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Departments of
1 Medicine
2 Cardiology
3 Pathology, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand
4 Department of Internal Medicine, University of the United Arab Emirates, Al Ain, United Arab Emirates
The time course of cardiac sympathetic nerve activity (CSNA) following acute myocardial infarction (MI) is unknown. We therefore undertook serial direct recordings of CSNA, arterial blood pressure (MAP) and heart rate (HR) in 11 conscious sheep before and after MI, and compared them with 10 controls. Conscious CSNA recordings were taken daily from electrodes glued into the thoracic cardiac nerves. Infarction was induced under pethidine and diazepam analgesia by applying tension to a coronary suture. MI size was assessed by left ventricular planimetry (%) at postmortem, peak troponin T and brain natriuretic peptide levels (BNP). Baroreflex slopes were assessed daily using phenylephrine-nitroprusside ramps. The mean infarcted area was 14.4 ± 2.9%, troponin T 1.88 ± 0.39 µg l–1 and BNP 8.4 ± 1.3 pmol l–1. There were no differences in haemodynamic parameters or CSNA between groups at baseline. MAP and HR remained constant following MI. CSNA burst frequency increased from baseline levels of 55.8 ± 7.1 bursts min–1 to levels of 77.5 ± 8.7 bursts min–1 at 2 h post-MI, and remained elevated for 2 days (P < 0.001). CSNA burst area also increased and was sustained for 7 days following MI (P= 0.016). Baroreflex slopes for pulse interval and CSNA did not change. CSNA increases within 1 h of the onset of MI and is sustained for at least 7 days. The duration of this response may be longer because the recording fields decrease with time. This result is consistent with a sustained cardiac excitatory sympathetic reflex.
(Received 27 December 2004;
accepted after revision 10 March 2005;
first published online 17 March 2005)
Corresponding author D. L. Jardine: Department of General Medicine, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand. Email: david.jardine{at}cdhb.govt.nz
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