Autonomic imbalance in the recovery period after myocardial infarction.

The aim of the study was to evaluate the responses to autonomic function tests during the healing period of myocardial infarction (AMI). In 24 patients, at 2 and 6 weeks after the acute event, Valsalva manoeuvre, deep breathing at 6 breaths per min, isometric handgrip and cold pressor tests were performed. Responses of arterial blood pressure (BP) and heart rate (HR) were measured. At 2 weeks post AMI a significant decrease in parasympathetic tone was noted: HR reduction during deep breathing: 18.5 +/- 5.7 beats.min-1 for controls vs 9.7 +/- 2.6 beats.min-1 for AMI, P < 0.001. Systolic BP response to handgrip and cold pressor test was only slightly (non significantly) increased: 30.6 +/- 12.9 mmHg (controls) vs 40.0 +/- 20.5 mmHg (AMI) for the handgrip test and 13.8 +/- 8.1 mmHg vs 18.0 +/- 10.1 mmHg respectively for the cold pressor test. At 6 weeks post AMI, the response to the deep breathing test (15.9 +/- 5.6 beats.min-1) no longer significantly differed from that in controls. In contrast, the sympathetic stressor tests showed a significant increase in systolic BP response: 63.8 +/- 21.9 mmHg, P < 0.001 and 26.1 +/- 14.9 mmHg, P < 0.05, respectively for the handgrip and cold pressor tests. It appeared that infarct localization had no effect on autonomic function tests. There is evidence of autonomic imbalance both at 2 and 6 weeks after AMI, with a rapid but transient decrease in vagal activity and enhancement of orthosympathetic nervous tone; this was markedly more pronounced at 6 weeks post AMI despite treatment with beta-blocking agents in all patients.

24 hour ambulatory blood pressure variability and cardiac parasympathetic function 2 and 6 weeks after acute myocardial infarction.

The aim of the study was to assess non-invasively circadian blood pressure rhythm as well as the influence of parasympathetic function 2 and 6 weeks after acute myocardial infarction treated with beta-blocking agents. Twenty-four patients with uncomplicated first myocardial infarction, and aged less than 60 years, underwent ambulatory blood pressure recordings every 15 min during the day (0900-2100 h) and every 30 min during the night (2100-0900 h), 2 and 6 weeks after infarction. The deep breathing test (6 breaths/min) was performed on each occasion. Normal circadian blood pressure rhythm was maintained with a nocturnal decline of 10 to 15%. Both for systolic and diastolic blood pressure a moderate increase was obtained after 6 weeks (107.8 +/- 9.2 mmHg vs. 111.8 +/- 10.3 mmHg; NS and 64.9 +/- 4.5 mmHg vs. 68.8 +/- 6.5 mmHg; p < 0.05). The respective blood pressure variations were significantly higher at that time (10.0 +/- 2.4 mmHg vs. 13.6 +/- 4.2 mmHg; p < 0.001 and 7.9 +/- 1.7 mmHg vs. 11.7 +/- 3.5 mmHg, p < 0.001). There was a close correlation (r = 0.60, p < 0.005) between 24-h diastolic blood pressure variability and the results of the parasympathetic function test (deep breathing) 2 weeks after infarction. We conclude that the circadian blood pressure rhythm persists after acute myocardial infarction. The correlation between blood pressure variability and parasympathetic function early after infarction suggests a role for vagal control in post-infarction blood pressure variability.