Prevention Of Fibrillation Research Articles

Профилактика фибрилляции предсердий после прямой реваскуляризации миокарда: рандомизированное сравнительное исследование

Профилактика фибрилляции предсердий после прямой реваскуляризации миокарда: рандомизированное сравнительное исследование

冠動脈バイパス術後心房細動の発生と予防

冠動脈バイパス術後心房細動の発生と予防

Cardiac Sympathetic Nerve Sprouting and Susceptibility to Ventricular Arrhythmias after Myocardial Infarction.

Ventricular arrhythmogenesis is thought to be a common cause of sudden cardiac death following myocardial infarction (MI). Nerve remodeling as a result of MI is known to be an important genesis of life-threatening arrhythmias. It is hypothesized that neural modulation might serve as a therapeutic option of malignant arrhythmias. In fact, left stellectomy or β-blocker therapy is shown to be effective in the prevention of ventricular tachyarrhythmias (VT), ventricular fibrillation (VF), and sudden cardiac death (SCD) after MI both in patients and in animal models. Results from decades of research already evidenced a positive relationship between abnormal nerve density and ventricular arrhythmias after MI. In this review, we summarized the molecular mechanisms involved in cardiac sympathetic rejuvenation and mechanisms related to sympathetic hyperinnervation and arrhythmogenesis after MI and analyzed the potential therapeutic implications of nerve sprouting modification for ventricular arrhythmias and SCD control.

冠動脈バイパス術後心房細動の予防と治療

冠動脈バイパス術後心房細動の予防と治療

Abstract 18114: Prevalence of Left Atrial Appendage Thrombus in Oncologic Patients with Atrial Fibrillation

Introduction: There is considerable evidence that the left atrial appendage (LAA) is a common site for thrombus formation and its characteristics pose varying risks for having embolic events. Furthermore, atrial fibrillation has been found to occur with an increased frequency in patients with malignancies. The lack of evidence of standardized treatment strategies in the cancer population forces physicians to take an individualized approach to atrial fibrillation and stroke prevention. Herein, we describe the LAA characteristics in a cancer population with atrial fibrillation. Hypothesis: Cancer patients have an increased risk of LAA thrombus formation in atrial fibrillation. Methods: This is a retrospective study to determine the prevalence of LAA thrombus in a cohort of oncologic patients with atrial fibrillation. Two hundred and forty-five patients underwent transesophageal echocardiogram (TEE) at MD Anderson Cancer Center during the period 2000-2013 for atrial fibrillation evaluation. Results: LAA thrombus was identified in 6.5% of patients (16 of 245). During follow up, three of these patients had experienced a stroke (19%). The mean age was 67 with 5 females (31%) and 11 males (69%). Fifteen patients were white. The majority of patients had solid tumors (75%, 12 of 16). The mean CHADS2 score was 1.3 +/- 0.9 and the mean left ventricular ejection fraction on transthoracic echo was 57 +/- 9%. Spontaneous echo contrast was noted on TEE in 56% of patients (9 of 16). Five patients were on antiplatelet therapy and 9 were on oral anticoagulants. Oncologic, TEE, and clinical data are detailed below (Table 1). Conclusions: The prevalence of LAA thrombus and stroke in cancer patients with atrial fibrillation is significant. These findings may be a reflection of the enhanced inflammatory state of cancer. This data suggest that LAA thrombus evaluation is critical in determining the anticoagulation strategy in atrial fibrillation patients with cancer.

The effect of lidocaine and amiodarone on prevention of ventricular fibrillation in patients undergoing coronary artery bypass grafting.

Ventricular fibrillation is common after aortic declamping in patients undergoing open heart surgery. This situation has a negative impact on morbidity and mortality. The aim of this prospective study was to compare the effect of administering lidocaine versus amiodarone before aortic declamping during elective coronary bypass grafting, paying close attention to when the initial effect of amiodarone sets in. In this double blind, prospective, randomized, controlled study, 86 patients who were candidates for elective coronary artery bypass grafting were recruited into three groups: group lidocaine (group L, n=29); group amiodarone (group A, n=27); and group placebo (group P, n=30). Group L patients received 1.5 mg/kg of lidocaine 2 minutes before aortic declamping and group A patients received 300 mg of amiodarone intravenously 15 minutes before release of the aortic cross clamp. The primary endpoints were the incidence of ventricular fibrillation and the number of shocks required to terminate ventricular fibrillation. The frequency of ventricular fibrillation occurrence was significantly higher in group P (70%) when compared with group A (37%) and group L (38%) (P=.017). There was no statistically significant difference between the amiodarone and the lidocaine groups regarding ventricular fibrillation. However, when ventricular fibrillation occurred, the percentage of patients requiring electrical defibrillation was significantly higher in both group L and group P when compared with group A (P=.023). We suggest that during coronary arterial bypass surgery, administration of an amiodarone regime before release of the aortic cross clamp, paying particular attention to the start of the initial effect of amiodarone, is no more effective than lidocaine for prevention from arrhythmia; however, amiodarone reduces the need for electrical defibrillation.

Advances in clinical cardiology.

Multiple, potentially practice-changing cardiology trials have been presented or published over the past year. In this paper, we summarize and place in clinical context, new data regarding management of acute coronary syndrome and ST-elevation myocardial infarction (copeptin assessment, otamixaban, cangrelor, prasugrel, sodium nitrite, inclacumab, ranolazine, preventive coronary intervention of non-culprit lesions, immediate thrombolytic therapy versus transfer for primary intervention), new coronary intervention data (thrombectomy, radial access, pressure wire fractional flow reserve, antiplatelet therapy duration and gene-guidance, permanent and biodegradable polymers, coronary bifurcation and strategies), and coronary artery bypass data (off pump vs. on pump). Latest trials in trans-aortic valve implantation, heart failure (eplerenone, aliskiren, spironolactone, sildenafil, dopamine, nesiritide, omecamtiv mecarbil, the algisyl left ventricular augmentation device, and echo-guided cardiac resynchronization), atrial fibrillation (edoxaban, dabigatran, and ablation), cardiac arrest (hypothermia, LUCAS™ mechanical chest compression), and cardiovascular prevention (vitamins, renal denervation for resistant hypertension, renal artery stenting, saxagliptin, alogliptin, and gastric banding) are also discussed.

Comparison of Plegisol and Modified ST Thomas Hospital Cardioplegic Solution in the Development of Ventricular Fibrillation after Declamping of the Aorta

Ventricular fibrillation seen just after declamping of the aorta is an undesirable condition causing myocardial injury. To return to normal rhythm, often internal shocks are applied. But defibrillation itself can also contribute to myocardial injury. So prevention of fibrillation is more important than treatment. 236 patients undergoing coronary artery by-pass surgery were included in this retrospective clinical study. 144 of those patients were operated using modified St. Thomas’ Hospital cardioplegic solution, for stopping the heart. In the other 92 patients, plegisol cardioplegic solution was used. We compared the two groups for the development of ventricular fibrilation after declamping of the aorta. In the modified St. Thomas’ Hospital group, ventricular fibrillation after declamping of the aorta was seen less frequently, this being statistically significant (22.2% vs. 52.2%, p = 0.026). This study shows that the modified St.Thomas’ Hospital cardioplegic solution is preferred for avoiding ventricular fibrillation occuring just after declamping of the aorta.

SECONDARY PREVENTION OF STROKE IN PATIENTS WITH NON-VALVULAR ATRIAL FIBRILLATION: THE CLINICIANS’ VIEWPOINT

Atrial fibrillation is one of the main risk factor of ischemic stroke. Current problems of the management of patients with stroke due to non-valvular atrial fibrillation and secondary stroke prevention in these patients are considered. Data of own author’s observation for patients of this type during 6 months after discharge from the hospital are presented. The problems which patients faced with are analyzed. Comparative assessment of warfarin and dabigatran therapies is given.

Amiodarone versus lidocaine for the prevention of reperfusion ventricular fibrillation: A randomized clinical trial.

Reperfusion ventricular fibrillation after aortic cross clamp is one of the important complications of open cardiac surgery and its prevention could reduce myocardial injuries. This study aimed to evaluate the efficacy of single dose of amiodarone or lidocaine by the way of pump circuit three minutes before aortic cross clamp release and compare the results with normal saline as placebo in a randomized double blinded controlled trial. One hundred fifty patients scheduled for first time elective coronary artery bypass graft surgery were randomly assigned to receive either single dose of amiodarone (150 mg), lidocaine (100 mg), or normal saline (5 ml) three minutes before aortic cross clamp release. The incidence of ventricular fibrillation and the need for reuse of drug were compared between these groups by chi-square, Student's t-test, Mann-Whitney test, and One-way ANOVA. SPSS software was used for statistical analysis. The incidence of ventricular fibrillation is higher in the placebo group (15.9%) compare to lidocaine (11.8%) and amiodarone (8.9%) groups; however, there was no statistical difference among the three groups (P = 0.41). Moreover, the reuse of amiodarone (22.7%) was statistically higher (P < 0.05) than lidocaine (5.9%). This study showed no difference among lidocaine, amiodarone, and placebo in preventing ventricular fibrillation after aortic cross clamp release.

SAFE Combinations Fail to Open the Door to Atrial Fibrillation Prevention

The prevalence of atrial fibrillation (AF) in the entire US population is ≈1%.1 The prevalence of AF increases substantially with age, with ≤9% of patients over the age of 80 years developing AF. The population presenting with permanent pacing requirements also increases with age, and the cumulative lifetime risk of developing paroxysmal AF in pacemaker patients may be as high as 40%.2 Article see p 687 Mechanisms for AF initiation and maintenance are multiple but are widely accepted to be a result of triggered initiation by atrial premature beats, and maintenance within the atrial substrate on the basis of multiple wavelets of reentry and rotors that depend on inhomogeneous atrial refractory periods and atrial conduction velocities. Atrial pacing may prevent both AF triggers and atrial substrate changes by suppressing atrial premature beats and inducing a more homogenous atrial landscape of refractory periods and conduction velocities. Atrial-based pacing is clearly superior to ventricular pacing alone in preventing atrial fibrillation with an 18% relative risk reduction with atrial-based pacing over a 3-year follow-up.3 This treatment effect has been postulated to be the result of atrial premature beat suppression and changes in atrial refractory periods and atrial conduction velocities as a result of atrial stretch attributed to higher atrial pressure from AV dyssynchronous pacing. The atrial changes associated with atrial-based pacing could possibly be enhanced by atrial overdrive pacing algorithms or by alternative site atrial pacing, such as the atrial septum. The role of alternative-site atrial pacing …

Abstract 288: Vitamin C Decreases Atrial Fibrillation In Cardiac Surgery Patients But Vitamin E May Decrease Response: A Randomized-controlled Trial Meta-analysis

Background: Due to the population aging, atrial fibrillation (AF) is becoming a more prevalent disease, it also commonly presents as a cardiac surgery complication. Randomized controlled trials (RCT) concerning anti-oxidant vitamins for atrial fibrillation (AF) prophylaxis have yielded inconsistent outcomes. Similar inconsistencies were found in other cardiovascular studies, as the HOPE and FATS studies, suggesting that vitamin E in special may not be helpful, perhaps harmful. Methods: All randomized controlled trials on anti-oxidant vitamins supplementation for atrial fibrillation prevention for patients undergoing cardiac surgery were sought in Medline and Cochrane databases during May 2012. Data was extracted by 3 reviewers. Results: Seven studies were found, three with vitamin C, two with Vitamin E and two combining both. We found an overall significant 60% decrease in the overall chance for AF occurrence mostly driven by (Figures1A and 1B) as the studies with vitamin E or vitamin C and E combined (Figures 1 C and 1D) did not show a statistically significant difference. When all studies with Vitamin E alone or in combination with Vitamin C (Figure 1E). Conclusions: Vitamin C supplementation decreases the incidence of post cardiac surgery AF but the data on Vitamin E is inconsistent, it may even decrease the Vitamin C benefit. As vitamin self-supplementation is extremely common in the US, large trials are extremely important not only for benefit confirmation but to exclude potential harms.

CHADS2 Score, Statin Therapy, and Risks of Atrial Fibrillation

ObjectiveLittle is known about the effectiveness of statins on primary prevention of atrial fibrillation in elderly patients. This study aimed to evaluate the efficacy of statin treatment for atrial fibrillation prevention in elderly patients with hypertension, and to determine if comorbidity or CHADS2 (Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus, prior Stroke or transient ischemic attack) score can predict the effectiveness of statin treatment. MethodsPatients aged ≥65 years with hypertension were identified from a National Health Insurance research database (a systemic sampling from 2000 to 2009 with a total of 1,000,000 subjects). Medical records of 27,002 patients were used in this study, in which 2400 (8.9%) were receiving statin therapy. Risk of new-onset atrial fibrillation in statin users and nonusers was analyzed. ResultsDuring the 9-year follow-up period, 2241 patients experienced new-onset atrial fibrillation. Statin users were younger than nonusers (72.4 vs 73.4 years) but had a higher prevalence of ischemic heart disease, diabetes mellitus, stroke, and chronic renal disease. Overall, statin therapy reduced the risk of atrial fibrillation by 19% (adjusted hazard ratio 0.81; 95% confidence interval, 0.69-0.95; P=.009). Subgroup analysis showed that statin use was beneficial in patients with or without a particular comorbidity. The effectiveness of statins was significant in patients with CHADS2 score ≥2 (adjusted hazard ratio 0.69; 95% confidence interval, 0.57-0.85; P <.001). However, statin therapy was not as beneficial in hypertensive patients without other cardiovascular comorbidities (CHADS2 score =1). ConclusionStatin therapy in elderly patients with hypertension reduces the risk of new-onset atrial fibrillation. Statins are more beneficial in patients with CHADS2 score ≥2 than in those with score of 1.

Anticoagulation du sujet âgé : nouveautés thérapeutiques

Vitamin-K antagonists (VKA) are the current standard for oral anticoagulation. However, they carry several problems in older patients: frequent bleeding complications, complex management, risk of interactions with multiple drugs. Two new classes of oral anticoagulants (NOA) are now available: direct thrombin inhibitors (dabigatran); and direct factor Xa inhibitors (rivaroxaban, apixaban) and others. Their management is easier: quickly effective after administration, they are given at fixed doses and do not need regular laboratory monitoring. Several randomized trials have shown that NOA are non-inferior to heparins and VKA for treating venous thromboembolic disease (prophylactic or curative treatment) and atrial fibrillation (prevention of associated embolisms). NOA are also being studied for long-term treatment after acute coronary syndromes. Data regarding older people is still sparse. No trial has specifically studied older patients. In the context of atrial fibrillation, subgroup analysis show similar results between patients above and below 75 years old, except for dabigatran which seems to carry more bleeding complications in people older than 75 years, specially with the highest dose employed. All NOA are eliminated at least partly by kidneys. Their dose must be reduced in moderate renal failure (filtration glomerular rate (FGR) 30 to 50 ml/min) and they are contra-indicated in severe renal failure (FGR<30 ml/min). Doses of dabigatran and apixaban should be reduced in older people too. NOA also have other unresolved problems: drug interactions are still possible, specific coagulation test to assess them must be developed, and no specific antidote is currently available in case of hemorrhagic complication.

How curcumin affords effective protection against amyloid fibrillation in insulin

Since the formation of amyloid structures from proteins was recognized in numerous diseases, many efforts have been devoted to the task of finding effective anti-amyloidogenic compounds. In a number of these investigations, the existence of "generic" compounds is implicitly acknowledged. Curcumin seems to be one of these compounds, possessing key structural components effective toward fibrillation prevention, and its anti-amyloidogenic property has been reported for a number of model and disease-related proteins such as lysozyme and alpha-synuclein. In this study, insulin amyloid formation has been shown to be effectively influenced by micromolar concentrations of curcumin. Under amyloidogenic conditions (pH 2.5 and 37 °C), the compound was observed to inhibit fibril formation of insulin in a dose-dependent manner. Moreover, addition of curcumin to the protein incubated under such conditions at different time points resulted in reduced amounts of final fibrils. Disaggregation of pre-formed fibrils was also observed upon addition of curcumin, as well as reduction in final fibril amounts after seeding. Overall, this compound appears to be able to interact with native, intermediate and fibrillar forms. Docking experiments suggest a potential interacting site with the B-chain of insulin, as well as the possibility for beta-sheet breaker activity.

Atrial fibrillation and stroke prevention: is warfarin still an option?—No

Atrial fibrillation is a common arrhythmia that increases the risk of stroke by 4.5 times. Anticoagulant/antithrombotic therapy in atrial fibrillation has been inconsistent and inappropriate. Warfarin enjoyed the monopoly of being the primary medication used to reduce the risk of thromboembolic events. Warfarin has many limitations in its use as an ideal anticoagulant. To overcome this difficulty, now there are two main alternative groups to warfarin namely, direct thrombin inhibitors (ximelagatran and dabigatran) and factor Xa inhibitors (apixaban, rivaroxaban, edoxaban, etc.). The advantages of the newer anticoagulants over the conventional warfarin are numerous. There are three landmark trials which have shown some light to the path of newer anticoagulant era, which include the following: RE-LY, ROCKET AF and ARISTOTLE. Head to head comparison of warfarin with newer anticoagulants showed the superiority of newer anticoagulants over warfarin in terms of efficacy and favorable side effect profile. After few decades of using warfarin, it's high time to enter into the era of newer anticoagulants and bid adieu to warfarin.

New Insights into the Beneficial Electrophysiologic Profile of Ranolazine in Heart Failure: Prevention of Ventricular Fibrillation With Increased Postrepolarization Refractoriness and Without Drug-Induced Proarrhythmia

BackgroundRanolazine inhibits late Na+ and K+ currents. Earlier studies have reported an antiarrhythmic effect. The aim of the present study was to understand whether ranolazine could still preserve its antiarrhythmic properties in the settings of chronic heart failure (CHF). Methods and ResultsIn 12 female rabbits, CHF was induced by 4 weeks of rapid ventricular pacing leading to a decrease in ejection fraction. Twelve rabbits underwent sham operation. Isolated hearts were Langendorff perfused and demonstrated a significant QT prolongation after induction of heart failure. Ranolazine caused a concentration-dependent (10 and 30 μmol/L) increase of action potential duration (APD90) in sham-operated and failing hearts. Eight endo- and epicardial monophasic action potentials revealed a nonsignificant increase in spatial and temporal dispersion of repolarization. The increase in APD90 was accompanied by a greater increase in refractory period, resulting in a significant increase in postrepolarization refractoriness in sham-operated (+29 ms and +55 ms; P < .01) and failing (+22 ms and +30 ms; P < .05) hearts. In control conditions, programmed ventricular stimulation and a burst pacing protocol led to ventricular fibrillation (VF) in 5 of the 12 sham-operated (6 episodes) and in 7 of the 12 failing (18 episodes) hearts. In the presence of ranolazine, VF was inducible in only 2 of 12 failing hearts (5 episodes). In the presence of low [K+], only 1 ranolazine-treated sham-operated heart developed early afterdepolarizations and ventricular tachyarrhythmias despite significant QT prolongation. ConclusionsRanolazine decreases inducibility of VF in the presence of a significant increase in postrepolarization refractoriness. This antiarrhythmic effect in the intact heart is preserved in CHF and is not associated with drug-induced proarrhythmia.

Endocardial Mapping and Catheter Ablation for Ventricular Fibrillation Prevention in Brugada Syndrome

Endocardial Mapping and Ablation of Brugada Syndrome. Brugada syndrome (BS) is characterized by ST-segment elevation in the right precordial electrocardiogram (ECG) leads and episodes of ventricular fibrillation (VF). This study aimed to observe the feasibility of substrate modification by radiofrequency catheter ablation and its effects on VF storm. Ten BS patients (all men; median age 36.5 years) with VF storm (group I, n = 4) and no VF storm (group II, n = 6) were enrolled in the study between August 2007 and December 2008. All patients underwent electrophysiological study using noncontact mapping. The multielectrode array was placed in the right ventricular outflow tract (RVOT). The isopotential map was analyzed during sinus rhythm and the region that had electrical activity occurring during J point to +60 (J+60) milliseconds interval of the V1 or V2 of surface ECG was considered as the late activation zone (LAZ) and also the substrate for ablation. LAZ was found in RVOT with variable distribution in both groups. Endocardial catheter ablation of the LAZ modified Brugada ECG pattern in 3 of 4 patients (75%) and suppressed VF storm in all 4 patients in group I during long-term follow-up (12-30 months). One patient had complete right bundle branch block from the ablation procedure. LAZ on RVOT identified by noncontact mapping may serve as potential VF substrate in BS patients with VF episodes. Radiofrequency ablation on LAZ normalized ECG, suppressed VF storm, and reduced VF recurrence. The procedure is safe and may prevent VF occurrence.

Ivabradine but not propranolol delays the time to onset of ischaemia-induced ventricular fibrillation by preserving myocardial metabolic energy status

ObjectiveHeart rate reduction (HRR) has shown a beneficial impact on the prevention of ventricular fibrillation, which could be explained by increased myocardial blood flow and preservation of mitochondrial structure. Here, we assessed the HRR impact on time to onset of ventricular fibrillation (TOVF) and myocardial metabolic energy status. Methods and resultsAn acute myocardial ischaemia was induced in pigs until ventricular fibrillation onset and TOVF was then measured. High-energy phosphates were measured in ventricular samples from the ischaemic region by nuclear magnetic resonance. Saline, ivabradine (IVA, a selective heart rate-lowering agent) and propranolol (PROPRA, a β-blocker) were administered intravenously, 30 and 60min respectively prior to ischaemia to ensure stable HRR. To study specifically the HRR impact, another set of animals received IVA and was submitted to rapid atrial pacing (200bpm) to abolish HRR. IVA and PROPRA induced a similar HRR (IVA: 22–26%, PRORA: 20–21%, p<0.01 vs. control), which was associated with a significant increase in TOVF with IVA (2325s) compared to PROPRA (682s) and saline (401s). This effect was abolished by atrial pacing performed during ischaemia and throughout the entire experimental session. Only IVA partially prevented the decrease in phosphocreatine-to-ATP ratio (CrP/ATP) ratio and the ADP accumulation at the onset of ventricular fibrillation. Finally, CrP/ATP ratio levels were correlated with TOVF (r=0.74, p<0.001). ConclusionUnlike PROPRA, IVA delayed the time to onset of ischaemia-induced ventricular fibrillation by preserving myocardial energy status, supporting the pertinence of IVA in the management of patients with coronary artery disease.

Comparison of intravenous and oral magnesium replacement in hospitalized patients with cardiovascular disease

The results of an investigation of serum magnesium concentrations (SMCs) after i.v. versus oral delivery of magnesium in cardiovascular critical care are presented. A retrospective case review was conducted to compare the net gain of magnesium after i.v. (n = 188) or oral (n = 164) magnesium therapy for the prevention of ventricular fibrillation and arrhythmias in patients hospitalized for serious cardiovascular disorders, as determined by assessing SMCs. The primary study outcome was the change from baseline SMC values 6-24 hours after the completion of magnesium courses; secondary outcomes included the impact of renal impairment, concomitant medication use, and other clinical variables on SMC changes. Although consistent elevations in SMC were produced by oral magnesium delivery, i.v. administration resulted in greater and more rapid elevations relative to baseline SMC. The degree of change in SMC was significantly influenced by the timing of SMC measurement after a magnesium course, by renal function, and by concomitant use of i.v. loop diuretics. A comparison of 24-hour courses of magnesium replacement therapy showed that magnesium sulfate 2 g i.v. was associated with larger changes in SMC than magnesium oxide 800, 1200, or 1600 mg orally when the baseline SMC was 1.4-1.8 mg/dL. At baseline SMCs of 1.4-1.8 mg/dL, oral magnesium oxide provided a consistent median increase in SMC of 0.1 mg/dL. The change in the number of bowel movements did not differ significantly between courses of i.v. magnesium sulfate and oral magnesium oxide.