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Biomedical subjects

Lennart Bergfeldt

Publications and source records attributed to Lennart Bergfeldt.

At least 19 recordsLinked to original sources
PubMed2006

Time relation between a syncopal event and documentation of atrioventricular block in patients with bifascicular block: clinical implications.

BACKGROUND: Transient high-degree atrioventricular (AV) block is a common cause of syncope in patients with bifascicular block (BFB) but the intermittent nature of AV block makes ECG documentation a challenge. A sensitive and safe tool to investigate BFB patients with syncope would be a bradycardia-detecting pacemaker, which provides a possibility of studying the time relation between the index syncopal episode and the development of high-degree AV block. METHODS: Twenty-seven patients with BFB and syncope were studied prospectively. All patients received a single-chamber ventricular-based pacemaker with bradycardia-detecting ability. A bradycardia episode was defined as a heart rate of < 30 beats/min lasting > or = 6 s. RESULTS: During a median follow-up of 60 months, a bradycardia event was detected in 14 patients (52%), of whom 13 also had documented high-degree AV block on ECG. The median time between the syncopal episode and the first pacemaker-detected bradycardia event was 5 months and after an additional median time of 6 months, high-degree AV block was documented on the ECG. In 10 of 13 patients (77%) high-degree AV block was documented within 24 months of the syncopal episode corresponding to an annual incidence of 19% during the first 2 years of follow-up in the study population. CONCLUSION: In this group of BFB patients a syncopal episode was highly predictive of the development of high-degree AV block within 24 months, justifying pacemaker therapy without prior ECG verification.

Aged↗
PubMed2006

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.

Aged↗
PubMed2006

T wave inversions following ablation of 125 posteroseptal accessory pathways.

BACKGROUND: Cardiac memory, electrophysiological remodeling induced by periods of altered ventricular activation, has been observed after resumption of normal activation following ablation of overt accessory pathways. We studied the occurrence and temporal characteristics of cardiac memory (inferior T wave inversions) after ablation of overt posteroseptal accessory pathways. METHODS: T wave changes were assessed in the frontal plane (leads II, aVF, and III) up to one year after the ablation in 125 consecutive patients. T wave polarity immediately after ablation was compared with the pre ablation delta wave polarity and the dominant QRS force in each lead. The number of inferior leads (0-3) with post ablation T wave changes (estimate of degree of cardiac memory) was analyzed in relation to estimates of the degree of preexcitation (accessory pathway refractoriness and QRS duration) prior to ablation. RESULTS: Electrocardiogram (ECG) signs of cardiac memory were present in 123 (98%) of the patients within one day after ablation. The post ablation T wave vector had the same direction as the vector of the pre-excited QRS complex (and delta wave) creating inferior T wave inversions. There was no correlation between the degree of preexcitation pre ablation and the extent of cardiac memory post ablation. A majority (about 90%) of ECGs recorded 3-6 months after the procedure, showed complete or almost complete normalization. CONCLUSIONS: T wave inversions were present in the vast majority of patients, persisted in some patients beyond 3 months, and might be misinterpreted as inferior wall ischemia.

Catheter Ablation↗
PubMed2005

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.

Adult↗
PubMed2005

Pacing-induced electrophysiological remodeling in hypertrophic obstructive cardiomyopathy--observations on cardiac memory.

BACKGROUND: Hypertrophic cardiomyopathy carries an increased risk for sudden cardiac death. While pacing therapy reduces the left ventricular outflow tract gradient and improves symptoms in a subgroup of hypertrophic obstructive cardiomyopathy (HOCM) patients, its electrophysiological consequences are unknown and were therefore assessed in this prospective study. METHODS AND RESULTS: Fifteen consecutive HOCM patients were studied and compared with 14 patients without HOCM paced because of sinus bradycardia. ECG intervals were measured before pacemaker implantation and after > or =3 months of DDD pacing in HOCM patients and > or =5 weeks in controls. Both groups showed similar ECG signs of cardiac memory development. In HOCM patients, with baseline QTc 447 +/- 33 ms, cardiac memory development was not associated with any significant changes in ECG intervals. In contrast, baseline repolarization in control patients was significantly prolonged by 6% (QTc 429 +/- 33 vs 454 +/- 46 ms; P < 0.05). Furthermore, in HOCM patients repolarization was 7% shorter during DDD pacing compared to sinus rhythm (JTc 329 +/- 25 vs 353 +/- 21 ms; P < 0.05), despite a significantly prolonged ventricular activation time (QRS duration 155 +/- 16 vs 91 +/- 9 ms; P < 0.01). CONCLUSIONS: Importantly, the development of cardiac memory-induced different repolarization responses depending on baseline structure and electrophysiology. In HOCM patients repolarization was shorter during right ventricular apical pacing than during normal activation despite prolonged activation time.

Adult↗
PubMed2004

Acute comparative effect of right and left ventricular pacing in patients with permanent atrial fibrillation.

We tested the hypothesis that left ventricular (LV) pacing is superior to right ventricular (RV) apical pacing in patients undergoing atrioventricular (AV) junction ablation and pacing for permanent atrial fibrillation. The potential benefit of LV over RV pacing needs to be evaluated without the confounding effect of other variables that can influence cardiac performance. An acute intrapatient comparison of the QRS width and echocardiographic parameters between RV versus LV pacing was performed within 24 h after ablation in 44 patients. Both modes of pacing were also compared with pre-implantation values. Compared with RV pacing, LV pacing caused a 5.7% increase in the ejection fraction (EF) and a 16.7% decrease in the mitral regurgitation (MR) score; the QRS width was 4.8% shorter with LV pacing. Similar results were observed in patients with or without systolic dysfunction and/or native left bundle branch block, except for a greater improvement in MR in the latter group. Compared with pre-ablation measures, the EF increased by 11.2% and 17.6% with RV and LV pacing, respectively; the MR score decreased by 0% and 16.7%; and the diastolic filling time increased by 12.7% and 15.6%.Rhythm regularization achieved with AV junction ablation improved EF with both RV and LV pacing; LV pacing provided an additional modest but favorable hemodynamic effect, as reflected by a further increase of EF and reduction of MR. The effect seems to be equal in patients with both depressed and preserved systolic functions and in those with and without native left bundle branch block.

Aged↗
PubMed2004

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.

Acute Disease↗
PubMed2003

Power spectral and Poincaré plot characteristics in sinus node dysfunction.

A salient feature of the normal sinus node activity is its prominent beat-to-beat variability, which shows self-similarity on different time scales (fractal dynamics). However, in patients with sinus node dysfunction, short-term time sinus cycles show exaggerated variability, the characteristics of which have not been analyzed. Therefore, Poincaré plots and power spectral analysis were applied to short-term variations of sinus cycles in 30 patients with and 30 patients without sinus node disease. Three patterns of behavior were observed in sick sinus patients: type 1, completely normal (n = 3); type 2, randomlike pattern in the Poincaré plots with "white noise" power spectra (n = 9); and type 3, a transitional pattern, characterized by remnants of normal behavior mixed with scattered points (n = 18). In control subjects, only type 1 (n = 27) and type 3 (n = 3) patterns were observed, P < 0.0001. The power spectral changes in sinus node dysfunction are thus characterized by a loss of the inverse power law relationship, which both has implications for heart rate variability analysis and might offer a new diagnostic approach.

Aged↗
PubMed2003

Rapid atrial pacing does not decrease the atrial defibrillation threshold.

The aim of the study was to evaluate the effect of preshock atrial pacing on the atrial defibrillation threshold (DFT) during internal cardioversion of AF. The implantable atrial defibrillator has been added to the therapeutic options for patients with recurrent episodes of persistent AF. Although the device is efficient in restoring sinus rhythm, patient discomfort is a limitation. Methods that lower the ADFT are needed. Eleven patients with AF underwent internal cardioversion. In a randomized, crossover design, ADFT testing was performed, applying a step-up protocol starting at 100 V. Rapid atrial pacing was performed with a right atrial catheter for 20 seconds at 90% of the average cycle length of the fibrillatory waves and was immediately followed by a biphasic defibrillation shock. At each energy level, pacing + shock was compared to shock only, until the level at which sinus rhythm was restored by both modes. The step-up protocol was thereafter repeated using the inverse sequence of the two modes. A total of 19 ADFTs were obtained. For 10 the ADFT was lower with pacing + shock, in 4 equal and in 5 higher, than with shock only. The ADFT (mean +/- SD) with pacing + shock was 260 +/- 84 V(3.4 +/- 2.9 J) and did not differ from shock only: 268 +/- 85 V(3.8 +/- 3.0 J) (P > 0.05). The coefficient of variation and the coefficient of reproducibility for pacing + shock was 16% and 60 V, respectively, and for shock only 17% and 61 V. Rapid atrial pacing did not influence the internal ADFT in AF. The randomized, crossover protocol used was reproducible between different modes, and seems useful when testing the impact of different interventions on the ADFT.

Atrial Fibrillation↗
PubMed2002

Repolarization measures and their relation to sex hormones in postmenopausal women with cardiovascular disease receiving hormone replacement therapy.

Women are more susceptible to the development of Torsades de Pointes ventricular tachycardia and have a longer heart rate-corrected QT interval than men. A causal role for estrogen has been implicated. The purpose of this study was to investigate if hormone replacement therapy (HRT) resulted in any changes in noninvasive depolarization and repolarization measurements, and to study their relation to circulating concentrations of sex hormones. Sixty postmenopausal women with cardiovascular disease (mean age 59 +/- 7 years; range 44 to 75) were randomized to receive oral conjugated estrogens, transdermal estradiol-17-beta (both with addition of progestins), or placebo. QRS, QT, and JT intervals and their dispersion on 12-lead electrocardiograms were analyzed at baseline, and after 6 and 12 treatment cycles of HRT. Blood samples for analyses of serum concentration of estrogens and androgens were obtained on the same occasions. Neither mean RR, QT, QTc, JT, and JTc intervals, nor QT and JT dispersion changed during treatment. There was a significant inverse relation between the mean JTc interval and the serum concentration of estradiol-17-beta, independent of age, testosterone levels, and abdominal obesity. There was also a significant inverse relation between the change in androstenedione levels and the change in QT interval (Spearman -0.35, p = 0.028) or JT interval (Spearman -0.41, p = 0.009) at 6 treatment cycles compared with baseline. In conclusion, treatment with oral conjugated estrogens or transdermal estradiol-17-beta combined with progestins did not alter depolarization or repolarization measurements. However, the inverse relation between repolarization and androgens fits with an effect of androgens on repolarization in postmenopausal women.

Administration, Cutaneous↗
PubMed2002

Comparison of actions of irbesartan versus atenolol on cardiac repolarization in hypertensive left ventricular hypertrophy: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA).

Left ventricular (LV) hypertrophy is associated with a substantial risk for malignant arrhythmias and sudden death. The effects of antihypertensive therapy on QT dispersion, which reflects cardiac repolarization heterogeneity, in relation to changes in LV mass has not been well studied. Repeat echocardiography and QT measurements (standard 12-lead electrocardiograms) were performed in hypertensive patients with LV hypertrophy, who were randomized double-blind to receive the angiotensin II type 1-receptor blocker irbesartan (n = 44) or the beta(1)-receptor blocker atenolol (n = 48) for 48 weeks, and in 37 matched hypertensive control subjects without LV hypertrophy. LV mass index was related to QT dispersion (r = 0.34, p <0.001). The reduction in LV mass was greater using irbesartan than using atenolol (-27 +/- 28 vs -15 +/- 21 g/m(2) at 48 weeks, p = 0.021), with similar reductions in blood pressure. Irbesartan decreased QT dispersion (from 56 +/- 24 ms to 45 +/- 20 ms at 48 weeks; p <0.001) and QTc dispersion (from 57 +/- 24 to 44 +/- 19 ms at 48 weeks; p <0.001). In contrast, atenolol had minor effects. The decreases in QT and QTc dispersions were greater using irbesartan than using atenolol (p = 0.001 and p = 0.011, respectively); the same results were found when changes in LV mass, blood pressure, and heart rate were also included in multivariate analyses. Thus, heterogeneity of ventricular repolarization is related to the degree of LV hypertrophy. Irbesartan, but not atenolol, reduces QT and QTc dispersions independent of changes in LV mass, blood pressure, or heart rate, and thus seems to induce structural and electrical remodeling in a direction that could decrease the risk of fatal events in hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed2002

Transient proarrhythmic state following atrioventricular junction radiofrequency ablation: pathophysiologic mechanisms and recommendations for management.

The induction of complete heart block by radiofrequency ablation of the atrioventricular junction combined with pacemaker implantation has become an established therapy for rate control in patients with atrial fibrillation who are unresponsive to drugs. Reports of ventricular arrhythmias and sudden death after ablation have, however, raised concerns about safety. Ventricular arrhythmias are usually polymorphic and related to a phase of electrical instability due to an initial prolongation and then slow adaptation of repolarization caused by the change in heart rate and activation sequence. Structural heart disease, and other factors that predispose for the acquired long QT syndrome, seem to add to the risk. Ventricular activation and repolarization stabilize during the first week after the procedure. Routine pacing at 80 beats per minute during this phase is recommended, as well as in hospital monitoring for at least 48 hours. Patients with high-risk features for arrhythmias, such as congestive heart failure or impaired left ventricular function, may require pacing at higher rates. Adjustment of the pacing rate-although rarely below 70 beats per minute-is usually undertaken after a week in most patients, preferably after an electrocardiographic evaluation for repolarization abnormalities at the lower rate.

Atrioventricular Node↗