The Syndrome of Alternating Bradycardia and Tachycardia

Short, David

doi:10.1136/hrt.16.2.208

Cited by 149 publications

(25 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The syndrome of alternating bradycardia and tachycardia was originally described in 4 patients by Short 12 in 1954. These patients had periods of atrial flutter or fibrillation with periods of sinus pauses at termination of the atrial arrhythmia leading to syncope.…”

Section: Tachycardia-bradycardia Syndromementioning

confidence: 99%

Sinus Node and Atrial Arrhythmias

2016

View full text Add to dashboard Cite

Sinus node dysfunction (SND) and atrial arrhythmias frequently coexist and interact to initiate and perpetuate each other. Atrial arrhythmias are present in 40% to 70% of patients at the time of diagnosis of SND.1,2 However, the complex relationship between the 2 remains ill defined. The documented degenerative changes in atrial myocardial structure relating to SND are primarily right atrial. Yet, the majority of triggers and substrates for atrial fibrillation (AF) originate from the left atrium. Although progressive biatrial fibrosis is a feature in patients with structural heart disease and in senescence, paroxysmal AF that occurs in patients with no structural heart disease may have a different pathophysiology. SND associated with this latter condition is likely to be primarily a result of electric remodeling and potentially reversible. The time course of the progression of SND and AF 3 and their individual clinical manifestations also vary depending on the underlying pathology. The purpose of this review is to summarize the state of our knowledge of sinus node (SN) function in both health and disease, and to understand the complex relationship between SN disease and atrial arrhythmias. Structure and Functional Components of the Sinus NodeIn the adult human heart, the SN is a crescent-shaped structure 1 to 2 cm long and 0.5 cm wide that lies at the junction of the superior vena cava with the right atrium and lies along the sulcus terminalis. The node itself is composed of clusters of pacemaker myocytes arranged in parallel rows with short digitations that frequently anastomose with the surrounding atrial tissue. The specialized pacemaker cells are interspersed with nerves and capillaries and scaffolded by dense connective tissue to form the SN pacemaker complex. The caudal portion fragments to merge with the atrial myocardium. The lack of a distinct encapsulation and the radiating sinoatrial connections explains the lack of a single breakthrough of the sinus impulse. The position of the leading pacemaker site shifts within the node and varies with sympathetic and vagal stimulation. 3The SN pacemaker cells are interspersed with interstitial collagen that varies in extent as a function of older age. 4 Collagen content increases from 24% in the infant to 70% in the adult heart.5 The fibrous matrix with surrounding fatty insulation of the SN together with distinct electrophysiological properties (see below) provides insulation and prevents the depression of pacemaker automaticity from the hyperpolarizing electric load of the surrounding atrial myocardium. 6 Multiple currents are involved in the activation of the SN. The predominant inward current in the center of the node is I CaL . Action potentials with slow upstrokes initiated in the center spreads peripherally and into the musculature of the terminal crest. However, in the periphery of the node, I Na is operative and is necessary for providing sufficient inward current to depolarize the larger mass of atrial tissue. Delayed rectifier potassium currents facili...

show abstract

Section: Tachycardia-bradycardia Syndromementioning

confidence: 99%

Sinus Node and Atrial Arrhythmias

2016

View full text Add to dashboard Cite

show abstract

“…Sinoatrial rhythm disorders, such as SSS, and their cardiac rhythm disturbance are causes of SAS. A literature review showed that, the original Stokes-Adams concept of cardiac arrhythmias resulting in syncope was described in 1829 and Levine reported sinoatrial block and paroxsymal atrial fibrillation in 1916, then Short described symptomatic brady-tachycardia in 1954 (8,9).…”

Section: Discussionmentioning

confidence: 99%

Adams-Stokes atakları: Epilepsi taklitçisi

Şengeze¹,

Yürekli²,

Gulcan³

et al. 2014

Ege Tıp Dergisi

View full text Add to dashboard Cite

SummaryStokes-Adams Syndrome is commonly seen in elderly patients and does not cause any symptoms in most cases. However, it may have convulsions that mimic epileptic seizures during periods of cerebral ischemia. These symptoms are often intermittent, changeable and unpredictable. The most common cause of this syndrome is cardiac arrhythmias. Despite numerous investigations for this syndrome, most diagnoses are made by 12-lead electrocardiography. Cardiac pacemaker implantation is the most powerful therapy.A patient who had stroke history, was admitted to the emergency department with repetitive convulsions that mimic epileptic seizures. Also these convulsions included loss of consciousness and tonic-clonic jerks. The convulsions were associated with cardiac arrhythmia and increased with antiepileptic therapy. The aim of this paper is to review the Stokes-Adams attack and its similarity to epileptic seizure with a case report.

show abstract

“…The indications for permanent pacemakers include primary treatment for AV block with Stokes-Adams syndrome and many other bradycardia and tachycardia arrhythmia problems. Our patient had an unusual arrhythmia which previously presented a dilemma in therapy.l3, [24][25][26][27][28][29][30][31][32][33] The bradycardia-tachycardia syndrome can be defined as a paroxysmal supraventricular tachycardia alternating with periods of sinus bradycardia, sinus block or sinus arrest. The therapeutic dilemma arises from the fact that treatment of either the tachycardia or bradycardia results in aggravation of the other.…”

Section: General Aspects Of Bradycardia-tachycardia Syndromementioning

confidence: 99%

“…Drug therapy often leads to a therapeutic dilemma. [24][25][26][27][28][29][30][31][32][33] The purpose of this communication is to report such a patient treated with a permanent demand transvenous ventricular pacemaker with complete control of symptoms without drug therapy.…”

Section: Introductionmentioning

confidence: 99%

Treatment of the Bradycardia-Tachycardia Syndrome with Permanent Demand Pacing

Pittman

1976

Angiology

View full text Add to dashboard Cite

The bradycardia-tachycardia syndrome (paroxysmal supraventricular tachycardia alternating with sinus bradycardia and episodes of sinus node arrest) has previously presented a complicated therapeutic dilemma when excitatory and suppressive drugs have been utilized. A patient with this syndrome successfully treated with a permanent ventricular transvenous demand pacemaker is presented. Various aspects of this syndrome as well as facets of diagnosis and treatment have been reviewed and discussed. Significant underlying cardiac disease was ruled out in this patient by the usual diagnostic methods including left heart catheterization and coronary angiography. An interesting possibility of the relationship of vagal stimulation secondary to hiatus hernia as an etiologic factor in this syndrome has been discussed. The opinion is expressed that the currently preferred method of treatment is the insertion of a permanent transvenous pacemaker alone or in conjunction with antiarrhythmic drugs, preferably digitalis and propranolol.

show abstract

The Syndrome of Alternating Bradycardia and Tachycardia

Cited by 149 publications

References 8 publications

Sinus Node and Atrial Arrhythmias

Sinus Node and Atrial Arrhythmias

Adams-Stokes atakları: Epilepsi taklitçisi

Treatment of the Bradycardia-Tachycardia Syndrome with Permanent Demand Pacing

Contact Info

Product

Resources

About