JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
QUICK SEARCH:   [advanced]


     

J Am Coll Cardiol, 1999; 34:1924-1931
© 1999 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Joho, S.
Right arrow Articles by Inoue, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Joho, S.
Right arrow Articles by Inoue, H.

CLINICAL STUDIES

Time-varying spectral analysis of heart rate and left ventricular pressure variability during balloon coronary occlusion in humans

A sympathoexcitatory response to myocardial ischemia

Shuji Joho, MD*, Hidetsugu Asanoi, MD*, Hosam A. Remah, MD*, Akihiko Igawa, MD*, Tomoki Kameyama, MD*, Takashi Nozawa, MD*, Katsumi Umeno, BS{dagger} and Hiroshi Inoue, MD, FACC*

* Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan
{dagger} the First Department of Physiology, Toyama Medical and Pharmaceutical University, Toyama, Japan

Manuscript received August 18, 1998; revised manuscript received July 1, 1999, accepted August 30, 1999.

Reprint requests and correspondence: Dr. Hidetsugu Asanoi, Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan
hidetugu{at}ms.toyama-mpu.ac.jp


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES

We assessed time-varying spectral components of heart rate and left ventricular (LV) pressure variability during coronary angioplasty to elucidate dynamic autonomic responses to transient myocardial ischemia.

BACKGROUND

Sympathoexcitatory reflexes elicited by acute coronary occlusion are rarely addressed in the clinical settings because of a lack of technique to monitor transient changes in sympathetic activation.

METHODS

RR interval and LV pressure and volume were serially recorded in 14 patients with effort angina during balloon coronary angioplasty. Wavelet analysis was applied for determination of nonstationary spectral components of RR interval and LV peak pressure variability.

RESULTS

The wavelet analysis revealed that coronary occlusion provoked low-frequency (LF) fluctuations of RR interval (seven patients) and LV peak pressure (six patients) at 0.06 ± 0.01 Hz, but not in the remaining patients. Following the balloon inflation, the LF component of RR interval began to increase after the onset of myocardial ischemia, peaked at about 80 s, and then declined in the late phase of inflation. Consequently, the ratio of low to high frequency component rose to be significantly greater in the LF augmentation group than in the no LF augmentation group in the middle phase of coronary occlusion. The patients with no LF augmentation had little evidence of myocardial ischemia as reflected by changes in ST segment and LV systolic function during coronary occlusion.

CONCLUSIONS

The wavelet analysis of RR interval and LV pressure variability clearly showed a dynamic profile of spectral components in response to transient coronary artery occlusion. The resultant regional myocardial ischemia elicited a profound sympathoexcitatory response followed by a gradual suppression. This method provides a useful tool to gain a new insight into the nonstationary autonomic influence on the cardiovascular system.

Abbreviations and Acronyms
  ECG = electrocardiogram
  HF = high-frequency
  LF = low-frequency
  LV = left ventricular
  RR = relative risk
  Tau = time constant of isovolumic left ventricular pressure

Experimental coronary occlusion elicits sympathoexcitatory reflexes through activation of sensory endings in the ischemic left ventricle (1–3) whose afferent fibers travel to the spinal cord via the sympathetic afferents (3,4). These reflexes could exaggerate myocardial ischemia further by increasing myocardial oxygen consumption while maintaining cardiac function transiently by enhancing contractility. In the clinical settings, this reflex is supposed to be responsible for hypertension and tachycardia frequently observed in the early stages of acute myocardial infarction (5). The recent introduction of spectral analysis of beat-by-beat heart rate variability has provided quantitative markers of sympathovagal balance and revealed that coronary occlusion elicits variable changes in heart rate variability (6–10). This is likely attributable to complex interaction between excitatory reflexes mediated by sympathetic afferent fibers and inhibitory reflex mediated by vagal afferent fibers (11). A relative contribution of these opposing reflexes on sympathetic efferent activity has been shown to depend on the severity and the site of myocardial ischemia. Therefore, the spectral components and their magnitude of cardiovascular variability could vary as the coronary occlusion time elapsed. To date, the dynamic nature of cardiac sympathetic activity during coronary occlusion has not been studied in clinical settings because of the lack of a technique to trace the nonstationary level of autonomic function.

The purpose of this study was to reveal the time-varying profile of autonomic balance while myocardial ischemia was progressing during balloon coronary occlusion in humans. We applied wavelet transform for RR interval and left ventricular (LV) pressure variability, which allowed valid and serial evaluation of transient changes in spectral components.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 References
 
Patient population.   The study group consisted of 14 patients (9 men and 5 women; mean age, 59 ± 10 years; range, 36 to 74 years). All patients had effort angina and an electrocardiographically positive, symptomatic exercise stress test. Three patients had electrocardiographic evidence of prior myocardial infarction. Elective coronary angioplasty was performed at 15 target lesions (6 left anterior descending coronary arteries, 7 left circumflex coronary arteries and 2 right coronary arteries). All antianginal agents had been withdrawn 24 h before the procedure. Beta-adrenergic blocking agents which had been given to eight patients were withdrawn more than 48 h before the coronary angioplasty. All patients provided written informed consent and the protocol was approved by our institute’s Committee on Clinical Investigation. All procedures were successfully performed, and no complications were encountered.

Study protocol.   An 8F conductance catheter (Sentron, Roden, the Netherlands) together with a 2F micromanometer-tipped catheter (Millar Instruments, Houston, Texas) was inserted from the left femoral artery and placed along the long axis of the left ventricle to the apex (12). The volume catheter was connected to Sigma-5/DF signal conditioner processor (Leycom Cardiodynamics Inc, Zoetermeer, the Netherlands) that used a dual excitation algorithm. Segmental volumes were summed to yield total conductance which was calibrated by actual volume derived from left ventriculogram.

Coronary angioplasty was performed through the right femoral sheath while electrocardiogram (ECG) and LV pressure and volume were serially recorded on digital tape (RD-130TE, TEAC Corp., Tokyo, Japan) for later analyses. Patients were advised to breath regularly and refrain from talking during balloon coronary occlusion. They were asked to grade the severity of chest pain according to Smokler’s numeral scale after balloon deflation (13): grade 1 was mild, grade 2 was moderate, grade 3 was moderately severe and grade 4 was maximally severe. In 12 patients, coronary collateral recruitment was graded by contralateral or ipsilateral coronary angiography during balloon coronary occlusion using Rentrop criteria (14).

Data acquisition and analysis.   We excluded the ECG and LV pressure-volume data obtained during the first balloon inflation from this analysis because myocardial ischemia had already been provoked by the first positioning of balloon catheter through the target lesion (15). Electrocardiogram, micromanometer pressure and conductance catheter volume were played back from the digital tape and digitalized at 1,000 Hz per channel by an analog-to-digital converter (DT31-EZ, Data Translation Inc., Marlboro, Massachusetts) and stored on a hard disk memory system using a computer (Optiplex-GXMT, Dell Computer Corp., Round Rock, Texas). Hemodynamic variables derived from digital pressure and volume data were analyzed with software developed in our laboratory as reported previously (8,16). The time constant of isovolumic LV pressure (Tau) decay was calculated by the derivative method of Raff and Glantz (17). Beat-to-beat RR interval and LV peak pressure were interpolated at 2 Hz to ensure equidistant sampling in each time series (8). The very low-frequency (LF) nonstationarity (<0.01 Hz) and the baseline trend were removed using a moving average function which did not affect the higher frequencies (HFs). The beat-to-beat spectral estimation analysis was based on the discrete wavelet transform using Gabor basis wavelet (18) and 256-event data. Theoretically, applying the basis wavelet to the original signal by dilution operations could result in a decreased time resolution in very LF. Nevertheless, this method has a great advantage over the traditional stationary spectral analysis in that the wavelet distribution enables one to decompose a signal in nonsteady states, into a function of time and frequency (19). The frequency contents were then classified as HF (HF: greater double equals0.15 Hz) and LF (LF: 0.04–0.14 Hz) components. In this study, the augmentation of power spectra was defined to be present if the peak power of fluctuation was above the level of mean +2 standard deviation of the baseline power (Fig. 1). Additionally, spectral components of the entire time series before and during balloon occlusion were examined using a conventional maximum entropy method (8). Power of the analyzed bands was expressed as absolute values and units normalized to the total power (7,8).



View larger version (49K):
[in this window]
[in a new window]
  		Figure 1 Original tracing of HR and LVP during coronary occlusion (upper panel). ST segment was elevated during coronary occlusion. HR and LVP oscillation appeared at 55 s after the balloon inflation (Inf) and disappeared after the balloon deflation (Def). Wavelet analysis (lower panel) clearly demonstrates augmentation of low-frequency fluctuation (0.05–0.06 Hz) of RR and LVSP during coronary occlusion. HR = heart rate; LVSP = left ventricular systolic pressure; LVP = left ventricular pressure; RR = RR intervals.

 
Statistical analysis.   Data are expressed as mean ± standard deviation unless otherwise indicated. Differences in time-series data obtained by wavelet analysis were analyzed with analysis of variance for repeated measures and with the Bonferroni’s method for multiple comparisons. Differences between the baseline and coronary occlusion were compared with paired t test, and differences between two groups were examined with unpaired t test. The level of statistical significance was set at p < 0.05.


   Results
Top
 Abstract
 Methods
 Results
Discussion
 References
 
Patient characteristics and time-varying spectral data.   A marked augmentation of LF fluctuation of RR interval variability was provoked with balloon coronary occlusion of eight target arteries in seven patients. In these patients, a concomitant increase in LF component of LV peak pressure variability was observed during coronary occlusion of five target lesions. There were no significant changes in these power spectral components in the remaining seven patients except one patient who showed an increase in LF component of LV peak pressure variability. Prior myocardial infarction was documented in one of seven patients with LF augmentation and in two of seven patients without LF augmentation. No significant differences were found in age (56 ± 13 vs. 63 ± 5 years), Canadian Cardiovascular Society angina class (1.7 ± 0.5 vs. 1.7 ± 1.0) and the distribution of coronary target lesions between LF augmentation and no LF augmentation groups, respectively. There was an insignificant trend for the grade of collateral recruitment to be less in LF augmentation group (1.3 ± 1.1 vs. 2.0 ± 1.0), whereas the magnitude of ST segment deviation (0.18 ± 0.09 vs. 0.04 ± 0.03 mV, p < 0.01) and the severity of chest pain (1.9 ± 1.5 vs. 0.6 ± 0.5, p < 0.05) during coronary occlusion were significantly greater in LF augmentation group.

The beat-to-beat dynamics of RR interval fluctuations in each patient are shown within the three-dimensional framework of time, frequency and power, where the augmentation of the LF fluctuation is readily defined at 0.06 ± 0.01 Hz (Fig. 2). In contrast, no appreciable changes in LF fluctuation of RR interval were seen in the remaining seven patients during coronary occlusion (Fig. 3). These differences were clearly recognized by serial changes in LF component averaged every 10 s (Fig. 4). In the LF augmentation group, the LF component began to rise at 48 ± 11 s of the balloon inflation after the critical ST deviation; either 0.1 mV elevation or 0.1 mV depression was documented at 30 ± 8 s. The LF power peaked at 81 ± 19 s and then gradually declined in the late phase of coronary occlusion while myocardial ischemia progressed. Following LF augmentation, HF component began to increase in the middle to late phase of coronary occlusion, but the changes did not reach statistical significance (Fig. 4). Consequently, the ratio of LF to HF component in the LF augmentation group rose to be significantly greater than that of the no LF augmentation group in the middle phase of coronary occlusion. Release of the occlusion was followed by prompt return of LF component to the control level. The time sequence of spectral components of LV peak pressure variability was similar to that of RR interval variability (Fig. 1). The LF power spectra obtained by the maximum entropy method were also increased in LF augmentation group (Table 1). Although a significant correlation (Y = 2.5X–0.7, r = 0.92, p < 0.001) was found between LF power (X) by maximum entropy method and the peak LF power (Y) by the wavelet analysis, the changes in spectral power were substantially higher in the wavelet analysis than the maximum entropy method.



View larger version (65K):
[in this window]
[in a new window]
  		Figure 2 Three-dimensional continuous plots (wavelet transforms) of RR interval in patients who showed an augmentation of low-frequency component during coronary occlusion. The low-frequency power around 0.06 Hz gradually increased as the occlusion period progressed. Patient initials and target coronary lesion are indicated in each figure. Def = balloon deflation; Inf = balloon inflation; LAD = left anterior descending artery; LCX = left circumflex artery; RCA = right coronary artery.

 


View larger version (45K):
[in this window]
[in a new window]
  		Figure 3 Three-dimensional continuous spectral plots (wavelet transform) of RR interval in patients who showed no augmentation of low-frequency component during coronary occlusion. Format and abbreviations are as in Figure 2.

 


View larger version (19K):
[in this window]
[in a new window]
  		Figure 4 Serial changes in low-frequency (LF) component of RR variability (0.04–0.14 Hz). Two groups could be definitely identified by the study design. In seven patients, the LF component began to rise within 1 min after balloon inflation and reached a peak at about 80 s (closed squares). In contrast, there were no appreciable changes in spectral components of RR interval variability in the remaining seven patients (open circles). Following LF augmentation, high-frequency (HF) component (≥0.15 Hz) began to increase in the middle to late phase of coronary occlusion, but the changes did not reach statistical significance. Consequently, the ratio of LF to HF component rose to be significantly greater in the LF augmentation group than the no LF augmentation group. Data are expressed as mean ± standard error of percent changes from the control value. *p < 0.05 vs. baseline value, #p < 0.05 vs. open circles at the corresponding time.

 

View this table:
[in this window]
[in a new window]
  		Table 1 Effects of Balloon Coronary Occlusion on Left Ventricular Function and Power Spectral Components Determined With Maximum Entropy Method

 
Ventricular hemodynamic changes.   Coronary occlusion resulted in significant differences in LV systolic and diastolic function while the baseline cardiac function was similar between the two groups (Table 1). Left ventricular systolic pressure and heart rate did not change appreciably in either group during coronary occlusion. In the LF augmentation group, coronary occlusion increased LV end-diastolic and end-systolic volumes by 11% (p < 0.01) and 34% (p < 0.01), respectively, resulting in a decline in LV ejection fraction by 12% (p < 0.05). Left ventricular peak +dP/dt fell, and LV end-diastolic pressure rose with a significant prolongation of Tau and a trend to decline for peak –dP/dt. In the no LF augmentation group, most of the hemodynamic variables did not show significant changes during coronary occlusion except Tau (+24%, p < 0.01), the most sensitive hemodynamic parameter to myocardial ischemia. Consequently, there was an inverse correlation (r = –0.61, p < 0.02) between changes in LV ejection fraction and in LF components during coronary occlusion.


   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The wavelet analysis employed in this study revealed a dynamic nature of cardiovascular variability provoked by brief periods of coronary artery occlusion. The major findings obtained by this new method include the following:

  1. LF components and the ratio of LF to HF component of RR interval and LV pressure variability began to increase after the onset of a significant ST deviation, peaked at the middle to late phase and then declined in the late phase of coronary occlusion.
  2. The magnitude of maximal LF component was related to the severity of regional myocardial ischemia.
  3. The maximal LF component detected by the wavelet analysis correlated well with the LF component of entire time series obtained by the maximum entropy method.

Sympathoexcitation during myocardial ischemia.   The average spectral changes by coronary angioplasty were quite concordant with those obtained from previous experimental and clinical studies. Rimoldi et al. (20) experimentally documented that regional myocardial ischemia provoked a powerful sympathoexcitatory response with a marked increase of the LF component of RR interval and arterial pressure variability. In clinical settings, ischemia-induced sympathetic overactivity was first described by Webb et al. (5) who found tachycardia and hypertension in the early phase of myocardial infarction. Recently, Lombardi et al. (21) applied autoregressive power spectral analysis of heart rate variability to detect autonomic disturbance within the first few hours of acute myocardial infarction in humans. They found a relative predominance of LF component independently from the infarct localization. The wavelet analysis employed in this study expanded these pioneering clinical findings to time-frequency representations of RR interval and LV peak pressure variability to reveal a dynamic profile of sympathovagal balance as the coronary occlusion time elapsed.

The possible mechanisms for a dome-shaped increase in LF component and a later increasing trend in HF components involve a complex neural, metabolic and mechanical interaction during myocardial ischemia. Generally, acute myocardial ischemia elicits both excitatory reflexes mediated by sympathetic afferent fibers and inhibitory reflexes mediated by vagal afferent fibers (1,3,22,23). The relative magnitude of these opposing reflexes was shown to be related to the site and severity of myocardial ischemia and the grade of ischemia-induced cardiac deterioration (5,11,24). Although the LV endings of all these fibers act as polymodal receptors, the effective stimulus to these receptors seems to differ considerably between sympathetic and vagal afferent fibers. Lombardi et al. (11) showed that global ischemia, by occluding the main left coronary artery, elicited early sympathoexcitation followed by a predominant vagal inhibitory reflex as the heart failed. These findings could be explained by other experimental observations that the vagal inhibitory receptors respond largely to the attendant increase in heart size with a latency of 20–40 s while ischemia per se seems to be of little or no importance (22). By contrast, myocardial ischemia is known to effectively stimulate sympathetic afferent receptors with a much shorter latency (10 to 20 s) (11). Therefore, localized ischemia without profound cardiac deterioration could elicit predominant sympathoexcitatory reflex rather than reflex vagal inhibition. They confirmed experimentally that regional ischemia, by occluding the distal coronary artery, produced a marked and sustained increase in sympathetic discharge. These previous data suggest that the LF augmentation observed in this study could faithfully reflect sympathosympathetic excitation provoked by regional ischemia during balloon coronary occlusion. However, the decline of LF augmentation in the late phase of coronary occlusion could attribute to the vagally-mediated sympathoinhibition manifested as ischemia-induced cardiac dysfunction progressed.

The mean heart rate did not change significantly during coronary occlusion despite a marked increase in LF fluctuation of RR interval. Similar findings were found in the previous experimental study where regional ischemia did not appreciably change mean heart rate while increasing cardiac sympathetic activity (11). Recently, Kawada et al. (25) found that tonic gain of heart rate by sympathetic stimulation was canceled by simultaneous vagal stimulation, whereas phasic gain from sympathetic stimulation was amplified. Our disparate responses of mean heart rate and RR interval variability might be attributable to such interaction between the sympathetic and vagal systems in controlling heart rate.

Clinical implications.   Cardiac sympathosympathetic reflex could result in two opposite consequences during coronary occlusion. For a short period following coronary occlusion, reflex-mediated increase in LV contractility might be able to support cardiac function to maintain normal arterial pressure, while potentially aggravating myocardial ischemia through an augmentation of myocardial oxygen consumption. Hereby, this reflex results in an underestimate of actual cardiac depression in the early phase of myocardial ischemia. However, total cardiac function deteriorates progressively as direct cardiodepressive action of myocardial ischemia gradually predominates over the reflex-mediated increase in LV contractility. Under these conditions, activation of afferent vagal receptors would occur and in turn suppress cardiac sympathetic nerve activity, resulting in a manifestation of actual deterioration of cardiac performance. As far as cardiac function is not severely compromised following acute coronary occlusion, early introduction of beta-blockers is rational for effective prevention of progression of myocardial ischemia.

Study limitations.   Most of the patients studied had the target lesion in the left anterior descending artery or circumflex artery. Therefore, these data could not determine the relationship between the location of ischemia and the prevalence of hemodynamic fluctuations. Secondly, the nature of the LF component is still controversial despite consistent evidence that the normalized LF component of heart rate variability serves as a marker of sympathetic modulation of the sinus node (6,7). We have also demonstrated that cardiovascular variability at the frequency of 0.06 to 0.07 Hz has a high coherence with corresponding components of muscle sympathetic nerve activity in humans (26). The normalized LF component showed a parallel increase with plasma norepinephrine levels during the course of tachycardia-induced heart failure (8). Finally, the response of hemodynamic variability to coronary occlusion was not uniform in some patients. This seems to be caused by heterogeneity of coronary legions and extent of ischemia, the presence of prior myocardial infarction or development of coronary collateral vessels. Destruction of nerve endings by myocardial infarction or repetitive ischemic insult could result in a loss of sympathetic reflexes originating from the ischemic area (27). Sympathoexcitation might be modified by another complex interaction with arterial baroreflex modulation accompanying hemodynamic changes or altered central mechanisms related to pain perception and to the stressful situation (28).

Conclusions.   The wavelet analysis of RR interval and LV pressure variability clearly showed a dynamic profile of sympathoexcitatory response to brief periods of coronary artery occlusion in humans. The regional myocardial ischemia elicited a profound sympathoexcitatory response followed by a gradual suppression which presumably attributed to vagal inhibitory reflex. Thus, the time-frequency analysis of cardiovascular variability provides a useful tool to gain new insight into the nonstationary autonomic influence on the cardiovascular system.


   Footnotes
 
This study was supported by Grant-in-Aid for General Scientific Research No. 09670706 from the Ministry of Education, Science and Culture of Japan.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

  1. Brown M. Excitation of afferent cardiac sympathetic nerve fibers during myocardial ischemia. J Physiol. 1967;190:35–53[Abstract/Free Full Text]
  2. Malliani A, Schwartz JP, Zanchetti A. A sympathetic reflex elicited by experimental coronary occlusion. Am J Physiol. 1969;217:703–709[Free Full Text]
  3. Casati R, Lombardi F, Malliani A. Afferent sympathetic unmyelinated fibers with left ventricular endings in cats. J Physiol. 1979;292:135–148[Abstract/Free Full Text]
  4. Malliani A, Peterson DF, Bishop VS, Brown AM. Spinal sympathetic cardiocardiac reflex. Circ Res. 1972;30:158–166[Abstract/Free Full Text]
  5. Webb SW, Adgey AA, Pantridge JF. Autonomic disturbance at onset of acute myocardial infarction. Br Med J. 1972;3:89–92[Medline]
  6. Pagani M, Lombardi F, Guzzetti S, et al. Power spectral analysis of heart rate and arterial pressure variabilities as a marker of sympathovagal interaction in man and conscious dog. Circ Res. 1986;59:178–193[Abstract/Free Full Text]
  7. Pagani M, Montano N, Porta A, et al. Relationship between spectral components of cardiovascular variabilities and direct measures of muscle sympathetic nerve activity in human. Circulation. 1997;95:1441–1448[Abstract/Free Full Text]
  8. Ishise H, Asanoi H, Ishizaka S, et al. The time course of sympathovagal imbalance and left ventricular dysfunction in conscious dogs with heart failure. J Appl Physiol. 1998;84:1234–1241[Abstract/Free Full Text]
  9. Airaksinen KEJ, Ikäheimo MJ, Huikuri HV, et al. Response of heart rate variability to coronary occlusion during coronary angioplasty. Am J Cardiol. 1993;72:1026–1030[CrossRef][Medline]
  10. Airaksinen KEJ, Ikäheimo MJ, Niemelä MJ, et al. Effect of beta blockade on heart rate variability during vessel occlusion at the time of coronary angioplasty. Am J Cardiol. 1996;77:40–44
  11. Lombardi F, Casalone C, Bella PD, et al. Global versus regional myocardial ischemia: differences in cardiovascular and sympathetic responses in cats. Cardiovasc Res. 1984;18:12–23
  12. Baan J, van der Velde ET, de Bruin HG, et al. Continuous measurement of left ventricular volume in animals and humans by conductance catheter. Circulation. 1984;70:812–823[Abstract/Free Full Text]
  13. Smokler PE, MacAlpin RN, Alvaro A, Kattus AA. Reproducibility of a multistage near maximal treadmill test for exercise tolerance in angina pectoris. Circulation. 1973;48:346–351[Abstract/Free Full Text]
  14. Rentrop KP, Cohen M, Blanke H, Phillips R. Changes in collateral filling immediately following controlled coronary artery occlusion by an angioplasty balloon in man. J Am Coll Cardiol. 1985;5:587–592[Abstract]
  15. Perry RA, Seth A, Hunt A, et al. Balloon occlusion during coronary angioplasty as a model of myocardial ischemia: reproducibility of sequential inflations. Eur Heart J. 1989;10:791–800[Abstract/Free Full Text]
  16. Asanoi H, Ishizaka S, Kameyama T, et al. Serial reproducibility of conductance catheter volumetry of left ventricle in conscious dogs. Am J Physiol. 1992;262:H911–H915
  17. Raff GL, Glantz SA. Volume loading slows left ventricular isovolumic relaxation rate. Circ Res. 1981;48:813–824[Free Full Text]
  18. Mallat SG. A theory for multiresolution signal decomposition: the wavelet representation. IEEE Trans Patt Anal Mach Intell. 1989;11:674–693[CrossRef]
  19. Crowe JA, Gibson NM, Woolfson MS, Somekh MG. Wavelet transform as a potential tool for ECG analysis and compression. J Biomed Eng. 1992;14:268–272[CrossRef][Medline]
  20. Rimoldi O, Pagani MR, Piazza S, et al. Restraining effects of captopril on sympathetic excitatory responses in dogs: a spectral analysis approach. Am J Physiol. 1994;267:H1608–H1618
  21. 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]
  22. Recordati G, Schwartz PJ, Pagani M, et al. Activation of cardiac vagal receptors during myocardial ischemia. Experientia. 1971;27:1423–1424[CrossRef][Medline]
  23. Thoren P. Left ventricular receptors activated by severe asphyxia and by coronary artery occlusion. Acta Physiol Scand. 1972;85:455–463[Medline]
  24. Barber MJ, Mueller M, Davies BG, Zipes DP. Phenol topically applied to canine left ventricular epicardium interrupts sympathetic but not vagal afferents. Circ Res. 1984;55:532–544[Abstract/Free Full Text]
  25. Kawada T, Sugimachi M, Shishido T, et al. Dynamic vagosympathetic interaction augments heart rate response irrespective of stimulation patterns. Am J Physiol. 1997;272:H2180–H2187
  26. Goso Y, Asanoi H, Ishise H, et al. Relationship between low-frequency cardiovascular variability and muscle sympathetic nerve activity in patients with cardiac dysfunction. J Cardiovasc Pharmacol [in press].
  27. Barber MJ, Mueller TM, Davies BG, et al. Interruption of sympathetic and vagal mediated afferent response by transmural myocardial infarction. Circulation. 1985;72:623–631[Abstract/Free Full Text]
  28. Malliani A, Lombardi F. Consideration of the fundamental mechanisms eliciting cardiac pain. Am Heart J. 1982;103:575–578[CrossRef][Medline]



This article has been cited by other articles:


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

Home page
 J. Pharmacol. Exp. Ther.Home page
D. E. Mager and D. R. Abernethy
Use of Wavelet and Fast Fourier Transforms in Pharmacodynamics
J. Pharmacol. Exp. Ther., May 1, 2007; 321(2): 423 - 430.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. Barbieri, E. C. Matten, A. A. Alabi, and E. N. Brown
A point-process model of human heartbeat intervals: new definitions of heart rate and heart rate variability
Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H424 - H435.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
E. Toledo, O. Gurevitz, H. Hod, M. Eldar, and S. Akselrod
Wavelet analysis of instantaneous heart rate: a study of autonomic control during thrombolysis
Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2003; 284(4): R1079 - R1091.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
S. Joho, H. Asanoi, J. Takagawa, T. Kameyama, T. Hirai, T. Nozawa, K. Umeno, M. Shimizu, H. Seto, and H. Inoue
Cardiac sympathetic denervationmodulates the sympathoexcitatoryresponse to acute myocardial ischemia
J. Am. Coll. Cardiol., February 6, 2002; 39(3): 436 - 442.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Joho, S.
Right arrow Articles by Inoue, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Joho, S.
Right arrow Articles by Inoue, H.

HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK