Abstract 2035: Effects of Ischemia and Reperfusion on Tonic Vagal Modulation: Deceleration Capacity in Patients Undergoing Direct PCI for Acute Myocardial Infarction
Recent findings indicate that decreased deceleration capacity (DC), a novel Holter-derived surrogate marker for tonic vagal activity, is a strong predictor for mortality in patients after myocardial infarction (MI). However, the early course of DC within the acute phase of MI, as well as the impact of reperfusion by direct percutaneous coronary intervention (PCI) has so far not been examined.
Methods and Results: We investigated DC in a total of 100 patients undergoing direct PCI for a first ST-segment elevation MI. Acceleration capacity (AC) and DC were determined before reperfusion, during the initial 2 hours after reperfusion, hours 12 and 20 after reperfusion from Holter-ECG-recordings started on hospital admission. After PCI, DC constantly increased within the following 12 hours and remained stable within the entire recording period (DC before PCI 3.8 ± 0.3ms vs. DC after 12 hours 5.3 ± 0.3ms; p<0.001). Likewise, AC constantly decreased after PCI, also exhibiting stable values after hour 12 (AC before PCI −3.9 ± 0.3ms vs. AC after 12 hours −5.9 ± 0.4ms; p<0.001).
Conclusion: The improvement of DC and AC after reperfusion is a previously unreported effect of early PCI for acute MI. In contrast to reflex cardiac autonomic modulation (i.e. baroreflex sensitivity), which has been shown to significantly increase within the initial hour after reperfusion, the characteristic time courses of DC and AC after PCI suggests a slow and constant recovery of tonic cardiac vagal modulation within 12 hours after reperfusion.