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Biomedical subjects

A John Camm

Publications and source records attributed to A John Camm.

At least 19 recordsLinked to original sources
PubMed2007

Prognostic value of blood pressure measured during hospitalization after acute myocardial infarction: an insight from survival trials.

BACKGROUND: The prognostic value of blood pressure measured during hospitalization after acute myocardial infarction (MI) has not been investigated, particularly with regard to arrhythmic death. METHODS: A total of 3311 placebo patients (2612 men, median age 64 years; range 23-92) from the EMIAT, CAMIAT, SWORD, TRACE and DIAMOND-MI studies with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia surviving more than 45 days after MI were pooled. Systolic and diastolic blood pressures and pulse pressures were measured soon after MI (median 6 days, range 0-53 days). Mortality up to 2 years was examined using Cox regression. RESULTS: At the 2-year follow-up, after adjustment for age, sex, smoking, previous MI, hypertension, heart rate, New York Heart Association functional class, baseline treatments, study effect and diastolic blood pressure, reduced systolic blood pressure measured during hospitalization after acute MI significantly increased the risk of all-cause mortality [hazard ratio (HR) for 10% increase in systolic blood pressure 0.80, 95% confidence interval (CI) 0.71-0.90; P < 0.001] and arrhythmic mortality (HR 0.73, 95% CI 0.61-0.86; P = 0.001). Reduced diastolic blood pressure significantly increased the risk of all-cause mortality (HR 0.87, 95% CI 0.77-0.98; P = 0.02) and arrhythmic mortality (HR 0.80, 95% CI 0.68-0.93; P = 0.005). CONCLUSION: In post-MI patients with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia, reduced blood pressure measured during hospitalization after MI significantly predicts all-cause mortality and arrhythmic mortality, and can be reliably used to identify patients who are at risk of dying after MI.

Adult↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death).

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Anti-Arrhythmia Agents↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Arrhythmias, Cardiac↗
PubMed2006

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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American Heart Association↗
PubMed2006

ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Algorithms↗
PubMed2006

Cumulative experience of azimilide-associated torsades de pointes ventricular tachycardia in the 19 clinical studies comprising the azimilide database.

OBJECTIVES: The purpose of this study was to assess the incidence, temporal characteristics, and risk factors associated with azimilide-associated torsades de pointes (TdP) ventricular tachycardia. BACKGROUND: Azimilide dihydrochloride is a class III antiarrhythmic drug possessing Ikr and Iks channel-blocking properties. METHODS: Oral azimilide (75 to 125 mg/day) was taken by 5,375 patients in 19 clinical trials conducted at 775 international centers. Of 3,964 patients in double-blind studies, 1,427 had a history of atrial fibrillation or other supraventricular arrhythmia, 510 had an implantable cardioverter-defibrillator, and 2,027 were post-myocardial infarction patients with a left ventricular ejection fraction < or =35%. RESULTS: The TdP occurred in 56 patients assigned to azimilide, was dose-related, and tended to occur earlier with an azimilide-loading regimen. Forty-three percent of TdP patients had a QT interval corrected by Bazett's formula, for heart rate, (QTc) > or =500 ms at the time of or before the TdP occurrence. Significant risk factors using logistic regression were increasing age, female gender, diuretic use, and lack of aspirin use. CONCLUSIONS: Azimilide-associated TdP has characteristics and risk factors similar to other Ikr blockers. However, there is a distinctive temporal profile. The TdP events are not concentrated in the first week. The azimilide-associated TdP rate is 1% (95% confidence interval 0.78 to 1.35) and is not increased in patients with low left ventricular ejection fraction, even in women.

Aged↗
PubMed2006

Cardiovascular outcomes with atrial-based pacing compared with ventricular pacing: meta-analysis of randomized trials, using individual patient data.

BACKGROUND: Several randomized trials have compared atrial-based (dual-chamber or atrial) pacing with ventricular pacing in patients with bradycardia. No trial has shown a mortality reduction, and only 1 small trial suggested a reduction in stroke. The goal of this review was to determine whether atrial-based pacing prevents major cardiovascular events. METHODS AND RESULTS: A systematic review was performed of publications since 1980. For inclusion, trials had to compare an atrial-based with a ventricular-based pacing mode; use a randomized, controlled, parallel design; and have data on mortality, stroke, heart failure, or atrial fibrillation. Individual patient data were obtained from 5 of the 8 identified studies, representing 95% of patients in the 8 trials, and a total of 35 000 patient-years of follow-up. There was no significant heterogeneity among the results of the individual trials. There was no significant reduction in mortality (hazard ratio [HR], 0.95; 95% confidence interval [CI], 0.87 to 1.03; P=0.19) or heart failure (HR, 0.89; 95% CI, 0.77 to 1.03; P=0.15) with atrial-based pacing. There was a significant reduction in atrial fibrillation (HR, 0.80; 95% CI, 0.72 to 0.89; P=0.00003) and a reduction in stroke that was of borderline significance (HR, 0.81; 95% CI, 0.67 to 0.99; P=0.035). There was no convincing evidence that any patient subgroup received special benefit from atrial-based pacing. CONCLUSIONS: Compared with ventricular pacing, the use of atrial-based pacing does not improve survival or reduce heart failure or cardiovascular death. However, atrial-based pacing reduces the incidence of atrial fibrillation and may modestly reduce stroke.

Arrhythmias, Cardiac↗
PubMed2006

Effect of fish oil on ventricular tachyarrhythmia and death in patients with implantable cardioverter defibrillators: the Study on Omega-3 Fatty Acids and Ventricular Arrhythmia (SOFA) randomized trial.

CONTEXT: Very-long-chain n-3 polyunsaturated fatty acids (omega-3 PUFAs) from fish are thought to reduce risk of sudden death, possibly by reducing susceptibility to cardiac arrhythmia. OBJECTIVE: To study the effect of supplemental fish oil vs placebo on ventricular tachyarrhythmia or death. DESIGN, SETTING, AND PATIENTS: The Study on Omega-3 Fatty acids and ventricular Arrhythmia (SOFA) was a randomized, parallel, placebo-controlled, double-blind trial conducted at 26 cardiology clinics across Europe. A total of 546 patients with implantable cardioverter-defibrillators (ICDs) and prior documented malignant ventricular tachycardia (VT) or ventricular fibrillation (VF) were enrolled between October 2001 and August 2004. Patients were randomly assigned to receive 2 g/d of fish oil (n = 273) or placebo (n = 273) for a median period of 356 days (range, 14-379 days). MAIN OUTCOME MEASURE: Appropriate ICD intervention for VT or VF, or all-cause death. RESULTS: The primary end point occurred in 81 (30%) patients taking fish oil vs 90 (33%) patients taking placebo (hazard ratio [HR], 0.86; 95% confidence interval [CI], 0.64-1.16; P = .33). In prespecified subgroup analyses, the HR was 0.91 (95% CI, 0.66-1.26) for fish oil vs placebo in the 411 patients who had experienced VT in the year before the study, and 0.76 (95% CI, 0.52-1.11) for 332 patients with prior myocardial infarctions. CONCLUSION: Our findings do not indicate evidence of a strong protective effect of intake of omega-3 PUFAs from fish oil against ventricular arrhythmia in patients with ICDs. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00110838.

Aged↗
PubMed2006

Delayed paced ventricular activation in the long QT syndrome is associated with ventricular fibrillation.

BACKGROUND: LQTS may cause sudden cardiac death (SCD), but the mechanisms linking gene mutations to ventricular fibrillation (VF) are unclear. OBJECTIVE: To determine whether ventricular activation delays in congenital long QT syndrome (LQTS) are associated with VF and to describe these delays clinically by measuring activation through ventricular myocardium after a premature extrastimulus. METHODS: Forty-six patients with LQTS, including 16 with VF (LQTS VF) were investigated, and the results were compared with those from 24 patients with hypertrophic cardiomyopathy and VF (HCM VF). Electrograms in response to premature stimuli were analyzed for increases in electrogram duration (DeltaED) and the S1S2 coupling intervals at which electrogram latency starts to increase (S1S2(delay)). Two piecewise continuous straight line segments were fitted to the last electrogram deflection as a function of S1S2 interval in the LQTS and HCM VF populations, and the difference in their gradient (alpha) was taken as an index of the abruptness of the onset of this delay. RESULTS: Thirteen LQTS VF and six LQTS non-VF patients had values of DeltaED and S1S2(delay) comparable to those in HCM VF patients, while the remainder (three LQTS VF and 24 LQTS non-VF) had lower values (P<.001). There was only a weak correlation between delay and the corrected QT interval. The HCM and LQTS VF patients could be separated by the value of alpha (P<.01), with the LQTS patients having a more abrupt onset of delay. CONCLUSIONS: Large delays in ventricular activation after an extrastimulus occur in patients with the LQTS, especially those with VF. The change in delay is abrupt in the LQTS, indicating sudden block to activation creating a dynamic substrate for arrhythmogenesis.

Adolescent↗
PubMed2006

Turbulence dynamics: an independent predictor of late mortality after acute myocardial infarction.

INTRODUCTION: The prognostic value of heart rate turbulence for predicting mortality after acute myocardial infarction is well established. This study investigates a new measure of heart rate turbulence, termed turbulence dynamics, which quantifies the relationship between turbulence slope and underlying heart rate (HR(VPC)). METHODS: Six hundred eight patients participating in the European Myocardial Infarction Amiodarone Trial had > or =25 ventricular premature complexes/24 h. During a follow-up period of 21 months (median), 120 patients died. Turbulence dynamics was assessed as the slope of the regression line between turbulence slope and HR(VPC). Survival analyses included age, history of previous myocardial infarction, presence of diabetes mellitus, mean normal-to-normal interval, heart rate variability index, presence of non-sustained ventricular tachycardia, left ventricular ejection fraction, turbulence onset and turbulence slope. All risk predictors were dichotomized at pre-defined cut-off points, turbulence dynamics was dichotomized at the median. Primary endpoint of the study was death of any cause. RESULTS: In most patients, turbulence slope was inversely correlated to HR(VPC). Univariately, turbulence dynamics was the second strongest risk predictor of mortality (relative risk 2.4 (95% confidence interval 1.6-3.6), p<0.001). Multivariately, turbulence dynamics was the third strongest risk predictor (1.7 (1.1-2.7, p<0.01)). CONCLUSION: In the patient population studied, turbulence dynamics was an independent predictor of mortality. The results indicate that in addition to the overall level of autonomic function the loss of autonomic adaptability contributes to prognosis.

Acute Disease↗
PubMed2006

Effect of slow pathway ablation in atrioventricular nodal reentrant tachycardia on the electrophysiologic characteristics of the inferior atrial inputs to the human atrioventricular node.

The inferior atrial extensions of the atrioventricular (AV) node have been related to the anatomic substrate of the slow pathway, but their role in AV nodal reentrant tachycardia (AVNRT) is unknown. Ten patients with slow-fast AVNRT were studied before and after successful slow pathway ablation. Simultaneous His bundle recordings from the right and left sides of the septum were made during right and left inferoparaseptal pacing. Longer stimulus to His (St-H) intervals were measured during right inferoparaseptal pacing than during left inferoparaseptal pacing (284 +/- 55 vs 246 +/- 46 ms, p = 0.005 for right His recordings and 283 +/- 56 vs 244 +/- 46 ms, p = 0.005 for left His recordings) at similar coupling intervals during AVNRT induction. After ablation, the St-H intervals at the maximum AV nodal conduction decrement were similar during right inferoparaseptal and left inferoparaseptal pacing (217 +/- 32 vs 207 +/- 21 ms, p = 0.10 for right His and 215 +/- 32 vs 206 +/- 20 ms, p = 0.13 for left His) at similar coupling intervals. The difference (DeltaSt-H) between St-H intervals during AVRNT induction or at the maximum conduction decrement and during constant pacing for right His recordings with right inferoparaseptal pacing were significantly greater than DeltaSt-H measured with left His during left inferoparaseptal pacing (173 +/- 64 vs 137 +/- 55 ms, p = 0.005) before ablation, but not after (117 +/- 39 vs 100 +/- 40 ms, p = 0.44). Resetting of AVNRT with delivery of left inferoparaseptal extrastimuli was achieved in 7 of 10 patients. In conclusion, the electrophysiologic characteristics of the right and left inferior atrial inputs to the human AV node in patients with AVNRT and their response to slow pathway ablation provide further evidence that the inferior nodal extensions represent the anatomic substrate of the slow pathway.

Adult↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Anti-Arrhythmia Agents↗
PubMed2006

Classification and differential diagnosis of atrioventricular nodal re-entrant tachycardia.

Recent evidence on atrioventricular nodal re-entrant tachycardia has identified several types of this common arrhythmia, with potential therapeutic implications. This article reviews the relevant new information, discusses the differential diagnosis of atrioventricular nodal re-entrant tachycardia, and summarizes the electrophysiological criteria for classification of the various forms of the arrhythmia.

Diagnosis, Differential↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Atrial Fibrillation↗
PubMed2006

Novel If current inhibitor ivabradine: safety considerations.

Ivabradine is a novel heart-rate-lowering agent that acts specifically on the sinoatrial node by selectively inhibiting the I(f) current, which is the current predominantly responsible for the slow diastolic depolarization of pacemaker cells. Unlike many rate-lowering agents, ivabradine reduces heart rate in a dose-dependent manner both at rest and during exercise without producing any negative inotropic or vasoconstrictor effect. The bradycardic effect of ivabradine is proportional to the resting heart rate, such that the effect tends to plateau. Thus, extreme sinus bradycardia is uncommon. Less than 1% of patients withdrew from therapy because of untoward sinus bradycardia. The QT interval is expectedly prolonged with the reduction in heart rate, but after appropriate correction for heart rate and in direct comparisons of the QT interval when the influence of the heart rate was controlled by atrial pacing, no significant effect of ivabradine on ventricular repolarization duration was demonstrated. Consequently, ivabradine has no direct torsadogenic potential, although, for obvious reasons, the specific bradycardic drug should not be administered with agents which have known rate-lowering and/or QTprolonging effects. Ivabradine has little effect on the atrioventricular node and ventricular refractoriness, but because of its effect on the sinus node, it should be avoided in patients with sick sinus syndrome. The physiological significance of upregulation of the I(f) current in the His-Purkinje system and ventricular myocardium due to ionic remodeling in pathophysiological conditions, such as end-stage heart failure, and the effects of ivabradine have yet to be explored. Because ivabradine also binds to hyperpolarization voltage-gated channels which carry the I(h) current in the eye, transient, dose-dependent changes of the electroretinogram resulting in mild to moderate visual side effects (phenomes) may occur in approximately 15% of patients exposed to ivabradine. Ivabradine does not cross the blood-brain barrier and therefore, has no effect on the I(h) current in central nervous system neurons. The safety of ivabradine has been assessed in a development program that enrolled over 3,500 patients and 800 healthy volunteers in 36 countries from Europe, North and South America, Africa, Asia and Australia, 1,200 of whom were exposed to ivabradine for over 1 year. Ivabradine has been associated with a good safety profile during its clinical development and its safety will be further assessed by postmarketing surveillance and during on-going clinical trials.

Adrenergic beta-Antagonists↗