[The risk of arrhythmia can be congenital or acquired].
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Arrhythmias, Cardiac↗
Biomedical subjects
Lennart Bergfeldt
Publications and source records attributed to Lennart Bergfeldt.
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↗
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↗
Differential diagnosis of cardiogenic syncope and seizure disorders.
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Anticonvulsants↗
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↗
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↗
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↗
Cardiovascular effects and cardiopulmonary plasma gradients following intravenous infusion of neuropeptide Y in humans: negative dromotropic effect on atrioventricular node conduction.
Neuropeptide Y (NPY) is co-released with noradrenaline from sympathetic nerves, has a strong vasoconstrictive action, and causes an attenuation of parasympathetic action in animal experiments. The plasma level of NPY is greatly elevated in patients with congestive heart failure, but the clinical relevance of this finding is unclear. Central haemodynamic effects, cardiac conduction system electrophysiology and coronary sinus blood flow were therefore studied in two sets of experiments, each carried out on seven healthy men. In the first series, NPY was given intravenously at doses of 3, 10 and 30 pmol.min(-1).kg(-1), and in the second it was given as a bolus injection of 90, 200 or 900 pmol/kg, which resulted in plasma concentrations similar to those seen in heart failure patients. During continuous infusion of NPY, systemic blood pressure increased slightly, but myocardial perfusion, cardiac output, pulmonary arterial pressure, cardiac conduction intervals and atrioventricular (AV) node functional measures remained unchanged. In contrast, the bolus injection of NPY evoked prolongation and block (in four out of seven subjects) of AV node conduction, but did not affect haemodynamic variables, apart from a minor increase in systemic blood pressure. Impaired AV node conduction is a novel observation, which might reflect a baroreceptor-mediated vagal reflex, or - more likely - an NPY-induced direct negative dromotropic effect, caused by a reduction of the L-type calcium current as observed in vitro, or a combination of the two.
Adult↗
Magnetocardiographic and magnetic resonance imaging for noninvasive localization of ventricular arrhythmia origin in a model of nonischemic cardiomyopathy.
Ventricular arrhythmia may in myocardial failure arise as a consequence of remodeling related to hypertrophy and dilatation. In surgically repaired tetralogy of Fallot (TOF), which carries a substantial risk for ventricular arrhythmias and sudden death, the situation is even more complex and several potential arrhythmia mechanisms exist. The authors wanted to test a completely noninvasive localization technique, magnetocardiography (MCG) and magnetic resonance imaging (MRI), to define the origin of ventricular ectopic beats (VEBs) in this model of nonischemic cardiomyopathy. The study included 84 patients with surgically repaired TOF, all 11 subjects with VEBs Lown grade > or = 2 on a 24-hour Holter were included. From 37-channel MCG registrations, the underlying current dipole was computed for the VEBs, and for anatomic correlation MRIs were produced. Eight patients had VEBs of altogether 11 morphologies during the MCG recording. The RVOT was the origin of 6 VEBs, while 4 originated from the RV free wall, and 1 VEB could not be localized. Applying this completely noninvasive technique, it was possible to define different origins of RV ectopies in a complex heart model. Thus, VEBs originated from the RVOT, suggesting a relation to surgical scars and from the nonoperated parts of the RV, supporting that ventricular remodeling might be of equal importance for arrhythmogenesis in this model of cardiomyopathy. This technique can assist in answering the important question of whether there is any difference in prognostic information depending on the origin and related mechanism of VEBs in this and other high risk conditions.
Adult↗
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.
Action Potentials↗