Sinus Node Dysfunction Treatment & Management

Updated: Nov 30, 2018
  • Author: Bharat K Kantharia, MD, FRCP, FAHA, FACC, FESC, FHRS; Chief Editor: Mikhael F El-Chami, MD  more...
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Approach Considerations

See also the Guidelines section for recommendations from the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society for the evaluation and management of bradycardia and disorders of cardiac conduction delay.

The only effective medical care in patients with sinus node dysfunction (SND) is correction of extrinsic causes. Admit patients for testing and pacemaker placement when indicated. Transfer patients for complicated dysrhythmias and pacemaker implantation.

No treatment is required for asymptomatic patients, even if they have abnormal SN recovery times (SNRTs) or sinoatrial conduction times (SACTs). If the patient is receiving medications that can provoke sinus bradyarrhythmias (eg, beta blockers), the medications should be stopped if possible.

Acute treatment consists of atropine (0.04 mg/kg intravenously [IV] every 2-4 h) and/or isoproterenol (0.05-0.5 mcg/kg/min intravenously [IV]). A transvenous temporary pacemaker is sometimes required despite medical therapy.

In patients with bradyarrhythmias-tachyarrhythmias, the tachyarrhythmias may be controlled with digoxin, propranolol, or quinidine. However, these patients should be monitored closely with frequent Holter monitoring to ensure that the bradyarrhythmias are not exacerbated or causing symptoms (eg, dizziness, syncope, congestive heart failure); if exacerbation of arrhythmias or symptoms occur, permanent pacemaker therapy is also required.


Patients with symptomatic SND who are not on pacemaker therapy should titrate their level of activity to minimize symptoms.


These include cardiac electrophysiology consultation.


Pacemaker Therapy

Pacemaker therapy is the only effective surgical care for patients with chronic, symptomatic sinus node dysfunction (SND). The major goal of pacemaker therapy in patients with SND is to relieve symptoms.

Recommendations for permanent pacing in SND

On the basis of the American College of Cardiology Foundation, American Heart Association, the Heart Rhythm Society (ACCF/AHA/HRS), and the European Society of Cardiology (ESC), general recommendations for cardiac pacing therapy for SND are outlined below. [1, 4, 32]

Class I recommendations (All level of evidence C)

Permanent pacemaker implantation is indicated for the following [1, 4, 32] :

  • SND with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms

  • Symptomatic chronotropic incompetence

  • Symptomatic sinus bradycardia that results from required drug therapy for medical conditions

Class IIa recommendations (All level of evidence C)

Permanent pacemaker implantation is reasonable for the following [1, 4, 32] :

  • SND with a heart rate below 40 bpm, when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented

  • Syncope of unexplained origin, when clinically significant abnormalities of SN function are discovered or provoked in electrophysiologic (EP) studies

Class IIb recommendation

Permanent pacemaker implantation may be considered in minimally symptomatic patients with a chronic heart rate below 40 bpm while awake (level of evidence: C). [1, 4, 32]

Class III recommendations (All level of evidence C)

Permanent pacemaker implantation is not indicated for SND in the following individuals [1, 4, 32] :

  • Asymptomatic patients

  • Those for whom the symptoms suggestive of bradycardia have been clearly documented to occur in the absence of bradycardia

  • Those with symptomatic bradycardia due to nonessential drug therapy

Single- versus dual-chamber pacemakers

In patients with SND, the annual incidence of complete heart block is about 0.6%. [33] In the United States, the implantation of dual-chamber pacemakers is preferred in practice because their use anticipates the possible subsequent development of conducting system dysfunction.

This practice is supported by data from the Danish Multicenter Randomized Trial on Single Lead Atrial Pacing versus Dual Chamber Pacing in Sick Sinus Syndrome (DANPACE) trial, in which 9.3% of patients with single-lead atrial pacing (AAI) required upgrade to a dual-chamber pacemaker (DDD) over 5.4 years of follow-up due to new development of significant atrioventricular (AV) conduction abnormalities. [34] This was necessary despite the fact that these patients had no significant intraventricular conduction abnormality, had PR intervals below 260 ms, and had no Wenckebach AV block with atrial pacing at 100 bpm at baseline. In addition, the incidence of atrial fibrillation (AF) was higher in patients in AAI mode than those in DDD mode. However, no significant mortality difference was noted between the groups in AAI and DDD modes. [34]

Arguably, a single-chamber atrial pacemaker with AAI mode is an acceptable alternative in patients with SND and normal AV and intraventricular conduction because of the added expense of, and the potential for, more lead extraction with a dual-chamber pacemaker.

In patients with SND and known AV conduction abnormality (including bundle branch block and bifascicular block), a dual-chamber pacemaker should be used due to the high risk of AV block (about 36% in a 5-year follow-up study).

In a collaborative pooled-analysis of 10 randomized trials (n = 6639) to evaluate the effect of existing pacing strategies on the risk of postimplantation AF and heart failure events in SND patients, Chen et al stratified the pooled-analysis into two subsets—AAI versus DDD, and minimal ventricular pacing (MinVP) versus DDD—and found that although composite AF and heart failure (HF) events were similar in the AAI versus DDD subset, there was a substantially reduced risk of composite AF and HF in the MinVP group receiving pacemaker as primary treatment. [35] Over the long term, however, the rate of AF and HF was similar in the MinVP versus DDD subset of patients who were scheduled for device replacement. The investigators indicated their findings supported the use of MinVP over conventional DDD in improving clinical outcomes for SND patients who received a pacemaker as primary treatment. [35]

Pacemaker programming features

Chronic right ventricular pacing has been shown to be associated with an increased incidence of AF, stroke, HF, and probably death. [21, 22, 36] A study suggested that right ventricular (RV) pacing is detrimental to left ventricular (LV) function even in patients with a normal LV ejection fraction (LVEF). [37] Therefore, avoiding RV pacing is advantageous in patients with SND treated with pacemaker therapy.

However, using the intrinsic AV conduction in patients with a very long intrinsic PR interval may not be beneficial clinically, as suggested by a trial in patients with an intracardiac defibrillator (ICD). [34] Theoretically, a very long PR interval may result in pacemaker syndrome during sinus tachycardia or a fast atrial pacing rhythm.

As noted above, in the DANPACE trial, about 65% of patients with a moderate AV delay setting in DDD mode with mean RV pacing had a lower incidence of AF and no increased rate of HF, as compared with patients in AAI mode. [34] The optimal AV delay settings in patients with SND are remain unknown, although various programming algorithms from different pacemaker companies are very effective in reducing RV pacing.

Mode switch is an important feature to monitor atrial flutter and AF events. Because more than 50% of patients with SND may develop tachy-brady syndrome over time, [21] it is very important to identify these patients through pacemaker monitoring and to anticoagulate them to reduce their risk of stroke. However, the most appropriate anticoagulant therapy is still uncertain for patients in whom AF is detected only as an incidental finding on pacemaker or ICD diagnostics.

Rate response features have been used in patients with SND, especially in the presence of chronotropic incompetence. However, the clinical benefits of this program feature are still controversial. [38]


Funny Current Blocker Ivabradine

Spontaneous depolarization of the sinus node involves "funny" (I(f)) current in sinoatrial (SA) node myocytes. This is an inward current that is activated on hyperpolarization to the diastolic range of voltages, thereby generating repetitive activity and modulating spontaneous rate. The degree of activation of the funny current determines the steepness of phase 4 depolarization and, hence, the frequency of action potential firing.

I(f) is controlled by intracellular cyclic adenosine monophosphate (cAMP) and is thus activated and inhibited by beta-adrenergic and muscarinic M2 receptor stimulation, respectively; it represents a basic physiologic mechanism for mediating autonomic regulation of the heart rate. Typically, given their exclusive role, f-channels are ideal targets of drugs aiming for pharmacologic control of the cardiac rate. Molecules able to bind specifically to and block f-channels can therefore be used as pharmacologic tools for heart rate control with little or no adverse cardiovascular side effects. 

In addition, several loss-of-function mutations of HCN4 (hyperpolarization-activated, cyclic-nucleotide gated 4), the major constitutive subunit of f-channels in pacemaker cells, are known to cause rhythm disturbances (eg, inherited sinus bradycardia). Finally, gene- or cell-based methods for in situ delivery of f-channels to silent or defective cardiac muscle represent novel approaches for the development of biologic pacemakers that may eventually be able to replace electronic devices.

Current status of ivabradine

A selective f-channel inhibitor, ivabradine, is now commercially available and used in patients with heart failure (HF) and sinus tachycardia.

The 2016 American College of Cardiology, American Heart Association, and the Heart Failure Society of America (ACC/AHA/HFSA) guideline update on new pharmacologic therapy for HF gives a class IIa recommendation for the use of ivabradine to reduce HF hospitalization in patients with symptomatic (New York Heart Association [NYHA] class II-III) stable chronic HF with reduced ejection fraction (HFrEF) (left ventricular ejection fraction [LVEF] ≤35%) receiving guideline-directed evaluation and management, including a beta blocker at the maximum tolerated dose, as well as who are in sinus rhythm with a resting heart rate of 70 bpm or more. [39] The guideline indicates that, "given the well-proven mortality benefits of beta-blocker therapy, it is important to initiate and up titrate these agents to target doses, as tolerated, before assessing the resting heart rate for consideration of ivabradine initiation." [39]

Ivabradine is contraindicated in patients with HF and SND without a permanent cardiac pacemaker.


Long-Term Monitoring

Asymptomatic patients with sinus node dysfunction (SND) should be observed for symptoms. In patients with a pacemaker, carry out the following on routine pacemaker interrogations:

  • Monitor leads and battery status

  • Ensure adequate heart rate support at rest, during daily activities, and during exercise

  • Monitor for pacemaker malfunction

  • Ensure minimal right ventricular (RV) pacing.

  • Monitor for atrial fibrillation and atrial flutter events


Patients with SND who become pregnant and take antiarrhythmic medications should have their medication levels measured because these drug regimens frequently require adjustment. In addition, medication with teratogenic effects (eg, amiodarone, which is associated with fetal thyroid dysfunction) should be avoided.

Patients with SND who become pregnant and have a pacemaker are advised to perform frequent pacemaker checks and make the appropriate adjustments.

Patients with SND who become pregnant and have ventricular dysfunction due to cardiomyopathy or a Mustard or Fontan procedure should have regular and close medical follow-ups with their obstetrician and cardiologist. This permits appropriate adjustment and implementation of anti-congestive heart failure (CHF) medication. If the CHF progresses despite medical management and becomes intractable, the mother and fetus are at risk and early delivery may be scheduled.


Future Directions

Certain genetic mutations have been linked to sinus node and conduction system disease. SCN5A, HCN4, RYR2, CASQ2, and ankyrin-B (ANKB) mutations are associated with sinus node dysfunction, whereas mutations of SN5A, SCN1B, KCNJ2, TBX5, and NKX2-5 are associated with conduction system disease. Neuromuscular genetic disorders including emerin (EMD), lamin A/C (LMNA), and myotonic dystrophy type 1 (DM1) are also associated with AV conduction disease.[7] Gene- and stem cell-based therapies are currently being investigated as therapeutic options for patients with genetic or degenerative abnormalities of the cardiac electrical conduction system.