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Published on: September 13, 2022
Elevated platelet activating factor level in ischemia-related arrhythmia and its electrophysiological effect on
Yong Kang Tao1, Shui Ping Zhao, Pu Lin Yu
1Emergency Department, China-Japan Friendship Hospital, Ministry of Health, Beijing 100029, China. taoyongkang@163.com
Insights
Platelet-activating factor (PAF) levels increase during acute myocardial infarction (AMI) and ischemia, correlating with fatal arrhythmias. PAF affects cardiac repolarization, potentially via ion channels.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Pharmacology
Background:
- The precise mechanism of platelet-activating factor (PAF) in cardiac electrical disturbances and arrhythmias post-acute myocardial infarction (AMI) remains unclear.
- Previous research suggests a role for ion channels in PAF's cardiac effects.
Purpose of the Study:
- To elucidate the role of PAF in fatal arrhythmias following AMI.
- To investigate the underlying electrophysiological mechanisms of PAF's action in the context of myocardial infarction and ischemia.
Main Methods:
- Measurement of blood PAF levels and continuous electrocardiogram (ECG) monitoring in 72 AMI patients.
- Ischemia simulation and ECG recording in 20 pigs, with concurrent PAF level measurements.
- In vitro studies using guinea pig papillary muscles involving PAF perfusion and microelectrode recordings.
Main Results:
- Elevated PAF levels were observed in human AMI patients and pigs with simulated ischemia, with significantly higher levels during fatal arrhythmias.
- In guinea pig myocardium, PAF induced action potential duration shortening (APD90) under both non-ischemic and simulated ischemic conditions.
- The effect of PAF on APD90 was more pronounced under simulated ischemic conditions.
Conclusions:
- Acute myocardial infarction and ischemia are linked to increased PAF levels in humans and pigs.
- Further elevation of PAF occurs when fatal arrhythmias develop post-AMI or ischemia.
- PAF's myocardial effects are likely mediated through interactions with multiple cardiac ion channels.
Objective:
The mechanism through which platelet activating factor (PAF) induces cardiac electrical activity and arrhythmia is not well understood and previous studies have suggested a potential involvement of ion channels in its action. The present study was aimed to clarify the role of PAF in fatal arrhythmias following acute myocardia infarction (AMI) and the underlying mechanism.
Methods:
(1) Blood PAF levels were measured among 72 AMI patients at the time of diagnosis with AMI and 48 h later, and their electrocardiogram (ECG) was recorded continuously. (2) Ischemia simulation and surface electrocardiogram were conducted in 20 pigs and their PAF levels were measured. (3) PAF perfusion and standard microelectrode recording were performed on guinea pig papillary muscles.
Results:
In both humans and pigs, elevated PAF levels were detected in AMI and simulated ischemia, respectively, and even higher PAF levels were found when fatal arrhythmias occurred. In guinea pig myocardium, PAF induced a shortening of action potential duration at 90% level of repolarization (APD90)under non-ischemic conditions and a more pronounced shortening under early simulated ischemic conditions.
Conclusion:
AMI and ischemia are associated with increased PAF levels in humans and pigs, which are further raised when fatal arrhythmia follows. The effects of PAF on the myocardium may be mediated by multiple ion channels.
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