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At least 1,693 records · Page 94Linked to original sources
PubMed2004

Antiarrhythmic drug therapy of atrial fibrillation.

In the post-AFFIRM era, treatment of AF has become the treatment of symptoms. In some patients, this will be simple rate control, but there remain a significant cohort of patients in whom rate control alone does not give acceptable symptom relief. In this group, antiarrhythmic therapy still has a role, and the AFFIRM trial indicates that this therapeutic strategy is without significant deleterious effect on mortality. The choice of antiarrhythmic agent must be individualized according to underlying cardiac pathologies and comorbidities, however. Most recently, the introduction of dofetilide has widened the therapeutic options in patients with severe heart disease, and the Canadian Trial of Atrial Fibrillation indicated the superior efficacy of amiodarone at low doses. The release/ development of newer Class III antiarrhythmic agents may offer hope for the benefits of amiodarone without the serious adverse effects with long-term therapy.

Amiodarone↗
PubMed2001

Medical therapy of neurocardiogenic syncope.

Neurocardiogenic syncope, alternatively called vasovagal, vasodepressor, or neurally mediated syncope, is a clinical syndrome faced by many clinicians. Its pathophysiology is complicated and not fully understood. Multiple pharmacologic therapies have been evaluated, with no clear ideal agent. Decisions regarding tilt-table testing, selection of pharmacotherapy, and assessment of drug efficacy are not straightforward. This article attempts to assess these issues.

Adolescent↗
PubMed1985

Discordance between ambulatory monitoring and programmed stimulation in assessing efficacy of class IA antiarrhythmic agents in patients with ventricular tachycardia.

Concordance between programmed stimulation and 24 hour ambulatory electrocardiographic (Holter) monitoring was studied in 54 patients with sustained ventricular tachycardia during 84 therapeutic trials with class IA antiarrhythmic agents. During baseline studies before treatment, all patients had frequent (greater than or equal to 30/h) ventricular premature complexes on Holter recordings and sustained ventricular tachycardia inducible by one to three extrastimuli. During treatment, programmed stimulation and Holter monitoring were repeated. Efficacy of treatment determined by programmed stimulation (ventricular tachycardia no longer inducible or nonsustained) was compared with three Holter criteria of efficacy: I = 83% or more reduction of ventricular premature complexes and abolition of ventricular tachycardia; II = 50% or more reduction of ventricular premature complexes and 90% or more reduction of couplets and abolition of ventricular tachycardia; III = abolition of ventricular tachycardia in patients with ventricular tachycardia during a baseline Holter recording. Treatments were judged effective by programmed stimulation criteria in only 25% of cases but in 51, 63 and 75% of cases by Holter criterion I, II and III, respectively. Results of programmed stimulation and Holter monitor were discordant (effective by one criterion but ineffective by the other) in 50% of cases using Holter criterion I, in 54% using Holter criterion II and in 61% using Holter criterion III. In the majority of discordant results, treatments appeared efficacious by Holter criteria but ineffective by programmed stimulation criteria, suggesting insensitivity of efficacy by Holter criteria or nonspecificity of induced ventricular tachycardia during treatment, or both.

Aged↗
PubMed1997

Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy--the lobster claw abnormality.

UNLABELLED: In many patients with obstructive hypertrophic cardiomyopathy, an abrupt mid-systolic drop in left ventricular ejection velocity can be detected. We analyzed 27 patients with obstructive hypertrophic cardiomyopathy who had 43 echocardiographic examinations (mean gradient 53 +/- 6 mm Hg). Exams showing a mid-systolic drop had higher mean outflow tract pressure gradients (90 +/- 6 compared with 29 +/- 4 mm Hg, p < 0.001). After medical elimination of obstruction, the mid-systolic drop was no longer seen. We measured 105 pulsed-wave Doppler tracings in the left ventricular cavity and compared them with 90 continuous-wave tracings through the outflow tract. There was a close temporal correlation between the nadir of the left ventricular velocity drop and the peak continuous-wave left ventricular outflow tract velocity (r = 0.99). There was also a close temporal correlation between the onset of the fall in pulsed velocity and the onset of M-mode mitral-septal contact (r = 0.95). CONCLUSIONS: The mid-systolic drop in left ventricular velocity is due to impedance to ejection and provides evidence of true obstruction. As left ventricular ejection velocity falls to its mid-systolic nadir because of impedance of ejection, velocity downstream in the left ventricular outflow tract actually rises to its peak. This disparity in the two velocities, deceleration in the left ventricular cavity and acceleration in the left ventricular outflow tract, indicates that the outflow orifice is progressively narrowed over time as the mitral valve is forced into the septum by the rising pressure difference. The obstruction phase is best described as a time-dependent, amplifying feedback loop. The orifice narrows over time because of the rising pressure difference; the pressure difference rises over time because of the narrowing orifice.

Acceleration↗
PubMed2005

[Atrial flutter and fibrillation].

This article summarizes current understandings and therapies for both arrhythmias. Atrial flutter is most often arising from a macroreentry circuit in the right atrium or around scar tissue in case or previous cardiothoracic surgery. As a macroreentrant tachycardia it is regular and can lead to higher heart rates, especially if occurring with 1:1 conduction. In contrast atrial fibrillation, especially when occurring paroxysmal at the beginning, is arising from triggers within the pulmonary veins. Ablation strategies to electrically isolate those triggers have a treatment success rate of 80%, which is much more than can be achieved with antiarrhythmic medication (success rates 30-50%). Emergency treatment of both arrhythmias include cardioversion and pacemaker implantation with AV node ablation if necessary.

Adrenergic alpha-Antagonists↗