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(Hypertension. 1996;28:16-21.)
© 1996 American Heart Association, Inc.
Articles |
Dispersion of the QT Interval and Autonomic Modulation of Heart Rate in Hypertensive Men With and Without Left Ventricular Hypertrophy
the Division of Cardiology, Department of Medicine, University of Oulu (Finland).
Correspondence to Juha S. Perkiomaki, MD, Division of Cardiology, Department of Medicine, Oulu University Central Hospital, 90220, Oulu, Finland.
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Abstract |
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Left ventricular hypertrophy is an independent risk factor for sudden cardiac death in hypertension, but the mechanisms of electrical instability associated with hypertrophy are not well known. We studied dispersion of the QT interval, an index of inhomogeneity of repolarization, and heart rate variability, a measure of cardiac autonomic modulation, in a randomly selected population of 162 men with systemic hypertension and made comparisons between the patients with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index
131 g/m2, n=44) and those without hypertrophy (left ventricular mass index <131 g/m2, n=118). The heart rate-corrected QT dispersion (67±37 versus 53±21 milliseconds, P<.05) and QT apex dispersion (55±22 versus 44±16 milliseconds, P<.01) were significantly longer in the patients with left ventricular hypertrophy than in those without hypertrophy. Thirteen of the 44 patients (30%) with hypertrophy versus 7 of the 118 patients (6%) without hypertrophy had an abnormally long QT apex dispersion (>70 milliseconds) (P<.001). The time and frequency domain measures of heart rate variability did not differ significantly between the patient groups with and without left ventricular hypertrophy. The measures of heart rate variability were not related to QT dispersion or left ventricular mass index but had a negative correlation with blood pressure values (eg, r=-.30 between the low-frequency component of heart rate variability and systolic pressure, P<.001). Age, body mass index, antihypertensive medication, and the other demographic variables were similar between the groups, but the patients with left ventricular hypertrophy had higher systolic (P<.01) and diastolic (P<.01) pressures compared with the patients without hypertrophy. Left ventricular hypertrophy in hypertensive men is associated with inhomogeneity of the early phase of ventricular repolarization, favoring susceptibility to reentrant ventricular tachyarrhythmias. Abnormalities in cardiac autonomic function, which may trigger a spontaneous onset of arrhythmias, are related to elevated blood pressure but not specifically to left ventricular hypertrophy.
Key Words: electrocardiography • heart rate • hypertension, chronic • hypertrophy
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Introduction |
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In hypertension, LVH is a risk factor for ventricular arrhythmias and sudden cardiac death.1 2 3 4 5 6 7 Several mechanisms have been proposed to explain the vulnerability of the hypertrophied ventricle to life-threatening arrhythmias,8 but the factors actually predisposing hypertensive patients with LVH to electrical instability and sudden cardiac death are not well established.
The variability in the QT interval duration between the different leads of a surface 12-lead ECG (QT dispersion) reflects local differences in the recovery time of the myocardium,9 10 11 12 13 14 and QT dispersion is increased in patients with a prior myocardial infarction, who have a susceptibility to ventricular tachyarrhythmias.15 Patients with hypertrophic cardiomyopathy have a broader QT dispersion than healthy subjects, and QT dispersion discriminates between patients with and without serious ventricular arrhythmias or sudden death in hypertrophic cardiomyopathy16 and congestive heart failure.17 Thus, a long QT dispersion indicates the presence of a substrate for ventricular tachyarrhythmias, most obviously by a reentry mechanism.15 Autonomic cardiac control has been shown to be altered in hypertensive patients compared with their normotensive counterparts.18 Reduced HRV, an indicator of abnormal cardiac autonomic control, may condition the heart to a spontaneous onset of ventricular arrhythmias, but it is not a specific marker of a substrate for ventricular tachyarrhythmias.19 In the present work, we studied the mechanisms of electrical instability in hypertensive patients with LVH by comparing QT dispersion and HRV in hypertensive men with and without LVH.
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Methods |
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The study comprised 250 hypertensive men between 40 and 60 years of age who were randomly selected from all men who had filed for reimbursement of antihypertensive medication in the register maintained by the Social Insurance Institute. Patients with symptoms of, taking medication for, or showing ECG evidence of coronary artery disease were excluded, as were those with diabetes mellitus, with echocardiographic findings of significant valvular lesions, on antiarrhythmic medication, or with atrial fibrillation. After these exclusions, the remaining 162 patients were divided into two groups on the basis of the echocardiographic measurement of LVMI. Forty-four patients fulfilled the criteria of LVH (LVMI
131g/m2, LVH+ group)20 21 ; LVMI was less than 131g/m2 in the remaining 118 patients (LVH- group). All patients went through a clinical examination, including height, weight, and waist and hip circumference measurements. Blood pressure was measured with an automatic oscillometric blood pressure recorder (Dinamap, Critikon Ltd). The patient was seated for at least 5 minutes, after which time blood pressure was measured three times at 1-minute intervals from the right arm. The mean of the three measurements was used in the analysis. A 12-lead surface ECG was taken from every patient. The study protocol was approved by the Ethics Committee of the University of Oulu.
Echocardiographic Measurements
The same experienced cardiologist was blinded to the clinical data of the patients and performed all echocardiographic measurements using a Hewlett-Packard 77020A ultrasound color system for M-mode, two-dimensional, and Doppler examinations. Standard techniques were used, and recordings were analyzed with a previously described method.22 23 The M-mode measurements were obtained as recommended by the American Society of Echocardiography.24 Left ventricular mass was calculated with the formula of Troy25 and LVMI by dividing left ventricular mass by body surface area. Fractional shortening was calculated by dividing the difference between left ventricular internal dimensions in diastole and systole by diastolic dimension and multiplying by 100.
Measurement of QT Interval and Dispersion
The QT and QTa intervals and the QRS complex duration were measured at each lead of the 12-lead surface ECG for two consecutive cycles. The details of the method of measuring the dispersion of the intervals have been previously described.15 The QT intervals were measured from the onset of the QRS to the end of the T wave by a tangential method. When U waves were present, the QT was measured to the nadir of the curve between the T and U waves, also with the aid of tangent. The QTa intervals were measured from the onset of the QRS to the apex of the T wave. The QRS complex duration was measured from the beginning of the QRS to its end. The Te interval (from the apex of the T wave to its end) was calculated from the equation Te=QT-QTa, and the JT interval (from the J point to the end of the T wave) from the equation JT=QT-QRS. The measurements were performed manually by an experienced observer blinded to the clinical data of the patients. The QT, QTa, Te, JT, and QRS dispersions were defined as the differences between the maximum and minimum QT, QTa, Te, JT, and QRS values, respectively, and the mean value of two consecutive cycles was calculated. Bazett's formula was used to obtain heart rate-corrected (c) values of the QT, QTa, Te, and JT intervals and dispersions. Also, the SD values of the QT and QTa intervals between the leads of the 12-lead ECG were calculated (QTSD and QTaSD, respectively). Only two patients, both in the LVH+ group, had features of a strain pattern on the ECG, one with T wave inversions at leads V4 through V6 and the other at leads V5 and V6. At the leads where the T wave was inverted, the QTa interval was not measured. Intraobserver and interobserver measurement errors of the QT and QTa dispersions were defined. Interobserver measurement error was avoided by using the measurements of the same experienced observer for statistical comparisons.
Analysis of HRV
All patients were examined with an ambulatory ECG recorder (Dynacord Holter Recorder, model 420, DM Scientific) for 45 minutes: 15 minutes while lying down quietly, 15 minutes while sitting, and 15 minutes while walking.
The ECG recordings were performed between 7 AM and 3 PM, and the ECG data were transferred from the Del Mar Avionics scanner (model 500) to a microcomputer for analysis of HRV by a method described in detail previously.26 27 A linear detrend was applied to the RR interval data in segments of the 512 samples to make the data more stationary, while premature beats and noise were excluded both automatically and manually, and the gaps were then refilled with an average value. Patients with segments with less than 85% qualified beats were excluded from the analysis.
An autoregressive model was used to estimate the power spectrum densities of the RR interval variability. Size 10 was used for the order of the model in the analysis of RR data. The computer program automatically calculates the autoregressive coefficients to define the power spectrum density. The power spectra were quantified by a measurement of the area in four frequency bands: total power less than 0.4 Hz, high-frequency power from 0.15 to 0.40 Hz, low-frequency power from 0.04 to 0.15 Hz, and very-low-frequency power from 0.005 to 0.04 Hz.27 The different spectral components were calculated (1) as absolute units (equal to the area under the curves for the spectral densities) and (2) as normalized units by dividing the powers of the low-frequency and high-frequency components by the total power, from which those components less than 0.04 Hz had been subtracted, and multiplying by 100. The ratios between the low- and high-frequency spectra in fractional units were also analyzed, as was the SD of successive RR intervals. The average 45-minute RR intervals, the SD of the RR intervals, and the power spectrum components of HRV were calculated from segments of 512 RR intervals.
Statistics
The Mann-Whitney two independent sample test was used for estimation of the differences in the data between the patient groups. Spearman's and Pearson's correlation coefficients were used in estimating the correlations between the variables. Because of the skewed distribution, a logarithmic transformation for HRV measures was performed before statistical analyses. Proportions were compared with Fisher's exact test. A value of P<.05 was considered significant.
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Results |
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Clinical and Echocardiographic Data
The clinical and echocardiographic data on the patients in the two study groups are presented in Table 1
. Age, body mass index, and waist-hip ratio were similar in the patient groups, but the LVH+ patients had higher systolic and diastolic pressures compared with the LVH- patients. The LVH+ patients had longer left ventricular internal diastolic diameter and left atrial diameter and thicker interventricular septa and left ventricular posterior walls but lower ratios of interventricular septum to left ventricular posterior wall compared with the LVH- patients. Fractional shortening did not differ between the groups. Medication did not differ significantly between the two groups.
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QT Intervals and QT Dispersion
QT intervals, QRS duration, and the average RR interval did not differ significantly between the study groups (Table 2).
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QTc, QTac, and JTc dispersions were significantly broader in the LVH+ patients compared with the LVH- patients. QRS dispersion was quite similar in the patient groups. The LVH+ patients had significantly higher QTSD and QTaSD values compared with the LVH- patients (Table 2
). QTac dispersion (r=.24, P=.002) and QTaSD (r=.28, P<.001) had a positive correlation with LVMI, but the correlations between QTc dispersion or QTSD and LVMI (r=.08, P=.33 and r=.08, P=.29, respectively), JTc dispersion and LVMI (r=.11, P=.17), and Tec dispersion and LVMI (r=.08, P=.29) did not reach statistical significance. QTac dispersion and QTaSD were significantly positively correlated with left ventricular posterior wall thickness (r=.16, P=.04 and r=.21, P=.006, respectively) and left ventricular internal diastolic diameter (r=.18, P=.02 and r=.16, P=.04, respectively). QTc, QTac, QRS, and JTc dispersions did not differ between patients using ß-blockers (n=74) compared with those not using ß-blockers (n=88) (57±22 versus 57±31 milliseconds, 46±18 versus 48±20, 29±9 versus 29±11, and 62±22 versus 63±31, respectively), and no correlation was observed between the measures of QT interval dispersion and other antihypertensive medication. When a cutoff value of 70 milliseconds was used for abnormal QTac dispersion,15 13 of the 44 patients (30%) with LVH versus 7 of the 118 patients (6%) without LVH had longer QTac dispersion (P<.001).
Intraobserver variability of QT dispersion and QTa dispersion measurements were 11 and 3.5 milliseconds, respectively; corresponding interobserver variabilities were 12 and 7.5 milliseconds.
Heart Rate Variability
Neither the average heart rate nor any of the time or frequency domain measures of HRV analyzed in either absolute or normalized units differed significantly between the patient groups (Table 3). HRV measures did not correlate with QTc, QTac, JTc, and Tec dispersions or LVMI. However, HRV measures correlated inversely with both systolic and diastolic pressures (Table 4).
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Discussion |
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Experimental studies provide powerful evidence for the significance of the dispersion of myocardial recovery times for the occurrence of ventricular arrhythmias.28 29 30 31 However, the current methods of measuring the recovery time dispersion, ie, the epicardial or endocardial monophasic action potentials, and body surface mapping are not very practical in routine clinical use. QT dispersion has been shown to be a useful noninvasive method for detection of the inhomogeneity of ventricular recovery times.9 10 11 12 13 14 The present population-based cross-sectional study of hypertensive men showed that QT dispersion is increased in the patients with echocardiographic evidence of LVH compared with those without LVH. In particular, QTa dispersion had a significant positive correlation to LVMI, indicating inhomogeneity of the early phase of repolarization in relation to LVH. In previous studies, QT dispersion has been shown to be increased in patients after acute myocardial infarction12 and in patients with the long QT syndrome,32 with chronic heart failure,17 and with hypertrophic cardiomyopathy.16 In these patient populations, broad QT dispersion has also been shown to be associated with susceptibility to ventricular arrhythmias or sudden cardiac death.9 16 17 33 Although we did not assess the arrhythmic susceptibility in the patients with and without LVH, the present observations suggest that LVH is associated with increased inhomogeneity in repolarization, probably predisposing the patients to life-threatening arrhythmias.
Possible Explanations for Broad QTa Dispersion in Hypertensive Patients With LVH
Hypertensive patients with LVH showed increased QTa dispersion, but the dispersion of the QRS complex duration or of Te did not differ significantly between the patient groups, demonstrating that LVH results in more marked inhomogeneity of the plateau phase of repolarization than the downslope phase of repolarization or the depolarization phase. Myocardial hypertrophy may alter the ion channels that are operative during the early repolarization phase.34 35 36 37 Abnormalities in the potassium channels in hypertrophied myocytes have been shown to contribute to the prolongation of action potential duration.37 The present findings concur with these experimental observations in that the QTa maximum interval tended to be longer in the LVH+ patients compared with the LVH- patients. Thus, changes in potassium channels due to the hypertrophy of myocytes may partly contribute to the increased QTa dispersion.
Animal studies have also shown that ischemia shortens the refractory period in the affected area of the ventricular muscle and increases the dispersion of the recovery time in the myocardium.29 In the present study, the QTa minimum interval tended to be shorter in the LVH+ patients compared with the LVH- patients, suggesting that local ischemia of the hypertrophied ventricle may also be one potential mechanism for the increased dispersion of repolarization. Increased anisotropy and stretching of myocardial fibers may also account for the increased QTa dispersion. In contrast to the present study, the postinfarction patients with arrhythmic susceptibility also have increased Te dispersion,15 indicating that there may be differences in the substrate for reentrant ventricular tachyarrhythmias between chronically infarcted and hypertrophied hearts.
Role of the Autonomic Nervous System
Increased QT dispersion did not correlate with measures of HRV, suggesting that abnormal autonomic cardiac control is not related to repolarization abnormalities in LVH. On the other hand, an analysis of HRV may not reveal the abnormalities in autonomic control at the ventricular level. Therefore, local ventricular denervation cannot be excluded as a cause of increased dispersion of repolarization.
In previous studies of hypertensive individuals, analyses of HRV have yielded variable results.18 38 39 40 41 In subjects with mild hypertension, no significant abnormalities in the HRV measures were observed compared with healthy individuals.38 39 In comparisons between untreated patients with borderline hypertension and age-matched normotensive control subjects, Guzzetti et al40 and Dassi et al41 have shown normalized low- and high-frequency components to be higher and lower than normal, respectively, in the hypertensive group. In contrast, Chakko et al18 reported that all the power spectral components are significantly reduced and the circadian fluctuation of HRV is blunted in hypertensive subjects with evidence of LVH compared with age-matched normotensive control subjects. The present study demonstrated that reduced HRV is related to elevated blood pressure in hypertensive patients. Elevated blood pressure was most closely related to a reduced low-frequency component of HRV, which is compatible with the observations that baroreflex sensitivity is reduced in patients with hypertension.42 43 44 However, impairment of HRV was not related to LVH per se, suggesting that structural cardiac abnormalities are not significant determinants of the autonomic modulation of heart rate. In contrast, Mandawat et al45 have reported an inverse correlation between the SD of RR intervals and LVMI in a mixed population of normotensive and hypertensive subjects, but they did not adjust their results for blood pressure, which seems to be a stronger determinant of HRV than LVH in a population of hypertensive males.
Altered autonomic cardiac control is known to predispose individuals to ventricular arrhythmias in several experimental and clinical conditions.19 26 46 Increased sympathetic and/or reduced vagal tone can facilitate the arrhythmogenesis by a reentrant mechanism, triggered activity, and increased automaticity. The present observations suggest that uncontrolled hypertension may alter the autonomic modulation of heart rate and thereby predispose to arrhythmogenesis. It will be important to establish whether reduced HRV is an irreversible abnormality or whether it can be normalized by a better control of elevated blood pressure.
Methodological Considerations
There are intraobserver and interobserver variabilities in the measurements of QT interval and QT dispersion.47 48 In the present study, both intraobserver and interobserver variabilities of QTa dispersion measurements were found to be smaller compared with those of QT dispersion measurements, perhaps partly explaining the stronger relation of LVMI to QTa dispersion than QT dispersion. Furthermore, the intraobserver error for QTa dispersion measurements was found to be 3.5 milliseconds. Therefore, the broader QTa dispersion in the patients with LVH compared with the patients without hypertrophy cannot be explained by measurement variability.
Conclusions
The present study demonstrates that LVH in hypertensive patients results in inhomogeneity of repolarization, especially the early phase, favoring the propensity to ventricular tachyarrhythmias, and that reduced HRV is more closely related to elevated blood pressure than to the degree of LVH in individuals with hypertension. Some of the values of QT dispersion overlapped between the patients with and without LVH, and the correlation between repolarization inhomogeneity and LVH was relatively weak. However, one third of the patients with LVH but very few of those without LVH had abnormal QTa dispersion. Therefore, it will be important to find out in future studies whether increased QT dispersion combined with impaired HRV can specifically identify the hypertensive patients with LVH who are at high risk for life-threatening arrhythmias and sudden death. It will also be important to resolve whether repolarization inhomogeneity and abnormal cardiac autonomic function can be corrected by antihypertensive treatment aimed at reducing blood pressure and regressing LVH.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by grants from the Finnish Foundation for Cardiovascular Research and the Medical Council of the Academy of Finland, Helsinki.
Received February 6, 1996; accepted February 13, 1996.
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References |
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