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  • 1
    Book
    Book
    Cardiac mechano-electric feedback and arrhythmias / (2005)
    Philadelphia, PA :Elsevier Saunders,
    Details
    Title: Cardiac mechano-electric feedback and arrhythmias /
    Author: Kohl, Peter
    Contributer: Sachs, Frederick , Franz, Michael R.
    Edition: 1st ed
    Publisher: Philadelphia, PA :Elsevier Saunders,
    Year of publication: 2005
    Pages: xxi, 423 p., [12] p. of plates : , ill. (some col.) ; , 24 cm
    ISBN: 1-416-00034-8
    Type of Medium: Book
    Language: English
    URL: 04
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  • 2
    Electronic Resource
    Electronic Resource
    Is Dispersion of Ventricular Repolarization Rate Dependent? (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 20 (1997), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 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 QTcmax-QTcmin or JT dispersion as fTcmax-fTcmin, 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1997.tb06078.x
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  • 3
    Electronic Resource
    Electronic Resource
    Timing of the Upper Limit of Vulnerability is Different for Monophasic and Biphasic Shocks: Implications for the Determination of the Defibrillation Threshold (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 20 (1997), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The upper limit of vulnerability (ULV) has been used in clinical studies to predict the DFT in patients with ICDs. Despite the ULV-DFT correlation, uncertainties about the optimal timing of the ULV determination remain. Previous studies using monophasic or biphasic shock waveforms reported differences in the ULV timing with respect to the electrocardiographic T wave. The purpose of this study was to directly compare the ULV timing for mono- versus biphasic T wave shocks. In ten isolated rabbit hearts, mono- and biphasic shocks were delivered randomly during the vulnerable window and at varying shock strengths to determine the ULV. The ULV timing was expressed as the coupling interval at the ULV, the myocardial repolarization state at the ULV measured by monophasic action potential recordings, and the relation between the ULV and the peak of the simultaneously recorded volume conducted T wave. The ULV for biphasic shocks occurred at longer coupling intervals than for monophasic shocks (188.0 ± 9.5 ms vs 173.5 ± 8.8 ms, P 〈 0.001). This resulted in a more repolarized myocardial state at the ULV for biphasic than for monophasic shocks (81.1%± 7.5% vs 66.9%± 9.0%, P = 0.002). The ULV for monophasic shocks occurred predominantly during the upslope of the T wave (8.0 ± 9.7 ms before the peak of the T wave) whereas the ULV for biphasic shocks occurred at or after the peak of the T wave (5.9 ± 9.3 ms after the peak of the T wave) (P 〈 0.001). Biphasic shocks delay the timing of the ULV as compared to monophasic shocks. This is important for the prediction of the DFT by ULV measurements.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1997.tb04234.x
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  • 4
    Electronic Resource
    Electronic Resource
    Dispersion of Ventricular Repolarization in the Voltage Domain (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 21 (1998), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Dispersion of ventricular repolarization, assessed as QT dispersion in the ECG or by multiple monophasic action potential (MAP) recordings, is defined as the difference between the earliest and latest repolarization. It is thus measured in the time domain. However, myocardial refractoriness is primarily a function of the membrane potential during phase 3 repolarization. The purpose of this study, therefore, was to measure dispersion of ventricular repolarization in the voltage domain and to study its relation to VF inducibility. To further validate this concept, the effects of chronic amiodarone treatment on the voltage dispersion were assessed. MAPs were recorded simultaneously at 10 epicardial and endocardial sites in isolated rabbit hearts, both under baseline conditions (n = 8) and after chronic amiodarone treatment (n = 8). Repolarization dispersion in the voltage domain was calculated as the difference between the highest and lowest repolarization level of all 10 MAPs at 10-ms steps, starting from the MAP plateau level to complete repolarization. Plotting these voltage differences along the time axis resulted in a dispersion curve, which rose during early repolarization, reached a peak during phase 3 repolarization, and thereafter declined toward zero. There was a close correlation between VF vulnerability in response to electrical field stimuli and the time during which voltage dispersion was maximal (r = 0.828, P 〈 0.0001). Amiodarone caused a right-ward shift of both the dispersion curve (P = 0.007) and VF vulnerability (P = 0.025), but did not change the magnitude nor the shape of the voltage dispersion curve and its relation to VF vulnerability. Repolarization dispersion in the voltage domain describes an alternate approach for evaluating the heterogeneity of ventricular repolarization and may help to characterize arrhythmia susceptibility under experimental conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1998.tb01067.x
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  • 5
    Electronic Resource
    Electronic Resource
    Myocardial Vulnerability to T Wave Shocks: Relation to Shock Strength, Shock Coupling Interval, and Dispersion of Ventricular Repolarization (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 7 (1996), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Myocardial Vulnerability to T Wave Shocks. Introduction: Induction of ventricular fibrillation (VF) by T wave shocks is of clinical interest due to the correlation between the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). However, the ULV bas not yet been defined precisely in reference to the entire “area of vulnerability” (AOV), which is defined bifunctionally by both shock strengths and shock coupling intervals, nor has it been related to the dispersion of ventricular repolarization, considered to be an important determinant of vulnerability. Methods and Results: In 11 isolated perfused rabbit hearts immersed in a tissue bath containing a 3-lead ECG recording system and two opposite plate electrodes for field shock administration, 7 monophasic action potentials (MAPs) were recorded simultaneously from different epicardial and endocardial regions of the right and left ventricles. An average of 90 ± 25 monophasic waveform shocks of varying shock strengths and coupling intervals were delivered to each heart to determine the horizontal and vertical boundaries of the AOV. The AOV approximated a rhomboid with homogenous VF inducibility. The ULV and lower limit of vulnerability (LLV) represented discrete corners of the AOV with significant changes in VF inducibility if either shock coupling intervals or shock strength were changed by only 10 msec or 10 V. respectively (P 〈 0.001). The ULV occurred at 7 ± 10 msec shorter coupling intervals than the LLV (P 〈 0.05), and VF-inducing shock strengths at the left corner of the AOV were 50 ± 67 V higher as compared to the right corner (P 〈 0.01). The maximal range of VF-inducing coupling intervals coincided (within 〈 2 msec) with the dispersion of MAPs at 70% repolarization, and the ULV coupling interval coincided (within 〈 4 msec) with the longest repolarization at 50%. Conclusions: (1) VF vulnerability to monophasic T wave shocks is defined by an AOV that bas the shape of a leftward tilted rhomboid. (2) Both the ULV and LLV are sharply defined upper and lower corners of the AOV rhomboid. (3) The width of the AOV corresponds to the dispersion of ventricular repolarization at the 70% level. (4) Considering the dispersion of ventricular repolarization may yield more precise ULV determinations and a better understanding of the correlation between the ULV and DFT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1996.tb00520.x
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  • 6
    Electronic Resource
    Electronic Resource
    Bridging the Gap Between Basic and Clinical Electrophysiology: (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 5 (1994), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Monophasic Action Potentials. With rapid advances occuring in both basic and clinical electrophysiology, the gap between the two disciplines appears to be widening rather than narrowing. In most instances, we cannot apply the knowledge derived from cellular studies directly to clinical practice. Monophasic action potential (MAP) recording by contact electrode technique allows us in measure basic electrophysiological phenomena in the human heart and thus provides an important bridge between basic and clinical electrophysiology. MAP recordings produce the lime course of cellular repolarization during cycle length changes and antiarrhythmic drug administration, lending insights into use dependency and reverse use dependency of antiarrhythmic drug effects in the clinical electrophsiology laboratory. The ability to deliver electrical stimuli at the MAI recording site further allows one to investigate drug-induced postrepolarization refractoriness. MAP recordings provide precise local activation times, important for mapping of abnormal ventricular activation, and detect areas of abnormal repolarization due to ischemia or scarring. MAP recordings are uniquely suited to detect early and delayed afterdepolarizations in the human heart, thereby helping to unravel the arrhythmia mechanisms in the long QT syndrome. By embedding the MAP electrode in a radiofrequency electrode, arrhythmogenic foci may be both detected and ablated. In many instances, MAP recordings are more accurate than KCG tracings in defining and distinguishing ventricular fibrillation and ventricular tachycardia. This can he of clinical importance during testing of the implantable cardioverler/delibrillator. An area of growing interest is stretch-activated arrhythmias. Here, MAP recordings are of particular value because no other method is available to record mechanically induced electrophysiological changes in the vigorously beating heart. It can be expected that MAP recordings will, in the future, provide this important bridge between “cell and bedside” also in atrial tachyarrhythmias, such as in atrial fibrillation and flutter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1994.tb01192.x
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  • 7
    Electronic Resource
    Electronic Resource
    Electrophysiologic Features of Torsades de Pointes: (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 8 (1997), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Torsades de Pointes in the Isolated Rabbit Heart. Introduction: The exact electrophysiologic mechanism of torsades de pointes (TdP) is under intense investigation. No isolated animal heart model of this particular arrhythmia exists. Methods and Results: In isolated rabbit hearts, TdP was induced by means of bradyeardia in the presence of a high concentration of d-sotalol (10−4 M) and shortly after lowering the concentration of potassium and magnesium in the perfusate. Multiple simultaneous epicardial and endocardial monophasic action potentials (MAPs) and volume-conducted 12-lead ECGs were recorded. d-Sotalol prolonged repolarization and increased dispersion of ventricular repolarization compared to baseline recordings. With the onset of low potassium and magnesium concentrations, repolarization was further prolonged and dispersion of repolarization was further increased followed by the occurrence of early afterdepolariZations (EADs) in the majority of MAP recordings, i.e., at both endocardial and epicardial locations of both ventricles, upon increase of EAD amplitude, triggered arrhythmias with TdP of up to 42 heats ensued in 10 of 11 hearts studied. MAP duration at 90% repolarization (APD90), dispersion of APD90, and the incidence of EADs as well as dispersion of the QT interval and T wave area were significantly higher in heats triggering higemini, couplets, or runs of TdP. Conclusion: TdP observed in this new isolated heart model was associated with markedly increased dispersion of ventricular repolarization and the occurrence of EADs in multiple locations of the heart. TdP is initiated when the amplitude of an EAD reaches threshold for initiation of the first beat of an episode.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1997.tb01001.x
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  • 8
    Electronic Resource
    Electronic Resource
    Comparison of ECG Variables of Dispersion of Ventricular Repolarization with Direct Myocardial Repolarization Measurements in the Human Heart (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 9 (1998), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Validation of ECG Variables of Dispersion. Introduction: QT dispersion (QTD) from the 12-tead ECG has been widely adopted as a noninvasive index of dispersion of ventricular repolarization (DVR). QTD, however, has never been validated by direct comparison with myocardial DVR in the human heart. Methods and Results: Monophasic action potential (MAP) recordings obtained in an earlier study were retrospectively matched with 12-lead ECGs available from within 24 hours of the invasive procedure. MAPs were available from an average of 8 ± 3 left endocardial sites in 4 patients with left ventricular hypertrophy (LVH) and 7 patients with normal ECGs, and 6 ± 2 epicardial sites in 3 patients of each group during normal ventricular activation. Local repolarization time (RT) was determined as MAP duration at 90% repolarization plus the local activation time. Dispersion of RT was calculated as the difference between the earliest and latest RT. ECGs were digitized and analyzed with recently described interactive QTD analysis software. In addition to standard QTD (defined as QTmax– QTmin), all currently proposed ECG dispersion variables were compared and correlated with the invasive measurements of DVR. QTD exhibited a reasonable correlation with dispersion of RT (R = 0.67; P 〈 0.01). Several other variables designed to measure DVR exhibited a similar, but not better, correlation. Among them, the QT peak/QT end ratio in V3 (R =−0.72; P 〈 0.01) and averaged over all analyzableleads (R =−0.59; P 〈 0.01) exhibited a good correlation with dispersion of RT, which was further improved when endocardial measurements were considered alone. T area measures did not correlate with dispersion of RT, but discriminated LVH. Conclusion: DVR can he assessed by means of a 12-lead surface ECG. Several of the variables under study exhibit a similar accuracy in determination of true myocardial dispersion of repolarization. Variables involving the terminal part of repolarization, such as the QT peak/QT ratio, even from a single lead, may add to the determination of DVR from the human heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1998.tb00103.x
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of Sustained Load on Dispersion of Ventricular Repolarization and Conduction Time in the Isolated Intact Rabbit Heart (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 7 (1996), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Effect of Sustained Load on EP Parameters. Introduction: It is well known that myocardial stretch can elicit ventricular arrhythmias in experimental models. However, previous reports have predominantly documented stretch-induced arrhythmias during short, pulsatile stretch. The arrhythmogenic mechanism of sustained static stretch is incompletely understood. Methods and Results: To examine the influence of sustained load on several electrophysiologic parameters, a latex balloon was placed into the left ventricle of ten isolated Langendorffperfused rabbit hearts and filled with a neutral volume of fluid. The heart was paced from a catheter inside the right ventricle (apicoseptal endocardial position), and the following parameters were studied during steady-state pacing with a cycle length of 500 msec (S1) and during extrastimulation (S2, base drive of 8 beats): monophasic action potential (MAP) durations at 90% repolarization (APD90) from 5 to 6 epicardial electrodes located on both ventricles and one right ventricular endocardial contact electrode; dispersion of APD90 (range of MAP durations from all electrodes); effective refractory period (ERP) and longest activation time (pacing stimulus to MAP upstroke). After baseline recordings, the balloon inside the left ventricle was filled with a volume of 1.0 mL of fluid by means of a servo-controlled pump. The ERP was significantly shortened from 198 ± 9 msec at baseline to 183 ± 8 msec during sustained load (P 〈 0.03). Similarly, the average APD90 was shortened from 180 ± 5 msec at baseline to 175 ± 6 msec during sustained load (P 〈 0.006) with steady-state pacing and from 178 ± 6 msec to 170 ± 8 msec during premature extrastimulation (P 〈 0.03). At the same time, dispersion of APD90 was increased from 27 ± 5 msec to 38 ± 6 msec (P 〈 0.002) during steady-state pacing and from 28 ± 4 msec to 38 ± 6 msec (P = 0.013) during premature extrastimulation. The longest activation time among all MAP recordings was increased from 39 ± 2 msec to 43 ± 3 msec (P = 0.003) during steady-state pacing and from 56 ± 6 msec to 69 ± 6 msec during premature extrastimulation (P 〈 0.003). Conclusions: Sustained load shortens the ERP and the mean APD90 and at the same time increases dispersion of APD90 and prolongs activation times. These findings provide additional insight into the arrhythmogenic mechanisms of sustained mechanical load.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1996.tb00455.x
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  • 10
    Electronic Resource
    Electronic Resource
    Shock-Induced Dispersion of Ventricular Repolarization: (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 8 (1997), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Shock-induced Dispersion and VF Induction. Introduction: Shock-induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction: however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear. Methods and Results: In eight Langendorff-perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV. SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 ± 15 msec for sbocks inducing VF. SIDR was 41 ± 17 msec for shocks delivered above the ULV, and 33 ± 14 and 27 ± 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P 〈 0.01 vs VF-inducing shocks). Although SIDR was larger for shocks delivered below the LLV(93 ± 24 msec, P 〈 0.01 vs VF-inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3%± 3.9% vs 16.3%± 4.9%, P 〈 0.01). Conclusion: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1997.tb00623.x
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