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Effect of the Ca2+ chelators EDTA and EGTA on sinoatrial-node activity and heart irritability
Insights
Calcium chelators EDTA and EGTA significantly disrupt sinoatrial node function, causing bradycardia and arrest. This leads to altered heart rhythms, including atrial and ventricular fibrillation, impacting cardiac electrophysiology.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Calcium ions (Ca²⁺) are crucial for cardiac electrical activity and contractility.
- Sinoatrial node (SAN) dysfunction can lead to serious arrhythmias.
- The role of calcium in SAN function and heart irritability requires further investigation.
Purpose of the Study:
- To investigate the effects of calcium chelators ethylenediaminetetraacetic acid (EDTA) and ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid (EGTA) on sinoatrial node activity.
- To assess the impact of these chelators on cardiac irritability and impulse conduction in canine hearts.
Main Methods:
- Experiments were conducted on dog hearts, perfusing the artery supplying the sinoatrial node.
- Standard ECG, epicardial electrograms (atrial, ventricular), His-bundle electrogram, and early SAN activity were recorded.
- Action potentials were recorded from the left auricle and right ventricle.
Main Results:
- Local application of EDTA and EGTA around the SAN and atrioventricular (AV) nodes induced rapid sinus bradycardia and sinus arrest.
- Junctional escape rhythms replaced sinus rhythm, followed by atrial premature beats, flutter, and fibrillation.
- AV nodal conduction was prolonged, and atrial and ventricular action potentials were depressed.
Conclusions:
- EDTA and EGTA significantly impair sinoatrial node automaticity and atrioventricular conduction.
- Calcium chelation can precipitate complex atrial and ventricular arrhythmias, highlighting calcium's critical role in maintaining normal cardiac rhythm.
Abstract:
The effect of the Ca-chelators EDTA and EGTA on sinoatrial activity and heart irritability was studied in dog experiments by perfusing the artery supplying the sinoatrial node. Beside the usual ECG recordings left and right atrial and left and right ventricular epicardial electrograms, His-bundle electrogram and the early activity of the sinoatrial node were recorded. In addition action potentials were recorded from the left auricle and right ventricle of the dog hearts. Local application around the sinoatrial and atrio-ventricular nodes of EDTA and EGTA caused sinus bradycardia and later sinus arrest within 1 min after introduction of the drugs. For substitution of the sinus rhythm junctional (seldom lower atrial) escape rhythm developed. One to two minutes later it was followed by atrial premature beats and even later atrial flutter and fibrillation could be recorded. In one third of the cases atrial fibrillation was followed by secondary ventricular fibrillation. Atrio-ventricular impulse conduction was prolonged in the av node by EDTA and EGTA. Atrial action potentials and the slow (Ca dependent) ventricular action potentials were depressed by EDTA and EGTA.