Several animal studies have shown that blood platelet contents released during acute myocardial infarction can induce ventricular fibrillation (VF). Previously, we have found that activated blood platelets products (ABPP) increase action potential duration of rabbit ventricular myocytes, increase L-type calcium current and intracellular calcium transients, and induce afterdepolarizations. One of the possible mechanisms of arrhythmia is triggered activity caused by afterdepolarizations.
To test if ABPP can induce VF on organ level we used a model of regional ischemia in Langendorff-perfused rabbit heart. Blood platelets were isolated from healthy volunteers. Platelets activation during isolation was controlled by CD62p (alpha-granule membrane glycoprotein) and CD63 (lysosomal integral membrane protein) labeling. We applied ABPP (or control solution) 5 min before and after coronary artery ligation. A recording multi-electrode grid (16x16) was situated on the left ventricular free wall. Three premature stimuli and burst pacing protocol were applied until 90 minutes post occlusion.
Ventricular activation - recovery interval was significantly prolonged after application of ABPP (before occlusion), confirming out previous finding of increased action potential duration in single myocytes. In four out of five hearts perfused with ABPP, and in none out of five control hearts, premature stimuli caused ventricular fibrillation at ~70 min of ischemia (P < 0.05 in Fisher's Exact Test versus control hearts). In one heart we were able to record conduction block after 65 min of ischemia, before VF. The size of myocardial infarction did not differ significantly between groups.
In summary, products secreted from activated human platelets in Langendorff-perfused rabbit heart prolong activation - recovery interval of nonischemic myocardium, increase incidence of VF at ~70 min after myocardial infarction, possibly by inducing conduction block.