Spatiotemporal repolarization dispersion before and after exercise in patients with long QT syndrome type 1 versus controls: probing into the arrhythmia substrate.

Congenital long QT syndrome (LQTS) carries an increased risk for syncope and sudden death. QT prolongation promotes ventricular extrasystoles, which, in the presence of an arrhythmia substrate, might trigger ventricular tachycardia degenerating into fibrillation. Increased electrical heterogeneity (dispersion) is the suggested arrhythmia substrate in LQTS. In the most common subtype LQT1, physical exercise predisposes for arrhythmia and spatiotemporal dispersion was therefore studied in this context. Thirty-seven patients (57% on ß-blockers) and 37 healthy controls (mean age, 31 vs. 35; range, 6-68 vs. 6-72 yr) performed an exercise test. Frank vectorcardiography was used to assess spatiotemporal dispersion as Tampl, Tarea, the ventricular gradient (VG), and the Tpeak-end interval from 10-s signal averages before and 7 ± 2 min after exercise; during exercise too much signal disturbance excluded analysis. Baseline and maximum heart rates as well as estimated exercise intensity were similar, but heart rate recovery was slower in patients. At baseline, QT and heart rate-corrected QT (QTcB) were significantly longer in patients (as expected), whereas dispersion parameters were numerically larger in controls. After exercise, QTpeakcB and Tpeak-endcB increased significantly more in patients (18 ± 23 vs. 7 ± 10 ms and 12 ± 17 vs. 2 ± 6 ms; P < 0.001 and P < 0.01). There was, however, no difference in the change in Tampl, Tarea, and VG between groups. In conclusion, although temporal dispersion of repolarization increased significantly more after exercise in patients with LQT1, there were no signs of exercise-induced increase in global dispersion of action potential duration and morphology. The arrhythmia substrate/mechanism in LQT1 warrants further study.NEW & NOTEWORTHY Physical activity increases the risk for life-threatening arrhythmias in LQTS type 1 (LQT1). The arrhythmia substrate is presumably altered electrical heterogeneity (a.k.a. dispersion). Spatiotemporal dispersion parameters were therefore compared before and after exercise in patients versus healthy controls using Frank vectorcardiography, a novelty. Physical exercise prolonged the time between the earliest and latest complete repolarization in patients versus controls, but did not increase parameters reflecting global dispersion of action potential duration and morphology, another novelty.

Accelerated QT adaptation following atropine-induced heart rate increase in LQT1 patients versus healthy controls: A sign of disturbed hysteresis.

Hysteresis, a ubiquitous regulatory phenomenon, is a salient feature of the adaptation of ventricular repolarization duration to heart rate (HR) change. We therefore compared the QT interval adaptation to rapid HR increase in patients with the long QT syndrome type 1 (LQT1) versus healthy controls because LQT1 is caused by loss-of-function mutations affecting the repolarizing potassium channel current IKs , presumably an important player in QT hysteresis. The study was performed in an outpatient hospital setting. HR was increased in LQT1 patients and controls by administering an intravenous bolus of atropine (0.04 mg/kg body weight) for 30 s. RR and QT intervals were recorded by continuous Frank vectorcardiography. Atropine induced transient expected side effects but no adverse arrhythmias. There was no difference in HR response (RR intervals) to atropine between the groups. Although atropine-induced ΔQT was 48% greater in 18 LQT1 patients than in 28 controls (p < 0.001), QT adaptation was on average 25% faster in LQT1 patients (measured as the time constant τ for the mono-exponential function and the time for 90% of ΔQT; p < 0.01); however, there was some overlap between the groups, possibly a beta-blocker effect. The shorter QT adaptation time to atropine-induced HR increase in LQT1 patients on the group level corroborates the importance of IKs in QT adaptation hysteresis in humans and shows that LQT1 patients have a disturbed ultra-rapid cardiac memory. On the individual level, the QT adaptation time possibly reflects the effect-size of the loss-of-function mutation, but its clinical implications need to be shown.

Noninvasive electrophysiological differences between women and men: differences in body size not an explanation.

There are numerous sex-related differences in cardiac electrophysiology and arrhythmia propensity but very little knowledge about the reasons. Difference in body size has been proposed as one reason and was tested in this study of >20 cardiac electrophysiology parameters in 319 (158 women) apparently healthy 50- to 64-yr-old subjects from a randomly enrolled population sample, the pilot SCAPIS (Swedish Cardiopulmonary Bioimaging Study), using Frank vectorcardiography. We studied conventional conduction intervals, parameters reflecting electrical heterogeneity (dispersion) in the ventricles, QRS- and T-vector directions, spatial QRS-T angles, and T-vector loop morphology. Body surface area (BSA; 2 methods) and lean body mass (LBM), both estimated from body weight and height, were used as body size parameters. According to multivariable linear regression analysis adjusted for sex, there was no association between electrophysiological parameters and body size apart from QRS duration and QRSarea. In conclusion, most electrophysiological parameters assessed completely noninvasively and showing statistically significant differences between women and men on the group level show no association with BSA or LBM. Scaling (indexing) the electrophysiological parameters for body size parameters is therefore not an option. Consequently, the explanation for the sex-related electrophysiological differences should be sought along other lines.NEW & NOTEWORTHY We sought explanations for sex-related differences in >20 cardiac electrophysiology parameters including conventional conduction intervals in 319 (158 women) apparently healthy 50- to 64-yr-old subjects using Frank vectorcardiography, a novelty. Our hypothesis that body size was partly explanatory for such differences had to be refuted apart from QRS duration and QRSarea. Scaling (indexing) electrophysiological parameters for body size is therefore not an option and explanations for electrophysiological sex-related differences are to be sought elsewhere.

Adaptation of ventricular repolarization dispersion during heart rate increase in humans: A roller coaster process.

BACKGROUND: Regional differences in ventricular activation sequence and action potential duration and morphology result in dispersion in ventricular repolarization (VR). VR dispersion is a key factor in arrhythmogenesis. We studied the adaptation of global VR dispersion in humans during normal and abnormal ventricular activation, and the relation to the QT adaptation (hysteresis). METHODS: We measured global VR dispersion as T amplitude, T area, and ventricular gradient (VG), using continuous Frank vectorcardiography, in response to abrupt and sustained atrial (AP) or ventricular pacing (VP) aiming at 120 bpm, in 21 subjects with permanent pacemakers. RESULTS: Following pacing start, VR adaptation showed an initially rapid and complex tri-phasic pattern, most pronounced for T amplitude. There were major differences in the patterns of VR dispersion adaptation following abrupt AP vs VP, confirming that the adaptation pattern is activation dependent. In response to AP, an instantaneous decrease in VR dispersion occurred, followed by an increase and then a slow decrease, all at a lower level than baseline. In contrast, following VP there was an immediate increase to ~4× baseline in T amplitude and T area (but not in VG), with a subsequent biphasic adaptation lasting longer during VP than AP. The initial rapid changes occurred within the time for QT adaptation to reach steady-state. CONCLUSIONS: Our results corroborate and expand data from animal and invasive human studies, showing similarities of the adaptation pattern on different scales. The initial rapidly changing VR adaptation phase presumably reflects a window of increased vulnerability to arrhythmias.

Adaptation of ventricular repolarization time following abrupt changes in heart rate: comparisons and reproducibility of repeated atrial and ventricular pacing.

Adequate adaptation of ventricular repolarization (VR) duration to changes in heart rate (HR) is important for cardiac electromechanical function and electrical stability. We studied the QT and QTpeak adaptation in response to abrupt start and stop of atrial and ventricular pacing on two occasions with an interval of at least 1 mo in 25 study subjects with permanent pacemakers. Frank vectorcardiography was used for data collection. Atrial or ventricular pacing was performed for 8 min aiming at a cycle length (CL) of 500 ms. We measured the immediate response (IR), the time constant (τ) of the exponential phase, and T90 End, the time to reach 90% change of QT and QTpeak from baseline to steady state during and after pacing. During atrial pacing, the CL decreased on average 45% from mean (SD) 944 (120) to 518 (46) ms and QT decreased on average 18% from 388 (20) to 318 (17) ms. For QT, T90 End was 103 (24) s and 126 (15) s after start versus stop of atrial pacing; a difference of 24 (27) s (P = 0.006). The response pattern was similar for τ but IR did not differ significantly between pacing start and stop. The response pattern was similar for QTpeak and also for QT and QTpeak following ventricular pacing start and stop. The coefficients of variation for repeated measures were 7%-21% for T90 End and τ. In conclusion, the adaptation of VR duration was significantly more rapid following increasing than decreasing HR and intraindividually a relatively reproducible process.NEW & NOTEWORTHY We studied the duration of ventricular repolarization (VR) adaptation and its hysteresis, following increasing and decreasing heart rate by abrupt start and stop of 8-min atrial or ventricular pacing in study subjects with permanent pacemakers and repeated the protocol with ≥1 mo interval, a novel approach. VR adaptation was significantly longer following decreasing than increasing heart rate corroborating previous observations. Furthermore, VR adaptation was intraindividually a reproducible and, hence, robust phenomenon, a novel finding.

Automatic identification of a stable QRST complex for non-invasive evaluation of human cardiac electrophysiology.

BACKGROUND: A vectorcardiography approach to electrocardiology contributes to the non-invasive assessment of electrical heterogeneity in the ventricles of the heart and to risk stratification for cardiac events including sudden cardiac death. The aim of this study was to develop an automatic method that identifies a representative QRST complex (QRSonset to Tend) from a Frank vectorcardiogram (VCG). This method should provide reliable measurements of morphological VCG parameters and signal when such measurements required manual scrutiny. METHODS: Frank VCG was recorded in a population-based sample of 1094 participants (550 women) 50-65 years old as part of the Swedish CArdioPulmonary bioImage Study (SCAPIS) pilot. Standardized supine rest allowing heart rate stabilization and adaptation of ventricular repolarization preceded a recording period lasting ≥5 minutes. In the Frank VCG a recording segment during steady-state conditions and with good signal quality was selected based on QRST variability. In this segment a representative signal-averaged QRST complex from cardiac cycles during 10s was selected. Twenty-eight morphological parameters were calculated including both conventional conduction intervals and VCG-derived parameters. The reliability and reproducibility of these parameters were evaluated when using completely automatic and automatic but manually edited annotation points. RESULTS: In 1080 participants (98.7%) our automatic method reliably selected a representative QRST complex where its instability measure effectively identified signal variability due to both external disturbances ("noise") and physiologic and pathophysiologic variability, such as e.g. sinus arrhythmia and atrial fibrillation. There were significant sex-related differences in 24 of 28 VCG parameters. Some VCG parameters were insensitive to the instability value, while others were moderately sensitive. CONCLUSION: We developed an automatic process for identification of a signal-averaged QRST complex suitable for morphologic measurements which worked reliably in 99% of participants. This process is applicable for all non-invasive analyses of cardiac electrophysiology including risk stratification for cardiac death based on such measurements.

Spatial peak and mean QRS-T angles: A comparison of similar but different emerging risk factors for cardiac death.

BACKGROUND: The spatial peak and mean QRS-T angles are scientifically but not clinically established risk factors for cardiovascular events including cardiac death. The study aims were to compare these angles, assess their association with hypertension (HT) and diabetes mellitus (DM), and explore the relation between the mean QRS-T angle and the ventricular gradient (VG; reflecting electrical heterogeneity), which both are derived from the QRSarea and Tarea vectors. METHODS: Altogether 1094 participants (aged 50-65 years, 550 women) from the pilot of the population-based Swedish CArdioPulmonary bioImage Study with Frank vectorcardiographic recordings were included and divided into 5 subgroups: apparently healthy n = 320; HT n = 311; DM n = 33; DM + HT n = 53; miscellaneous conditions n = 377. Abnormal peak and mean QRS-T angles were defined as >95th percentile. RESULTS: Peak QRS-T angles were generally narrower than the mean QRS-T angles; both were narrower in women than in men. Abnormal peak (>124°) and/or mean (>119°) QRS-T angles were found in 73 participants (6.7%). The concordance regarding abnormal versus normal-borderline QRS-T angles was good (Cohen's kappa 0.61). The prevalence of abnormal angles varied from 2.5% in healthy to 21.2% in DM. There was an inverse logarithmical relation between the mean QRS-T angle and the VG. CONCLUSIONS: The peak and mean QRS-T angles are not interchangeable but complementary. DM, HT, sex and absence of disease are important determinants of both QRS-T angles. The mean QRS-T angle and the VG relationship is complex. All three VCG derived measures reflect related but differing electrophysiological properties and have potential prognostic value vis-à-vis cardiovascular events.

Adaptation of ventricular repolarization duration and dispersion during changes in heart rate induced by atrial stimulation.

BACKGROUND: The duration of ventricular repolarization (VR) and its spatial and temporal heterogeneity are central elements in arrhythmogenesis. We studied the adaptation of VR duration and dispersion and their relationship in healthy human subjects during atrial pacing. METHODS: Patients 20-50 years of age who were scheduled for ablation of supraventricular tachycardia without preexcitation but otherwise healthy were eligible. Vectorcardiography recordings with Frank leads were used for data collection. Incremental atrial pacing from a coronary sinus electrode was performed by decrements of 10ms/cycle from just above sinus rate, and then kept at a fixed heart rate (HR) just below the Wenckebach rate for ≥5min and then stopped. VR duration was measured as QT and VR dispersion as T area, T amplitude and ventricular gradient. The primary measure (T90 End) was the time to reach 90% change from baseline to the steady state value during and after pacing. RESULTS: A complete study protocol was accomplished in 9 individuals (6 women). VR duration displayed a monophasic adaptation during HR acceleration lasting on average 20s. The median (Q1-Q3) T90 End for QT was 85s (51-104), a delay by a factor >4. All dispersion measures displayed a tri-phasic response pattern during HR acceleration and T90 End was 3-5 times shorter than for VR duration. CONCLUSIONS: Even during close to "physiological" conditions, complex and differing response patterns in VR duration and dispersion measures followed changes in HR. Extended knowledge about these responses in disease conditions might assist in risk evaluation and finding therapeutic alternatives.

Ventricular repolarization duration and dispersion adaptation after atropine induced rapid heart rate increase in healthy adults.

BACKGROUND: Proper adaptation of ventricular repolarization (VR) to rapid heart rate (HR) increase is crucial for cardiac electro-mechanical function. The pattern and temporal aspects of this adaptation and its components (duration and dispersion) during normal conduction are, however, incompletely known in humans and were the topic of this study. METHODS & RESULTS: The VR duration (QT & QTpeak) and dispersion (Tamplitude, Tarea & ventricular gradient; VG) responses were studied by continuous vectorcardiogram after a bolus injection of atropine 0.04mg/kg b.w. in 31 healthy young adults (16 men). The primary measure (T90 End) was the time to reach 90% change from baseline to end value 300s later. Mean (SD) of T90 End was 23 (9) s for a 41% RR decrease, 130 (35) s for a 16% QTend decrease and 110 (36) s for a 19% QTpeak decrease; the response was single-exponential for these measures. For 35-43% decreases of Tamplitude, Tarea & VG, mean (SD) of T90 End were 21 (10), 38 (20) and 40 (23) s and the response pattern was double-exponential with varying overshoot. CONCLUSIONS: VR duration and dispersion responses to a very rapid HR increase during normal conduction differed substantially. In contrast to the well-known single-exponential delay in VR duration adaptation the responses of VR dispersion measures were double-exponential and much more rapid. We describe a new and completely non-invasive phenotypic characterization of different components of VR adaptation.

Instability of repolarization in LQTS mutation carriers compared to healthy control subjects assessed by vectorcardiography.

BACKGROUND: Potassium channel dysfunction in congenital and acquired forms of long QT syndrome types 1 and 2 (LQT1 and LQT2) increases the beat-to-beat variability of the QT interval. OBJECTIVE: To study about the little known variability (instability) of other aspects of ventricular repolarization (VR) in humans by using vectorcardiography. METHODS: Beat-to-beat analysis was performed regarding vectorcardiography derived RR, QRS, and QT intervals, as well as T vector- and T vector loop-based parameters during 1-minute recordings of uninterrupted sinus rhythm at rest in 41 adult LQT1 (n = 31) and LQT2 (n = 10) mutation carriers and 41 age- and sex-matched control subjects. The short-term variability for each parameter, describing the mean orthogonal distance to the line of identity on the Poincaré plot, was calculated. RESULTS: Mutation carriers showed significantly larger (by a factor 2) instability in most VR parameters compared to controls despite higher instantaneous heart rate variability (STVRR) in the control group. The longer the QT interval, the greater was its instability, and the instability of VR dispersion measures. CONCLUSIONS: A greater instability of most aspects of VR already at rest seems to be a salient feature in both LQT1 and LQT2, which might pave the way for early afterdepolarizations and torsades de pointes ventricular tachycardia. In contrast, no signs of increased VR dispersion per se were observed in mutation carriers.

Vectorcardiography shows cardiac memory and repolarization heterogeneity after ablation of accessory pathways not apparent on ECG.

BACKGROUND: Pacing induced cardiac memory is an established phenomenon, but following successful WPW ablation, cardiac memory was present on ECG in variable proportions of patients depending on accessory pathway (AP) location. We hypothesized that vectorcardiography (VCG), which is more sensitive than ECG, would show cardiac memory after WPW ablation independent of AP location. METHODS: Thirty-six patients were followed after successful AP ablation, 11 with overt posteroseptal (PS), 13 with overt left-sided (LS) and 12 with concealed APs (controls). VCGs were recorded the day before and after the procedure, ≥ once/week for 6-8 weeks and after ≥ 3 months. T vector and T-vector loop parameters were analyzed and compared. RESULTS: After ablation of overt APs, there was a correlation between the directions of the preexcited maximum QRS-vector and the post-ablation maximum T-vector, confirming the presence of cardiac memory. Ablation of overt APs was followed by cardiac memory apparent in different directions. Thus, ablation of PS APs was followed by most pronounced changes in T-vector elevation and LS APs with significant changes only in T-vector azimuth. Cardiac memory disappeared within a month in > 80% of cases. Furthermore, T-vector loop morphology changes suggested a period of repolarization heterogeneity immediately after ablation of overt APs. CONCLUSIONS: According to VCG analysis cardiac memory was present after ablation of overt APs independent of location as consistently as after ventricular pacing, and disappeared within a similar time frame during normal ventricular activation. In addition, signs of transient repolarization heterogeneity were observed after ablation of overt APs.

Maximal aerobic power versus performance in two aerobic endurance tests among young and old adults.

BACKGROUND: Aerobic fitness is of great value for reducing risk of mortality and cardiovascular diseases. OBJECTIVE: This study evaluated the performance in and correlations between a new test (five-minute pyramid test, 5MPT), the six-minute walk-test (6MWT) and maximal oxygen uptake (VO2max) among old and young adults. METHODS: Forty-four habitually active adults (females and males), 23 old (64-79 years) and 21 young (20-32 years) participated. In the 5MPT, the participants moved back and forth along a short walkway (5.5 m) over boxes (height: 'old people' 0.42 m, 'young people' 0.62 m) arranged like an elongated step pyramid for 5 min. Power in the pyramid test (5MPT(power)) was calculated as the product of numbers of laps, body weight, gravity and highest box level divided by time. A 6MWT and a maximal cycle ergometer test for direct measurements of VO2max were also performed. In all tests heart rate, with on-line electrocardiography, and perceived exertion were recorded. RESULTS: There was a strong correlation between the 5MPT(power) and VO2max for the entire group studied (r = 0.98), and each of the four subgroups old and young females and males separately (r = 0.78-0.98). Contrary to several earlier studies, especially involving people with various diseases, the present data showed that 6MWT cannot be used to predict VO2max among old females and young adults. The correlation with VO2max was weaker for the 6MWT than for the 5MPT(power). The relative performance values for the old compared to the young (ratio old/young × 100) were considerably lower in 5MPT(power) and VO2max (47-55%) than in distance and 'work' in the 6MWT (82-86%). CONCLUSIONS: The results, with age and gender variations, can be valuable information in health-fitness contexts, since measuring physical aerobic capacity is very significant in connection with risk evaluations of mortality and various diseases. The 5MPT is a rapid, functional, easy and inexpensive tool for predicting assessed maximal aerobic power.

Ischemia-induced repolarization response in relation to the size and location of the ischemic myocardium during short-lasting coronary occlusion in humans.

BACKGROUND: The ventricular repolarization (VR) response to short-lasting coronary occlusion has been characterized by 3-dimensional vectorcardiography (VCG) in humans; the T vector loop becomes distorted and more circular. The purpose of this study was to relate these changes to the size of the myocardium at risk (MAR) and its location. METHODS: Continuous VCG was applied during transient coronary occlusion in 35 elective angioplasty patients, and the size of the MAR was estimated by single-photon emission computed tomography. Three VR aspects were assessed at baseline vs maximum ischemia: the ST segment, the T vector angles, and the T vector loop morphology. RESULTS: The T loop morphology changes were significantly associated with MAR size, but also dependent of its location. In contrast, the early phase of VR reflected by the ST segment responded to acute ischemia in relation to the MAR size independent of location. CONCLUSION: The VR changes were related both to the size and the location of the MAR and most pronounced during occlusion of the left anterior descending artery.

Right ventricular pacing-induced electrophysiological remodeling in the human heart and its relationship to cardiac memory.

BACKGROUND: Right ventricular apical (RVA) pacing induces electrophysiological and structural remodeling. Cardiac memory (CM) evolves during the course of pacing and is readily apparent on electrocardiography (ECG) or vectorcardiography (VCG) when normal ventricular activation resumes. OBJECTIVE: This study sought to assess ventricular repolarization (VR) changes during pacing and intermittent normal ventricular conduction by ECG and VCG and to determine the temporal and conformational evolution of CM. METHODS: Twenty sick sinus patients received a dual-chamber rate-adaptive (DDD-R) pacemaker and were paced from the RVA endocardium. The pacemakers were programmed to a short AV delay to maximize ventricular preexcitation. The ECG and VCG were recorded before and 1 day after implantation, and then daily for the first week (n=6) or weekly for 5 to 8 weeks (n=14), with the pacemakers temporarily programmed to AAI (normal ventricular activation). RESULTS: The first parameters to change were T-vector amplitude, T(area), and T(peak)-T(end) (T(p-e)), which decreased within 1 day after initiating pacing. CM became apparent between day 1 and day 3, was fully established after 1 week, and then remained stable. Signs of increased VR heterogeneity were observed as the T loop became more circular (decreased T(egenv)) and distorted (increased T(avplan)), which have previously been observed in conditions with increased risk for arrhythmias. Over weeks, VR duration was prolonged (increased QTc). In contrast, during ventricular pacing, a gradual shortening of the repolarization time was observed, suggesting a stabilizing adaptive process. CONCLUSION: In sick sinus syndrome patients in whom ventricular pacing is indicated, switching between normal AV conduction and ventricular pacing should be minimized to avoid periods of repolarization instability.

Ischemia induces aggravation of baseline repolarization abnormalities in left ventricular hypertrophy: a deleterious interaction.

Epidemiological studies show that left ventricular hypertrophy (LVH) and hypertension (HT) in coronary artery disease increases the risk for cardiovascular events including sudden cardiac death (SCD). According to experimental studies, myocardial hypertrophy is associated both with altered electrophysiological properties (including prolonged repolarization) and increased vulnerability to ischemia. However, human data to support a repolarization-related mechanism for the increased SCD risk has not been provided. We therefore studied 187 patients undergoing three-dimensional vectorcardiographic monitoring during coronary angioplasty. Eight parameters reflecting different aspects of ventricular repolarization were used: 1) the ST segment (ST-VM and STC-VM), 2) the T vector (QRS-T angle, Televation, and Tazimuth), and 3) the T vector loop (Tavplan, Teigenv, and Tarea). Data collection was performed at rest and at the time of maximum ischemia during coronary occlusion. The patients were divided into three groups: 33 patients with ECG signs of LVH (18 with HT), 54 with HT but without LVH signs, and 100 patients with neither. Coronary artery disease patients with LVH not only had the most abnormal baseline repolarization (as expected) but also a significantly more pronounced repolarization response during coronary occlusion, whereas HT patients had mean parameter values between LVH patients and those without neither HT nor LVH signs. Because there is a relation between increased SCD risk and repolarization disturbances in various clinical settings, the results of the present study are in agreement with animal data and epidemiological observations, although other factors than disturbed repolarization might be of importance.

Temporal characteristics of cardiac memory in humans: vectorcardiographic quantification in a model of cardiac pacing.

OBJECTIVES: The purpose of this study was to assess the temporal characteristics of cardiac memory in a human pacing model. BACKGROUND: Cardiac memory is induced by periods of altered ventricular activation and in the canine pacing model develops in 2 to 3 weeks. METHODS: Cardiac memory development (phase 1) and resolution (phase 2) was followed qualitatively (ECG) and quantitatively (vectorcardiography [VCG]) in 20 patients with symptomatic sinus bradycardia receiving DDD-R pacing at physiologic rates. During phase 1, maximum ventricular pacing in the right ventricular apical endocardium was achieved by short AV delay. ECG and VCG were recorded during normal ventricular activation prior to implantation (sinus rhythm), 1 day after and then weekly for 5 to 8 weeks during AAI pacing (n = 14, "long-term"), and daily during 1 week (n = 6, "short-term"). In phase 2, the remaining cardiac memory was related to the amount of ventricular pacing. A long AV delay was chosen to reduce ventricular pacing, and 14 patients were seen once after 4 to 5 weeks. RESULTS: ECG and VCG showed marked changes in all patients within 1 week's pacing and remained stable during phase 1. Of the 14 long-term patients, 13 showed significant change in T vector azimuth (mean -150 degrees ) and 11 in T vector elevation (mean 63 degrees ). At the end of phase 2, a linear relation existed between remaining cardiac memory (%) and amount (%) of delivered ventricular pacing. CONCLUSIONS: Cardiac memory developed and reached steady state within 1 week of right ventricular endocardial pacing at physiologic rates in man, was preserved in proportion to delivered ventricular pacing, and completely resolved within 1 month in its absence.

T vector and loop characteristics in coronary artery disease and during acute ischemia.

OBJECTIVE: Three-dimensional characterization of the ventricular repolarization by the T vector and T vector loop morphology in coronary artery disease (CAD), and their response to short-term (no flow) ischemia induced by coronary occlusion during a percutaneous intervention (PCI). BACKGROUND: The risk for sudden cardiac death is increased in conditions of acute or permanently heterogeneous ventricular repolarization, for which ischemia is a risk factor. METHODS: Fifty-six CAD patients without visible collateral circulation were studied during an elective single-vessel PCI, and 10 healthy controls twice at rest. T vector parameters (Televation, Tazimuth, and QRS-T angle), and T loop parameters (Tarea, Tavplan, and Teigenv) were measured by vectorcardiography. ST vector magnitude (ST-VM) and its change (STC-VM) were used for reference. RESULTS: At rest, T vector loop morphology (Tarea, Teigenv) was significantly different in CAD patients and controls, while T vector angles did not separate the groups. Ischemia induced significant changes in T loop parameters in the entire CAD group, whereas in the LAD subgroup significant changes were seen also in T vector angle. The T loop morphology was significantly different at baseline and a more pronounced response to ischemia (Tarea) was seen in patients with, than in those without, a history of hypertension. CONCLUSION: T loop morphology, rather than the T vector angle, separated CAD patients from healthy controls. Coronary occlusion had significant impact on ventricular repolarization, as assessed by T vector and morphology analysis, and most prominently in the LAD group. Hypertensive patients appeared especially vulnerable to ischemia.