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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 24-28

A study on hospitalized patients of junctional rhythm with reference to the prevalence of different underlying etiologies


1 BM Birla Heart Research Centre, Kolkata, West Bengal, India
2 Department of Medicine, North Bengal Medical College, Darjeeling, West Bengal, India
3 Department of Cardiology, Bankura Sammilani Medical College, Bankura, West Bengal, India

Date of Submission20-Nov-2020
Date of Decision05-Jan-2021
Date of Acceptance25-Feb-2021
Date of Web Publication30-Mar-2021

Correspondence Address:
Dr. Avijit Moulick
Flat 2F, Spandan Apartment, 1/14 Extn Chittaranjan Colony, Jadavpur, Kolkata - 700 032, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_51_20

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  Abstract 


Introduction: Junctional rhythm (JR) is a rescue rhythm where the upstream impulse generators fail to pace the heart and atrioventricular (AV) junction takes up that function. The presentation is variable ranging from totally asymptomatic cases, where it is a manifestation of heightened vagal tone, to life-threatening bradycardia, resulting from some serious underlying pathologies. JR results from diverse causes such as sick sinus syndrome, acute myocardial infarction (AMI), dyselectrolytemia, drugs, and toxins. Understanding the etiologic factor has immense implication in the management as the prognosis is related mainly to the primary pathology rather than JR itself.
Subjects and Methods: In this observational study, we evaluated 100 hospitalized patients of JR over a period of 1 year regarding their symptoms, signs, and underlying pathology.
Results: Among 100 patients, 38 had a history of syncope and 42 had angina. Twenty-four patients had hyperkalemia (22 of them had renal dysfunction). Thirty patients had elevated troponin-T and/or CK-MB. The most common etiology was AMI responsible in 28% patients followed by hyperkalemia (24%), sick sinus syndrome (20%), and medication drug use (16%) as the principal causes of JR. Myocarditis, toxin, and hypothyroidism were uncommon association. Accelerated JR and junctional tachycardia were associated with AV nodal ablation and postsurgical patients, respectively.
Conclusion: JR is a manifestation of several diverse etiopathologies, and elucidation of them is extremely important for the patient management. We estimated the prevalence of various underlying etiologies which should be considered during the management of such patients.

Keywords: Junctional rhythm, prevalence study, underlying etiology


How to cite this article:
Sinha P, Moulick A, Majhi B. A study on hospitalized patients of junctional rhythm with reference to the prevalence of different underlying etiologies. Heart India 2021;9:24-8

How to cite this URL:
Sinha P, Moulick A, Majhi B. A study on hospitalized patients of junctional rhythm with reference to the prevalence of different underlying etiologies. Heart India [serial online] 2021 [cited 2021 Apr 14];9:24-8. Available from: https://www.heartindia.net/text.asp?2021/9/1/24/312491




  Introduction Top


If sinoatrial node fails to be the default impulse generator and area around the atrioventricular (AV) junction takes over as the heart's escape pacemaker, the rhythm is called junctional. In junctional rhythm (JR), the ventricular rate is 40–60 per min and the P wave may occur before, during or just after the QRS complex. P wave occurring before the QRS complex may be negative, and the PR interval is short. QRS complexes are regular and narrow.

An accelerated JR (rate >60 but <100/min) is a narrow complex rhythm that often supersedes a clinically slower sinus rate. Less commonly, the AV junction develops abnormal automaticity and exceeds the sinus rate at a time when the sinus rate would be normal, resulting in junctional tachycardia (rate >100/min). Junctional tachycardia is most often observed in the setting of digitalis toxicity and recent cardiac surgery.

This rhythm may occur in persons of any age, equally in males and females. The symptoms in JR are principally determined by the actual heart rate. The common symptoms include palpitations, fatigue or poor exercise tolerance, dyspnea, presyncope/syncope, and neck venous pulsation (cannon a wave). It may be associated with increased mortality and morbidity which is directly related to the underlying cause, for example, complete heart block or sick sinus syndrome, and not to JR itself. Young healthy individuals, especially those with increased vagal tone during sleep, often have the periods of JR that is completely benign, not requiring any intervention.

The causes of JR include sick sinus syndrome, digoxin toxicity, ischemia of the AV node, electrolyte imbalance, postcardiac surgery, acute inflammatory processes such as diphtheria, certain drugs such as beta-blockers, calcium channel blockers, and antiarrhythmic agents.

Data are sparse in the literature on the prevalence of different causes of JR. In the present study, we sought to explore the prevalence of different etiologies of JR.


  Subjects and Methods Top


In this “cross-sectional, observational study,” we evaluated 100 randomly selected patients of JR admitted in the department of cardiology between May 2016 and April 2017. Details of clinical history were obtained and meticulous clinical examination performed regarding the cause of JR, symptoms, and signs at presentation. Basic biochemical tests and imaging were performed to establish the diagnosis and etiology of JR. JR was diagnosed with the help of standard 12-lead electrocardiogram (ECG).

Particular emphasis was given on a history of medication intake, presence of renal and thyroid dysfunction and electrolyte abnormalities, ischemic biomarkers such as troponin and CK-MB. 2D echocardiography and 24 h' Holter monitoring were done in all patients. Coronary angiography (CAG) and cardiac magnetic resonance imaging were performed in selected patients as per standard indication. Statistical analysis was done, and data were presented as charts and tables. The quantitative data were presented as mean ± standard deviation.

Ethical clearance was obtained from the Institutional Ethics Committee.


  Results Top


Among the 100 patients under evaluation, 54 were male and 46 were female. [Table 1] shows the basic characteristics of the studied patients. Exposure to drugs and/or toxins was found in 32 patients [Table 2]. Beta-blockers were associated with most of the cases.
Table 1: Baseline characteristics of the study population

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Table 2: Distribution of patients who had exposure to drug/toxin

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The minimum pulse rate was 36, and the maximum 138 per min with a mean of 46.56 ± 14.60 per min. The systolic and diastolic blood pressures of patients were 129.60 ± 21.15 and 83.08 ± 7.21 mmHg, respectively.

[Table 3] shows basic biochemical parameters of the patients. Twenty-two patients had renal dysfunction and 24 had hyperkalemia. Six patients had hypothyroidism, and among them, two were on beta-blockers and another two patients had sick sinus syndrome on 24 h' Holter monitoring.
Table 3: Biochemical parameters of patients

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Calculated left ventricular (LV) ejection fraction by Simpson's method was 53.96% ± 8.29%. Thirty-six patients had regional wall motion abnormality, whereas 10 patients had global LV hypokinesia. CAG was performed in 56 patients among whom 36 had significant obstructive coronary artery disease (CAD) and two had minor CAD [Table 4]. Acute myocardial infarction (AMI) from occlusion of right coronary artery (RCA) or dominant left circumflex artery (LCx) was seen in 28 patients.
Table 4: Coronary angiography findings in the patients studied

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Twenty patients had evidence of sick sinus syndrome in 24 h' Holter monitoring [Table 5]; which were performed after stopping all drugs that may affect interpretation. Two of them were also hypothyroid and four were taking beta-blockers at the time of presentation.
Table 5: Holter monitoring results of the studied patients

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Several patients had multiple factors under consideration [Table 6]. Finally, distribution of all study patients according to etiology of JR is given in [Table 7].
Table 6: Distribution of combined factors

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Table 7: Distribution of different etiology of junctional rhythm

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  Discussion Top


The study was conducted to find out the prevalence of different etiologies of JR by evaluating hundred such patients attending this institution, a high-volume cardiac center, in order to get an overall estimate of such etiologic factors in this part of the country as this hospital has a large catchment area including most of Eastern India.

The study revealed AMI as the leading cause of JR and coronary occlusion was found in 28% in the form of RCA occlusion or a dominant LCx occlusion that can result in ischemia in AV node. In AMI, the specialized conduction system can be affected directly by ischemia, necrosis, or autonomic imbalance.[1] Sinus bradycardia, junctional bradycardia, and AV block with idioventricular rhythm occur frequently after myocardial infarction, especially inferior wall AMI.[2],[3],[4] The blood supply for each component of conduction system plays an important role in ischemic hearts, and the type of bradycardia depends on which epicardial vessel is affected as well as the level of obstruction.[1],[5],[6] Overall, the incidence of bradyarrhythmia has decreased in the era of thrombolysis and early invasive revascularization.[2]

Hyperkalemia is considered an important cause of JR. Serum potassium >6.5 mEq/L is associated with progressive paralysis of the atria. Serum potassium >7.0 mEq/L is associated with conduction abnormalities and bradycardia, high-grade AV block with slow junctional, and ventricular escape rhythms.[7] An increased likelihood of short-term adverse event was found for hyperkalemic patients whose ECG demonstrated QRS prolongation, bradycardia (HR <50), and/or JR.[8] In a study on patients of symptomatic bradycardia, Chon et al. found hyperkalemia in 21% patients similar to us.[9] Most of our patients had renal dysfunction and 10 of them were also receiving beta-blockers; a commonly encountered concurrent factors in patients with bradycardia.[10],[11] In all of these patients, sinus rhythm was restored with the correction of serum potassium level, including those who were receiving beta-blockers, and the drug could be resumed in most patients with compelling indication during follow-up, usually at a lower dosage. It was therefore concluded hyperkalemia, and not beta blocker was responsible for JR in them. Beta-blockers, mainly nonselective ones, can potentiate hyperkalemia in patients with renal insufficiency and should be used with caution in such patients.[12]

Sinus node dysfunction may present as severe sinus bradycardia, sinus pause or arrest, periods of JR, and/or alternating tachycardia-bradycardia episodes. In the study by Eraut and Shaw, JR was observed in 33% patients of sinus node dysfunction.[13] We found sick sinus syndrome, as diagnosed by 24 h Holter monitoring, in 20% patients. Majority of these patients had h/o syncope and drug history was positive in four of them (drug was stopped before proceeding to Holter recording); and two had subclinical hypothyroidism. They required permanent pacemaker implantation. Several medications (beta blockers, antiarrhythmic, etc.,) depress sinus node function and can result in the features consistent with sinus node dysfunction. However, persistent sinus node dysfunction after withdrawal of offending agent suggests an unmasking effect rather than a causal effect of the drug.

Because of their depressant effects on the sinus rate and on the conduction time at the more proximal (AV nodal) segments, beta-blockers and nondihydropyridine calcium channel antagonists (verapamil and diltiazem) are considered a common cause of JR (bradycardia).[14],[15] Both junctional bradycardia and nonparoxysmal junctional tachycardia have been described in digoxin toxicity. In their study, Zeltser et al. demonstrated that only 15% of all AV block was “truly caused by drugs” in their studied patients and concluded AV block is commonly “related to drugs” but is rarely “caused by drugs.”[16] Similarly, in our study, drugs were found to be responsible in 16% patients. Sinus bradycardia with junctional escape beats was the most common ECG finding in drug-related bradycardia as observed by Lee et al.[17] Majority of them returned to sinus rhythm after withdrawal of the offending drug. Two patients receiving beta-blocker also had hypothyroidism; however, sinus rhythm was restored after withdrawing beta-blocker.

Hypothyroidism may be associated with bradycardia as well as AV block, and there are only a few case reports in the literature.[18],[19] It is postulated to be caused by edema (myxedema) compressing on AV node and levothyroxine probably improves AV conduction by resolving this edema. No data are available regarding the prevalence of JR in hypothyroidism. We found JR exclusive to hypothyroidism in only two patients. These two patients of overt hypothyroidism responded to levothyroxine replacement.

Bradycardia, usually sinus, may be seen in viral myocarditis, especially when caused by influenza and JR as well as complete AV block can occur.[20] Isolated case reports have documented the use of temporary endocardial pacing in myocarditis caused by other viruses such as mumps, coxsackie B2, and adenovirus. JR seems to be uncommon in viral myocarditis. In the present study, myocarditis was diagnosed in four patients with JR which responded to conservative treatment.

Accelerated JR has been described in post-radiofrequency (RF) ablation of AVNRT.[21] This rhythm typically develops within a few seconds of RF delivery at the ablation site and is likely to be secondary to enhanced automaticity in AV nodal tissue because of thermal injury. The occurrence of this rhythm is strongly correlated with successful ablation. A malignant variant of accelerated JR is junctional ectopic tachycardia (JET) which occurs almost exclusively in neonates or young children undergoing major cardiac surgery.[22],[23] JET is associated with marked tachycardia (>180 beats/min), significant hemodynamic compromise, and increased mortality rate. In the majority of cases, JET occurred immediately after surgery or during the 1st postoperative day.[23] In the present study, we had two such patients in each category.

There are numerous toxins that can cause ECG changes in patients without a history of cardiac pathology. Some of them are aconitine (plants from genus aconitum), grayanotoxins (some rhododendron plants), ostreolysin (oyster mushrooms) and a wide variety of snakes and other animal toxins. Yellow Oleander contains at least eight different cardiac glycosides.[24] All parts of the plant are dangerous, especially the seeds. We had two patients having junctional bradycardia with h/o yellow oleander ingestion and in the absence of any other factors.


  Conclusion Top


After thorough analysis of the data, CAD was found to be the underlying etiology in 28%, hyperkalemia in 24%, sinus node dysfunction in 20%, and drugs and toxin in 18% patients presenting with JR. Beta-blocker in the setting of hyperkalemia and renal failure was frequently found to be associated with JR. Because multiple coexistent factors (in an individual patient) are common, meticulous analysis of pathophysiologic mechanisms is essential for etiologic diagnosis and management of such patients. Most of the time, the underlying causes are reversible and do not require implantation of permanent pacemaker.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical approval

Ethical clearance was obtained from the Institutional Ethics Committee.

Authors' contributions

All the authors have contributed significantly in preparation of the manuscript.



 
  References Top

1.
Zimetbaum PJ, Joseph EM. Conduction abnormalities after myocardial infarction. In: Knight BP, Gersh BJ, Hoekstra J, editors. UpToDate. Copyright 2020; Available from: http://www.uptodate.com. [Last accessed on 2019 Mar 25].  Back to cited text no. 1
    
2.
Archbold RA, Sayer JW, Ray S, Wilkinson P, Ranjadayalan K, Timmis AD. Frequency and prognostic implications of conduction defects in acute myocardial infarction since the introduction of thrombolytic therapy. Eur Heart J 1998;19:893-8.  Back to cited text no. 2
    
3.
Meine TJ, Al-Khatib SM, Alexander JH, Granger CB, White HD, Kilaru R, et al. Incidence, predictors, and outcomes of high-degree atrioventricular block complicating acute myocardial infarction treated with thrombolytic therapy. Am Heart J 2005;149:670-4.  Back to cited text no. 3
    
4.
Brady WJ Jr., Harrigan RA. Diagnosis and management of bradycardia and atrioventricular block associated with acute coronary ischemia. Emerg Med Clin North Am 2001;19:371-84, xi-xii.  Back to cited text no. 4
    
5.
Josephson ME, Zimetbaum P. The bradyarrhythmias: Disorders of sinus node function and AV conduction disturbances. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Kasper DL, Longo DL, Jameson JL. editors. Harrison's Principles of Internal Medicine. 16th ed. New York: McGraw-Hill; 2006:1333-41.  Back to cited text no. 5
    
6.
Tjandrawidjaja MC, Fu Y, Kim DH, Burton JR, Lindholm L, Armstrong PW, et al. Compromised atrial coronary anatomy is associated with atrial arrhythmias and atrioventricular block complicating acute myocardial infarction. J Electrocardiol 2005;38:271-8.  Back to cited text no. 6
    
7.
Mirvis DM, Goldberger AL. Electrocardiography: The abnormal electrocardiogram. In: Zipes DP, Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 11th ed. Philadelphia: Elsevier; 2019. p. 146-7.  Back to cited text no. 7
    
8.
Durfey N, Lehnhof B, Bergeson A, Durfey SN, Leytin V, McAteer K, et al. Severe hyperkalemia: Can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med 2017;18:963-71.  Back to cited text no. 8
    
9.
Chon SB, Kwak YH, Hwang SS, Oh WS, Bae JH. Severe hyperkalemia can be detected immediately by quantitative electrocardiography and clinical history in patients with symptomatic or extreme bradycardia: A retrospective cross-sectional study. J Crit Care 2013;28:1112.e7-1112.e13.  Back to cited text no. 9
    
10.
Isabel J, Champion JC. Junctional escape rhythm secondary to acute hyperkalemic renal failure in the setting of concurrent beta-blocker therapy. JAAPA 2006;19:78.  Back to cited text no. 10
    
11.
Simmons T, Blazar E. Synergistic bradycardia from beta blockers, hyperkalemia, and renal failure. J Emerg Med 2019;57:e41-e44.  Back to cited text no. 11
    
12.
Hawboldt J, McGrath D. Possible metoprolol-induced hyperkalemia. J Pharm Pract 2006;19:320-5.  Back to cited text no. 12
    
13.
Eraut D, Shaw DB. Sinus bradycardia. Br Heart J I971;33:742-9.  Back to cited text no. 13
    
14.
Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000;342:703-9.  Back to cited text no. 14
    
15.
Olgin JE, Zipes DP. Heart block. In: Braunwald E, Zipes DP, Libby P, editors. Braunwald's Heart Disease. A Textbook of Cardiovascular Medicine. 6th ed. Philadelphia, PA: W.B. Saunders Company; 2001:871-9.  Back to cited text no. 15
    
16.
Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, et al. Drug-induced atrioventricular block: Prognosis after discontinuation of the culprit drug. J Am Coll Cardiol 2004;44:105-8.  Back to cited text no. 16
    
17.
Lee JH, Ryu HM, Bae MH, Kwon YS, Lee JH, Park Y, et al. Prognosis and natural history of drug-related bradycardia. Korean Circ J 2009;39:367-71.  Back to cited text no. 17
    
18.
Schoenmakers N, de Graaff WE, Peters RH. Hypothyroidism as the cause of atrioventricular block in an elderly patient. Neth Heart J 2008;16:57-9.  Back to cited text no. 18
    
19.
Nakayama Y, Ohno M, Yonemura S, Uozumi H, Kobayakawa N, Fukushima K, et al. A case of transient 2:1 atrioventricular block, resolved by thyroxine supplementation for subclinical hypothyroidism. Pacing Clin Electrophysiol 2006;29:106-8.  Back to cited text no. 19
    
20.
Verel D, Warrack AJ, Potter CW, Ward C, Rickards DF. Observations on the A2 England influenza epidemic: A clinicopathological study. Am Heart J 1976;92:290-6.  Back to cited text no. 20
    
21.
Kawaguchi N, Kobayashi Y, Miyauchi Y, Atarashi H, Takano T, Hayakawa H. Incidence and clinical significance of junctional rhythm remaining after termination of radiofrequency current delivery in patients with atrioventricular nodal reentrant tachycardia. Jpn Circ J 1999;63:865-72.  Back to cited text no. 21
    
22.
Cools E, Missant C. Junctional ectopic tachycardia after congenital heart surgery. Acta Anaesthesiol Belg 2014;65:1-8.  Back to cited text no. 22
    
23.
Hoffman TM, Bush DM, Wernovsky G, Cohen MI, Wieand TS, Gaynor JW, et al. Postoperative junctional ectopic tachycardia in children: Incidence, risk factors, and treatment. Ann Thorac Surg 2002;74:1607-11.  Back to cited text no. 23
    
24.
Eddleston M, Ariaratnam CA, Meyer WP, Perera G, Kularatne AM, Attapattu S, et al. Epidemic of self-poisoning with seeds of the yellow oleander tree (Thevetia peruviana) in northern Sri Lanka. Trop Med Int Health 1999;4:266-73.  Back to cited text no. 24
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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