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296 results on '"Garratt, Clifford"'

53. PREVALENCE AND PREDICTORS OF PACEMAKER PLACEMENT IN ADULT FONTAN PATIENTS

Author

Agarwal, Anushree, primary, Sabanayagam, Aarthi, additional, Kheiwa, Ahmed, additional, Cunnington, Colin, additional, Gerstenfeld, Edward, additional, McCulloch, Charles, additional, Harris, Ian, additional, Tseng, Zian, additional, Foster, Elyse, additional, Jenkins, Petra, additional, Dua, Jaspal, additional, Karunaratne, Devinda, additional, Muhyaldeen, Sahrkaw, additional, Zaidi, Amir, additional, Fitzpatrick, Adam, additional, Garratt, Clifford, additional, Clarke, Bernard, additional, Hoschtitzky, Andreas, additional, and Mahadevan, Vaikom, additional

Published
2017
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54. PREVALENCE AND PREDICTORS OF ATRIAL TACHYARRHYTHMIAS IN ADULT FONTAN PATIENTS

Author

Agarwal, Anushree, primary, Sabanayagam, Aarthi, additional, Kheiwa, Ahmed, additional, Cunnington, Colin, additional, Harris, Ian, additional, Gerstenfeld, Edward, additional, McCulloch, Charles, additional, Foster, Elyse, additional, Tseng, Zian, additional, Zier, Lucas, additional, Jenkins, Petra, additional, Dua, Jaspal, additional, Karunaratne, Devinda, additional, Muhyaldeen, Sahrkaw, additional, Zaidi, Amir, additional, Fitzpatrick, Adam, additional, Garratt, Clifford, additional, Clarke, Bernard, additional, Hoschtitzky, Andreas, additional, and Mahadevan, Vaikom, additional

Published
2017
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55. Effects of persistent atrial fibrillation-induced electrical remodeling on atrial electro-mechanics – insights from a 3D model of the human atria

Author

Adeniran, Ismail, Maclver, David H., Garratt, Clifford J., Ye, Jianqiao, Hancox, Jules C., Zhang, Henggui, Adeniran, Ismail, Maclver, David H., Garratt, Clifford J., Ye, Jianqiao, Hancox, Jules C., and Zhang, Henggui

Abstract

A 3D electromechanical model of the human atria was developed to investigate the effects of AFER on atrial electro-mechanics. Simulations were carried out in 3 conditions for 4states: (i) the control condition, representing the normal tissue (state 1) and the tissue 2–3months after cardio version (state 2) when the atrial tissue recovers its electrophysiological properties after completion of reverse electrophysiological remodelling; (ii) AFER-SR condition for AF-remodelled tissue with normal sinus rhythm (SR) (state 3); and (iii) AFER-AF condition for AF-remodeled tissue with re-entrant excitation waves (state 4). Our results indicate that at the cellular level, AFER (states 3 & 4) abbreviated action potentials and reduced the Ca2+content in the sarcoplasmic reticulum, resulting in a reduced amplitude of the intracellular Ca2+transient leading to decreased cell active force and cell shortening as compared to the control condition (states 1 & 2). Consequently at the whole organ level, atrial contraction in AFER-SR condition (state 3) was dramatically reduced. In the AFER-AF condition (state 4) atrial contraction was almost abolished.

Published
2015

56. Comparison of Atrial Fibrillation in the Young versus That in the Elderly: A Review

Author

Sankaranarayanan, Rajiv, Kirkwood, Graeme, Dibb, Katharine, and Garratt, Clifford J.

Subjects
Article Subject
Abstract

The incidence and prevalence of atrial fibrillation (AF) are projected to increase significantly worldwide, imposing a significant burden on healthcare resources. The disease itself is extremely heterogeneous in its epidemiology, pathophysiology, and treatment options based on individual patient characteristics. Whilst ageing is well recognised to be an independent risk factor for the development of AF, this condition also affects the young in whom the condition is frequently symptomatic and troublesome. Traditional thinking suggests that the causal factors and pathogenesis of the condition in the young with structurally normal atria but electrophysiological “triggers” in the form of pulmonary vein ectopics leading to lone AF are in stark contrast to that in the elderly who have AF primarily due to an abnormal substrate consisting of fibrosed and dilated atria acting in concert with the pulmonary vein triggers. However, there can be exceptions to this rule as there is increasing evidence of structural and electrophysiological abnormalities in the atrial substrate in young patients with “lone AF,” as well as elderly patients who present with idiopathic AF. These reports seem to be blurring the distinction in the pathophysiology of so-called idiopathic lone AF in the young versus that in the elderly. Moreover with availability of improved and modern investigational and diagnostic techniques, novel causes of AF are being reported thereby seemingly consigning the diagnosis of “lone AF” to a rather mythical existence. We shall also elucidate in this paper the differences seen in the epidemiology, causes, pathogenesis, and clinical features of AF in the young versus that seen in the elderly, thereby requiring clearly defined management strategies to tackle this arrhythmia and its associated consequences.

Published
2013
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60. What are the thromboembolic risks of heart failure combined with chronic or paroxysmal AF?

Author

Caldwell, Jane Cochrane, Mamas, Mamas A., Neyses, Ludwig, Garratt, Clifford J., Caldwell, Jane Cochrane, Mamas, Mamas A., Neyses, Ludwig, and Garratt, Clifford J.

Abstract

BACKGROUND: Heart failure (HF) and atrial fibrillation (AF) are common disorders that frequently occur together and are associated with an increased risk of thromboembolism. This thromboembolic risk may be reduced by anticoagulation with warfarin but not without introducing new hemorrhagic risks. METHODS AND RESULTS: Current guidelines recommend the use of anticoagulation in patients with HF and chronic AF and paroxysmal AF (PAF) that is symptomatic or frequent and prolonged enough to be detected by electrocardiogram. However, the evidence supporting these recommendations is weak and does not take account of research indicating that the prothrombotic risk is higher in more severe HF. CONCLUSIONS: An area not addressed by current guidelines is anticoagulation in patients with HF and short, asymptomatic episodes of AF. These issues need to be resolved with further studies using implanted devices to detect such asymptomatic PAF.

Published
2010

65. Comparison of adenosine and verapamil for termination of paroxysmal junctional tachycardia

Author

Garratt, Clifford, Linker, Nicholas, Griffith, Michael, Ward, David, and Camm, A. John

Subjects
Arrhythmia -- Drug therapy, Adenosine -- Evaluation, Anti-arrhythmia drugs -- Evaluation, Paroxysmal tachycardia -- Drug therapy, Verapamil -- Evaluation, Health
Abstract

Paroxysmal junctional tachycardia is a rapid heart beat which starts and ends suddenly. These abnormal heart beats can be terminated with physical maneuvers or with drugs. Verapamil is the drug most commonly used, while adenosine is also effective in terminating abnormal electrical conduction in the heart. The effectiveness of both drugs was compared in 20 patients during electrophysical heart testing. With respect to ending the arrhythmia or preventing the development of significant arrhythmias, adenosine worked well on all 20 patients, while six patients on verapamil had subsequent undesirable arrhythmias. Therefore adenosine was more effective in ending paroxysmal junctional ventricular tachycardia without causing other types of arrhythmias. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1989

82. Misuse of verapamil in pre-excited atrial fibrillation

Author

Garratt, Clifford, Ward, David, Antoniou, Anna, and Camm, A. John

Subjects
Electrocardiography -- Analysis, Atrial fibrillation -- Drug therapy, Verapamil -- Dosage and administration, Arrhythmia -- Diagnosis
Published
1989

96. Atrial proarrhythmia due to increased inward rectifier current (I K1) arising from KCNJ2 mutation – A simulation study

Author

Kharche, Sanjay, Garratt, Clifford J., Boyett, Mark R., Inada, Shin, Holden, Arun V., Hancox, Jules C., and Zhang, Henggui

Subjects
*ATRIAL fibrillation, *ION channels, *ACTION potentials, *ELECTROPHYSIOLOGY
Abstract

Abstract: Atrial fibrillation (AF) has been linked to increased inward rectifier potassium current, I K1, either due to AF-induced electrical remodelling, or from functional changes due to the Kir2.1 V93I mutation. The aim of this simulation study was to identify at cell and tissue levels'' mechanisms by which increased I K1 facilitates and perpetuates AF. The Courtemanche et al. human atrial cell action potential (AP) model was modified to incorporate reported changes in I K1 induced by the Kir2.1 V93I mutation in both heterozygous (Het) and homozygous (Hom) mutant forms. The modified models for wild type (WT), Het and Hom conditions were incorporated into homogeneous 1D, 2D and 3D tissue models. Restitution curves of AP duration (APD), effective refractory period (ERP) and conduction velocity (CV) were computed and both the temporal and the spatial vulnerability of atrial tissue to re-entry were measured. The lifespan and tip meandering pattern of re-entry were also characterised. For comparison, parallel simulations were performed by incorporating into the Courtmanche et al. model a linear increase in maximal I K1 conductance. It was found that the gain-in-function of V93I ‘mutant’I K1 led to abbreviated atrial APs and flattened APD, ERP and CV restitution curves. It also hyperpolarised atrial resting membrane potential and slowed down intra-atrial conduction. V93I ‘mutant’I K1 reduced the tissue''s temporal vulnerability but increased spatial vulnerability to initiate and sustain re-entry, resulting in an increased overall susceptibility of atrial tissue to arrhythmogenesis. In the 2D model, spiral waves self-terminated for WT (lifespan < 3.3 s) tissue, but persisted in Het and Hom tissues for the whole simulation period (lifespan > 10 s). The tip of the spiral wave meandered more in WT tissue than in Het and Hom tissues. Increased I K1 due to augmented maximal conductance produced similar results to those of Het and Hom Kir2.1 V93I mutant conditions. In the 3D model the dynamic behaviour of scroll waves was stabilized by increased I K1. In conclusion, increased I K1 current, either by the Kir2.1 V93I mutation or by augmented maximal conductance, increases atrial susceptibility to arrhythmia by increasing the lifespan of re-entrant spiral waves and the stability of scroll waves in 3D tissue, thereby facilitating initiation and maintenance of re-entrant circuits. [Copyright &y& Elsevier]

Published
2008
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97. Upstream Management of Atrial Fibrillation.

Author

Caldwell, Jane and Garratt, Clifford J.

Subjects
*ATRIAL fibrillation, *DISEASE management, *ARRHYTHMIA, *HEART diseases, *ELECTROPHYSIOLOGY, *ANIMAL models in research
Abstract

The article discusses the upstream management of atrial fibrillation (AF) which involves treating the abnormalities that are thought to predispose certain patient groups to this arrhythmia. It examines the predisposing clinical factors for AF. It also explains the underlying electrophysiological mechanisms of AF, AF development in animal models, and effects of therapies in animal models of AF in the setting of structural heart disease or inflammation.

Published
2008

98. Role of up-regulation of I K1 in action potential shortening associated with atrial fibrillation in humans

Author

Zhang, Henggui, Garratt, Clifford J., Zhu, Jiujiang, and Holden, Arun V.

Subjects
*ATRIAL fibrillation, *COMPUTER simulation, *MEMBRANE proteins, *ACTIVE biological transport
Abstract

Abstract: Objectives: Although previous studies in dogs have indicated a minimal role for changes in I K1 in the shortening of action potential duration (APD) associated with atrial fibrillation (AF), in humans, there is evidence for significant AF-induced up-regulation of this current. In this computer model study, we investigated the relative contributions of the remodeling of I K1, L-type calcium current, and other remodeled ionic channel currents to AF-induced APD reduction in human atrium. Methods: Two computer models of electrical activity of human atrial cell were modified by incorporating experimental data of AF-induced changes in human atrial ionic channel conductance and kinetics reported by Bosch et al. (I CaL, I to, I K1, and I Na) (AF-1) and Workman et al. (I CaL, I to, and I K1) (AF-2). The roles and relative importance of individually remodeled ion channels in the APD reduction in human atrium were evaluated by the removal and exclusive methods, in which remodeling of specific currents was omitted, or considered in isolation, in the two models. Results: When tested together, previously reported AF-induced changes in sarcolemmal ion currents result in marked shortening of atrial APD90. With the AF-1 remodeled parameters, there is a 62% reduction in APD90 for the Nygren et al. model, and a 68% reduction for the Courtemanche et al. model, which are comparable to experimental results of 60% reduction seen in humans. When tested individually, AF-1-induced changes in I CaL, I K1, or I to alone result in APD90 reduction of 20%, 64%, and −10%, respectively, for the Nygren et al. model, and 27%, 40%, and 11.6%, respectively, for the Courtemanche et al. model. With the AF-2 remodeled parameters, there is a 47% reduction in APD90 for the Nygren et al. model and a 49% reduction for the Courtemanche et al. model, which are also comparable to experimental results of 45% reduction. When tested individually, AF-2-induced changes in I CaL or I K1 alone result in APD90 reduction of 20% and 40%, respectively, for the Nygren et al. model, and 14% and 21%, respectively, for the Courtemanche et al. model. Conclusion: Previously reported changes in L-type Ca2+ current are insufficient to account for the observed reduction in atrial APD associated with persistent AF. Up-regulation of I K1 has a greater influence on atrial APD in the human model. [Copyright &y& Elsevier]

Published
2005
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