Supraventricular Tachycardia—Part I

doi:10.1016/j.cpcardiol.2008.06.002

Current Problems in Cardiology

Volume 33, Issue 9, September 2008, Pages 467-546

https://doi.org/10.1016/j.cpcardiol.2008.06.002 Get rights and content

Abstract

Supraventricular tachycardias (SVTs) affect all age groups and are a source of significant morbidity. They are frequently encountered in otherwise healthy individuals without structural heart disease. Advances in the understanding of their mechanisms and anatomical locations have led to highly effective pharmacologic and nonpharmacologic treatment strategies. Recognition, identification, and differentiation of the various SVTs are of great importance in formulating an effective treatment strategy. Developments over the past four decades have made possible the accurate diagnosis of SVTs. Today, advances in catheter design, energy delivery systems, mapping systems, and remote navigation systems have rendered the ablation of most SVTs safe and effective. This monograph provides an in-depth discussion of the history, presentation, mechanism, and treatment strategies of the most commonly encountered SVTs. The monograph is divided into two parts. The first part is presented here.

Section snippets

Brief Historical Perspective

The clinical and ECG features of paroxysmal tachycardias have long piqued the interest of investigators. In 1867 British physician Richard Cotton¹¹ first reported a case of paroxysmal tachycardia involving a 42-year-old man who developed the sudden onset of palpitations with presyncope and dyspnea.¹¹ A sphygmograph revealed the patient's pulse to be regular with a rate of 232 bpm. The author reported that the patient's rhythm abnormality would begin and end abruptly. In 1887 British physician

Classification

SVTs denote all tachyarrhythmias that originate from supraventricular tissue or require it to be a part of the reentrant circuit. Paroxysmal supraventricular tachycardia denotes a clinical syndrome characterized by a rapid tachycardia with an abrupt onset and termination. While most SVTs are due to reentry, a small proportion is due to triggered activity or automaticity.¹⁷ To provide a framework for a coherent discussion of the wide array of SVTs, a classification is needed. Table 1 shows a

Epidemiology

Orejarena et al¹⁸ published an epidemiologic study of SVT in the general population. Based on 1990 census data, the incidence of SVT is estimated to be 36/100,000 person-years and the prevalence is 2.29/1000 persons. Extrapolating the results to the entire U.S. population, it is estimated that close to 570,000 individuals have SVT with about 89,000 new cases annually.¹⁸ Based on data from the Marshfield Epidemiologic Study Area study, the average age of SVT onset is 57 years (range, infancy to

Presentation

SVT is usually regular with a heart rate of 160 to 200 bpm, although the rate can range from 80 to 240 bpm.⁴¹ Tachycardias are usually not life-threatening and are associated with an aborted sudden death rate of 2-4.5%.35, 42, 43, 44, 45 However, they are responsible for a wide spectrum of symptoms including very serious ones.46, 47 Based on a study of 167 consecutive subjects referred to a specialized arrhythmia center for radiofrequency (RF) ablation over a 2-year period, Wood et al⁴² found

Specific Arrhythmias

While atrial flutter and atrial fibrillation are included in the list of SVTs, these arrhythmias have distinctly different mechanisms and management strategies and are not discussed in the current monograph. Recently, both arrhythmias have been reviewed in detail by Lee et al,⁶⁹ Hersi and Wyse,⁷⁰ and Riley and Marrouche.⁷¹ Regular paroxysmal SVTs comprise AVNRT in 51% of cases (up to 60-70% in some studies), AVRT in 34% of cases, and various other mechanisms in the remaining 15% of cases.⁷

Historical Perspective

AVNRT is the most common regular, narrow-complex tachycardia and has a rich history.72, 73, 74 Reentry as the mechanism of the arrhythmia was first postulated by Mines¹⁶ as early as 1913 and subsequently by Iliescu and Sebastiani⁷⁵ in 1923. Two decades later, investigative work by Barker et al⁷⁶ pointed to the AV node as the site of reentry. Detailed studies on canine hearts by Moe et al⁷⁷ and on rabbit heart preparations by Mendez and Moe⁷⁸ established dual AV nodal pathways as the

Historical Perspective

The term “preexcitation” was first used by Öhnell in 1944 to denote premature activation of the ventricle by an atrial impulse using an accessory conduction system.¹⁹⁰ The peculiar finding of preexcitation on the surface ECG and its associated tachyarrhythmias has long piqued the interest of clinician-scientists. Detailed works by countless investigators over the past century have resulted in substantial advances in the understanding and treatment of this syndrome.

Initial description of the

Acknowledgments

The authors thank Kathy Lenihan and William Chu for helping obtain the surface ECGs, Ms. Ann Seley for her superb secretarial assistance, and Dr. Yanfei Yang for some of the diagrams. The authors are also greatly indebted to the dedicated EP fellows, attendings, nurses, and support staff at UCSF for helping to conduct the EP studies.

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Narrow complex supraventricular tachycardia. What is the mechanism?
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Electrophysiological evaluation of supraventricular tachycardia using various maneuvers is routinely performed before the attempted ablation.1,2
Left posterior fascicular ventricular tachycardia in a young infant with a structurally normal heart: Clinical course and caveats to electrocardiographic diagnosis
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AV nodal re-entrant tachycardia (AVNRT) is uncommon during infancy and is unlikely to present with AV dissociation as noted here. In retrospect, the absence of any effect of Adenosine on the tachyarrhythmia during the first presentation also argues against an AV node dependent tachycardia mechanism (i.e. AVRT and AVNRT) [2]. Thus in the setting of AV dissociation, the plausible diagnosis was either a junctional ectopic tachycardia (JET) with aberrancy or VT.
In this illustrative case report, we describe a rare case of left posterior fascicular ventricular tachycardia (LPFVT) in a 2 month-old infant with emphasis on electrocardiographic caveats to diagnosis. The clinical course, treatment, and eventual resolution of the VT over a 2 year follow-up is comprehensively compared and contrasted to a modicum of individual such case reports of infants. The corpus of each such case of infantile LPVT is systematically reviewed and succinctly summarized in a tabular compendium. The collective knowledge compiled here should allow for a refined approach to diagnosis and management of this unusual arrhythmia.
Interference dissociation in the presence of dual atrioventricular nodal physiology
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Findings compatible with simultaneous conduction along 2 pathways in response to a ventricular premature complex were noted in our patient’s ECG (Figure 3), indicating presence of underlying dual AV nodal physiology. Dual AV nodal physiology can manifest itself as normal sinus rhythm, spontaneous shortening or lengthening of the PR interval persisting for varying periods of time, PR interval alternans,2–7 PR interval alternans with Wenckebach sequence of the slowly and rapidly conducting pathways, and conduction along both pathways in response to a single sinus impulse.8–12 In the presence of sinus rhythm the presenting ECG (Figure 1) and continuous rhythm strip (Figure 2) illustrate an unusual presentation masquerading as dual AV nodal physiology.
Dual atrioventricular nodal pathways physiology: A review of relevant anatomy, electrophysiology, and electrocardiographic manifestations
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Dual pathway physiology can be electrocardiographically “silent” with no manifestations whatsoever. The prevalence of dual pathways physiology is variably reported as being demonstrable in 10 to 35% of normal people [25-28] including children [29], but may become less common with aging [30]. A multitude of electrocardiographic manifestations [19,31,32] may be explained by dual pathways physiology (see Table 1).
More than half a century has passed since the concept of dual atrioventricular (AV) nodal pathways physiology was conceived. Dual AV nodal pathways have been shown to be responsible for many clinical arrhythmia syndromes, most notably AV nodal reentrant tachycardia. Although there has been a considerable amount of research on this topic, the subject of dual AV nodal pathways physiology remains heavily debated and discussed. Despite advances in understanding arrhythmia mechanisms and the widespread use of invasive electrophysiologic studies, there is still disagreement on the anatomy and physiology of the AV node that is the basis of discontinuous antegrade AV conduction. The purpose of this paper is to review the concept of dual AV nodal pathways physiology and its varied electrocardiographic manifestations.
Aqueous fraction from Costus spiralis (Jacq.) Roscoe leaf reduces contractility by impairing the calcium inward current in the mammalian myocardium
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Brazilian folk medicine uses infusion of Costus spiralis leaf to help people to treat arterial hypertension and syndromes of cardiac hyperexcitability.
Evaluate the aqueous fraction (AqF) effect on atrial contractility and investigate its mechanism of action.
The AqF effect on the cardiac contractility was studied on isolated electrically driven guinea pig left atria. Atropine and tetraethylammonium (TEA) were employed to investigate whether potassium contributes for the inotropic mechanism of the AqF. The role of calcium in this effect was also studied. This was done by analysing the AqF effect on the Bowditch's phenomenon, as well as by studying whether it could interfere with the concentration–effect curve for CaCl₂, isoproterenol, and BAY K8644. Mice isolated cardiomyocytes were submitted to a whole-cell patch-clamp technique in order to evaluate whether the L-type calcium current participates on the AqF effect. Furthermore, the intracellular calcium transient was studied by confocal fluorescence microscopy.
AqF depressed the atrial contractile force. It was the most potent fraction from C. spiralis leaf (EC₅₀ = 305 ± 41 mg/l) (crude extract: EC₅₀ = 712 ± 41; ethyl acetate: EC₅₀ = 788 ± 121; chloroform: EC₅₀ = 8948 ± 1346 mg/l). Sodium and potassium content in the AqF was 0.15 mM and 1.91 mM, respectively. Phytochemical analysis revealed phenols, tannins, flavones, xanthones, flavonoids, flavonols, flavononols, flavonones, and saponins. Experiments with atropine and TEA showed that potassium does not participate of the inotropic mechanism of AqF. However, this fraction decreased the force overshoot characteristic of the Bowditch's phenomenon, and shifted the concentration–response curve for CaCl₂ (EC₅₀ from 1.12 ± 0.07 to 7.23 ± 0.47 mM) indicating that calcium currents participate on its mechanism of action. Results obtained with isoproterenol (1–1000 pM) and BAY K8644 (5–2000 nM) showed that AqF abolished the inotropic effect of these substances. On cardiomyocytes, 48 mg/l AqF reduced (∼23%) the L-type calcium current density from −6.3 ± 0.3 to −4.9 ± 0.2 A/F (n = 5 cells, p < 0.05) and reduced the intracellular calcium transient (∼20%, 4.7 ± 1.2 a.u., n = 42 cells to 3.7 ± 1.00 a.u., n = 35 cells, p < 0.05). However, the decay time of the fluorescence was not changed (control: 860 ± 32 ms, n = 42 cells; AqF: 876 ± 26 ms, n = 35 cells, p > 0.05).
The AqF of C. spiralis leaf depresses myocardial contractility by reducing the L-type calcium current and by decreasing the intracellular calcium transient. Despite the lack of data on the therapeutic dose of AqF used in folk medicine, our results support, at least in part, the traditional use of this plant to treat cardiac disorders.
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The P-P interval can be marched out in lead aVR (Fig. 4) without any change in its rate and falls at the expected time after the PVC. The lack of reset in the atrium following early coupled PVC (Fig. 4) makes retrograde conduction over an accessory pathway unlikely [2]. To summarize, sinus tachycardia in this neonate was associated with narrow and wide QRS complexes simulating a tachyarrhythmia.
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: The authors have no conflicts of interest to disclose.

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Supraventricular Tachycardia—Part I

Abstract

Section snippets

Brief Historical Perspective

Classification

Epidemiology

Presentation

Specific Arrhythmias

Historical Perspective

Historical Perspective

Acknowledgments

Lancet

J Am Coll Cardiol

Heart Rhythm

Am J Cardiol

Am J Cardiol

Am Heart J

Heart Rhythm

J Am Coll Cardiol

Chest

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

Am Heart J

Lancet

J Am Coll Cardiol

J Am Coll Cardiol

Chest

Am J Cardiol

Am J Cardiol

Cardiol Clin

Am J Med

Am J Cardiol

Curr Probl Cardiol

Curr Probl Cardiol

Curr Probl Cardiol

Am Heart J

Am J Cardiol

Am Heart J

J Am Coll Cardiol

Am J Cardiol

The role of premature beats in the initiation and the termination of supraventricular tachycardia in the Wolff-Parkinson-White syndrome

Circulation

Tachycardie permanente par rhythme reciproque

Arch Mal Coeur

Electrical Stimulation of the Heart in the Study and Treatment of Tachycardias

Catheter technique for recording His bundle activity in man

Circulation

Successful surgical interruption of the bundle of Kent in a patient with Wolff-Parkinson-White syndrome

Circulation

Catheter-induced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias

JAMA

Clinical Cardiac Electrophysiology: Techniques and Interpretations

Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current

New Engl J Med

Localization of the origin of arrhythmias for ablation: from electrocardiography to advanced endocardial mapping systems

J Cardiovasc Electrophysiol

Three-dimensional electromagnetic catheter technology: electroanatomical mapping of the right atrium and ablation of ectopic atrial tachycardia

J Cardiovasc Electrophysiol

Notes and observation upon a case of unusually rapid action of the heart (232 per minute)

BMJ

On recurrent palpitations of extreme rapidity in persons otherwise apparenty healthy

Brain

Classic Description Disease

Paroxysmal Tachycardie

Paroxysmal tachycardia

Heart (Br Cardiac Soc)

On dynamic equilibrium in the heart

J Physiol