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Indian Pacing and Electrophysiology... Aug 2010After initial documentation of excellent efficacy with radiofrequency ablation, this procedure is being performed increasingly in more complex situations and for more...
After initial documentation of excellent efficacy with radiofrequency ablation, this procedure is being performed increasingly in more complex situations and for more difficult arrhythmia. In these circumstances, an accurate knowledge of the anatomic basis for the ablation procedure will help maintain this efficacy and improve safety. In this review, we discuss the relevant anatomy for electrophysiology interventions for typical right atrial flutter, atrial fibrillation, and outflow tract ventricular tachycardia. In the pediatric population, maintaining safety is a greater challenge, and here again, knowing the neighboring and regional anatomy of the arrhythmogenic substrate for these arrhythmias may go a long way in preventing complications.
PubMed: 20811537
DOI: No ID Found -
Cureus Jul 2023Atrial flutter is characterized by rapid atrial activity, causing an abnormal heart rhythm. Recognition and prompt management are of utmost importance since this cardiac...
Atrial flutter is characterized by rapid atrial activity, causing an abnormal heart rhythm. Recognition and prompt management are of utmost importance since this cardiac arrhythmia could increase the risk of thromboembolic stroke and atrial fibrillation, which may lead to disability and death. Risk factors include myocardial infarction, surgery, medication, and structural heart abnormalities. One distinctive structural abnormality is dextrocardia. Herein, we present a case of a 47-year-old male who initially complains of difficulty in ambulation. Further workup showed atrial flutter with rapid ventricular response on electrocardiogram (ECG) and dextrocardia on imaging. This case tackles the possible association between dextrocardia and arrhythmias, which was an atrial flutter, its management, and treatment outcomes.
PubMed: 37602138
DOI: 10.7759/cureus.42177 -
Heart Rhythm Mar 2015Stellate ganglion nerve activity (SGNA) is important in ventricular arrhythmogenesis. However, because thoracotomy is needed to access the stellate ganglion, it is...
BACKGROUND
Stellate ganglion nerve activity (SGNA) is important in ventricular arrhythmogenesis. However, because thoracotomy is needed to access the stellate ganglion, it is difficult to use SGNA for risk stratification.
OBJECTIVE
The purpose of this study was to test the hypothesis that subcutaneous nerve activity (SCNA) in canines can be used to estimate SGNA and predict ventricular arrhythmia.
METHODS
We implanted radiotransmitters to continuously monitor left stellate ganglion and subcutaneous electrical activities in 7 ambulatory dogs with myocardial infarction, complete heart block, and nerve growth factor infusion to the left stellate ganglion.
RESULTS
Spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) was documented in each dog. SCNA preceded a combined 61 episodes of VT and VF, 61 frequent bigeminy or couplets, and 61 premature ventricular contractions within 15 seconds in 70%, 59%, and 61% of arrhythmias, respectively. Similar incidence of 75%, 69%, and 62% was noted for SGNA. Progressive increase in SCNA [48.9 (95% confidence interval [CI] 39.3-58.5) vs 61.8 (95% CI 45.9-77.6) vs 75.1 (95% CI 57.5-92.7) mV-s] and SGNA [48.6 (95% CI 40.9-56.3) vs 58.5 (95% CI 47.5-69.4) vs 69.0 (95% CI 53.8-84.2) mV-s] integrated over 20-second intervals was demonstrated 60 seconds, 40 seconds, and 20 seconds before VT/VF (P <.05), respectively. The Pearson correlation coefficient for integrated SCNA and SGNA was 0.73 ± 0.18 (P <.0001 for all dogs, n = 5). Both SCNA and SGNA exhibited circadian variation.
CONCLUSION
SCNA can be used as an estimate of SGNA to predict susceptibility to VT and VF in a canine model of ventricular arrhythmia and sudden cardiac death.
Topics: Adipose Tissue; Animals; Disease Models, Animal; Dogs; Electrocardiography; Heart Block; Heart Rate; Incidence; Locomotion; Monitoring, Physiologic; Myocardial Infarction; Nerve Growth Factor; Predictive Value of Tests; Prostheses and Implants; Stellate Ganglion; Sympathetic Nervous System; Telemetry; Ventricular Fibrillation; Ventricular Flutter; Ventricular Premature Complexes
PubMed: 25460171
DOI: 10.1016/j.hrthm.2014.11.007 -
Journal of the American College of... Jul 2020Atrial flutter (AFL) and atrial fibrillation (AF) are associated with AF-promoting atrial remodeling, but no experimental studies have addressed remodeling with...
BACKGROUND
Atrial flutter (AFL) and atrial fibrillation (AF) are associated with AF-promoting atrial remodeling, but no experimental studies have addressed remodeling with sustained AFL.
OBJECTIVES
This study aimed to define the atrial remodeling caused by sustained atrial flutter (AFL) and/or atrial fibrillation (AF).
METHODS
Intercaval radiofrequency lesions created a substrate for sustained isthmus-dependent AFL, confirmed by endocavity mapping. Four groups (6 dogs per group) were followed for 3 weeks: sustained AFL; sustained AF (600 beats/min atrial tachypacing); AF superimposed on an AFL substrate (AF+AFLs); sinus rhythm (SR) with an AFL substrate (SR+AFLs; control group). All dogs had atrioventricular-node ablation and ventricular pacemakers at 80 beats/min to control ventricular rate.
RESULTS
Monitoring confirmed spontaneous AFL maintenance >99% of the time in dogs with AFL. At terminal open-chest study, left-atrial (LA) effective refractory period was reduced similarly with AFL, AF+AFLs and AF, while AF vulnerability to extrastimuli increased in parallel. Induced AF duration increased significantly in AF+AFLs and AF, but not AFL. Dogs with AF+AFLs had shorter cycle lengths and substantial irregularity versus dogs with AFL. LA volume increased in AF+AFLs and AF, but not dogs with AFL, versus SR+AFLs. Optical mapping showed significant conduction slowing in AF+AFLs and AF but not AFL, paralleling atrial fibrosis and collagen-gene upregulation. Left-ventricular function did not change in any group. Transcriptomic analysis revealed substantial dysregulation of inflammatory and extracellular matrix-signaling pathways with AF and AF+ALs but not AFL.
CONCLUSIONS
Sustained AFL causes atrial repolarization changes like those in AF but, unlike AF or AF+AFLs, does not induce structural remodeling. These results provide novel insights into AFL-induced remodeling and suggest that early intervention may be important to prevent irreversible fibrosis when AF intervenes in a patient with AFL.
Topics: Animals; Atrial Fibrillation; Atrial Flutter; Atrial Remodeling; Catheter Ablation; Dogs; Electrocardiography; Fibrosis; Heart Atria
PubMed: 32703507
DOI: 10.1016/j.jacc.2020.05.062 -
Indian Heart Journal 2023The benefit of prior statin use to reduce the incidence of arrhythmia in acute coronary syndrome (ACS) is still a matter of debate. Statins have multiple pleiotropic... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The benefit of prior statin use to reduce the incidence of arrhythmia in acute coronary syndrome (ACS) is still a matter of debate. Statins have multiple pleiotropic effects, which may reduce the incidence of in-hospital arrhythmia. A systematic review and meta-analysis were performed to evaluate prior statin use and the incidence of in-hospital arrhythmia in ACS.
METHODS
This systematic review was conducted as per the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA). We performed a literature search through Pubmed, Proquest, EBSCOhost, and Clinicaltrial.gov. A random-effect model was used due to moderate heterogeneity. Quality assessment was performed using Newcastle Ottawa Scale. Sensitivity analysis was performed by using leave one or two out method. PROSPERO registration number: CRD42022336402.
RESULTS
Nine eligible studies consisting of 86,795 patients were included. A total of 22,130 (25.5%) patients were in statin use before the index ACS event. The prevalence of old myocardial infarction, heart failure, hypertension, diabetes mellitus, and chronic renal failure and concomitant treatment with aspirin, clopidogrel, and beta blocker was higher in the prior statin group compared to no previous statin. Overall, prior statin use was associated with a significantly lower incidence of in-hospital arrhythmia during ACS compared to no previous statin (OR 0.60; 95% CI 0.49-0.72; P < 0.00001; I = 54%, P-heterogeneity = 0.03). In subgroup analysis, previous statin use reduced the incidence of atrial fibrillation or atrial flutter (OR 0.64; 95% CI 0.43-0.95; P = 0.03; I = 73%, P-heterogeneity = 0.01) and ventricular tachycardia or ventricular fibrillation (OR 0.57; 95% CI 0.49-0.65; P < 0.00001; I = 8%, P-heterogeneity = 0.35).
CONCLUSIONS
Based on aggregate patient data, prior statin use may reduce the incidence of in-hospital arrhythmia during ACS, particularly atrial fibrillation or atrial flutter and ventricular tachycardia or ventricular fibrillation.
Topics: Humans; Atrial Fibrillation; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Acute Coronary Syndrome; Incidence; Atrial Flutter; Ventricular Fibrillation; Tachycardia, Ventricular
PubMed: 36642406
DOI: 10.1016/j.ihj.2023.01.004 -
Journal of Cardiovascular Magnetic... Nov 2022Although Chagas cardiomyopathy is related to thromboembolic stroke, data on risk factors for cerebrovascular events in Chagas disease is limited. Thus, we assessed the...
BACKGROUND
Although Chagas cardiomyopathy is related to thromboembolic stroke, data on risk factors for cerebrovascular events in Chagas disease is limited. Thus, we assessed the relationship between left ventricular (LV) impairment and cerebrovascular events and sources of thromboembolism in patients with Chagas cardiomyopathy.
METHODS
This retrospective cohort included patients with chronic Chagas cardiomyopathy who underwent cardiovascular magnetic resonance (CMR). CMR was performed with a 1.5 T scanner to provide LV volumes, mass, ejection fraction (LVEF), and myocardial fibrosis. The primary outcome was a composite of incident ischemic cerebrovascular events (stroke or transient ischemic attack-TIA) and potential thromboembolic sources (atrial fibrillation (AF), atrial flutter, or intracavitary thrombus) during the follow-up.
RESULTS
A total of 113 patients were included. Median age was 56 years (IQR: 45-67), and 58 (51%) were women. The median LVEF was 53% (IQR: 41-62). LV aneurysms and LV fibrosis were present in 38 (34%) and 76 (67%) individuals, respectively. The median follow-up time was 6.9 years, with 29 events: 11 cerebrovascular events, 16 had AF or atrial flutter, and two had LV apical thrombosis. In the multivariable model, only lower LVEF remained significantly associated with the outcomes (HR: 0.96, 95% CI: 0.93-0.99). Patients with reduced LVEF lower than 40% had a much higher risk of cerebrovascular events and thromboembolic sources (HR: 3.16 95% CI: 1.38-7.25) than those with normal LVEF. The combined incidence rate of the combined events in chronic Chagas cardiomyopathy patients with reduced LVEF was 13.9 new cases per 100 persons-year.
CONCLUSIONS
LV systolic dysfunction is an independent predictor of adverse cerebrovascular events and potential sources of thromboembolism in patients with chronic Chagas cardiomyopathy.
Topics: Humans; Female; Middle Aged; Male; Chagas Cardiomyopathy; Retrospective Studies; Atrial Flutter; Predictive Value of Tests; Ventricular Function, Left; Cardiomyopathies; Ventricular Dysfunction, Left; Stroke Volume; Atrial Fibrillation; Thromboembolism; Stroke; Heart Diseases
PubMed: 36329520
DOI: 10.1186/s12968-022-00885-x -
World Journal of Cardiology Oct 2021Dipeptidyl peptidase-4 (DPP-4) inhibitors are a generally safe and well tolerated antidiabetic drug class with proven efficacy in type 2 diabetes mellitus (T2DM)....
BACKGROUND
Dipeptidyl peptidase-4 (DPP-4) inhibitors are a generally safe and well tolerated antidiabetic drug class with proven efficacy in type 2 diabetes mellitus (T2DM). Recently, a series of large, randomized controlled trials (RCTs) addressing cardiovascular outcomes with DPP-4 inhibitors have been published.
AIM
To pool data from the aforementioned trials concerning the impact of DPP-4 inhibitors on surrogate cardiovascular efficacy outcomes and on major cardiac arrhythmias.
METHODS
We searched PubMed and grey literature sources for all published RCTs assessing cardiovascular outcomes with DPP-4 inhibitors compared to placebo until October 2020. We extracted data concerning the following "hard" efficacy outcomes: fatal and non-fatal myocardial infarction, fatal and non-fatal stroke, hospitalization for heart failure, hospitalization for unstable angina, hospitalization for coronary revascularization and cardiovascular death. We also extracted data regarding the risk for major cardiac arrhythmias, such as atrial fibrillation, atrial flutter, ventricular fibrillation and ventricular tachycardia.
RESULTS
We pooled data from 6 trials in a total of 52520 patients with T2DM assigned either to DPP-4 inhibitor or placebo. DPP-4 inhibitors compared to placebo led to a non-significant increase in the risk for fatal and non-fatal myocardial infarction [risk ratio (RR) = 1.02, 95%CI: 0.94-1.11, = 0%], hospitalization for heart failure (RR = 1.09, 95%CI: 0.92-1.29, = 65%) and cardiovascular death (RR = 1.02, 95%CI: 0.93-1.11, = 0%). DPP-4 inhibitors resulted in a non-significant decrease in the risk for fatal and non-fatal stroke (RR = 0.96, 95%CI: 0.85-1.08, = 0%) and coronary revascularization (RR = 0.99, 95%CI: 0.90-1.09, = 0%), Finally, DPP-4 inhibitors demonstrated a neutral effect on the risk for hospitalization due to unstable angina (RR = 1.00, 95%CI: 0.85-1.18, = 0%). As far as cardiac arrhythmias are concerned, DPP-4 inhibitors did not significantly affect the risk for atrial fibrillation (RR = 0.95, 95%CI: 0.78-1.17, = 0%), while they were associated with a significant increase in the risk for atrial flutter, equal to 52% (RR = 1.52, 95%CI: 1.03-2.24, = 0%). DPP-4 inhibitors did not have a significant impact on the risk for any of the rest assessed cardiac arrhythmias.
CONCLUSION
DPP-4 inhibitors do not seem to confer any significant cardiovascular benefit for patients with T2DM, while they do not seem to be associated with a significant risk for any major cardiac arrhythmias, except for atrial flutter. Therefore, this drug class should not be the treatment of choice for patients with established cardiovascular disease or multiple risk factors, except for those cases when newer antidiabetics (glucagon-like peptide-1 receptor agonists and sodium-glucose co-transporter-2 inhibitors) are not tolerated, contraindicated or not affordable for the patient.
PubMed: 34754403
DOI: 10.4330/wjc.v13.i10.585 -
Anticoagulation of Cardiovascular Conditions in the Cancer Patient: Review of Old and New Therapies.Current Oncology Reports Apr 2019The anticoagulation strategies for various cardiac-specific pathologies including atrial fibrillation are changing. Applying these strategies in patients with... (Review)
Review
PURPOSE OF REVIEW
The anticoagulation strategies for various cardiac-specific pathologies including atrial fibrillation are changing. Applying these strategies in patients with concomitant active cancer requires additional considerations. Here, we review the most recent changes in the anticoagulation management of common cardiac diseases and their application in cancer patients.
RECENT FINDINGS
There are a range of indications for therapeutic anticoagulation in cancer patients including venous thromboembolism (VTE), atrial fibrillation/flutter (AF/AFL), prosthetic heart valves, and intracardiac thrombi. Certain cancer therapeutics such as ibrutinib and anthracycline chemotherapy increase the risk of developing AF/AFL and pose unique challenges in anticoagulation management. Anticoagulation decisions for AF/AFL often utilize the CHADS2 or the CHA2DS2-VASc score with annualized stroke risk; however, these risk stratification models may be inadequate in cancer patients. Cancer type, stage, prognosis, and bleeding risk are all relevant when considering whether to initiate therapeutic anticoagulation. Moreover, thrombocytopenia may limit the ability to provide anticoagulation. Subsequent analyses of direct oral anticoagulants (DOACs) show fewer bleeding complications and thromboembolic events compared to warfarin in AF/AFL with apixaban and edoxaban particularly promising in this population for VTE, pulmonary embolism, and AF/AFL. There is a lack of data regarding ablation therapy and left atrial occlusion devices in this population. There is a growing experience of DOACs for intracardiac thrombi. Warfarin is still appropriate for patients with prosthetic heart valves and left ventricular assist devices. Anticoagulation management in the cancer patient can be challenging. DOACs are often a safe alternative to warfarin in cancer-associated DVT/PE and AF/AFL, and may be preferable in certain circumstances. Other cardiac indications for anticoagulation including the presence of a mechanical heart valve remain unchanged and dependent on warfarin or heparin-based products.
Topics: Anticoagulants; Antineoplastic Agents; Atrial Fibrillation; Atrial Flutter; Cardiotoxicity; Cardiovascular Diseases; Heart Valve Prosthesis; Humans; Neoplasms; Thrombosis
PubMed: 30949848
DOI: 10.1007/s11912-019-0797-z -
Proceedings (Baylor University. Medical... Jul 2018Flecainide, a class Ic antiarrhythmic, is used for the prevention of paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation/flutter, and sustained...
Flecainide, a class Ic antiarrhythmic, is used for the prevention of paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation/flutter, and sustained ventricular tachycardia. Flecainide is primarily metabolized by the liver and to a lesser extent (30%) is excreted unchanged in the kidney. We present a case of flecainide toxicity in the setting of renal impairment that was successfully treated with intravenous sodium bicarbonate.
PubMed: 29904301
DOI: 10.1080/08998280.2018.1463042 -
International Journal of Clinical and... 2015To study various types of supraventricular arrhythmias in patients with Brugada Syndrome.
OBJECTIVE
To study various types of supraventricular arrhythmias in patients with Brugada Syndrome.
METHODS
Forty six patients with ECG of spontaneous type Brugada and with ventricular and/or supraventricular tachyarrhythmia, without structural heart diseases which were excluded by echocardiography, underwent 24 h-Holter recording, electrophysiological study and/or radiofrequency ablation.
RESULTS
There were thirty-nine male and seven female (mean age 37.44 years) among total forty-six patients. Twenty one patients had family histories of tachycardia, twentythree patients experienced episodes of syncope, and three patients were resuscitated from cardiac arrest. One patient had ventricular fibrillation and third degree atrioventricular block, eleven patients had polymorphic ventricular tachycardia and five patients had monomorphic ventricular tachycardia. Fourteen patients had atrial tachyarrhythmia, paroxysmal supraventricular tachycardia was found in five patients including four Wolf-Parkinson-White syndrome, two patients hadventricular tachycardia and third degree atrioventricular block, one of them had atrial fibrillation, two patients had both supraventricular tachycardia and ventricular tachycardia, three patients had both atrial tachyarrhythmia and supraventricular tachycardia, two third degree atrioventricular block patients had atrial flutter, one patienthad both atrial tachyrhythmia and ventricular tachycardia. Radiofrequency blation was performed in thirty-nine patients and succeed in thirty-two, four patients were implanted with pacemakers, and four patients had implantable cardioverter defibrillators.
CONCLUSION
In addition to ventricular tachycardia and ventricular fibrillation, patients with Brugada syndrome exhibit various supraventricular tachyarrhythmia and third degree atrioventricular block. In patients with Brugada syndrome, the dysfunction of the cardiac ion channel, which related to mutation of cardiac sodium channelgene, is not limited in His Purkinje system and ventricular myocardium, but also in the atrium and atrioventricular node, which may serves as a cause of dispersion of repolarization and phase 2 reentry leading to various arrhythmias.
PubMed: 26550443
DOI: No ID Found