Relationship Between Spectral Measures of Heart Rate Variability and Ventricular Ectopic Activity in Patients with Idiopathic Ventricular Tachycardia JASWINDER S. GILL, FEI LU, DAVID E. WARD, and A. JOHN GAMM From the Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom
GILL, J.S., ET AL.: Relationship Between Spectral Measures of Heart Rate Variability and Ventricular Ectopic Activity in Patients with Idiopathic Ventricular Tachycardia. This study examines the reJation-
ship of hourJy spectraJ measures of heart rate variability (HHV) to the occurrence of ventricular ectopic (VEJ activity in 20 patients with idiopathic ventricular tachycardia and frequent VE's. Spectral measures of HHV were obtained from 24-hour Holter recordings from the patients in a drug free state and included the total energies in (he spectrum, the Jowfrequency components (L) (0.04-0.15 Hz) representing predo;minantly sympathetic tone with some contribution from Ihe parasympathetic and high frequency components (H) (0.15-0.4 Hz) representing mainly parasympathetic tone. A high H component fparasympathetic) was defined as area > 12 msec and high L components fsympathetjcj as area > 30 msec. On an hourly analysis of spectral components in reiation to VE activity, VE's occurred significantly more frequently during periods of low H and low L(F = 20.5, DF = 3, P < 0.0001). The number of VE's did not differ statistically in the other combinations of H and L components (Joiv H, low L = 612.8 (50.1); high H, low L = 180.1 (36,8); low H, high L = 338.4 f58.9); high H, high L - 204.9 (17.7) VE's/hr (SEM). The results suggest that VE's are more jrequent during periods of low H and low L and are diminished when either H or L are increased in patients with idiopathic ventricular tachycardia. The results would be consistent with the hypothesis Ihat the parasympalhetic nervous system has an electrophysiologicaJJy stabilizing effect on the myocardium. (PACE, Vol. 15, November, Part II 1992) heart rate variability, ventricular tachycardia
Introduction In approximately 10% of cases of ventricular tachycardia (VT) seen in hospital, no obvious underlying disease is apparent on clinical examination and noninvasive investigations.^ These patients constitute the group with idiopathic ventricular tachycardia. Such patients are, generally, young and the male/female ratio is approximately equal, unlike the male excess ohserved in ischemic VT. The onset of episodes of VT are frequently related to exercise, and in many such pa-
Address for reprints: J.S. Gill, M.D., Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SWI7 ORE, UK.
2206
tients, the arrhythmia can he induced by isoprenaline infusion, though the rates of induction by programmed ventricular stimulation (PVS) are generally lower than for ischemic VT.^ The arrhythmia may be terminated hy vagal maneuvers, adenosine, or calcium antagonists.^ These features suggest that the occurrence of VT in such patients is under strong autonomic control, and that the mechanism of VT may differ from that of reentrant VT secondary to ischemic heart disease. Recently, there has been increasing interest in the role of the autonomic nervous system in the genesis of ventricular arrhythmias.^"^ The riso in interest comes from the easy availability of Holter monitoring and analysis of heart rate variability (HRV). Beat to beat variations in R-R interval are
November, Part II 1992
PACE, Vol. 15
HEART RATE VARIABILITY IN IDIOPATHIC VENTRICULAR TACHYCARDIA
transformed into a frequency domain using fast Fourier transformation, and spectral measures are computed as square root of areas under the power spectrum.^ Several studies suggest that individual spectral components represent the activity of different elements of the cardiac autnomic nervous system. The area on the HRV spectrum hetween the frequencies 0.04 and 0.15 Hz (low frequencies) represents sympathetic inputs, with contribution from the parasympathetic system,^® The area in the frequencies 0.15 to 0.4 Hz represents almost solely parasympathetic inputs.^'^ This method may therefore allow a means of examining the relative activities of the sympathetic and parasympathetic inputs, which regulate myocardial electrical and contractile activity. This study examines whether the changes in the sympathetic/ parasympathetic balance to the myocardium are important in determining ventricular ectopic activity in patients with idiopathic ventricular tachycardia. Patients and Methods Patients No patient had a previous history of underlying cardiac disease, and all had ventricular arrhythmias documented on multiple ECG leads. Patients had a normal clinical examination, normal chest radiograph (cardiothoracic ratio < 50%) and normal resting ECG (apart from minor T wave abnormalities). No patient had angiographic evidence of coronary artery disease, reduced ejection fraction of the left ventricle, or regional wall motion abnormality during left ventricular cine-angiography and routine echocardiography as assessed by two independent observers. All patients underwent recording of a signal averaged ECG, detailed echocardiography and biopsy of the right ventricle. No patient had atrial fibrillation or a pacemaker. The morphology of the VT was defined from lead Vl-QRS > 120 msec and predominantly negative being left bundle branch block-like (LBBB) and predominanuy positive being right bundle branch hlock-like (RBBB). The frontal plane axis of the clinical tachycardia was defined from the limb leads as as left-ward (< - 30°), right-ward (> + 90°), or normal ( - 30° to + 90°) from the vector
PACE, Vol. 15
perpendicular to the lead with the most isoelectric QRS complexes. The episodes of tachycardia were defined as sustained if VT lasted > 30 seconds or required termination because of hemodynamic compromise and nonsustained if VT lasted > 5 beats to < 30 seconds and terminated spontaneously. Patients were studied in a drug free state in all cases.
Heart Rate Variability Analysis Twenty-four hour Holter tapes were obtained on the patients using the Reynolds Tracker' recorders (Reynolds Medical Inc., Hertford, UK) or Marquette 8500 recorders and analyzed on the Marquette laser XP 1200 system (Marquette, Milwaukee, WI, USA) allowing detection of normal sinus beats, supraventricular, and ventricular extrasystoles, singly or in runs. Each tape was manually edited to ensure the correct classification of each QRS complex. The spectral HRV output from the Marquette program was used. Spectral plot and areas under the total frequency distribution (Total), low frequencies (L) and high frepuencies (H) were obtained for the whole tape and for each individual hour of the tape (Fig. 1). The numbers of ventricular ectopic beats within each corresponding hour of the tape were also enumerated. High H was defined as an area in the 0.04-0.15 Hz band > 30 msec and high L as area in the 0.15-0.4 Hz band exceeding 12 msec. This allowed reasonable numbers of hours to be present in each of the categories below. Statistical Analysis Each hour of the Holter spectral analysis was defined in terms of the quantity of H and L components resulting in four categories: high H and high L, high H and low L, low H and high L, and low H and low L. The four groups were compared using analysis of variance.
Results Twenty-two patients were studied (mean age 38.6 ± 8.6 years, 13 males). However, two patients had < 50 VE's/24 hours and these were excluded from the analysis. The spontaneous VT was classified of LBBB-like morphology in 16 patients and
November, Part II 1992
2207
GILL, ET AL.
30 ms
ms 0 . 0 1 - 1 . 0 0 Hz ms 0 . 0 4 - 0 . 1 5 Hz ms 0 . 1 5 - 0 . 4 0 Hz
SOAWN SO rMSSD pNNS0
30 ms 1 \ \ 0 ms ^
I9-APR-90 08:00
—
•
1
I
-
09:00
.
157 ms 86 ms 46 ms 25.6 I
70 34 19 _
54 30 17 —-—
Figure 1. Heart rate variability spectra obtained /rom tbe Marquette program. The numbers in tbe upper Jeft corner of each spectrum are from above downwards, the total area of the distribution, ihe high frequency component area and the low frequency component area.
of RBBB-like morphology in four patients. The axis of the VT was left-ward in 7 patients, normal in 3 patients, and right-ward in 8 patients. Patient details are given in Table I. The mean length of the Holter tape was 23.5 ± 2.2 hours. The mean numbers of VE's within each combination of H and L components are given in Table 11. The numbers of ventricular ectopic beats were highest when H and L components were low. The numbers of VE's were lower in all the other categories of H and L components and did not differ from each other. The VE's did not represent ventricular escape beats because the coupling interval of the VE to the previous normal beats was less than the previous normal to normal R-R interval.
Discussion The results of this study suggest that the occurrence of VE's in this group of patients occurs when H and L components are low. Periods of increased H and L component have reduced VE activity. Many lines of evidence suggest that ventric-
2208
ular ectopic activity in patients with idiopathic VT is highly influenced by the activity of the autonomic nervous system. In many patients episodes of VT are inducible by exercise, and although in the majority these are nonsustained, some patients have sustained episodes. The VT occurs either at near peak exercise or in the recovery period following exercise.^ The VT is inducible by isoprenaline infusion in many patients with exercise-induced episodes. In a small proportion of patients, there are frequent nonsustained runs of VT at rest and these disappear during exercise only to return again in recovery. Such patients form Ihe subgroup with repetitive monomorphic VT.^'^ Conversely, the VT can be terminated by vagal maneuvers, adenosine (which has an anti-catecholaminergic effect in the ventricle),^^ and calcium antagonists.^^ These effects also suggest that the mechanism of these forms of VT may be due to triggered activity. Early after depolarizations appear to occur at low heart rates, where late afterdepolarizations increase in magnitude during accelerations of pacing rate.'^ This mechanism inay
November, Part II 1992
PACE. Vol. 15
HEART RATE VARIABILITY IN IDIOPATHIC VENTRICULAR TACHYCARDIA
Tabie i. Clinical Characteristics of the Patients in the Study Patient
Sex
VT morph
VT axis
CL
1 2 3 4 5
42 54 35 41
6 7 8
50
F M F M M M
L L L L L L L L L R L L R L L L R L R L
Ri Le Ri Ri Le N
180 210 330 300 240 400 440 280 340 330 280 300 240 300 320 340 360 200 280 300
12 13 14 15
16 17
18 19 20
57 32 52 28 25 37 30 28 16 20 43 30 64 42
LL.
9 10 11
38
Ll_
Age
F M M M M M M M F F M M
Ri Ri N Le Ri
N Le Le Ri Le Le
Ri N Ri
Ex indue NS 0 NS NS NS NS NS S NS 0 0 S NS NS NS S S 0 0 0
Biopsy A
A No No
A No No No No No A No No A No A No No No No
VT morph = VT morphology; CL = cycle length (msec); Ex indue = exercise induction; L = left bundle branch block-like; R = right bundle branch block-like; Le = left-ward; Bi = right-ward; N = normal; 0 = no VT; S = sustained; NS = non-sustained VT; No = normal; A = abnormal.
therefore lead to ventricular ectopic activity either during periods of bradycardia or during tachycardia. A number of acute interventions lead to cbanges in the relative high and low frequency areas in the HRV power spectral distribution, of
Tabie ii. Mean Number of Ventricular Ectopics (VE) Beats in Spectral Components of Heart Rate Variability Spectrai Components Low L, low H High H. low L Low H, high L High H, high L
VE's/hr
SEM
612.8 180,1 338.4 204.9
50.1 36.8 58.9 17.7
H = high frequency component; L = low frequency component.
PACE, Vol. 15
which exercise is the most relevant to these patients. Arai et al,,^*' reported tbat in normal subjects, there was a progressive decrease in the high and low frequency spectra! power during exercise, and these returned towards normal levels during tbe recovery period. These results are similar to those obtained by other workers^^'^^ who report that both low and high frequency components decrease during exercise, but recover in tbe period following exercise, with a greater increase in the low frequency component in comparison to the high frequency. The results from our study are consistent with the occurrence of ventricular ectopic activity during exercise and periods of decreased low and high frequency spectral components of HRV. It might be expected tbat tbe low frequency peak would increase during exercise with increasing sympathetic activity. This appears to not occur, presumably because a significant proportion of this component is due to parasympatbetic tone that diminishes during tbe exercise pe-
November, Part II 1992
2209
GILL. ET AL.
® It is notable that in patients with myocardial ischemia, the presence of diminished heart rate variability, which manifests as a diminution of the total, low and high frequency components is associated with an increased incidence of sudden death, presumably due to ventricular tachyarrhythmia or fibrillation.^'^ We conclude that the occurrence of ventricu-
lar ectopic activity in patients with idiopathic ventricular tachycardia is associated with diminished low and high frequency components of heart rate variability. The results would be consistant with the concept that increased parasympathetic tone is protective to the myocardium,^^ in these patients as well as in individuals with ischemic heart disease.
References Froment R. Gallavardin L, Cahen P. Paroxysmal ventricular tachycardia: A clinical classification. Br Heart J 1953; 15:172^178. Lerman BB. Ventricular tachycardia unassociated with coronary artery disease. Progress in Cardiology 1990; 1:255-279. Corr PB, Yamada KA, Witkowski FX. Mechanisms controlling cardiac autonomic function and their relationship to arrhythmogenesis. In HA Fozzard, E Haher, RB Jennings. AM Katz (eds.): The Heart and Cardiovascular System. New York, NY, Raven, 1986. pp. 1343-1404. Kleiger RE, Miller JP, Bigger ]T. et al. Heart rate variability: A predictor of mortality following acute myocardial infarction. Am J Cardiol 1987; 59:256-262. Farrell TG, Bashir Y, Cripps T. et al. Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability, ambulatory electrocardiographic variables and the signal-averaged electrocardiogram. J Am Coll Cardiol 1991; 18:687-697. Axselrod S, Gordon D. Ubel FA, et al. Power spectrum analysis of heart rate variability: A quantitative probe of beat to beat cardiovascular control. Science 1981; 213:220-222. Shin SJ, Tapp WN, Reisman SS, et al. Assessment of autonomic regulation of heart rate variability by the method of complex demodulation. IEEE Trans Biomed End 1989; 36:274-283. Lipsitz LA, Mietus }, Moody GB, et al. Spectral characteristics of heart rate variability before and during postural tilt. Relations to aging and risk of syncope. Circulation 1990; 81:1803-1810.
2210
9. Vybiral T. Bryg RI, Maddens ME, et al. Effect of passive tilt on sympathetic and parasympathetic components of heart rate variability in normal subjects. Am J Cardiol 1990; 63:391-393. 10. Rahilly GM, Prystowsky EN, Zipes DP, et al. Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram. Am I Cardiol 1982; 50:459-468. 11. Lerman BB, BelardineUi L, West A, et al. Adenosine-sensitive ventricular tachycardia: Evidence suggesting cyclic AMP-mediated triggered activity. Circulation 1986; 74:270-280. 12. Wu D, Kou HC, Hung IS. Exercise-triggered paroxysmal ventricular tachycardia. A repetitive rhythmic activity possibly related to afterdepoltirization. Ann Int Med 1981; 95:410-414. 13. Rosen MR, Wit AL. Triggered activity. Progress in Cardiology 1990; 1:39-46. 14. Arai Y, Saul P, Albrecht P, et al. Modulation of cardiac autonomic activity during and immediately after exercise. Am | Physiol 1989; 256:Hl:32H141. 15. Kamath MV, Fallen EL. McKelvie R. Effects of steady state exercise on the power spectrum of heart rate variability. Med Sci Sports Exerc 1991; 23:428-434. 16. Berbardi L, Salvucci F. Suardi R. et al. Evidence for an intrinsic mechanism regulating heart rate variability in the transplanted and intact heart during submaxlmal dynamic exercise. Cardiovasc Res 1990; 24:969-981. 17. Zuanetti C. De Ferrari GM, Priori SG, et al. Protective effect of vagal stimulation on reperfusion arrhythmias in cats. Girc Res 1987; 61:429-435.
November. Part Ii 1992
PACE. Vol. 15
GILL, J.S., ET AL.: Relationship Between Spectral Measures of Heart Rate Variability and Ventricular Ectopic Activity in Patients with Idiopathic Ventricular Tachycardia. This study examines the reJation-
ship of hourJy spectraJ measures of heart rate variability (HHV) to the occurrence of ventricular ectopic (VEJ activity in 20 patients with idiopathic ventricular tachycardia and frequent VE's. Spectral measures of HHV were obtained from 24-hour Holter recordings from the patients in a drug free state and included the total energies in (he spectrum, the Jowfrequency components (L) (0.04-0.15 Hz) representing predo;minantly sympathetic tone with some contribution from Ihe parasympathetic and high frequency components (H) (0.15-0.4 Hz) representing mainly parasympathetic tone. A high H component fparasympathetic) was defined as area > 12 msec and high L components fsympathetjcj as area > 30 msec. On an hourly analysis of spectral components in reiation to VE activity, VE's occurred significantly more frequently during periods of low H and low L(F = 20.5, DF = 3, P < 0.0001). The number of VE's did not differ statistically in the other combinations of H and L components (Joiv H, low L = 612.8 (50.1); high H, low L = 180.1 (36,8); low H, high L = 338.4 f58.9); high H, high L - 204.9 (17.7) VE's/hr (SEM). The results suggest that VE's are more jrequent during periods of low H and low L and are diminished when either H or L are increased in patients with idiopathic ventricular tachycardia. The results would be consistent with the hypothesis Ihat the parasympalhetic nervous system has an electrophysiologicaJJy stabilizing effect on the myocardium. (PACE, Vol. 15, November, Part II 1992) heart rate variability, ventricular tachycardia
Introduction In approximately 10% of cases of ventricular tachycardia (VT) seen in hospital, no obvious underlying disease is apparent on clinical examination and noninvasive investigations.^ These patients constitute the group with idiopathic ventricular tachycardia. Such patients are, generally, young and the male/female ratio is approximately equal, unlike the male excess ohserved in ischemic VT. The onset of episodes of VT are frequently related to exercise, and in many such pa-
Address for reprints: J.S. Gill, M.D., Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SWI7 ORE, UK.
2206
tients, the arrhythmia can he induced by isoprenaline infusion, though the rates of induction by programmed ventricular stimulation (PVS) are generally lower than for ischemic VT.^ The arrhythmia may be terminated hy vagal maneuvers, adenosine, or calcium antagonists.^ These features suggest that the occurrence of VT in such patients is under strong autonomic control, and that the mechanism of VT may differ from that of reentrant VT secondary to ischemic heart disease. Recently, there has been increasing interest in the role of the autonomic nervous system in the genesis of ventricular arrhythmias.^"^ The riso in interest comes from the easy availability of Holter monitoring and analysis of heart rate variability (HRV). Beat to beat variations in R-R interval are
November, Part II 1992
PACE, Vol. 15
HEART RATE VARIABILITY IN IDIOPATHIC VENTRICULAR TACHYCARDIA
transformed into a frequency domain using fast Fourier transformation, and spectral measures are computed as square root of areas under the power spectrum.^ Several studies suggest that individual spectral components represent the activity of different elements of the cardiac autnomic nervous system. The area on the HRV spectrum hetween the frequencies 0.04 and 0.15 Hz (low frequencies) represents sympathetic inputs, with contribution from the parasympathetic system,^® The area in the frequencies 0.15 to 0.4 Hz represents almost solely parasympathetic inputs.^'^ This method may therefore allow a means of examining the relative activities of the sympathetic and parasympathetic inputs, which regulate myocardial electrical and contractile activity. This study examines whether the changes in the sympathetic/ parasympathetic balance to the myocardium are important in determining ventricular ectopic activity in patients with idiopathic ventricular tachycardia. Patients and Methods Patients No patient had a previous history of underlying cardiac disease, and all had ventricular arrhythmias documented on multiple ECG leads. Patients had a normal clinical examination, normal chest radiograph (cardiothoracic ratio < 50%) and normal resting ECG (apart from minor T wave abnormalities). No patient had angiographic evidence of coronary artery disease, reduced ejection fraction of the left ventricle, or regional wall motion abnormality during left ventricular cine-angiography and routine echocardiography as assessed by two independent observers. All patients underwent recording of a signal averaged ECG, detailed echocardiography and biopsy of the right ventricle. No patient had atrial fibrillation or a pacemaker. The morphology of the VT was defined from lead Vl-QRS > 120 msec and predominantly negative being left bundle branch block-like (LBBB) and predominanuy positive being right bundle branch hlock-like (RBBB). The frontal plane axis of the clinical tachycardia was defined from the limb leads as as left-ward (< - 30°), right-ward (> + 90°), or normal ( - 30° to + 90°) from the vector
PACE, Vol. 15
perpendicular to the lead with the most isoelectric QRS complexes. The episodes of tachycardia were defined as sustained if VT lasted > 30 seconds or required termination because of hemodynamic compromise and nonsustained if VT lasted > 5 beats to < 30 seconds and terminated spontaneously. Patients were studied in a drug free state in all cases.
Heart Rate Variability Analysis Twenty-four hour Holter tapes were obtained on the patients using the Reynolds Tracker' recorders (Reynolds Medical Inc., Hertford, UK) or Marquette 8500 recorders and analyzed on the Marquette laser XP 1200 system (Marquette, Milwaukee, WI, USA) allowing detection of normal sinus beats, supraventricular, and ventricular extrasystoles, singly or in runs. Each tape was manually edited to ensure the correct classification of each QRS complex. The spectral HRV output from the Marquette program was used. Spectral plot and areas under the total frequency distribution (Total), low frequencies (L) and high frepuencies (H) were obtained for the whole tape and for each individual hour of the tape (Fig. 1). The numbers of ventricular ectopic beats within each corresponding hour of the tape were also enumerated. High H was defined as an area in the 0.04-0.15 Hz band > 30 msec and high L as area in the 0.15-0.4 Hz band exceeding 12 msec. This allowed reasonable numbers of hours to be present in each of the categories below. Statistical Analysis Each hour of the Holter spectral analysis was defined in terms of the quantity of H and L components resulting in four categories: high H and high L, high H and low L, low H and high L, and low H and low L. The four groups were compared using analysis of variance.
Results Twenty-two patients were studied (mean age 38.6 ± 8.6 years, 13 males). However, two patients had < 50 VE's/24 hours and these were excluded from the analysis. The spontaneous VT was classified of LBBB-like morphology in 16 patients and
November, Part II 1992
2207
GILL, ET AL.
30 ms
ms 0 . 0 1 - 1 . 0 0 Hz ms 0 . 0 4 - 0 . 1 5 Hz ms 0 . 1 5 - 0 . 4 0 Hz
SOAWN SO rMSSD pNNS0
30 ms 1 \ \ 0 ms ^
I9-APR-90 08:00
—
•
1
I
-
09:00
.
157 ms 86 ms 46 ms 25.6 I
70 34 19 _
54 30 17 —-—
Figure 1. Heart rate variability spectra obtained /rom tbe Marquette program. The numbers in tbe upper Jeft corner of each spectrum are from above downwards, the total area of the distribution, ihe high frequency component area and the low frequency component area.
of RBBB-like morphology in four patients. The axis of the VT was left-ward in 7 patients, normal in 3 patients, and right-ward in 8 patients. Patient details are given in Table I. The mean length of the Holter tape was 23.5 ± 2.2 hours. The mean numbers of VE's within each combination of H and L components are given in Table 11. The numbers of ventricular ectopic beats were highest when H and L components were low. The numbers of VE's were lower in all the other categories of H and L components and did not differ from each other. The VE's did not represent ventricular escape beats because the coupling interval of the VE to the previous normal beats was less than the previous normal to normal R-R interval.
Discussion The results of this study suggest that the occurrence of VE's in this group of patients occurs when H and L components are low. Periods of increased H and L component have reduced VE activity. Many lines of evidence suggest that ventric-
2208
ular ectopic activity in patients with idiopathic VT is highly influenced by the activity of the autonomic nervous system. In many patients episodes of VT are inducible by exercise, and although in the majority these are nonsustained, some patients have sustained episodes. The VT occurs either at near peak exercise or in the recovery period following exercise.^ The VT is inducible by isoprenaline infusion in many patients with exercise-induced episodes. In a small proportion of patients, there are frequent nonsustained runs of VT at rest and these disappear during exercise only to return again in recovery. Such patients form Ihe subgroup with repetitive monomorphic VT.^'^ Conversely, the VT can be terminated by vagal maneuvers, adenosine (which has an anti-catecholaminergic effect in the ventricle),^^ and calcium antagonists.^^ These effects also suggest that the mechanism of these forms of VT may be due to triggered activity. Early after depolarizations appear to occur at low heart rates, where late afterdepolarizations increase in magnitude during accelerations of pacing rate.'^ This mechanism inay
November, Part II 1992
PACE. Vol. 15
HEART RATE VARIABILITY IN IDIOPATHIC VENTRICULAR TACHYCARDIA
Tabie i. Clinical Characteristics of the Patients in the Study Patient
Sex
VT morph
VT axis
CL
1 2 3 4 5
42 54 35 41
6 7 8
50
F M F M M M
L L L L L L L L L R L L R L L L R L R L
Ri Le Ri Ri Le N
180 210 330 300 240 400 440 280 340 330 280 300 240 300 320 340 360 200 280 300
12 13 14 15
16 17
18 19 20
57 32 52 28 25 37 30 28 16 20 43 30 64 42
LL.
9 10 11
38
Ll_
Age
F M M M M M M M F F M M
Ri Ri N Le Ri
N Le Le Ri Le Le
Ri N Ri
Ex indue NS 0 NS NS NS NS NS S NS 0 0 S NS NS NS S S 0 0 0
Biopsy A
A No No
A No No No No No A No No A No A No No No No
VT morph = VT morphology; CL = cycle length (msec); Ex indue = exercise induction; L = left bundle branch block-like; R = right bundle branch block-like; Le = left-ward; Bi = right-ward; N = normal; 0 = no VT; S = sustained; NS = non-sustained VT; No = normal; A = abnormal.
therefore lead to ventricular ectopic activity either during periods of bradycardia or during tachycardia. A number of acute interventions lead to cbanges in the relative high and low frequency areas in the HRV power spectral distribution, of
Tabie ii. Mean Number of Ventricular Ectopics (VE) Beats in Spectral Components of Heart Rate Variability Spectrai Components Low L, low H High H. low L Low H, high L High H, high L
VE's/hr
SEM
612.8 180,1 338.4 204.9
50.1 36.8 58.9 17.7
H = high frequency component; L = low frequency component.
PACE, Vol. 15
which exercise is the most relevant to these patients. Arai et al,,^*' reported tbat in normal subjects, there was a progressive decrease in the high and low frequency spectra! power during exercise, and these returned towards normal levels during tbe recovery period. These results are similar to those obtained by other workers^^'^^ who report that both low and high frequency components decrease during exercise, but recover in tbe period following exercise, with a greater increase in the low frequency component in comparison to the high frequency. The results from our study are consistent with the occurrence of ventricular ectopic activity during exercise and periods of decreased low and high frequency spectral components of HRV. It might be expected tbat tbe low frequency peak would increase during exercise with increasing sympathetic activity. This appears to not occur, presumably because a significant proportion of this component is due to parasympatbetic tone that diminishes during tbe exercise pe-
November, Part II 1992
2209
GILL. ET AL.
® It is notable that in patients with myocardial ischemia, the presence of diminished heart rate variability, which manifests as a diminution of the total, low and high frequency components is associated with an increased incidence of sudden death, presumably due to ventricular tachyarrhythmia or fibrillation.^'^ We conclude that the occurrence of ventricu-
lar ectopic activity in patients with idiopathic ventricular tachycardia is associated with diminished low and high frequency components of heart rate variability. The results would be consistant with the concept that increased parasympathetic tone is protective to the myocardium,^^ in these patients as well as in individuals with ischemic heart disease.
References Froment R. Gallavardin L, Cahen P. Paroxysmal ventricular tachycardia: A clinical classification. Br Heart J 1953; 15:172^178. Lerman BB. Ventricular tachycardia unassociated with coronary artery disease. Progress in Cardiology 1990; 1:255-279. Corr PB, Yamada KA, Witkowski FX. Mechanisms controlling cardiac autonomic function and their relationship to arrhythmogenesis. In HA Fozzard, E Haher, RB Jennings. AM Katz (eds.): The Heart and Cardiovascular System. New York, NY, Raven, 1986. pp. 1343-1404. Kleiger RE, Miller JP, Bigger ]T. et al. Heart rate variability: A predictor of mortality following acute myocardial infarction. Am J Cardiol 1987; 59:256-262. Farrell TG, Bashir Y, Cripps T. et al. Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability, ambulatory electrocardiographic variables and the signal-averaged electrocardiogram. J Am Coll Cardiol 1991; 18:687-697. Axselrod S, Gordon D. Ubel FA, et al. Power spectrum analysis of heart rate variability: A quantitative probe of beat to beat cardiovascular control. Science 1981; 213:220-222. Shin SJ, Tapp WN, Reisman SS, et al. Assessment of autonomic regulation of heart rate variability by the method of complex demodulation. IEEE Trans Biomed End 1989; 36:274-283. Lipsitz LA, Mietus }, Moody GB, et al. Spectral characteristics of heart rate variability before and during postural tilt. Relations to aging and risk of syncope. Circulation 1990; 81:1803-1810.
2210
9. Vybiral T. Bryg RI, Maddens ME, et al. Effect of passive tilt on sympathetic and parasympathetic components of heart rate variability in normal subjects. Am J Cardiol 1990; 63:391-393. 10. Rahilly GM, Prystowsky EN, Zipes DP, et al. Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram. Am I Cardiol 1982; 50:459-468. 11. Lerman BB, BelardineUi L, West A, et al. Adenosine-sensitive ventricular tachycardia: Evidence suggesting cyclic AMP-mediated triggered activity. Circulation 1986; 74:270-280. 12. Wu D, Kou HC, Hung IS. Exercise-triggered paroxysmal ventricular tachycardia. A repetitive rhythmic activity possibly related to afterdepoltirization. Ann Int Med 1981; 95:410-414. 13. Rosen MR, Wit AL. Triggered activity. Progress in Cardiology 1990; 1:39-46. 14. Arai Y, Saul P, Albrecht P, et al. Modulation of cardiac autonomic activity during and immediately after exercise. Am | Physiol 1989; 256:Hl:32H141. 15. Kamath MV, Fallen EL. McKelvie R. Effects of steady state exercise on the power spectrum of heart rate variability. Med Sci Sports Exerc 1991; 23:428-434. 16. Berbardi L, Salvucci F. Suardi R. et al. Evidence for an intrinsic mechanism regulating heart rate variability in the transplanted and intact heart during submaxlmal dynamic exercise. Cardiovasc Res 1990; 24:969-981. 17. Zuanetti C. De Ferrari GM, Priori SG, et al. Protective effect of vagal stimulation on reperfusion arrhythmias in cats. Girc Res 1987; 61:429-435.
November. Part Ii 1992
PACE. Vol. 15
