Relevant bibliographies by topics / QT variability

Academic literature on the topic 'QT variability'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "QT variability"

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Berger, Ronald D. "QT variability." Journal of Electrocardiology 36 (December 2003): 83–87. http://dx.doi.org/10.1016/j.jelectrocard.2003.09.019.

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Dobson, Craig P., Andrew Kim, and Mark Haigney. "QT Variability Index." Progress in Cardiovascular Diseases 56, no. 2 (September 2013): 186–94. http://dx.doi.org/10.1016/j.pcad.2013.07.004.

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Berger, Ronald D. "QT Interval Variability." Journal of the American College of Cardiology 54, no. 9 (August 2009): 851–52. http://dx.doi.org/10.1016/j.jacc.2009.06.007.

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Magnano, Massimo, Cristina Gallo, Pier Paolo Bocchino, Marco Briguglio, Anna Rivetti, Fiorenzo Gaita, and Matteo Anselmino. "QT prolongation and variability." Journal of Cardiovascular Medicine 20, no. 4 (April 2019): 180–85. http://dx.doi.org/10.2459/jcm.0000000000000773.

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Zareba, Wojciech, and Antoni Bayes de Luna. "QT Dynamics and Variability." Annals of Noninvasive Electrocardiology 10, no. 2 (April 2005): 256–62. http://dx.doi.org/10.1111/j.1542-474x.2005.10205.x.

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Tereshchenko, Larisa G., and Ronald D. Berger. "Towards a better understanding of QT interval variability." Therapeutic Advances in Drug Safety 2, no. 6 (September 27, 2011): 245–51. http://dx.doi.org/10.1177/2042098611421209.

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The International Conference on Harmonization of Technical Requirements for Registration of Pharmaceuticals for Human Use (ICH) Guideline E14 recommends ‘Thorough QT Study’ as a standard assessment of drug-induced QT interval prolongation. At the same time, the value of drug-induced QTc prolongation as a surrogate marker for risk of life-threatening polymorphic ventricular tachycardia known as torsades des pointes remains controversial. Beat-to-beat variability of QT interval was recently proposed as an alternative metric. The following review addresses mechanisms of beat-to-beat QT variability, methods of QT interval variability measurements, and its prognostic value in clinical studies.
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Yunisova, A. S. "Athletic heart and QT variability." Academy of medicine and sports 2, no. 4 (January 20, 2022): 20–23. http://dx.doi.org/10.15829/2712-7567-2021-38.

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This review provides detailed data on the diagnosis, prevalence, classification, and etiology. The variety of causes leading to long QT syndrome (LQTS) creates difficulties in the differential diagnosis of this condition and, as a result, LQTS often remains outside the sports medicine physicians’ attention. As a result, it is necessary to introduce non-invasive screening methods for studying the cardiac electrophysiological characteristics and select high-risk groups.
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HAIGNEY, MARK C. P., SHAMA ALAM, SCOT TEBO, GREGARY MARHEFKA, AHMED ELKASHEF, ROBERTA KAHN, C. NORA CHIANG, FRANK VOCCI, and LOUIS CANTILENA. "Intravenous Cocaine and QT Variability." Journal of Cardiovascular Electrophysiology 17, no. 6 (June 2006): 610–16. http://dx.doi.org/10.1111/j.1540-8167.2006.00421.x.

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Baumert, Mathias, Gavin W. Lambert, Tye Dawood, Elisabeth A. Lambert, Murray D. Esler, Mariee McGrane, David Barton, and Eugene Nalivaiko. "QT interval variability and cardiac norepinephrine spillover in patients with depression and panic disorder." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H962—H968. http://dx.doi.org/10.1152/ajpheart.00301.2008.

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Suggestions were made that increased myocardial sympathetic activity is reflected by elevated QT variability (dynamic changes in QT interval duration). However, the relationship between QT variability and the amount of norepinephrine released from the cardiac sympathetic terminals is unknown. We thus attempted to assess this relationship. The study was performed in 17 subjects (12 with major depressive disorder and 5 with panic disorder). Cardiac norepinephrine spillover (measured by direct catheter technique coupled with norepinephrine isotope dilution methodology) was assessed before and 4 mo after treatment with selective serotonin reuptake inhibitor (SSRI) antidepressants. The distribution of the cardiac norepinephrine spillover was bimodal, with the majority of patients having values of ≤10 ng/min. There was a positive correlation between cardiac norepinephrine spillover and corrected QT interval ( r = 0.7, P = 0.03) but not with any of the QT variability measures. However, in a subgroup of five patients who had high levels of cardiac norepinephrine spillover (>20 ng/min) a tendency for a strong positive correlation with variance of QT intervals ( r = 0.9, P = 0.08) was observed. There were significant correlations between the severity of depression and QT variability indexes normalized to the heart rate [QTVi and QT interval/R-R interval (QT/RR) coherence] and between the severity of anxiety and the QT/RR residual and regression coefficient, respectively. Treatment with SSRI antidepressants substantially reduced depression score but did not affect any of the QT variability indexes. We conclude that in depression/panic disorder patients with near-normal cardiac norepinephrine levels QT variability is not correlated with cardiac norepinephrine spillover and is not affected by treatment with SSRI.
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Yunisova, A. S., and A. V. Smolensky. "QT interval variability and athlete's heart remodeling." Clinical Medicine (Russian Journal) 100, no. 7-8 (October 31, 2022): 377–81. http://dx.doi.org/10.30629/0023-2149-2022-100-7-8-377-381.

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At present, the prevention of sudden cardiac death in athletes is of great interest. A large amount of literature data concerning the correlation between the length of the QT interval and the proarrhythmic potential of the myocardium has been accumulated. However, new potential predictors of the fatal arrhythmias occurrence in athletes have emerged in recent years — an increase in the dispersion of the QT interval, as well as short-term variability in repolarization. This review provides detailed data on the diagnosis, prevalence, classifi cation, etiology of long QT as one of the manifestations of QT variance. The variety of causes leading to long QT syndrome (LQTS) causes diffi culties in the diff erential diagnosis of this condition and, and as a result, LQTS often remains outside the attention of practitioners. The data of recent studies of the athlete’s heart remodelling are presented as well.
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Dissertations / Theses on the topic "QT variability"

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Schmidt, Martin, Mathias Baumert, Hagen Malberg, and Sebastian Zaunseder. "T Wave Amplitude Correction of QT Interval Variability for Improved Repolarization Lability Measurement." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-217300.

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Objectives: The inverse relationship between QT interval variability (QTV) and T wave amplitude potentially confounds QT variability assessment. We quantified the influence of the T wave amplitude on QTV in a comprehensive dataset and devised a correction formula. Methods: Three ECG datasets of healthy subjects were analyzed to model the relationship between T wave amplitude and QTV. To derive a generally valid correction formula, linear regression analysis was used. The proposed correction formula was applied to patients enrolled in the Evaluation of Defibrillator in Non-Ischemic Cardiomyopathy Treatment Evaluation trial (DEFINITE) to assess the prognostic significance of QTV for all-cause mortality in patients with non-ischemic dilated cardiomyopathy. Results: A strong inverse relationship between T wave amplitude and QTV was demonstrated, both in healthy subjects (R2 = 0.68, p < 0.001) and DEFINITE patients (R2 = 0.20, p < 0.001). Applying the T wave amplitude correction to QTV achieved 2.5-times better group discrimination between patients enrolled in the DEFINITE study and healthy subjects. Kaplan-Meier estimator analysis showed that T wave amplitude corrected QTVi is inversely related to survival (p < 0.01) and a significant predictor of all-cause mortality. Conclusion: We have proposed a simple correction formula for improved QTV assessment. Using this correction, predictive value of QTV for all-cause mortality in patients with non-ischemic cardiomyopathy has been demonstrated.
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Lee, Shirleatha T. "The effects of glucose tolerance, hypertension, and race on heart rate variability, QT interval duration, and left ventricular hypertrophy in overweight-obese adolescents." View the abstract Download the full-text PDF version, 2009. http://etd.utmem.edu/ABSTRACTS/2009-005-Lee-index.htm.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2009.
Title from title page screen (viewed on August 27, 2009). Research advisor: Patricia A. Cowan, Ph.D. Document formatted into pages (x, 71). Vita. Abstract. Includes bibliographical references (p. 56-70).
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Crotti, Lia. "An investigation of the clinical profile and extent of Long QT Syndrome (LQTS) associated with the KCNQ1-A341V mutation in South Africa and with the KCNH2-A1116V mutation in an Italian family and the role that autonomic nervous system (ANS) activity and genetics play in clinical variability." Thesis, Stellenbosch : University of Stellenbosch, 2007. http://hdl.handle.net/10019.1/1417.

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Thesis (DMed (Medicine. Internal Medicine))--University of Stellenbosch, 2007.
Background Although great progress has been made in defining genes conferring the majority of genetic risk in Long QT Syndrome (LQTS) patients, there remains a substantial challenge to explain the widely observed variability in disease expression and phenotype severity, even among family members, sharing the same mutation. Identifying clinical and genetic variables capable of influencing/predicting the clinical phenotype of LQTS patients would allow a more accurate risk stratification, important for determining prognosis, selecting patients for the most appropriate therapy, and counseling asymptomatic mutation carriers (MCs). To address these questions an Italian LQT2 family and a South African Founder LQT1 population have been used. Methods and Results Italian LQT2 family. The proband, a 44-yr-old white woman, presented with ventricular fibrillation and cardiac arrest. Intermittent QT prolongation was subsequently observed and LQT2 was diagnosed following the identification of a missense KCNH2 mutation (A1116V). The proband also carried the common KCNH2 polymorphism K897T on the non-mutant allele. Relatives who carried A1116V without K897T were asymptomatic but some exhibited transient mild QTc prolongation suggesting latent disease. Expression studies in Chinese Hamster Ovary (CHO) cells, demonstrated that the presence of KCNH2-K897T is predicted to exaggerate the IKr reduction caused by the A1116V mutation. These data explain why symptomatic LQTS occurred only in the proband carrying both alleles. South African LQT1 population. The study population involved 320 subjects, 166 MCs and 154 non mutation carriers (NMCs). Off ß-blocker therapy, MCs had a wide range of QTc values (406-676 ms) and a QTc>500 ms was associated with increased risk for cardiac events (OR=4.22; 95%CI 1.12-15.80; p=0.033). We also found that MCs with a heart rate <73 bpm were at significantly lower risk (OR=0.23; 95%CI 0.06-0.86; p=0.035). In a subgroup of patients Baroreflex Sensitivity (BRS) was determined both in presence and absence of ß-blocker therapy. BRS, analyzed in subjects in the 2nd and 3rd age quartiles (age 26-47) to avoid the influence of age, was lower among asymptomatic than symptomatic MCs (11.8±3.5 vs 20.1±10.9 ms/mmHg, p<0.05). A BRS in the lower tertile carried a lower risk of cardiac events (OR 0.13, 95%CI 0.02-0.96; p<0.05). This study also unexpectedly determined that KCNQ1-A341V was associated with greater risk than that reported for large databases of LQT1 patients: A341V MCs were more symptomatic by age 40 (79% vs 30%) and became symptomatic earlier (7±4 vs 13±9 years), both p<0.001. Accordingly, functional studies of KCNQ1-A341V in CHO cells with KCNE1, identified a dominant negative effect of the mutation on wild-type channels. Conclusion Our findings indicate that risk stratification for LQTS patients must be more individually tailored and may have to take into account the specific mutation and probably additional clinical and genetic variables capable of influencing/predicting the clinical phenotype of LQTS patients. As a matter of fact, we have provided evidence that a common KCNH2 polymorphism may modify the clinical expression of a latent LQT2 mutation and the availability of an extended kindred with a common mutation allowed us to highlight that KCNQ1-A341V is associated with an unusually severe clinical phenotype and to identify two autonomic markers, HR and BRS, as novel risk factors.
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Margara, Francesca. "Elucidating the phenotypic variability of a single cardiac sodium channel mutation: a multiscale computational approach." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amslaurea.unibo.it/15563/.

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Descritta per la prima volta nel 1999, la mutazione SCN5A-1795insD compromette l'inattivazione veloce della corrente del sodio e ne riduce drasticamente il picco. Ciò si riflette in una insolita combinazione di sintomi tipici delle sindromi long-QT-tipo 3 e Brugada (BrS). Attualmente si registrano ancora numerose questioni irrisolte relative agli aspetti biofisici di questa condizione e alla variabilità fenotipica attraverso cui questa patologia si manifesta. Utilizzando un approccio computazionale e multi-scala abbiamo acquisito una conoscenza più approfondita circa questa condizione potenzialmente mortale. Partendo dalla versione aggiornata del modello di elettrofisiologia cellulare O'Hara-Rudy dynamic e sfruttando la metodologia delle popolazioni di modelli, abbiamo costruito quattro popolazioni di cellule e due popolazioni di fibre rappresentanti soggetti sani e malati, incorporando nella modellazione dati sperimentali e clinici. I risultati delle simulazioni riproducono la variabilità fenotipica di questa patologia. Tali risultati sottolineano il ruolo della componente veloce della corrente di sodio nel sostenere il complesso QRS e di entrambe le componenti della corrente di sodio, lenta e veloce, nel determinare il prolungamento dell'intervallo QT. Lo studio degli effetti transmurali della mutazione mostra una dispersione nella durata del potenziale d'azione che si riflette in tessuto attraverso una maggiore dispersione transmurale di ripolarizzazione (TDR). La TDR potrebbe rappresentare un nuovo biomarker per la diagnosi clinica. Questo studio individua potenziali target terapeutici, supportando l'utilizzo di bloccanti della componente lenta della corrente di sodio e della corrente transitoria uscente di potassio. Questo studio fornisce inoltre evidenze in supporto alla teoria di depolarizzazione come meccanismo causale per la BrS. Le analisi confermano il ruolo della frequenza cardiaca nel prolungare l'intervallo QT nei pazienti portatori della mutazione.
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Metzner, Sarah Maria [Verfasser], Karl Jürgen [Gutachter] Bär, Bernhard [Gutachter] Blanz, and Marcus-Willy [Gutachter] Agelink. "Untersuchungen der Herzratenvariabilität, der Baroreflexsensitivität und der QT-Intervall-Variabilität bei Angehörigen ersten Grades von Patienten mit Schizophrenie / Sarah Maria Metzner ; Gutachter: Karl Jürgen Bär, Bernhard Blanz, Marcus-Willy Agelink." Jena : Friedrich-Schiller-Universität Jena, 2009. http://d-nb.info/1178249131/34.

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Jourdan, Géraldine. "Conséquences des altérations induites et spontanées du système nerveux autonome sur la fonction cardiovasculaire : approches physiologiques et pharmacologiques." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/425/.

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Durant ces 20 dernières années, de nombreuses études réalisées chez l'homme ont montré une relation significative entre les altérations du système nerveux autonome (SNA) et la mortalité. Le système nerveux bien qu'autonome, ne restant pas moins un élément physiopathologique central dans les affections et la morbidité cardiovasculaires, certains marqueurs traduisant directement ou indirectement les altérations de ce dernier ont ainsi pu être identifiés et permettre une stratification du risque en terme de mortalité. Notre travail a donc consisté à étudier in vivo les altérations du SNA et ses conséquences cardiovasculaires dans trois situations distinctes, reflétant des affections morbides : les effets cardiovasculaires des aminochromes, dérivés oxydatifs des catécholamines endogènes, chez le chien et la souris ; les effets cardiovasculaires d'une combinaison médicamenteuse chez le chien ; les modifications de la variabilité de la fréquence cardiaque et de la repolarisation ventriculaire (étude de l'espace QT) dans un modèle canin d'obésité nutritionnelle. Une première étude réalisée chez la souris démontre clairement l'existence de modifications cardiaques morbides - électriques et échocardiographiques - propres aux aminochromes. Si ces résultats se confirment au travers d'études cliniques de dosage plasmatique de ces composés chez l'homme, les aminochromes per se pourraient être consacrés comme un nouveau facteur concourant à la physiopathologie et au risque de mortalité cardiovasculaire. Une deuxième étude suggère que l'utilisation conjointe de la midodrine et de la dihydroergotamine dans le traitement de l'hypotension orthostatique sévère chez l'homme doit être évitée et confirme, chez le chien, les observations cliniques d'une aggravation de ce symptôme en cas d'association de ces deux médicaments. .
Over the past 20 years numerous studies in humans have shown a significant relationship between alterations in the autonomic nervous system (ANS) and mortality. Although the nervous system is autonomous, it is a key physiopathological element in diseases and morbidity of the cardiovascular system. Some factors, directly or indirectly, linked to alterations of the ANS have thus been indentified and allow for a stratification of risk in terms of mortality. Our work, therefore, has consisted in examining the alterations of the ANS in vivo and investigating their consequences on the cardiovascular system in three distinct situations that reflect morbid affectations : the effect of aminochromes, oxidative derivatives of endogenous catecholamines, on the cardiovascular system of dogs and mice; the cardiovascular effect of a combination of two drugs in dogs; modifications in heart rate variability and ventricular repolarisation (study of the QT space) in a canine model of nutritional obesity. A primary study conducted with mice, clearly shows the existence of morbid cardiac modifications - electric and echocardiographic - specific to aminochromes. If these results are confirmed through clinical studies of plasmatic dosage of these compounds in humans, aminochromes per se could be used as a dedicated novel factor combining physiopathology and cardiovascular risk of mortality. A second investigation suggests that combined use of midodrine and dihydroergotamine in the treatment of severe orthostatic hypotension in humans must be avoided and confirms in dogs, the clinical observations of a worsening of this symptom when these two drugs are given in association. .
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Schmidt, Martin, Marco Kircher, Alexander Noack, Hagen Malberg, and Sebastian Zaunseder. "Challenges to QT Interval Variability Analysis in Mobile Applications." 2015. https://tud.qucosa.de/id/qucosa%3A33162.

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The QT interval in an electrocardiogram (ECG) reflects complex processes affecting the repolarization of ventricular myocardium. Increased QT interval variability (QTV) is thought to be caused by ventricular repolarization lability and has been associated with cardiac mortality. Recent publications have shown that template-based methods are more robust than traditional methods for QT interval extraction on a beat-to-beat basis. However, most studies are limited to non-movement ECG recordings, we want to analyze in this study the power of QT interval extraction for mobile non-stationary ECG recordings. The records of 7 test subjects are at least 65 min long and contain about 25 minutes of sport exercise such as running, cycling, sport climbing or acrobatic training. 2DSW was used to extract QT interval and best-fit distance of matched template for signal quality evaluation for each beat. Potential relations between QTV, motion and signal quality are segmentally compared. To determine motion activity we calculated normalized signal magnitude area (SMA). QTV was increased in patients during sport exercise, possibly reflects sympathetic activity in these specific physiological conditions. However, increased QTV could also be caused by low signal quality.
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Rizkalla, Theodore Sami. "QT variability calculation using a template matching algorithm and power spectral analysis." Thesis, 2006. http://library1.njit.edu/etd/fromwebvoyage.cfm?id=njit-etd2006-014.

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Nayyar, Sachin. "High density mapping of ventricular scar: insights into mechanisms of ventricular tachycardia." Thesis, 2014. http://hdl.handle.net/2440/93913.

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Ventricular tachyarrhythmias related to structural heart disease are the most common cause of sudden cardiac death. Many of these occur in patients with ventricular scarring, related predominantly to coronary artery disease or dilated cardiomyopathies. These regions of scarring remodel over time with ongoing collagen turnover and do not stay stable, such that patients are often subject to repeated episodes of the arrhythmia. Ventricular scars are composed of variable regions of dense interstitial fibrosis that create conduction block, interspersed with viable myocyte channels with diminished coupling which produce substrate for circuitous slow conduction pathways that promote reentry. During sinus rhythm, these channels can be identified by the presence of late potentials and long stimulus to QRS intervals during pacing in the channel. A high density of sampling in the left ventricle allows recording of small amplitude electrograms that are of fundamental emphasis in ventricular substrate mapping. Several studies have characterized channels in patients with ventricular scar and ventricular tachycardia (VT). However, there has been no assessment on the functional characteristics of these channels and whether channels that are critical to the VT circuit differ from non-VT channels. Chapter 1 reviews literature on arrhythmic burden and epidemiology of scar related VT, its cellular mechanisms, substrate characterization, techniques of VT mapping and gaps in the current knowledge. Chapter 2 presents the high density characterization of substrate in ischemic cardiomyopathy (lCM) patients with W and compares the features of VT supporting channels with channels that do not support VT. This study showed that compared to non-VT channels, VT channels are more often located in the dense scar, longer in length, have long stimulus to QRS latencies and slower conduction velocity. Chapter 3 describes the electrogram properties in regions of VT channels, and development of a stepwise model from multiple electrogram properties to ensemble regions supporting VT(s) during sinus rhythm. It also discusses the application of Shannon entropy, a fundamental measure of information content in signals, to map VT channels in sinus rhythm. This system of ablation along with high density mapping will significantly advance VT mapping and help individualize substrate based ablation. Chapter 4 presents data on high density characterization of substrate in ICM patients with W and compares with those who do not have spontaneous VT. It showed that patients without spontaneous VT have fewer channels with shorter lengths and faster conduction, compared to VT patients. These observations partly explain the relative higher predilection of few selected surviving myocyte channels in the post infarct ventricles to sustain VT. Structural heterogeneity in the scar produces spatial and temporal disturbances in ventricular repolarization over multiple time scales. Chapter 5 evaluates the role of acute autonomic modulation on beat-to-beat QT variability in patients with heart failure with and without VT and contrasts it with patients without structural heart disease. It showed that acute pacing and humoral modulation including beta-blockade fail to bring down high repolarization instability in heart failure patients and VT. Catheter ablation is the mainstay for treatment of recurrent ventricular arrhythmias in patients with structural heart disease. Chapter 6 analyses published literature on ventricular arrhythmia storm ablation in a systematic review and meta-analysis. It showed that the interventions are safe and patients often need multiple procedures including non-radiofrequency ablation measures. Although patients who had successful ablation had good long-term outcomes, a failed procedure portended an early and high rate of mortality compared with medically managed historic controls. It raised a pertinent concern of possible harmful effects of catheter ablation in a high risk patient population. In summary, this thesis has developed innovative insights into the surviving myocyte channels in patients with ischemic cardiomyopathy. It describes a novel tool for ventricular substrate mapping that is readily applicable in the clinical laboratory. The repolarization instability is elevated in these patients and is resistant to modulation by acute beta-blocker treatment. Finally, catheter ablation is safe and should be advised in most patients with ventricular arrhythmia storm.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2014
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Abbushi, Oliver [Verfasser]. "Zirkardiane Variabilität der QT-Dispersion bei Gesunden und Herzkranken / vorgelegt von Oliver Abbushi." 2004. http://d-nb.info/973166487/34.

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Book chapters on the topic "QT variability"

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Osterhues, Hans-H. "QT-Variability: Clinical Results and Prognostic Significance." In Advances in Noninvasive Electrocardiographic Monitoring Techniques, 143–53. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4090-4_13.

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Martynenko, A. V., N. Yabluchansky, A. Yabluchansky, B. Verheyden, F. Beckers, and A. E. Aubert. "Nonlinear Analysis of RR and QT Variability for Cosmonauts Data." In IFMBE Proceedings, 393–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-23508-5_102.

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Yabluchansky, N., A. V. Martynenko, A. Yabluchansky, B. Verheyden, F. Beckers, and A. E. Aubert. "Stability Analysis of RR and QT Variability for Cosmonauts Data." In IFMBE Proceedings, 412–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-23508-5_107.

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Coumel, Philippe, and Pierre Maison-Blanche. "Heart rate variability and QT interval: their relationships with the cardiac frequency." In Cardiac Pacing and Electrophysiology, 63–72. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0872-0_7.

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Baumert, M. "QT variability versus sympathetic cardiac activity in patients with major depression and patients with panic disorder." In IFMBE Proceedings, 1318–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03882-2_349.

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Negoescu, R. "Beat-by-Beat Variability of QT ECG-Interval Holds a Well-Founded Promise for Clinical Cardiology: A Review." In IFMBE Proceedings, 40–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-22586-4_10.

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Vrtovec, Bojan, and Gregor Poglaje. "QT Interval and QT Variability." In Advances in Electrocardiograms - Methods and Analysis. InTech, 2012. http://dx.doi.org/10.5772/21888.

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Zareba, Wojciech, Iwona Cygankiewicz, and Antonio Bayes de Luna. "Q-T Interval, QT Dynamicity, and QT Variability." In Electrophysiological Disorders of the Heart, 945–56. Elsevier, 2012. http://dx.doi.org/10.1016/b978-1-4377-0285-9.00070-3.

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Tereshchenko, Larisa G. "QT variability and QRST integral." In Sex and Cardiac Electrophysiology, 117–23. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-817728-0.00010-3.

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"Beat-to-Beat QT Interval Variability and Autonomic Activity." In ECG Time Series Variability Analysis, 403–16. Taylor & Francis Group, 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-2742: CRC Press, 2017. http://dx.doi.org/10.1201/9781315372921-21.

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Conference papers on the topic "QT variability"

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De Maria, Beatrice, Gabriele Mora, Kalliopi Marinou, Riccardo Sideri, Vlasta Bari, Beatrice Cairo, Emanuele Vaini, Laura Adelaide Dalla Vecchia, and Alberto Porta. "QT Interval Variability and QT-HP Coupling Strength in Amyotrophic Lateral Sclerosis Patients." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.268.

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Zaunseder, S., M. Schmidt, H. Malberg, and M. Baumert. "Measurement of QT variability by two-dimensional warping." In 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847570.

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Almeida, R., J. P. Martinez, A. P. Rocha, S. Olmos, and P. Laguna. "Improved QT variability quantification by multilead automatic delineation." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588148.

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Porta, Alberto, Vlasta Bari, Andrea Marchi, Beatrice De Maria, and Sergio Cerutti. "Wiener-Granger causality in QT-HP variability interactions." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318724.

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Karjalainen, P. A., M. P. Tarvainen, and T. Laitinen. "Principal Component Regression Approach for QT Variability Estimation." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616624.

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Porta, A., E. Tobaldini, V. Magagnin, T. Bassani, T. Gnecchi-Ruscone, and N. Montano. "Open loop linear parametric modeling of the qt variability." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333541.

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Nguyen, LinhLan, Steven Su, and Hung T. Nguyen. "Effects of hyperglycemia on variability of RR, QT and corrected QT intervals in Type 1 diabetic patients." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609876.

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Khandoker, Ahsan, Veena Luthra, Yousef Abouallaban, Muhammad Hasan, Nayeefa Chowdhury, and Herbert Jelinek. "Reduced QT Variability and increased QT/RR slope in ECG signals of Depressed Patients with Suicidal Ideation." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.114-190.

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Cuomo, S., M. A. Ribani, F. Marciano, M. L. Migaux, P. Cortelli, G. Pierangeli, P. E. Russo, A. D'Andrea, and R. Calabro. "Abnormal QT interval variability in patients with multiple system atrophy." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588143.

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Orini, Michele, Peter Taggart, and Pier D. Lambiase. "A multivariate time-frequency approach for tracking QT variability changes unrelated to heart rate variability." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7590852.

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Journal articles
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