Is Dispersion of Ventricular Repolarization Rate Dependent?

QT dispersion has been adopted as a new index for the noninvasive assessment of the inhomogeneity of repolarization and has been evaluated in several clinical studies as an index of arrhythmia propensity. In most of these studies, indices of dispersion of repolarization were rate corrected by the Bazett formula calculating QT dispersion as QT_cmax-QT_cmin or JT dispersion as fT_cmax-fT_cmin, implying that dispersion of repolarization also changes with heart rate. This study aimed to determine in the electrically paced isolated heart whether dispersion of ventricular repolarization is rate dependent. Multiple (5–7) monophasic action potentials (MAPs) were recorded simultaneously from the epicardium and endocardium of both ventricles in 18 isolated Langendorff-perfused rabbit hearts. Hearts were paced from a right ventricular site at basic cycle lengths (CL) between 1,200 and 300 ms in 100-ms decrements. Action potential duration was measured at 90% repolarization (APD₉₀), and recovery time (RT) was defined as the sum of APD₉₀ and activation time in each of the simultaneous MAP recordings. The dispersion of APD₉₀ ond RT, respectively, were calculated as the maximal difference among all recordings. APD₉₀ and RT shortened continuously throughout the range of paced steady-state CLs from 1,200 to 300 ms. APD₉₀ was 197.6 ± 6.1 ms at a CL of 1,200 ms and decreased to 148.5 ± 2.5 ms at a CL of 300 ms (P < 0.0001). RT was 228.2 ± 6.2 ms at a CL of 1,000 ms and decreased to 175.9 ± 2.9 at a CL of 300 ms (P < 0.0001). In contrast, dispersion of APD₉₀ and RT did not change significantly. Dispersion of APD₉₀ was 24.8 ± 2.3 ms at a CL of 1,200 ms, 26.1 ± 1.9 msec at a CL of 1,000 ms, and 21.6 ± 2.1 at a CL of 300 ms (NS). Dispersion of RT was 29.7 ± 3.4 ms at a CL of 1,200 ms, 29.0 ± 3.0 ms at a CL of 1,000 ms, and 32.7 ± 3.2 ms at a CL of 300 ms (NS). In contrast to the duration of the QT interval, dispersion of ventricular repolarization does not change significantly with pacing induced changes in CL. Assuming that the rate-dependent behavior of action potential duration is similar between the rabbit and human heart, a rate correction of parameters of dispersion of repolarization is probably unnecessary.     

Time Dependent Changes in Duration of Ventricular Repolarization After AV Node Ablation: Insights into the Possible Mechanism of Postprocedural Sudden Death

DIZON, J., et al. : Time Dependent Changes in Duration of Ventricular Repolarization After AV Node Ablation: Insights into the Possible Mechanism of Postprocedural Sudden Death. Although effective, there is a disturbing incidence of sudden death after AV node ablation. The mechanism may be related to proarrhythmia associated with prolongation in ventricular repolarization from the sudden decrease in heart rate. To examine this issue, we studied 15 patients undergoing complete radiofrequency ablation of the AV node for rapid atrial arrhythmias. Twelve‐lead ECGs of paced rhythms at rates of 60, 80, 100, and 120 beats/min were recorded at time points of 30 minutes, 24 hours, 1 week, and 1 month after ablation. The QT interval was measured in the limb and precordial leads with the best T wave offset. The change in the QT interval (ΔQT) relative to the measurement at 30‐minute postablation was calculated. For comparison, a similar procedure was performed on patients receiving pacemakers for primary bradycardia (n = 5 ). The mean QT interval at 60 beats/min, 30‐minutes postablation was significantly longer than at time points thereafter (482 ± 39 vs 446 ± 28 ms at 1 month, limb leads, for example, P < 0.05 ). Analysis of ΔQT revealed a significant shortening of the QT interval at nearly every paced rate at every time point relative to the value at 30‐minute postablation. The QT intervals shortened and stabilized after 24 hours. Neither the QT interval nor ΔQT changed significantly in patients paced for primary bradycardia. We conclude that there is a relative increase in the duration of ventricular repolarization after AV node ablation, which then decreases and stabilizes after 24 hours. Such changes are not seen in patients being paced for primary bradycardia. This data is consistent with the hypothesis that sudden death after AV node ablation may be related to proarrhythmia from prolonged ventricular repolarization.     

QT interval dispersion in ventricular beats: a noninvasive marker of susceptibility to sustained ventricular arrhythmias

Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well-established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 +/- 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 +/- 30 vs 63.0 +/- 29 ms vs 53.9 +/- 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 +/- 31 vs 42.1 +/- 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 +/- 35 vs 46.7 +/- 13 ms, P = 0.008, and QTd-paced ventricular beats: 104.8 +/- 32 vs 65.9 +/- 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.     

Transient proarrhythmic state following atrioventricular junctional radiofrequency ablation

This study was designed to prospectively assess ventricular de- and repolarization by the QRS, QT, and JT intervals, and their dispersion in the 12-lead ECG during right ventricular pacing at 60, 70, and 80 beats/min during the first month after AV junctional RF ablation. Previous reports have found early polymorphic ventricular arrhythmia after RF AV junctional ablation. Our hypothesis was that there is a proarrhythmic state following this procedure, which depends on the paced rate and time after ablation. The analysis of the immediate changes was based on 17 patients (10 men) with a mean age of 64 years (SD 14) (range 38-82 years). A 12-lead ECG was recorded during right ventricular pacing at 60, 70, and 80 beats/min within 24 hours (day 1), between 24 and 48 hours (day 2), and 1 week after ablation (day 7). For analysis of changes beyond 1 week, 13 additional patients with a mean age of 73 years (SD 8) (range 62-90 years) were analyzed on days 1, 7, and 30. All intervals were measured with a digitizing table. The mean QRS duration shortened by 2.4% at 60 beats/min (P <0.01), and the mean QT and JT intervals shortened by 5-7% between days 1 and 7 (P < 0.001). The mean QT was 9% shorter and the mean JT interval was 13% shorter at 80 compared to 60 beats/min on day 1 (P < 0.001). QT dispersion was reduced by 13% when the stimulation rate was increasedfrom 60 to 80 beats/min on day 1 (P < 0.05). There were no significant changes beyond the first week. The study results point to the induction of a proarrhythmic state immediately after AV junctional RF ablation resolving during the first week. Repolarization shortened gradually between 80 and 60 beats/min to an extent that is suggestive of a clinically important antiarrhythmic effect at the higher rate, which was supported also by clinical experience.     

Paced QT dispersion and QT morphology after radiofrequency atrioventricular junction ablation: impact of left ventricular function

Catheter ablation of the atrioventricular junction (AVJ) is a widely accepted treatment for drug refractory atrial fibrillation. Unfortunately, there have been some reports of pause dependent ventricular arrhythmias associated with QT interval prolongation, mainly in patients with reduced LV function. The present investigation evaluates the association of LV function with QT dispersion in response to a sudden rate drop. ECGs were' recorded on 20 patients (13 with normal LV function) on the day following AVJ ablation while paced at a range of ventricular rates (40-120 beats/min), and during a sudden drop from 80 to 40 beats/min. The maximum QT interval (QTmax), minimum QT interval (QTmin), and QT interval dispersion (QTdisp) were compared. In both groups, the QTmax and QTmin increased at slower paced heart rates while the QTdisp did not change. In response to a sudden rate drop from 80 to 40 beats/min, the QTmax increased in both groups of LV function (trend), while the QTmin increased in those with normal LV function (24 +/- 22 ms), but not in those with reduced LV function (0 +/- 14 ms; P = 0.01). Consequently, the QTdisp increased significantly in those with reduced LV function (31 +/- 23 ms) but not in normal LV function (-5 +/- 29 ms; P = 0.01). Morphological QTU changes developed following the sudden rate drop in 67% of the reduced LV versus 8% of the normal LV (P = 0.02) function groups. Following AVJ ablation, QTdisp increased during a sudden rate drop in patients with reduced LV function, but not in patients with normal LV function.     

Increased heterogenity of ventricular repolarization in obese nonhypertensive children

Objective: Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on ventricular repolarization, excluding the influence of possible comorbidities. The QTc dispersion (QTc‐d), JTc dispersion (JTc‐d), and transmural dispersion of repolarization (TDR) have been suggested to be electrocardiographic indexes reflecting the physiological variability of regional ventricular repolarization. The aim of our study is to define the effects of obesity on the ventricular repolarization in obese children who have no other clinically appreciable cause of heart disease. Methods: The study involved 70 subjects (48 male, 22 female), with a mean age (± standard deviation) of 13 ± 2 years. A total of 35 individuals were obese (Group A: 24 male, 11 female, mean body mass index [BMI] of 38.2 ± 5.8 kg/m²), and 35 participants were healthy lean children (Group C: 24 male, 11 female, mean BMI of 22.3 ± 0.3 kg/m²). Heart rate; QRS duration; maximum and minimum QT interval; and QTc‐d, JTc‐d, and TDR measurement were performed. Results: Compared with the healthy control group, obese children presented increased values of the QTc‐d, JTc‐d, and TDR (31.1 ± 10.6 vs 46.2 ± 15.3 ms, P < 0.003; 29.8 ± 8.5 vs 40.1 ± 10.3 ms, P < 0.04; 83.2 ± 13.5 vs 100.7 ± 16.3 ms, P < 0.05). A statistically significant correlation was found between the values of QTc‐d, insulin serum concentration (r = 0.46, P = 0.04), and homeostasis model assessment of insulin resistance (r = 0.34, P = 0.03). Conclusions: Our data suggest that obese nonhypertensive children have an increased ventricular repolarization heterogeneity in relation to controls. (PACE 2010; 33:1533–1539)     

Noninvasive Evidence of Shortened Atrial Refractoriness during Sinus Rhythm in Patients with Paroxysmal Atrial Fibrillation

Background: Shortening of the atrial refractory period is the key feature of atrial electrical remodeling during atrial fibrillation (AF). During sinus rhythm (SR), assessment of the atrial refractoriness is hampered by the fact that the atrial repolarization wave (Ta wave) is largely obscured by the following QRST complex. The purpose of this study was to study the Ta wave in subjects with paroxysmal AF during SR with third‐degree atrioventricular (AV) block, and in matched controls. Methods: Fifteen patients (mean age 70 ± 10 years, five males) with paroxysmal AF undergoing AV‐nodal ablation were studied. Fifteen age‐ and gender‐matched subjects (mean age 71 ± 9 years, five males) with third‐degree AV block, without a history of heart disease, were used as controls. Standard 12‐lead electrocardiograms (ECGs) were recorded and transformed to orthogonal leads and studied using P‐wave signal averaging technique. Results: The P to Ta interval was shorter (408 ± 47 ms vs 451 ± 53 ms, P = 0.017) and in Lead Y the Ta peak location was earlier (156 ± 31 ms vs 187 ± 34 ms, P = 0.002) in subjects with paroxysmal AF than in the controls. The P‐wave duration (126 ± 15 ms vs 129 ± 17 ms, P = 0.59) and morphology was similar in AF patients and controls. Conclusions: In this study, the ECG signs of shorter atrial refractoriness associated with a history of AF are visualized for the first time during SR. The finding of the earlier location of the PTa peak in AF subjects implies that a possible indicator of increased arrhythmia susceptibility may be visible already in the unprocessed ECG.     

Magnetocardiographic QT Interval Dispersion in Postmyocardial Infarction Patients with Sustained Ventricular Tachycardia: Validation of Automated QT Measurements

T dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum — minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QT_apex dispersions were 127 ± 26 versus 83 ± 21 ms (P = 0.004) and QT_end dispersions 130 ± 37 versus 82 ± 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QT_apex and 27% for QT_end dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

Dispersion in ventricular repolarization in patients with severe intraventricular conduction disturbances

Increased dispersion of repolarization, measured invasively or by QT interval measurements, is associated with an increased risk for ventricular arrhythmias and sudden death. Most studies on this issue have included patients with normal intraventricular conduction, and it is not known if this finding has a predictive value also in patients with intraventricular conduction disorders. An invasive electrophysiological study, including programmed ventricular stimulation and assessment of effective refractory periods at two RV sites, was performed in 103 patients with bifascicular block (mean age 67 +/- 12 years). QT dispersion was measured from standard 12-lead ECGs. In patients with inducible sustained polymorphic VT or VF the dispersion in refractoriness between the two RV sites was significantly greater (46 +/- 11 ms, n = 13) than in noninducible patients (14 +/- 14 ms, n = 84) and in patients with inducible sustained monomorphic VT (16 +/- 5 ms, n = 6) (P < 0.01). Similarly, QT dispersion was 104 +/- 46 ms, 66 +/- 31 ms, and 77 +/- 33 ms, respectively, in the three groups (P < 0.05). Dispersion in repolarization, neither measured invasively nor by QT interval measurements, predicted sudden death, all cause mortality, or ventricular arrhythmia during a mean follow-up period of 3 years. In patients with bifascicular block, there is a relation between the degree of dispersion of ventricular repolarization and the inducibility of polymorphic ventricular arrhythmia, but this outcome did not occur during follow-up.     

QT dispersion from body surface ECG does not reflect the spatial dispersion of ventricular repolarization in sheep

The correlation between the QT dispersion on body surface ECG and the dispersion in ventricular repolarization from the cardiac surface was studied in six sheep anesthetized with pentobarbital. The standard 12-lead body surface ECG and multiple ventricular epicardial ECGs were simultaneously recorded. The activation-recovery interval (ARI) was measured from the unipolar epicardial ECGs. The pooled QT dispersion from the six animals was significantly smaller than the pooled ARI dispersion (22.7 +/- 2.6 vs 33.0 +/- 6.9 ms, P < 0.01). There was no correlation between the QT and ARI dispersion. The unipolar epicardial ECGs were then converted into bipolar ECGs and epicardial QT intervals were subsequently acquired from these ECGs. The average value of epicardial QT dispersion from the six animals was similar to that of body surface ECG, but was less than the ARI dispersion (27.5 +/- 6.8 vs 33.0 +/- 6.9, P < 0.01). A good correlation between the epicardial QT dispersion and ARI dispersion was identified (r = 0.84, P < 0.05). In addition, a prolongation in ventricular repolarization, induced by an increase in coronary flow, elicited a pooled ARI dispersion of 62.3 +/- 6.2 ms (n = 6), which was larger than the simultaneously recorded body surface QT dispersion (28.3 +/- 9.8 ms, n = 6, P < 0.01). No correlation between the ARI and QT dispersion was found in the presence of the prolonged ventricular repolarization. In conclusion, QT dispersion from a 12-lead body surface ECG seems to underestimate the spatial dispersion of ventricular repolarization acquired from sheep epicardium.     

Acute effect of methylphenidate on QT interval duration and dispersion in children with attention deficit hyperactivity disorder

Among childhood psychiatric disorders, attention deficit hyperactivity disorder (ADHD) is of greatest interest to practitioners. Methylphenidate (MPH) is a drug that is widely used in the treatment of children in whom ADHD has been diagnosed. Although this treatment has been used for years, its effects on the heart remain the subject of debate. The QT interval comprises the ventricular activation and recovery periods as seen on electrocardiogram (ECG). The acute effect of MPH on QT interval dispersion is unknown. Researchers in the present study sought to investigate the acute effects of MPH on QT interval as seen on ECG. A total of 25 patients with ADHD (mean age, 9.4±2.1 y) who were treated with MPH were enrolled in the study. Twelve-lead derivation ECGs were taken before and 2 h after administration of 10 mg of MPH. Maximum QT interval, minimum QT interval, and interval durations were measured, and QT dispersion was calculated, for each ECG. QT dispersion measured after medication administration decreased significantly from 59.6±16.3 ms to 50.8±10.9 ms (P=.016); corrected QT dispersion decreased significantly from 70.9±17.6 ms to 61.3±13.3 ms (P=.011). Maximum QT interval duration decreased from 373.7±21.8 ms to 361.8±29.0 ms (P=.006); minimum QT interval duration rose from 317.0±23.3 ms to 322.3±21.6 ms (P=.312). In conclusion, the findings of this study show that MPH reduces QT dispersion during the acute period shortly after its administration.     

The Ventricular Paced QT Interval—The Effects of Rate and Exercise

Changes in the QT and QTc intervals in 19 patients were studied at a ventricular paced rate difference of 50 beats/min. In all patients the measured QT interval shortened as the pacing rate was increased, from a mean value of 441 ms to 380 ms (p < 0.001), but when correct ed for heart rate the QTc- lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT in terval was measured at rest and immediately following exercise sufficient to increase the atrial rate by approximately 50 beats/min at identical ventricular paced rates. In all patients exercise-induced QT interval shortening from a mean value of 433 ms to 399 ms (p < 0.001). These results show first that Bazett's formula is unsuitable for correction of QT interval changes induced by ventricular pacing, and second that heart rate and changes in sympathetic tone independently influence the duration of the QT interval. It is suggested that these resuits are relevant to the design of physiological pacemakers in which the duration of the QT interval influences the discharge frequency of the pacemaker and to the consideration of ventricular pacing for the treatment of abnormal repolarization syndromes. (PACE, Vol. 5, May-June, 1982)     

Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

BARANOWSKI, R., et al .: Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy. This study examined ventricular repolarization before the onset of 37 episodes of nonsustained ventricular tachycardia (NSVT) in 26 untreated patients with hypertrophic cardiomyopathy (HCM). Fourteen episodes were recorded in patients with a history of cardiac arrest or patients who died suddenly during follow-up. The QT interval was measured beat-by-beat on 24-hour ambulatory electrocardiograms. Mean 24-hour, hourly QTc and QTc of the last 10 beats prior to NSVT, consisted of 4–50 cycles (mean   9 ± 10   ), at the fastest rates of 100–175 beats/min (mean 122 ± 22) were analyzed. NSVT was more prevalent during nighttime (23 episodes), than during daytime (14 episodes,   P < 0.05   ). No significant differences were observed between mean 24-hour, mean hourly QTc during the hour with NSVT, and QTc of the last 10 cycles prior to onset of NSVT. QTc was significantly longer in patients with a history of sudden cardiac death (SCD) or who died suddenly during follow-up than in survivors. The 24-hour QT variability was higher in nonsurvivors than in survivors (   -39 ± 6   vs   33 ± 6 ms, P = 0.03   ). Episodes of NSVT in untreated patients with hypertrophic cardiomyopathy were more frequent during the nighttime. The 24-hour QT variability was higher in nonsurvivors than in survivors. (PACE 2003; 26[Pt. II]:387–389)     

Interatrial conduction correlates with optimal atrioventricular timing in cardiac resynchronization therapy devices

Background: Echocardiographic optimization of the atrioventricular delay (AV) may result in improvement in cardiac resynchronization therapy (CRT) outcome. Optimal AV has been shown to correlate with interatrial conduction time (IACT) during right atrial pacing. This study aimed to prospectively validate the correlation at different paced heart rates and examine it during sinus rhythm (Sinus). Methods: An electrophysiology catheter was placed in the coronary sinus (CS) during CRT implant (n = 33). IACT was measured during Sinus and atrial pacing at 5 beats per minute (bpm) and 20 bpm above the sinus rate as the interval from atrial sensing or pacing to the beginning of the left atrial activation in the CS electrogram. P‐wave duration (PWd) was measured from 12‐lead surface electrocardiogram, and the interval from the right atrial to intrinsic right ventricular activation (RA‐RV) was measured from device electrograms. Within 3 weeks after the implant patients underwent echocardiographic optimization of the sensed and paced AVs by the mitral inflow method. Results: Optimal sensed and paced AVs were 129 ± 19 ms and 175 ± 24 ms, respectively, and correlated with IACT during Sinus (R = 0.76, P < 0.0001) and atrial pacing (R = 0.75, P < 0.0001), respectively. They also moderately correlated with PWd (R = 0.60, P = 0.0003 during Sinus and R = 0.66, P < 0.0001 during atrial pacing) and RA‐RV interval (R = 0.47, P = 0.009 during Sinus and R = 0.66, P < 0.0001 during atrial pacing). The electrical intervals were prolonged by the increased atrial pacing rate. Conclusion: IACT is a critical determinant of the optimal AV for CRT programming. Heart rate‐dependent AV shortening may not be appropriate for CRT patients during atrial pacing. (PACE 2011; 34:443–449)     

Circadian Profile of QT Interval and QT Interval Variability in 172 Healthy Volunteers

BONNEMEIER, H., et al .: Circadian Profile of QT Interval and QT Interval Variability in 172 Healthy Volunteers. The limited prognostic value of QT dispersion has been demonstrated in recent studies. However, longitudinal data on physiological variations of QT interval and the influence of aging and sex are few. This analysis included 172 healthy subjects (89 women, 83 men; mean age   38.7 ± 15   years). Beat-to-beat QT interval duration (QT, QTapex [QTa], T_end[Te]), variability (QTSD, QTaSD), and the mean R-R interval were determined from 24-hour ambulatory electrocardiograms after exclusion of artifacts and premature beats. All volunteers were fully active, awoke at approximately 7:00 am , and had 6–8 hours of sleep. QT and R-R intervals revealed a characteristic day-night-pattern. Diurnal profiles of QT interval variability exhibited a significant increase in the morning hours (6–9 am ; P < 0.01) and a consecutive decline to baseline levels. In female subjects the R-R and T_end intervals were significantly lower at day- and nighttime. Aging was associated with an increase of QT interval mainly at daytime and a significant shift of the T wave apex towards the end of the T wave. The circadian profile of ventricular repolarization is strongly related to the mean R-R interval, however, there are significant alterations mainly at daytime with normal aging. Furthermore, the diurnal course of the QT interval variability strongly suggests that it is related to cardiac sympathetic activity and to the reported diurnal pattern of malignant ventricular arrhythmias. (PACE 2003; 26[Pt. II]):377–382)     

AV interval optimization using pressure volume loops in dual chamber pacemaker patients with maintained systolic left ventricular function

Background

Atrioventricular (AV) interval optimization is often deemed too time-consuming in dual-chamber pacemaker patients with maintained LV function. Thus the majority of patients are left at their default AV interval.

Objective

To quantify the magnitude of hemodynamic improvement following AV interval optimization in chronically paced dual chamber pacemaker patients.

Patients and methods

A pressure volume catheter was placed in the left ventricle of 19 patients with chronic dual chamber pacing and an ejection fraction >45?% undergoing elective coronary angiography. AV interval was varied in 10?ms steps from 80 to 300?ms, and pressure volume loops were recorded during breath hold.

Results

The average optimal AV interval was 152?±?39?ms compared to 155?±?8?ms for the average default AV interval (range 100–240?ms). The average improvement in stroke work following AV interval optimization was 935?±?760?mmHg/ml (range 0–2,908; p?p?=?0.01).

Conclusion

The overall hemodynamic effect of AV interval optimization in patients with maintained LV function is in the same range as for patients undergoing cardiac resynchronization therapy for several parameters. The positive effect of AV interval optimization also applies to patients who have been chronically paced for years.     

窦性心动过缓患者阿托品试验前后QTd变化

目的　探讨迷走神经对QT间期离散度的影响。方法　观察 12 2例窦性心动过缓者阿托品试验前后QTd和QTcd的变化。结果　注射阿托品后 3分钟内单纯窦性心动过缓组QTd和QTcd虽然缩短 ( 19.72± 12 .82ms对 2 5 .99± 10 .33ms ;17.5 4± 10 .18ms对 2 2 .84± 11.34ms) ,但无统计学差异 (P >0 .0 5 ) ;急性胆囊炎组明显缩短 ( 16 .6 6± 10 .0 0ms对2 8.89± 13.33ms ,P <0 .0 5 ;15 .0 9± 11.18ms对 2 4.35± 8.92ms ,P <0 .0 1) ;胆囊炎并缺血性心脏病组则显著延长 ( 6 6 .9± 14 .18ms对 2 9.78± 12 .5 4ms ;6 4.2 1± 15 .0 6ms对 2 6 .10± 10 .10ms ,P <0 .0 5 )。结论　提示迷走神经兴奋对缺血性心肌具有保护作用。     

Distinct impacts of heart rate and right atrial‐pacing on left atrial mechanical activation and optimal AV delay in CRT

1 Background

Controversy exists regarding how atrial activation mode and heart rate affect optimal atrioventricular (AV) delay in cardiac resynchronization therapy. We studied these questions using high‐reproducibility hemodynamic and echocardiographic measurements.

2 Methods

Twenty patients were hemodynamically optimized using noninvasive beat‐to‐beat blood pressure at rest (62 ± 11 beats/min), during exercise (80 ± 6 beats/min), and at three atrially paced rates: 5, 25, and 45 beats/min above rest, denoted as A_paced,r+5, A_paced,r+25, and A_paced,r+45, respectively. Left atrial myocardial motion and transmitral flow were timed echocardiographically.

3 Results

During atrial sensing, raising heart rate shortened optimal AV delay by 25 ± 6 ms (P < 0.001). During atrial pacing, raising heart rate from A_paced,r+5 to A_paced,r+25 shortened it by 16 ± 6 ms; A_paced,r+45 shortened it 17 ± 6 ms further (P < 0.001). In comparison to atrial‐sensed activation, atrial pacing lengthened optimal AV delay by 76 ± 6 ms (P < 0.0001) at rest, and at ～20 beats/min faster, by 85 ± 7 ms (P < 0.0001), 9 ± 4 ms more (P  =  0.017). Mechanically, atrial pacing delayed left atrial contraction by 63 ± 5 ms at rest and by 73 ± 5 ms (i.e., by 10 ± 5 ms more, P < 0.05) at ～20 beats/min faster. Raising atrial rate by exercise advanced left atrial contraction by 7 ± 2 ms (P  =  0.001). Raising it by atrial pacing did not (P  =  0.2).

4 Conclusions

Hemodynamic optimal AV delay shortens with elevation of heart rate. It lengthens on switching from atrial‐sensed to atrial‐paced at the same rate, and echocardiography shows this sensed‐paced difference in optima results from a sensed‐paced difference in atrial electromechanical delay. The reason for the widening of the sensed‐paced difference in AV optimum may be physiological stimuli (e.g., adrenergic drive) advancing left atrial contraction during exercise but not with fast atrial pacing.     

New Insight into Repolarization Abnormalities in Patients with Congenital Long QT Syndrome: the Increased Transmural Dispersion of Repoiarization

There is evidence from experimental studies that the time interval from the peak to the end of T-wave reflects the transmural dispersion in repolarization (electrical gradient) between myocardial "layers" (epicardial, M-cells, endocardial). Since Congenital Long QT Syndrome (LQTS) is considered to be classical disease or repolarisation abnormalities, we performed the present study to assess the transmtiral dispersion of repolarization in LQTS patients. The study group consisted of 17 patients: 7 LQTS pts and 10 pts from the control group. In each patient the 24-hour ECG recording was performed on magnetic tape. The interval from the peak to the end of the T-wave (TpTo) was automatically measured by Holter system during every hour as a measure of transmural dispersion of repolarisation. Thereafter the mean TpTo from 24-hours was calculated. In addition the spatial QT dispersion was measured from 12 lead ECG and 3 channel Holter tape as a difference between the shortest and the longest QT interval between leads. The values were compared between groups using the Anova test.
TpTo was 79,6±9,6 ms (72–92 ms) in LQTS group and 62,4±7,5 ms (51–70) in the control group (p< 0.001). In LQTS group TpTo was significantly longer at night hours 72,5±2 when compared to day hours 87,4±8 (p<0.01). The spatial QT dispersion was significantly higher in LQTS patients when compared to control, both in 12-lead standard and Holter ECG.
Congenital long QT syndrome is associated with increase in both transmural and spatial dispersion of repolarization. The extent of prolongation of the terminal portion of QT in patients with congenital long QT syndrome is greater at night sleep hours compared to daily activity.     

QTc Dispersion in Hyperthyroidism and Its Association with Pulmonary Hypertension

Background: Several studies have reported that hyperthyroidism is associated with prolonged QT interval corrected by the heart rate (QTc) and pulmonary hypertension (PHT). Methods: Forty‐seven patients with newly diagnosed overt hyperthyroidism and 20 healthy people were enrolled in the study. Transthoracic echocardiography, 12‐lead surface electrocardiogram, and thyroid hormone levels were studied at the time of enrollment and after achievement of euthyroid state with propylthiouracil treatment. Results: Baseline clinical characteristics were similar. However, heart rate (90.5±19.6 vs 79.2±13.7 bpm, P = 0.024), pulmonary artery systolic pressure (PASP) (26.0±12.0 vs 10.6±4.0 mmHg, P < 0.001), E deceleration time (DT) (191.8±25.6 vs 177.0±10.7 ms, P = 0.016), isovolumetric relaxation time (IVRT) (91.38±12.3 vs 79.6±10.5 ms, P < 0.001), and QTc dispersion (QTcD) (50.3±17.2 vs 38.9±11.6 ms, P = 0.009) were significantly higher in hyperthyroid patients compared to control group. Heart rate (to 74.1±13.8, P < 0.001), QTcD (to 37.3±10.1 ms, P < 0.001), DT (to 185.3±19.7 ms, P = 0.008), IVRT (to 88.6±10.3 ms, P = 0.056), and PASP (23.1±10.1 mmHg P < 0.001) were significantly decreased after achievement of euthyroid state. Although PHT was present in 16 patients before treatment only six patients still had PHT during euyhyroid state. Compared to patients with normal PASP, QTcD was significantly longer in patients with PHT (56.5±15.8 vs 37.9±12.8 mmHg P < 0.001). There were also significant correlations between QTcD and presence of PHT (r = 0.516, P < 0.001) and PASP (r = 0.401, P = 0.009). Conclusions: Hyperthyroidism is a reversible cause of PHT and diastolic dysfunction. Increased QTcD observed in hyperthyroidism may be associated with PHT and diastolic dysfunction. These abnormal findings in hyperthyroidism often normalize with the achievement of euthyroid state.