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      Early Time Course of Heart Rate Variability after Thrombolytic and Delayed Interventional Therapy for Acute Myocardial Infarction

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          In 89 of 97 consecutive patients with myocardial infarction (MI) undergoing thrombolysis and delayed early coronary angiography with PTCA, if indicated, heart rate variability (HRV) in time domain was evaluable 40 ± 11 h after the onset of chest pain using 24-hour ECG recordings. Patients with anterior MI (n = 40) had lower values for HRV and left ventricular ejection fraction (p < 0.05). The mean of all 5-min standard deviations of RR intervals (SDNNi) and the root-mean-square difference of successive RR intervals (rMSSD) decreased significantly (p < 0.001 each), whereas the standard deviation of all normal RR intervals and the percentage of absolute differences between successive RR intervals only showed a tendency to lower values 4 weeks after MI (p = 0.20 and 0.08, respectively). The decreases in SDNNi and rMSSD were more evident in inferior than in anterior MI. The time course of HRV following MI was similar in patients with and without PTCA. These results indicate an initial vagal hyperactivity in inferior MI, which is quickly predominated by sympathetic activation and a prolonged recovery of the cardiac autonomic imbalance after MI despite a successful combined reperfusion therapy.

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          Heart rate variability as an index of sympathovagal interaction after acute myocardial infarction.

          By analysis of spectral components of heart rate variability, sympathovagal interaction was assessed in patients after acute myocardial infarction (AMI). At 2 weeks after AMI (n = 70), the low-frequency component was significantly greater (69 +/- 2 vs 53 +/- 3 normalized units [NU], p less than 0.05) and the high-frequency component was significantly smaller (17 +/- 1 vs 35 +/- 3 NU) than in 26 age-matched control subjects. This difference was likely to reflect an alteration of sympathovagal regulatory outflows with a predominance of sympathetic activity. At 6 (n = 33) and 12 (n = 29) months after AMI, a progressive decrease in the low- (62 +/- 2 and 54 +/- 3 NU) and an increase in the high-frequency (23 +/- 2 and 30 +/- 2 NU) spectral components was observed, which suggested a normalization of sympathovagal interaction. An increase in sympathetic efferent activity induced by tilt did not further modify the low-frequency spectral component (78 +/- 3 vs 74 +/- 3 NU) in a subgroup of 24 patients at 2 weeks after AMI. Instead, 1 year after AMI, this maneuver was accompanied by an increase in the low-frequency component (77 +/- 3 vs 53 +/- 3 NU, p less than 0.05) of a magnitude similar to the one observed in control subjects (78 +/- 3 vs 53 +/- 3 NU). These data indicate that the sympathetic predominance that is detectable 2 weeks after AMI is followed by recovery of vagal tone and a normalization of sympathovagal interaction, not only during resting conditions, but also in response to a sympathetic stimulus.
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            Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality.

            Clinical and experimental evidence suggest that sympathoadrenal activation contributes to mortality in patients with ischemic heart disease. To determine the level of sympathoadrenal activation in the very early phase of acute myocardial infarction (AMI) and to determine if location of infarction (anterior versus inferior) was related to sympathoadrenal activation, we studied norepinephrine (NE) and epinephrine (E) within 4 hours after the onset of symptoms and prior to any rise in plasma creatine kinase (CK). Mean (+/- SE) initial (NE = 591 +/- 111 pg/ml and E = 73 +/- 19 pg/ml), peak (NE = 1356 +/- 178 and E +/- 1098 +/- 608) and average (NE = 815 +/- 142 and E = 252 +/- 68) plasma catecholamine concentrations were considerably above normal (NE = 228 +/- 10 and E = 34 +/- 2 pg/ml, n 60) and values were similar for inferior and anterior infarctions. During an 18-month follow-up, three patients died in whom the AMI mean NE and E and peak CK were higher than in the eight late survivors. Thus the three AMI patients with peak EP values greater than 1000 died, whereas the eight AMI patients with peak EP values less than 1000 survived (p less than 0.01). The magnitude of sympathoadrenal activation early in the course of clinical AMI appeared related to the extent of myocardial damage and late mortality.

              Author and article information

              S. Karger AG
              April 2000
              19 April 2000
              : 92
              : 4
              : 256-263
              Departments of Internal Medicine III, aFriedrich Schiller University, Jena and bUniversity Hospital of the Saarland, Homburg, and cDepartment of Cardiology, District Hospital, Völklingen, Germany
              6983 Cardiology 1999;92:256–263
              © 2000 S. Karger AG, Basel

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              Page count
              Tables: 6, References: 33, Pages: 8
              Coronary Care


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