Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Circulation. 2004;109:2285-2289
Published online before print April 26, 2004, doi: 10.1161/01.CIR.0000129252.96341.8B
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
109/19/2285    most recent
01.CIR.0000129252.96341.8Bv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Graham, L. N.
Right arrow Articles by Mary, D. A.S.G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Graham, L. N.
Right arrow Articles by Mary, D. A.S.G.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Heart Attack
Related Collections
Right arrow Acute myocardial infarction

(Circulation. 2004;109:2285-2289.)
© 2004 American Heart Association, Inc.

Clinical Investigation and Reports

Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction

Lee N. Graham, MB, ChB; Paul A. Smith, MB, ChB; Robert J. Huggett, MBBS; John B. Stoker, BSc, MB, ChB; Alan F. Mackintosh, MA, MD; David A.S.G. Mary, MB, ChB, PhD

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

Received November 5, 2003; de novo received January 19, 2004; accepted February 13, 2004.


*    Abstract
up arrowTop
 *Abstract
down arrowIntroduction
 down arrowMethods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Background— The sympathetic activation that follows acute myocardial infarction (AMI) has been associated with increased morbidity and mortality. Because the prognosis after anterior AMI (ant-AMI) is worse than that after inferior AMI (inf-AMI), we planned to determine whether the magnitude of sympathetic hyperactivity differs between the two.

Methods and Results— Thirty-nine patients with uncomplicated AMI, comprising 2 matched groups of 17 patients with ant-AMI, and 22 patients with inf-AMI were examined. Measurements were obtained 2 to 4 days after AMI and compared with 20 normal subjects (NC) who were matched in terms of age and body weight to the AMI groups. Resting muscle sympathetic nerve activity was quantified from multiunit bursts (MSNA) and from single units (s-MSNA). Both groups of AMI patients were matched with regard to hemodynamic variables, left ventricular function, and infarct size. Both groups had greater (at least P<0.01) sympathetic nerve activity than NC (60±4.3 bursts/100 cardiac beats and 68±4.9 impulses/100 cardiac beats), but the magnitude of sympathetic nerve hyperactivity in ant-AMI (81±4.0 bursts/100 cardiac beats and 91±4.9 impulses/100 cardiac beats) was similar (P>0.05) to that in inf-AMI (80±3.2 bursts/100 cardiac beats and 90±4.0 impulses/100 cardiac beats)

Conclusions— Both ant-AMI and inf-AMI resulted primarily in a similar magnitude of sympathetic nerve hyperactivity. These findings suggest that the worse prognosis after ant-AMI compared with after inf-AMI would not be related primarily to the degree of sympathetic hyperactivity.


Key Words: nervous system, sympathetic • myocardial infarction • action potentials


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowMethods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Sympathetic hyperactivity has been shown to occur early after acute myocardial infarction (AMI),1–4 although very little is known about whether its magnitude differs between anterior wall (ant-AMI) and inferior wall (inf-AMI) infarction. This information is important because it may be relevant to the prognosis after AMI and to the mechanisms of associated sympathetic activation.

Adverse prognosis after AMI has been associated with factors such as advanced age, larger infarcts, and left ventricular systolic dysfunction,5–12 conditions in which a disproportionate sympathetic activation is known to occur.1,2,13 However, although the prognosis after ant-AMI is poorer than after inf-AMI,5,8,14,15 it is as yet unknown whether sympathetic nerve hyperactivity occurs to a greater extent in the former than the latter. The only available information has been derived from experimental studies in animals. For instance, after the demonstration of a sympatho-sympathetic cardiac reflex,16 other reports have reported that excitation of left ventricular sympathetic afferents is a significant mechanism leading to sympathetic activation after acute myocardial ischemia and infarction.17–19 These afferents are evenly distributed in the walls of the left ventricle, such that their excitation at any site causes similar reflex efferent sympathetic activation.20 Indeed, in humans, plasma norepinephrine levels have been reported to increase to a similar extent in patients who sustain either an ant-AMI or inf-AMI.21 However, plasma norepinephrine levels are a crude estimate of sympathetic output,22 and there are no available data from direct measurements of sympathetic nerve activity.

The present investigation was therefore designed to determine whether the magnitude of sympathetic nerve hyperactivity early after ant-AMI is different from that after inf-AMI. For this purpose, we quantified sympathetic nerve hyperactivity relative to normal controls in 2 groups of patients within 4 days of sustaining ant-AMI or inf-AMI who were closely matched in terms of age, body weight, left ventricular systolic function, and peak cardiac enzyme levels.


*    Methods
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 *Methods
down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Subjects
A total of 59 white subjects were examined (Table). They comprised 39 patients who had uncomplicated AMI, 17 with ant-AMI and 22 with inf-AMI. In addition, 20 normal control subjects (NC) were examined. All patients were screened by history, physical, and laboratory examination. They were excluded if there was a history of previous myocardial infarction, hypertension, diabetes, or other chronic disease that might influence the autonomic nervous system. Patients with evidence of arrhythmia, conduction abnormalities, heart failure, or cardiogenic shock were also excluded.


View this table:
[in this window]
[in a new window]
  		Details of the 3 Study Groups

AMI was confirmed by the following criteria: (1) a clinical history of ischemic-type chest pain, (2) changes on serially obtained ECGs, and (3) a rise in serum creatine kinase (CK) levels to >400 IU/L and their subsequent fall. The location of the infarct was obtained from analysis of the ECG according to the Minnesota code23 and was subsequently confirmed by the finding of a regional wall motion abnormality with 2D echocardiography and by coronary angiography and left ventriculography. In all patients, coronary artery disease was confirmed by both exercise treadmill testing and coronary angiography. A positive exercise test was defined by horizontal ST-segment depression of at least 2 mm during exercise with associated chest pain. Coronary angiography demonstrated significant coronary artery disease in these patients (>70% stenosis of at least 1 major epicardial coronary artery).

All patients were in Killip class I, and none had frequent ventricular ectopic beats or conduction defects, chest rales, or radiographic evidence of pulmonary vascular congestion. Also, none had a left ventricular ejection fraction (LVEF) of <40% as determined by echocardiography. Patients with ant-AMI and inf-AMI received conventional therapy in the form of thrombolysis (n=15 and 21), ß-blockers (n=15 and 18), and ACE inhibitors (n=13 and 15). None had undergone any revascularization procedure. The 2 groups, respectively, had single-vessel disease (n=10 and 14), 2-vessel disease (n=4 and 7), and 3-vessel disease (n=3 and 1). The investigation was performed with the approval of St James’s University Hospital Ethics Committee, and all subjects provided informed written consent.

General Protocol
Sympathetic activity in AMI patients was assessed at 2 to 4 days after admission. The same protocol was performed between the hours of 9:00 AM and 12:00 noon for all groups as previously reported.4 Subjects were asked to have a light breakfast and to empty their bladder before commencing the study and were requested to avoid alcohol, nicotine, and caffeine products for 12 hours before investigation.

During each session, the subjects were studied in the semisupine position. Measurements were made in a darkened laboratory in which the temperature was constant at 22°C to 24°C. Resting blood pressure was measured from the arm with a standard mercury sphygmomanometer. Heart rate and arterial blood pressure were monitored and recorded with a standard ECG and a Finapres device, and blood flow to the muscle of the left calf was obtained by use of standard strain-gauge plethysmography.

Microneurography
Postganglionic muscle sympathetic nerve activity (MSNA) was recorded from the right peroneal nerve for 5 minutes after subjects had attained steady state for at least 30 minutes with regard to measured variables as previously described.4 The neural signal was amplified (x50 000), and for the purpose of generating bursts representing multiunit discharge, the signal was filtered (bandwidth of 700 to 2000 Hz) and integrated (time constant, 0.1 second). The output of action potentials and bursts from this assembly were passed to a data-acquisition system, which digitized the action potentials at 12 000 samples per second and other data channels at 2000 samples per second (8 bits).

Single units (s-MSNA) in the raw action potential neurogram were obtained by adjusting the electrode position while using fast monitor sweep and online storage oscilloscope to confirm the presence of a consistent action potential morphology, as previously described.24,25 Only vasoconstrictor units were accepted and examined, the criteria of acceptance being appropriate responses to spontaneous changes in arterial blood pressure, the Valsalva maneuver, and isometric hand-grip exercise. Simultaneous measurement of calf vascular resistance confirmed the vasoconstrictor function of the observed neural activity. During the Valsalva maneuver, sympathetic activity increased during the latter part of phase II and/or phase III and decreased during phase IV (increase and overshoot of blood pressure). Isometric hand-grip exercise, performed with a dynamometer, produced a late increase in arterial blood pressure and sympathetic neural activity.

An electronic discriminator was used objectively to count the spikes of s-MSNA and was quantified as mean frequency of impulses/min and also as impulses/100 cardiac beats to avoid any interference by the length of the cardiac cycle.26 The bursts of MSNA were identified by inspection when the signal-to-noise ratio was >3 and were quantified in a similar manner. The variability of measuring both s-MSNA and MSNA in this laboratory did not exceed 10%.25 LVEF was determined by 2D echocardiography (Toshiba SSA-380A, Toshiba Corp). Briefly, left ventricular wall motion was assessed visually by use of a 9-segment model and graded as previously described in patients with myocardial infarction.27,28 The following scores were used: 3 for hyperkinesia, 2 for normokinesia, 1 for hypokinesia, 0 for akinesia, and –1 for dyskinesia. Wall motion index was calculated by dividing the sum of the scores in each individual segment by 9. Wall motion index multiplied by 0.3 gave the estimate of LVEF.

Statistics
One-way ANOVA with Newman-Keuls post hoc tests was used to compare data between the 3 groups of subjects. Student’s t test was used to compare unpaired data available only in patients with ant-AMI and inf-AMI. The least-squares technique was used for assessing the linear relationship between variables. Values of P<0.05 were considered statistically significant. Data are presented as mean±SEM.


*    Results
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 *Results
down arrowDiscussion
 down arrowReferences
 
The 3 groups of subjects were not significantly different with regard to age, body weight, body mass index, or heart rate (Table). Also, there were no significant differences in the gender ratio between the 3 groups ({chi}2=0.58; P>0.1). The indices of arterial blood pressure in ant-AMI were similar to those with inf-AMI, although as expected, they were lower in the 2 AMI groups than in NC. There were also no significant differences between ant-AMI and inf-AMI with regard to LVEF or peak CK levels (Table).

All indices of sympathetic nerve activity were significantly greater in ant-AMI and inf-AMI than in NC. However, all indices of sympathetic activity in ant-AMI were similar to those in inf-AMI (Table; Figure). In both of the AMI groups, there was a significant negative correlation between indices of sympathetic activity and LVEF (at least r=–0.45, P<0.02), although there was no correlation between sympathetic activity and peak CK levels (at least r=0.06; P>0.40).



View larger version (24K):
[in this window]
[in a new window]
  		Values of s-MSNA (top) and MSNA (bottom) in 17 patients with ant-AMI, 22 patients with inf-AMI, and corresponding values obtained in 20 matched normal subjects (NC). Height of column indicates mean value of group, and bars, SEM. *P<0.001, {dagger}P<0.01 vs NC. Sympathetic nerve activity in ant-AMI was similar to that in inf-AMI.

In each of the 3 groups, the indices of sympathetic nerve activity were positively correlated to age (at least r=0.59; P<0.008) but not to indices of arterial blood pressure (at least r=0.34; P>0.07).


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
down arrowReferences
 
The present investigation has shown for the first time that the site of infarction does not affect the magnitude of sympathetic nerve hyperactivity seen 2 to 4 days after uncomplicated AMI. These findings indicate that sympathetic nerve hyperactivity alone would not primarily account for the poorer prognosis observed after ant-AMI compared with inf-AMI. Furthermore, the findings are consistent with the proposals that the mechanism of efferent sympathetic hyperactivity to the periphery after AMI involves excitation of ventricular sympathetic afferents, which are evenly distributed within the walls of the left ventricle.

Although MSNA is limited to exploring efferent peripheral discharge, our findings that both groups of AMI had greater MSNA than normal controls is consistent with previous reports using different techniques, showing sympathetic activation early after AMI.1–3 All 3 groups in the present study were examined under the same laboratory conditions to avoid confounding influences related to circadian variation,29 alcohol,30 visceral distension, and a large meal.31,32 In addition, all groups were closely matched to avoid confounding factors such as age, gender,13 race,33 body weight,34 and heart rate.26 Unavoidably, the 2 groups with AMI were receiving ß-blocker or ACE inhibitor therapy and as a result had a slightly lower arterial pressure than the NC subjects. However, we found no correlation between sympathetic nerve activity and indices of arterial pressure as previously reported in other clinical conditions,4,25 supporting the proposal that sympathetic excitation was independent of baroreceptor reflex function.19 Also, we have previously shown that the sympathetic hyperactivity early after AMI persisted for at least 3 months despite normalization of arterial pressure.4 With regard to therapy, it has been reported in patients with heart failure that ACE inhibitors decrease sympathetic nerve activity35 and that ß-blockers have no effect on MSNA.36 Also, we have previously shown that after AMI, MSNA was greater than in control groups receiving the same therapeutic agents, including patients with stable coronary artery disease and patients hospitalized with chest pain in whom AMI was excluded.4 These treated control groups had the same level of MSNA as that in untreated matched normal controls.4 These considerations make it likely that no single factor other than AMI could have resulted in the observed sympathetic hyperactivity.

With regard to the site of the infarct, our findings were obtained 2 to 4 days after AMI, at a time when patients had no discernible clinical complications and their LVEF was >40%. Both groups were closely matched to avoid interfering effects on sympathetic nerve activity by factors including arterial pressure,25,37 peak serum CK levels, and degree of left ventricular dysfunction.1,2 In addition, both groups received similar therapy. Such considerations make it unlikely that confounding factors would have unequivocally explained the similarity of the magnitude of sympathetic hyperactivity between ant-AMI and inf-AMI.

Our findings have implications with regard to the mechanism of the sympathetic nerve hyperactivity observed after AMI. One of the postulated mechanisms of sympathetic activation after acute myocardial ischemia or infarction has involved chemical activation or impairment of sympathetic or vagal afferents, respectively, and their interaction.17–19 There has been experimental evidence showing that sympathetic afferents are evenly distributed throughout the anterior and inferoposterior walls of the left ventricle and that their activation by chemicals or ischemia in any of these locations leads to a similar reflex sympathetic activation.20 In contrast, the chemosensitive vagal afferents, the excitation of which leads to sympathetic inhibition, are located primarily in the inferoposterior walls of the left ventricle.38

Reports in humans seem to support the view that excitation of ventricular sympathetic afferents is the predominant mechanism of efferent sympathetic activation after AMI. For instance, plasma norepinephrine levels increase to a similar extent in patients developing either ant-AMI or inf-AMI.21 Within the first hours of developing infarction, excessive vagal discharge has been related to bradyarrhythmia and sudden death that occur in the case of posterior AMI.39 Using changes in heart rate and arterial pressure that occurred within 1 hour after the onset of posterior AMI, a predominance of parasympathetic effects was found to occur early, whereas sympathetic predominance occurred late within the hour after ant-AMI.40 In addition, sympathetic activation and diminished vagal modulation of the heart period have been reported {approx}3 hours after ant-AMI and inf-AMI, although they occurred to a greater extent in ant-AMI.3 Taken together, these reports3,39,40 indicate that any vagal overactivity and its confounding effect on sympathetic activation was short-lasting.3 The present study was therefore conducted 2 to 4 days after AMI, with the patients in a stable condition, to avoid the volatile phase of autonomic disturbance very early after infarction and also any other confounding factors that might interfere with the sympathetic drive, such as the complications of arrhythmia and heart failure. Our finding in each of the 2 AMI groups of an inverse correlation between sympathetic hyperactivity and LVEF is consistent with a predominant effect of excitation of sympathetic over vagal afferents, because the former leads to efferent sympathetic activation, whereas the latter leads to sympathetic inhibition. These considerations make it possible to propose that the efferent sympathetic activation after AMI has involved excitation of ventricular sympathetic afferents.

The other implications of the present study relate to reported factors that may potentially result in a greater mortality and morbidity in association with ant-AMI than with inf-AMI.5,8,14,15 These factors have included age, extent of left ventricular dysfunction, infarct size, and development of heart failure.41–44 It is notable that most of these factors result in sympathetic activation,1,2,13 which in turn is believed to lead to an adverse outcome.1,2,21 In addition, it is known that the increased mortality associated with ant-AMI occurs during the first few hours after the onset of infarction.40 However, both AMI groups in the present study were clinically stable, had no complications, and were matched for confounding factors, particularly LVEF and peak CK levels. Therefore, our data that were obtained 2 to 4 days after AMI indicate that the site of infarction alone does not influence the magnitude of sympathetic nerve hyperactivity and suggest that the eventual poorer prognosis after ant-AMI than inf-AMI is not related primarily to differences in the magnitude of sympathetic hyperactivity.

In conclusion, the findings of the present study indicate that the magnitude of sympathetic nerve hyperactivity seen 2 to 4 days after uncomplicated AMI is similar between ant-AMI and inf-AMI. The findings suggest that excitation of the evenly distributed sympathetic afferents within the left ventricle constitute an important mechanism for efferent sympathetic activation.


*    Acknowledgments
 
This work was funded by the British Heart Foundation (grant FS/2000069). The authors thank J. Bannister, J. Corrigan, and G. McGawley for technical assistance.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 up arrowDiscussion
 *References
 

  1. McAlpine HM, Cobbe SM. Neuroendocrine changes in acute myocardial infarction. Am J Med. 1988; 84: 61–66.[CrossRef][Medline] [Order article via Infotrieve]
  2. Sigurdsson A, Held P, Swedberg K. Short- and long-term neurohumoral activation following acute myocardial infarction. Am Heart J. 1993; 126: 1068–1076.[CrossRef][Medline] [Order article via Infotrieve]
  3. Lombardi F, Sandrone G, Spinnler MT, et al. Heart rate variability in the early hours of an acute myocardial infarction. Am J Cardiol. 1996; 77: 1037–1044.[CrossRef][Medline] [Order article via Infotrieve]
  4. Graham LN, Smith PA, Stoker JB, et al. Time course of sympathetic neural hyperactivity after uncomplicated acute myocardial infarction. Circulation. 2002; 106: 793–797.[Abstract/Free Full Text]
  5. Beaune J, Touboul P, Boissel JP, et al. Quantitative assessment of myocardial infarction prognosis to 1 and 6 mth from clinical data. Eur J Cardiol. 1978; 8: 629–647.[Medline] [Order article via Infotrieve]
  6. Hands ME, Rutherford JD, Muller JE, et al. The in-hospital development of cardiogenic shock after myocardial infarction: incidence, predictors of occurrence, outcome and prognostic factors. The MILIS Study Group. J Am Coll Cardiol. 1989; 14: 40–46.[Abstract]
  7. Kober L, Torp-Pedersen C, Ottesen M, et al. Influence of age on the prognostic importance of left ventricular dysfunction and congestive heart failure on long-term survival after acute myocardial infarction. TRACE Study Group. Am J Cardiol. 1996; 78: 158–162.[Medline] [Order article via Infotrieve]
  8. Danchin N, Vaur L, Genes N, et al. Management of acute myocardial infarction in intensive care units in 1995: a nationwide French survey of practice and early hospital results. J Am Coll Cardiol. 1997; 30: 1598–1605.[Abstract]
  9. French JK, Hyde TA, Patel H, et al. Survival 12 years after randomization to streptokinase: the influence of thrombolysis in myocardial infarction flow at three to four weeks. J Am Coll Cardiol. 1999; 34: 62–69.[Abstract/Free Full Text]
  10. Capewell S, Livingston BM, MacIntyre K, et al. Trends in case-fatality in 117 718 patients admitted with acute myocardial infarction in Scotland. Eur Heart J. 2000; 21: 1833–1840.[Abstract/Free Full Text]
  11. Webber BJ, McLaughlin SC, Whitlock RM, et al. Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction. J Am Coll Cardiol. 2000; 35: 1516–1524.[Abstract/Free Full Text]
  12. Marchioli R, Avanzini F, Barzi F, et al, for the GISSI-Prevenzione Investigators. Assessment of absolute risk of death after myocardial infarction by use of multiple-risk-factor assessment equations: GISSI-Prevenzione mortality risk chart. Eur Heart J. 2001; 22: 2085–2103.[Abstract/Free Full Text]
  13. Ng AV, Callister R, Johnson DG, et al. Age and gender influence muscle sympathetic nerve activity at rest in healthy humans. Hypertension. 1993; 21: 498–503.[Abstract/Free Full Text]
  14. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico. GISSI-2: a factorial randomised trial of alteplase versus streptokinase and heparin versus no heparin among 12,490 patients with acute myocardial infarction. Lancet. 1990; 336: 65–71.[Medline] [Order article via Infotrieve]
  15. Behar S, Rabinowitz B, Zion M, et al. Immediate and long-term prognostic significance of a first anterior versus first inferior wall Q-wave acute myocardial infarction. Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) Study Group. Am J Cardiol. 1993; 72: 1366–1370.[CrossRef][Medline] [Order article via Infotrieve]
  16. Malliani A, Schwartz PJ, Zanchetti A. A sympathetic reflex elicited by experimental coronary occlusion. Am J Physiol. 1969; 217: 703–709.[Free Full Text]
  17. Thames MD, Dibner-Dunlap ME, Minisi AJ, et al. Reflexes mediated by cardiac sympathetic afferents during myocardial ischaemia: role of adenosine. Clin Exp Pharmacol Physiol. 1996; 23: 709–714.[Medline] [Order article via Infotrieve]
  18. Longhurst JC, Tjen-A-Looi SC, Fu LW. Cardiac sympathetic afferent activation provoked by myocardial ischemia and reperfusion: mechanisms and reflexes. Ann N Y Acad Sci. 2001; 940: 74–95.[Abstract/Free Full Text]
  19. Malliani A, Montano N. Emerging excitatory role of cardiovascular sympathetic afferents in pathophysiological conditions. Hypertension. 2002; 39: 63–68.[Abstract/Free Full Text]
  20. Minisi AJ, Thames MD. Distribution of left ventricular sympathetic afferents demonstrated by reflex responses to transmural myocardial ischemia and to intracoronary and epicardial bradykinin. Circulation. 1993; 87: 240–246.[Abstract/Free Full Text]
  21. Karlsberg RP, Cryer PE, Roberts R. Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality. Am Heart J. 1981; 102: 24–29.[CrossRef][Medline] [Order article via Infotrieve]
  22. Esler MD, Jennings G, Lambert G, et al. Overflow of catecholamines neurotransmitters to the circulation: source, fate and functions. Physiol Rev. 1990; 70: 963–985.[Free Full Text]
  23. Rose GA, Blackburn H. Cardiovascular Survey Methods. WHO Monograph Series, No 56. Geneva, Switzerland: World Health Organization; 1968.
  24. Macefield VG, Wallin BG, Vallbo AB. The discharge behaviour of single vasoconstrictor motoneurones in human muscle nerves. J Physiol (Lond). 1994; 481: 799–809.[Medline] [Order article via Infotrieve]
  25. Greenwood JP, Stoker JB, Mary DASG. Single-unit sympathetic discharge: quantitative assessment in human hypertensive disease. Circulation. 1999; 100: 1305–1310.[Abstract/Free Full Text]
  26. Sundlöf G, Wallin BG. The variability of muscle nerve sympathetic activity in resting recumbent man. J Physiol (Lond). 1977; 272: 383–397.[Abstract/Free Full Text]
  27. Heger JJ, Weyman AE, Wann LS, et al. Cross-sectional echocardiographic analysis of left ventricular asynergy in acute myocardial infarction. Circulation. 1980; 61: 1113–1118.[Free Full Text]
  28. Berning J, Rokkedal Nielson J, Launbjerg J, et al. Rapid estimation of left ventricular ejection fraction in acute myocardial infarction by echocardiographic wall motion analysis. Cardiology. 1992; 80: 257–266.[Medline] [Order article via Infotrieve]
  29. Hartikainen J, Tarkiainen I, Tahvanainen K, et al. Circadian variation of cardiac autonomic regulation during 24-h bed rest. Clin Physiol. 1993; 13: 185–196.[Medline] [Order article via Infotrieve]
  30. Grassi GM, Somers VK, Renk WS, et al. Effects of alcohol intake on blood pressure and sympathetic nerve activity in normotensive humans: a preliminary report. J Hypertens. 1989; 7 (suppl): S20–S21.
  31. Fagius H, Karhuvaara S. Sympathetic activity and blood pressure increases with bladder distension in humans. Hypertension. 1989; 14: 511–517.[Abstract/Free Full Text]
  32. Cox HS, Kaye DM, Thompson JM, et al. Regional sympathetic nervous activation after a large meal in humans. Clin Sci (Colch). 1995; 89: 145–154.[Medline] [Order article via Infotrieve]
  33. Calhoun DA, Mutinga ML, Collins AS, et al. Normotensive blacks have heightened sympathetic response to cold pressor test. Hypertension. 1993; 22: 801–805.[Abstract/Free Full Text]
  34. Scherrer U, Randin D, Tappy L, et al. Body fat and sympathetic nerve activity in healthy subjects. Circulation. 1994; 89: 2634–2640.[Abstract/Free Full Text]
  35. Grassi G, Cattaneo BM, Servalle G, et al. Effects of chronic ACE inhibition on sympathetic nerve traffic and baroreflex control of circulation in heart failure. Circulation. 1997; 96: 1173–1179.[Abstract/Free Full Text]
  36. Azevedo ER, Kubo T, Mak S, et al. Nonselective versus selective ß-adrenergic receptor blockade in congestive heart failure: differential effects on sympathetic activity. Circulation. 2001; 104: 2194–2199.[Abstract/Free Full Text]
  37. Anderson EA, Sinkey CA, Lawton WJ, et al. Elevated sympathetic nerve activity in borderline hypertensive humans: evidence from direct intraneural recordings. Hypertension. 1989; 14: 177–183.[Abstract/Free Full Text]
  38. Inoue H, Zipes DP. Increased afferent vagal responses produced by epicardial application of nicotine on the canine posterior left ventricle. Am Heart J. 1987; 114: 757–764.[CrossRef][Medline] [Order article via Infotrieve]
  39. Adgey AA, Geddes JS, Mulholland HC, et al. Incidence, significance, and management of early bradyarrhythmia complicating acute myocardial infarction. Lancet. 1968; 2: 1097–1101.[Medline] [Order article via Infotrieve]
  40. Pantridge JF, Webb SW, Adgey AA. Arrhythmias in the first hours of acute myocardial infarction. Prog Cardiovasc Dis. 1981; 23: 265–278.[CrossRef][Medline] [Order article via Infotrieve]
  41. Stadius ML, Davis K, Maynard C, et al. Risk stratification for 1 year survival based on characteristics identified in the early hours of acute myocardial infarction. The Western Washington Intracoronary Streptokinase Trial. Circulation. 1986; 74: 703–711.[Abstract/Free Full Text]
  42. Hands ME, Lloyd BL, Robinson JS, et al. Prognostic significance of electrocardiographic site of infarction after correction for enzymatic size of infarction. Circulation. 1986; 73: 885–891.[Abstract/Free Full Text]
  43. Maisel AS, Gilpin E, Hoit B, et al. Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction. J Am Coll Cardiol. 1985; 6: 731–736.[Abstract]
  44. Thanavaro S, Kleiger RE, Province MA, et al. Effect of infarct location on the in-hospital prognosis of patients with first transmural myocardial infarction. Circulation. 1982; 66: 742–747.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
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]

Home page
 J. Appl. Physiol.Home page
R. Hainsworth and M. J. Drinkhill
COUNTERPOINT: ACTIVE VENOCONSTRICTION IS NOT IMPORTANT IN MAINTAINING OR RAISING END-DIASTOLIC VOLUME AND STROKE VOLUME DURING EXERCISE AND ORTHOSTASIS
J Appl Physiol, October 1, 2006; 101(4): 1264 - 1265.
[Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
REBUTTAL FROM DRS. HAINSWORTH AND DRINKHILL
J Appl Physiol, October 1, 2006; 101(4): 1266 - 1266.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
109/19/2285    most recent
01.CIR.0000129252.96341.8Bv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Graham, L. N.
Right arrow Articles by Mary, D. A.S.G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Graham, L. N.
Right arrow Articles by Mary, D. A.S.G.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Heart Attack
Related Collections
Right arrow Acute myocardial infarction

Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.