Published online before print July 22, 2002, doi: 10.1161/01.CIR.0000025610.14665.21
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2002;106:793.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
Time Course of Sympathetic Neural Hyperactivity After Uncomplicated Acute Myocardial Infarction
From the Department of Cardiology, St James’s University Hospital, Leeds, UK.
Correspondence to Dr Lee N. Graham, Department of Cardiology, St James’s University Hospital, Beckett Street, Leeds, UK. E-mail lee{at}graham93.fsnet.co.uk
Background— Little information is available on sympathetic activity after acute myocardial infarction (AMI), despite the belief that sympathetic drive is important in relation to morbidity and mortality. Indirect indices such as plasma catecholamines are transiently elevated after uncomplicated AMI, whereas other prognostically important autonomic indices may be affected longer. We planned to quantify central sympathetic output to the periphery after uncomplicated AMI and to investigate its progress over time.
Methods and Results— After uncomplicated AMI, 13 patients had muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). Measurements were obtained 2 to 4 days after AMI and were repeated after 3 and 6 months. We also examined 3 matched control groups comprising normal subjects, patients with coronary artery disease, and hospitalized patients without AMI. MSNA and s-MSNA after AMI (84±4.6 bursts/100 beats and 95±5.8 impulses/100 beats) were unchanged at 3 months but decreased (P<0.01 and P<0.001) after 6 months (75±4.0 bursts/100 beats and 80±4.4 impulses/100 beats). These were still greater (at least P<0.01) than values in normal subjects, patients with coronary artery disease, and hospitalized patients without AMI (51±3.9 bursts/100 beats, 58±4.7 impulses/100 beats; 56±2.2 bursts/100 beats, 61±2.2 impulses/100 beats; and 55±3.6 bursts/100 beats, 61±3.3 impulses/100 beats, respectively). This sympathetic hyperactivity was inversely correlated to left ventricular ejection fraction but not to changes in blood pressure.
Conclusions— A protracted state of sympathetic hyperactivity was shown to occur after uncomplicated AMI. It is suggested that this hyperactivity may explain delayed cardiovascular morbidity and mortality and that it arises because of an impairment of reflexes from cardiac receptors.
Key Words: nervous system, sympathetic • myocardial infarction • action potentials
This article has been cited by other articles:
 |
|
 |
|
  N. Charkoudian and J. A. Rabbitts Sympathetic Neural Mechanisms in Human Cardiovascular Health and Disease Mayo Clin. Proc., September 1, 2009; 84(9): 822 - 830. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Floras Sympathetic nervous system activation in human heart failure: clinical implications of an updated model. J. Am. Coll. Cardiol., July 28, 2009; 54(5): 375 - 385. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Hogarth, L. N. Graham, D. A.S.G. Mary, and J. P. Greenwood Gender differences in sympathetic neural activation following uncomplicated acute myocardial infarction Eur. Heart J., July 2, 2009; 30(14): 1764 - 1770. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Parrish, K. Gritman, D. M. Van Winkle, W. R. Woodward, M. Bader, and B. A. Habecker Postinfarct sympathetic hyperactivity differentially stimulates expression of tyrosine hydroxylase and norepinephrine transporter Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H99 - H106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Jardine, C. J. Charles, C. M. Frampton, and A. M. Richards Cardiac sympathetic nerve activity and ventricular fibrillation during acute myocardial infarction in a conscious sheep model Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H433 - H439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. Jankowska, P. Ponikowski, M. F. Piepoli, W. Banasiak, S. D. Anker, and P. A. Poole-Wilson Autonomic imbalance and immune activation in chronic heart failure - Pathophysiological links Cardiovasc Res, June 1, 2006; 70(3): 434 - 445. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kamiya, T. Kawada, K. Yamamoto, D. Michikami, H. Ariumi, T. Miyamoto, S. Shimizu, K. Uemura, T. Aiba, K. Sunagawa, et al. Dynamic and static baroreflex control of muscle sympathetic nerve activity (SNA) parallels that of renal and cardiac SNA during physiological change in pressure Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2641 - H2648. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Kamiya, T. Kawada, K. Yamamoto, D. Michikami, H. Ariumi, T. Miyamoto, K. Uemura, M. Sugimachi, and K. Sunagawa Muscle Sympathetic Nerve Activity Averaged Over 1 Minute Parallels Renal and Cardiac Sympathetic Nerve Activity in Response to a Forced Baroreceptor Pressure Change Circulation, July 19, 2005; 112(3): 384 - 386. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. L. Jardine, C. J. Charles, R. K. Ashton, S. I. Bennett, M. Whitehead, C. M. Frampton, and M. G. Nicholls Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model J. Physiol., May 15, 2005; 565(1): 325 - 333. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. N. Graham, P. A. Smith, R. J. Huggett, J. B. Stoker, A. F. Mackintosh, and D. A.S.G. Mary Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction Circulation, May 18, 2004; 109(19): 2285 - 2289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Malliani, N. Montano, L. N. Graham, P. A. Smith, J. B. Stoker, A. F. Mackintosh, and D. A.S.G. Mary Time Course of Sympathetic Neural Hyperactivity After Uncomplicated Acute Myocardial Infarction * Response Circulation, February 25, 2003; 107 (7): e53 - e53. [Full Text] [PDF]
|
|