Author: Jaime Pospishil, Esteban Davila

Peer Editor: Alec Feuerbach

Faculty Editor: Mark Silverberg

A 58-year-old male with a past medical history of diabetes and hypertension presents to the ED for several months of headache and neck pain following a motor vehicle collision. The patient is bradycardic and the triage ECG is as follows:

ECG interpretation: Sinus bradycardia with premature supraventricular bigeminy with aberrancy; T-wave inversions in I, aVL, V5, and V6. 

On this ECG we identify premature supraventricular bigeminy. What do we need to know about this? 

 

Definition of Premature Supraventricular Complex

A premature, supraventricular complex (PSVCs) is depolarization of atrial tissue originating from a focus other than the sinus node that typically occurs earlier in the cardiac cycle than the sinus node. Although the mechanism is not well established, PSVCs are thought to be the result of abnormal automaticity of cardiac myocytes, chemical or physical triggers, or reentry of retrograde impulses.[1,2] These complexes originate above the level of the left and right fascicles from the left atrium, right atrium, interatrial septum, or the AV node. This term encompasses both premature atrial complexes (PAC) and premature junctional complexes (PJC). 

The ECG in this case demonstrates a premature, narrow complex without a preceding P wave, identifying this as a likely PJC. A premature junctional complex differs from a premature ventricular complex (PVC), which has a prolonged QRS > 120 ms. A PJC differs from a PAC, which has an ectopic P wave arising from a focus distinct from the sinus node.

Premature complexes are characterized on a spectrum. When two premature complexes occur in succession, they are termed a doublet. Three in a row is a triplet.[2] More than three premature ventricular complexes is a salvo. They are termed unifocal where they originate from the same focus, or multifocal when they arise from separate foci. 

When a premature complex follows every successive conducted sinus impulse, it is termed bigeminy. If it follows every 2nd beat it is termed trigeminy, and if it follows every 3rd beat it is defined as quadrigeminy. 


Clinical Importance of Premature Supraventricular Complexes

Now that we’ve learned how to name these, why do I need to care? 

The etiology of premature complexes is commonly idiopathic, benign, and does not require treatment. Common triggers include alcohol, tobacco, increased catecholamines, electrolyte abnormalities, an extensive list of medications, and more.[2] Often, patients will present either asymptomatic or with a chest flutter or palpitation sensation. Young, generally healthy patients, with minimal PSVCs can be safely discharged. If a trigger is found, counsel the patient to avoid the trigger. 

However, there are more nefarious causes such as underlying structural heart disease and ischemia linked with PSVCs. PSVCs could also be a sign of atrial circuit re-entry or abnormal automaticity. Patients with more consistent premature complexes may have shortness of breath, anxiety, or even symptoms consistent with heart failure.[3] Structural heart diseases most commonly associated with PACs and PSVCs are those involving dilatation of LA or RA, such as mitral stenosis and hypertrophic cardiomyopathies.[4] 

In patients without known structural heart disease, identification of frequent PSVCs is important, as these patients are at increased risk of development of atrial fibrillation (AF), supraventricular tachycardia (SVT) such as AVNRT and AVRT, and, more rarely, ventricular tachycardias (VT).[5,6] Possible mechanisms for tachydysrhythmia induction include reentry or triggered (i.e. “R on T” event). Two large, prospective cohort studies found that the presence of frequent PSVCs was independently associated with increased long-term risk of AF, stroke, and cardiovascular death.[7,8] 

Patients with persistent symptoms from PSVCs may be placed on low-dose beta-blockers. More uncommon options include type IA, type IC, and type III antidysrhythmic agents.[1] Patients that fail these treatments or have severe symptoms that precipitate heart failure or atrial tachydysrhythmias warrant electrophysiology evaluation for possible atrial pacing or ablations. 

In summary, PSVCs are important when they are causing severe symptoms or when there is underlying heart disease. 

 

What happened to our patient? 

The patient in this case had no known underlying heart disease and did not have palpitations, lightheadedness, chest pain, or syncope that could be attributed to PSVCs. No immediate intervention was required, and he was encouraged to follow-up with a cardiologist. Assuming this patient does not develop severe symptoms, they will likely not require any intervention. For another example of a premature complex, check out this post.  

 

References

[1] Heaton J, Yandrapalli S. Premature Atrial Contractions. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 8, 2022.

[2] Farzam K, Richards JR. Premature Ventricular Contraction. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 8, 2022.

[3] Vervueren PL, Delmas C, Berry M, Rollin A, Sadron M, Duparc A, Mondoly P, Honton B, Lairez O, Maury P. Reversal of Dilated Cardiomyopathy After Successful Radio-Frequency Ablation of Frequent Atrial Premature Beats, a New Cause for Arrhythmia-Induced Cardiomyopathy. J Atr Fibrillation. 2012 Dec 16;5(4):627. doi: 10.4022/jafib.627. PMID: 28496791; PMCID: PMC5153155.

[4] Ramsdale DR, Arumugam N, Singh SS, Pearson J, Charles RG. Holter monitoring in patients with mitral stenosis and sinus rhythm. Eur Heart J. 1987 Feb;8(2):164-70. doi: 10.1093/oxfordjournals.eurheartj.a062244. PMID: 2436916.

[5] Belhassen B, Shapira I, Kauli N, Keren A, Laniado S. Initiation of ventricular tachycardia by supraventricular beats. Cardiology. 1982;69(4):203-13. doi: 10.1159/000173505. PMID: 7172169.

[6] Vincenti A, Brambilla R, Fumagalli MG, Merola R, Pedretti S. Onset mechanism of paroxysmal atrial fibrillation detected by ambulatory Holter monitoring. Europace. 2006 Mar;8(3):204-10. doi: 10.1093/europace/euj043. Epub 2006 Feb 13. PMID: 16627441.

[7] Binici Z, Intzilakis T, Nielsen OW, Køber L, Sajadieh A. Excessive supraventricular ectopic activity and increased risk of atrial fibrillation and stroke. Circulation. 2010 May 4;121(17):1904-11. doi: 10.1161/CIRCULATIONAHA.109.874982. Epub 2010 Apr 19. PMID: 20404258.

[8] Murakoshi N, Xu D, Sairenchi T, Igarashi M, Irie F, Tomizawa T, Tada H, Sekiguchi Y, Yamagishi K, Iso H, Yamaguchi I, Ota H, Aonuma K. Prognostic impact of supraventricular premature complexes in community-based health checkups: the Ibaraki Prefectural Health Study. Eur Heart J. 2015 Jan 14;36(3):170-8. doi: 10.1093/eurheartj/ehu407. Epub 2014 Oct 29.

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