Evaluation of Effects of Intra Aortic Balloon Counterpulsation on Autonomic Nervous System Functions by Heart Rate Variability Analysis

Abstract

Background: In patients with acute myocardial infarction (AMI), intraaortic balloon counterpulsation (IABC) may improve cardiac performance, decrease the incidence of recurrent ischemia, and improve survival. Although there have been several reports concerning circulatory maintenance with the IABC, response of the autonomic nervous system to these hemodynamic changes is not clear. Heart rate variability (HRV) analysis has been extensively used to evaluate autonomic modulation of sinus node and to identify patients at risk for an increased cardiac mortality. In this study, we evaluated effects of the IABC on autonomic nervous system functions by HRV analysis. Methods: The study group was composed of 32 consecutive patients (13 female, 19 male aged 61.8 +/- 8.8 years) undergoing IABC. Transthoracic echocardiography and 1-hour Holter recordings for HRV analysis in each IAB pumping mode were obtained. Results: The IABC improved left ventricular diastolic and systolic functions as well as caused an increase in SDNN1, PNN50(1), RMSSD1, and HF1 and a decrease in LF1, LF/HF1, mean heart rate, and the number of ventricular extrasystoles. The improvements in HRV parameters were correlated with some hemodynamic changes such as the increase in MAP and CO during counterpulsation. The only independent factors affecting in-hospital mortality were the change in LF/HF1 ratio (Delta LF/HF1) and the change in the number of ventricular extrasystole (Delta VES). The decrease in LF/HF1 >= 4.9 decreased the mortality by 1.7-folds (RR = 0.6, P = 0.04, 95% CI: 0.1-2.3). The decrease in VES >= 27/15 minutes resulted in mortality reduction by 16-folds (RR = 0.06, P = 0.02, 95% CI: 0.01-0.4). Conclusions: As a result, the IABC, especially in 1:1 support, causes an increase in HRV, decrease in sympathetic overactivity, and improvement in sympathovagal balance besides the favorable hemodynamic changes, and these electrophysiologic changes may explain the role of the IABC in the treatment of ventricular arrhythmias.