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Articles by J Cooper
Total Records ( 10 ) for J Cooper
  J. F Roux , E Zado , D. J Callans , F Garcia , D Lin , F. E Marchlinski , R Bala , S Dixit , M Riley , A. M Russo , M. D Hutchinson , J Cooper , R Verdino , V Patel , P. S Joy and E. P. Gerstenfeld

Background— Atrial arrhythmias are common early after atrial fibrillation (AF) ablation. We hypothesized that empirical antiarrhythmic drug (AAD) therapy for 6 weeks after AF ablation would reduce the occurrence of atrial arrhythmias.

Methods and Results— We randomized consecutive patients with paroxysmal AF undergoing ablation to empirical antiarrhythmic therapy (AAD group) or no antiarrhythmic therapy (no-AAD group) for the first 6 weeks after ablation. In the no-AAD group, only atrioventricular nodal blocking agents were prescribed. All patients wore a transtelephonic monitor for 4 weeks after discharge and were reevaluated at 6 weeks. The primary end point of the study was a composite of (1) atrial arrhythmias lasting more than 24 hours; (2) atrial arrhythmias associated with severe symptoms requiring hospital admission, cardioversion, or initiation/change of antiarrhythmic drug therapy; and (3) intolerance to antiarrhythmic agent requiring drug cessation. Of 110 enrolled patients (age 55±9 years, 71% male), 53 were randomized to AAD and 57 to no-AAD. There was no difference in baseline characteristics between groups. During the 6 weeks after ablation, fewer patients reached the primary end point in the AAD compared with the no-AAD group (19% versus 42%; P=0.005). There remained fewer events in the AAD group (13% versus 28%; P=0.05) when only end points of AF >24 hours, arrhythmia-related hospitalization, or electrical cardioversion were compared.

Conclusions— AAD treatment during the first 6 weeks after AF ablation is well tolerated and reduces the incidence of clinically significant atrial arrhythmias and need for cardioversion/hospitalization for arrhythmia management.

  R Sofat , A. D Hingorani , L Smeeth , S. E Humphries , P. J Talmud , J Cooper , T Shah , M. S Sandhu , S. L Ricketts , S. M Boekholdt , N Wareham , K. T Khaw , M Kumari , M Kivimaki , M Marmot , F. W Asselbergs , P van der Harst , R. P.F Dullaart , G Navis , D. J van Veldhuisen , W. H Van Gilst , J. F Thompson , P McCaskie , L. J Palmer , M Arca , F Quagliarini , C Gaudio , F Cambien , V Nicaud , O Poirer , V Gudnason , A Isaacs , J. C.M Witteman , C. M van Duijn , M Pencina , R. S Vasan , R. B D'Agostino , J Ordovas , T. Y Li , S Kakko , H Kauma , M. J Savolainen , Y. A Kesaniemi , A Sandhofer , B Paulweber , J. V Sorli , A Goto , S Yokoyama , K Okumura , B. D Horne , C Packard , D Freeman , I Ford , N Sattar , V McCormack , D. A Lawlor , S Ebrahim , G. D Smith , J. J.P Kastelein , J Deanfield and J. P. Casas

Background— Cholesteryl ester transfer protein (CETP) inhibitors raise high-density lipoprotein (HDL) cholesterol, but torcetrapib, the first-in-class inhibitor tested in a large outcome trial, caused an unexpected blood pressure elevation and increased cardiovascular events. Whether the hypertensive effect resulted from CETP inhibition or an off-target action of torcetrapib has been debated. We hypothesized that common single-nucleotide polymorphisms in the CETP gene could help distinguish mechanism-based from off-target actions of CETP inhibitors to inform on the validity of CETP as a therapeutic target.

Methods and Results— We compared the effect of CETP single-nucleotide polymorphisms and torcetrapib treatment on lipid fractions, blood pressure, and electrolytes in up to 67 687 individuals from genetic studies and 17 911 from randomized trials. CETP single-nucleotide polymorphisms and torcetrapib treatment reduced CETP activity and had a directionally concordant effect on 8 lipid and lipoprotein traits (total, low-density lipoprotein, and HDL cholesterol; HDL2; HDL3; apolipoproteins A-I and B; and triglycerides), with the genetic effect on HDL cholesterol (0.13 mmol/L, 95% confidence interval [CI] 0.11 to 0.14 mmol/L) being consistent with that expected of a 10-mg dose of torcetrapib (0.13 mmol/L, 95% CI 0.10 to 0.15). In trials, 60 mg of torcetrapib elevated systolic and diastolic blood pressure by 4.47 mm Hg (95% CI 4.10 to 4.84 mm Hg) and 2.08 mm Hg (95% CI 1.84 to 2.31 mm Hg), respectively. However, the effect of CETP single-nucleotide polymorphisms on systolic blood pressure (0.16 mm Hg, 95% CI –0.28 to 0.60 mm Hg) and diastolic blood pressure (–0.04 mm Hg, 95% CI –0.36 to 0.28 mm Hg) was null and significantly different from that expected of 10 mg of torcetrapib.

Conclusions— Discordance in the effects of CETP single-nucleotide polymorphisms and torcetrapib treatment on blood pressure despite the concordant effects on lipids indicates the hypertensive action of torcetrapib is unlikely to be due to CETP inhibition or shared by chemically dissimilar CETP inhibitors. Genetic studies could find a place in drug-development programs as a new source of randomized evidence for drug-target validation in humans.

  M. P Riley , E Zado , R Bala , D. J Callans , J Cooper , S Dixit , F Garcia , E. P Gerstenfeld , M. D Hutchinson , D Lin , V Patel , R Verdino and F. E. Marchlinski

The endocardial substrate for ventricular arrhythmias in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is thought to be caused by a progressive degenerative process. Many clinical decisions and treatment plans are guided by this pathophysiologic assumption, but the extent of progression of macroscopic endocardial scar and right ventricular (RV) dilatation have not been assessed.

Methods and Results—

Eleven patients with ARVD/C and ventricular tachycardia had 2 detailed sinus rhythm electroanatomic endocardial voltage maps (average, 291±122 points per map; range, 114 to 558 points) performed a mean of 57 months apart (minimum, 9 months) as part of ventricular tachycardia ablation procedures. Voltage-defined scar (<1.5 mV) and RV volume were measured by area and volume measurement software and compared. Two of the 11 patients had a clear increase in scar area (47 cm2; 32 cm2) confirmed by visual inspection. The remaining 9 (81%; 95% CI, 48% to 98%) patients had no increase (<10-cm2 difference) in scar area between studies. In contrast, 10 of the 11 patients had a significant increase in RV volume, with an average increase of 24% (212±67 mL to 263±52 mL; P≤0.01).


In patients with ARVD/C and ventricular tachycardia, progressive RV dilatation is the rule, and rapid progression of significant macroscopic endocardial scar occurs in only a subset of patients. These results have important management implications, suggesting that efforts to prevent RV dilatation in this population are needed and that an aggressive substrate-based ablation strategy offers the potential to provide long-term ventricular tachycardia control.

  P Leong Sit , E Zado , D. J Callans , F Garcia , D Lin , S Dixit , R Bala , M. P Riley , M. D Hutchinson , J Cooper , E. P Gerstenfeld and F. E. Marchlinski

Young patients with atrial fibrillation (AF) tend to be more symptomatic and less willing to take long-term medications, yet catheter ablation remains recommended as second-line therapy for AF regardless of age. This study seeks to characterize the effectiveness and risk of AF ablation in the young.

Methods and Results—

Consecutive (n=1548) patients who underwent 2038 AF ablation procedures were included. Major procedural complications and efficacy were analyzed on the basis of age at the initial procedure: <45 years (group 1), 45 to 54 years (group 2), 55 to 64 years (group 3), and ≥65 years (group 4). AF control was defined as no or rare AF on or off antiarrhythmic drugs. The primary outcome of AF control was similar in all groups; it was achieved in 87% in group 1, 88% in group 2, 88% in group 3, and 82% in group 4 (P=0.06). However, more group 1 patients demonstrated freedom from AF off antiarrhythmic drugs (76%) compared with group 2 at 68%, group 3 at 65%, and group 4 at 53% (P<0.001). There were no major complications in group 1, 10 (1.7%) in group 2, 14 (1.4%) in group 3, and 10 (2.6%) in group 4 (P=0.01).


In patients younger than 45 years, there is a lower major complication rate and a comparable efficacy rate, with a greater chance of being AF free without antiarrhythmic drugs. These findings suggest that it may be appropriate to consider ablative therapy as first-line therapy in this age group.

  V. W Tsai , J Cooper , H Garan , A Natale , L. M Ptaszek , P. T Ellinor , K Hickey , R Downey , P Zei , H Hsia , P Wang , S Hunt , F Haddad and A. Al Ahmad

Background— Sudden cardiac death among orthotopic heart transplant recipients is an important mechanism of death after cardiac transplantation. The role for implantable cardioverter-defibrillators (ICDs) in this population is not well established. This study sought to determine whether ICDs are effective in preventing Sudden cardiac death in high-risk heart transplant recipients.

Methods and Results— We retrospectively analyzed the records of all orthotopic heart transplant patients who had ICD implantation between January 1995 and December 2005 at 5 heart transplant centers. Thirty-six patients were considered high risk for sudden cardiac death. The mean age at orthotopic heart transplant was 44±14 years, the majority being male (n=29). The mean age at ICD implantation was 52±14 years, whereas the average time from orthotopic heart transplant to ICD implant was 8 years ±6 years. The main indications for ICD implantation were severe allograft vasculopathy (n=12), unexplained syncope (n=9), history of cardiac arrest (n=8), and severe left ventricular dysfunction (n=7). Twenty-two shocks were delivered to 10 patients (28%), of whom 8 (80%) received 12 appropriate shocks for either rapid ventricular tachycardia or ventricular fibrillation. The shocks were effective in terminating the ventricular arrhythmias in all cases. Three (8%) patients received 10 inappropriate shocks. Underlying allograft vasculopathy was present in 100% (8 of 8) of patients who received appropriate ICD therapy.

Conclusions— Use of ICDs after heart transplantation may be appropriate in selected high-risk patients. Further studies are needed to establish an appropriate prevention strategy in this population.

  K Hawton , H Bergen , S Simkin , J Cooper , K Waters , D Gunnell and N. Kapur


Self-poisoning is a common method of suicide and often involves ingestion of antidepressants. Information on the relative toxicity of antidepressants is therefore extremely important.


To assess the relative toxicity of specific tricyclic antidepressants (TCAs), a serotonin and noradrenaline reuptake inhibitor (SNRI), a noradrenergic and specific serotonergic antidepressant (NaSSA), and selective serotonin reuptake inhibitors (SSRIs).


Observational study of prescriptions (UK), poisoning deaths involving single antidepressants receiving coroners’ verdicts of suicide or undetermined intent (England and Wales) and non-fatal self-poisoning episodes presenting to six general hospitals (in Oxford, Manchester and Derby) between 2000 and 2006. Calculation of fatal toxicity index based on ratio of rates of deaths to prescriptions, and case fatality based on ratio of rates of deaths to non-fatal self-poisonings.


Fatal toxicity and case fatality indices provided very similar results (rho for relative ranking of indices 0.99). Case fatality rate ratios showed greater toxicity for TCAs (13.8, 95% CI 13.0–14.7) than the SNRI venlafaxine (2.5, 95% CI 2.0–3.1) and the NaSSA mirtazapine (1.9, 95% CI 1.1–2.9), both of which had greater toxicity than the SSRIs (0.5, 95% CI 0.4–0.7). Within the TCAs, compared with amitriptyline both dosulepin (relative toxicity index 2.7) and doxepin (2.6) were more toxic. Within the SSRIs, citalopram had a higher case fatality than the other SSRIs (1.1, 95% CI 0.8–1.4 v. 0.3, 95% CI 0.2–0.4).


There are wide differences in toxicity not only between classes of antidepressants, but also within classes. The findings are relevant to prescribing decisions, especially in individuals at risk, and to regulatory policy.

  N Kapur , J Cooper , O Bennewith , D Gunnell and K. Hawton

Self-harm is a major public health problem and universal interventions such as contacting individuals by post or telephone following a self-harm episode have received much attention recently. They may also appeal to service providers because of their low cost. However, a widespread introduction of these interventions cannot be justified without a better understanding of whether they work, and if so how.

  H Bergen , K Hawton , K Waters , J Cooper and N. Kapur


Self-harm is a common reason for presentation to a general hospital, with a strong association with suicide. Trends in self-harm are an important indicator of community psychopathology, with resource implications for health services and relevance to suicide prevention policy. Previous reports in the UK have come largely from single centres.


To investigate trends in non-fatal self-harm in six general hospitals in three centres from the Multicentre Study of Self-harm in England, and to relate these to trends in suicide.


Data on self-harm presentations to general hospital emergency departments in Oxford (one), Manchester (three) and Derby (two) were analysed over the 8-year period 1 January 2000 to 31 December 2007.


Rates of self-harm declined significantly over 8 years for males in three centres (Oxford: –14%; Manchester: –25%; Derby: –18%) and females in two centres (Oxford: –2% (not significant); Manchester: –13%; Derby: –17%), in keeping with national trends in suicide. A decreasing proportion and number of episodes involved self-poisoning alone, and an increasing proportion and number involved other self-injury (e.g. hanging, jumping, traffic related). Episodes involving self-cutting alone showed a slight decrease in numbers over time. Trends in alcohol use at the time of self-harm and repetition within 1 year were stable.


There were decreasing rates of non-fatal self-harm over the study period that paralleled trends in suicide in England. This was reflected mainly in a decline in emergency department presentations for self-poisoning.

  J. F Tien , N. T Umbreit , D. R Gestaut , A. D Franck , J Cooper , L Wordeman , T Gonen , C. L Asbury and T. N. Davis

The Dam1 complex, regulated by aurora B phosphorylation, confers a more stable microtubule association for the Ndc80 complex at kinetochores (see also related paper by Lampert et al. in this issue).

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