2015.04.012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26115830 }} </ref> | *[[A1 receptors]], which are present more in the [[AV node]] than the [[SA node]], impose an '''[[antiadrenergic]] action''' by antagonizing [[Βeta receptors|β1 receptors]], the [[sympathetic nervous system]], [[hyperpolarizing]] the SA and [[AV nodes]] through [[potassium channels]] and lowering [[intracellular]] [[Cyclic adenosine monophosphate|cAMP]] levels. <ref name="pmid26115830">{{cite journal| author=Brignole M, Deharo JC, Guieu R| title=Syncope and Idiopathic (Paroxysmal) AV Block. | journal=Cardiol Clin | year= 2015 | volume= 33 | issue= 3 | pages= 441-7 | pmid=26115830 | doi=10.1016/j.ccl.2015.04.012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26115830 }} </ref> | ||
*Therefore, in such patients an injection of adenosine or adenosine triphosphate (ATP) may reproduce the attack and adenosine antagonists such as theophylline may be an efficacious treatment option. | *Therefore, in such patients an [[injection]] of [[adenosine]] or [[adenosine triphosphate]] (ATP) may reproduce the attack and [[adenosine]] [[antagonists]] such as [[theophylline]] may be an efficacious treatment option. | ||
*On an ECG, there is an absence of signs of vagal stimulation, atrial/ventricular premature beats and there may be a presence of narrow QRS complexes prior to the period of complete AV Block/ asystole | *On an [[ECG]], there is an absence of signs of [[vagal]] stimulation, [[atrial]]/[[ventricular premature beats]] and there may be a presence of narrow [[QRS complexes]] prior to the period of complete [[AV Block]]/ [[asystole]] | ||
*Certain studies have also noticed '''genetic polymorphisms in A2A | *Certain studies have also noticed '''[[genetic]] [[polymorphisms]] in [[Adenosine A2A receptor|A2A receptor]]<nowiki/>s''' in a population of people experiencing recurrent unexplained [[syncope]]. .<ref name="pmid19386617">{{cite journal| author=Saadjian AY, Gerolami V, Giorgi R, Mercier L, Berge-Lefranc JL, Paganelli F | display-authors=etal| title=Head-up tilt induced syncope and adenosine A2A receptor gene polymorphism. | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 12 | pages= 1510-5 | pmid=19386617 | doi=10.1093/eurheartj/ehp126 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19386617 }} </ref> | ||
==References== | |||
Latest revision as of 18:46, 27 June 2020
Overview
Individuals with low levels of adenosine are susceptible to sudden surges in adenosine levels which act on the AV node and cause episodes of presyncope or syncope. This would be seen on an ECG as a sudden increase in sinus rate with narrow QRS complexes just prior to the period of asystole.
Pathophysiology
- The pathogenesis of extrinsic idiopathic paroxysmal AV block (EI-AVB) can be correlated to adenosine plasma levels (APL) and increased affinity of adenosine A1 receptors.
- There is a recurrent history of unexplained syncope, absence of ECG and cardiac abnormalities and a good prognosis.
- Due to innately low APL values seen in these patients, there is an upregulation of A1 receptors, such that even during a mild transient surge in endogenous adenosine levels, AV block occurs.
- A1 receptors, which are present more in the AV node than the SA node, impose an antiadrenergic action by antagonizing β1 receptors, the sympathetic nervous system, hyperpolarizing the SA and AV nodes through potassium channels and lowering intracellular cAMP levels. [1]
- Therefore, in such patients an injection of adenosine or adenosine triphosphate (ATP) may reproduce the attack and adenosine antagonists such as theophylline may be an efficacious treatment option.
- On an ECG, there is an absence of signs of vagal stimulation, atrial/ventricular premature beats and there may be a presence of narrow QRS complexes prior to the period of complete AV Block/ asystole
- Certain studies have also noticed genetic polymorphisms in A2A receptors in a population of people experiencing recurrent unexplained syncope. .[2]
References
- ↑ Brignole M, Deharo JC, Guieu R (2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.
- ↑ Saadjian AY, Gerolami V, Giorgi R, Mercier L, Berge-Lefranc JL, Paganelli F; et al. (2009). "Head-up tilt induced syncope and adenosine A2A receptor gene polymorphism". Eur Heart J. 30 (12): 1510–5. doi:10.1093/eurheartj/ehp126. PMID 19386617.