Sick sinus syndrome

Definition: Sick sinus syndrome (sinus node dysfunction) is a constellation of electrocardiographic abnormalities — sinus bradycardia, chronotropic incompetence (inadequate sinus response to exercise), sinoatrial exit block, and sinus arrest, particularly following paroxysms of atrial tachyarrhythmia (tachy-brady syndrome).

It is primarily a disease of older people. The substrate is age-related loss of specialised pacemaker myocytes in the sinoatrial node with collagen and fibrous tissue deposition, compounded by ischaemic and degenerative change from hypertension and coronary atherosclerosis.

Associations: both paroxysmal and chronic atrial fibrillation are commonly associated with sinus node disease; dysfunction may progress until no sinus beats occur at all, and conduction disease frequently coexists at the AV node.

Secondary/reversible causes must be excluded first: drugs (beta blockers including topical eye drops, verapamil/diltiazem, digoxin, amiodarone), hypothyroidism, hyperkalaemia and hypokalaemia, obstructive sleep apnoea, raised intracranial pressure, increased vagal tone, hypothermia, infiltrative disease (sarcoid, amyloid, haemochromatosis), infective endocarditis, Lyme and Chagas disease.

Clinical features (Essentials, Table 11-15) reflect reduced organ perfusion: syncope, dizziness, palpitations, angina pectoris, congestive heart failure, insomnia and memory loss. Falls and confusion are common atypical presentations in the elderly.

Diagnosis depends on correlating symptoms with documented bradycardia. Holter monitoring is the standard first test; longer monitoring (patch, event recorder, implantable loop recorder) is matched to symptom frequency. Exercise testing demonstrates chronotropic incompetence.

Key caveat: mild nocturnal bradycardia (>50 bpm) is normal and reflects increased overnight parasympathetic tone; sustained bradycardia in the absence of medication is not a normal finding in older people.

Prognosis: mortality appears unaffected by sinus node dysfunction itself; survival is determined by associated pathology such as ischaemic heart disease. Pacemakers relieve symptoms but do not reduce mortality.

Treatment: withdraw culprit drugs and correct reversible causes. Essentials states there is no satisfactory medical therapy; symptomatic patients require a permanent pacemaker. A pacemaker also permits continued use of rate-controlling drugs in tachy-brady syndrome.

Pacing indications (2018 ACC/AHA/HRS, as quoted in Pathy's): Class I — symptoms directly attributable to sinus node dysfunction, and bradycardia caused by clinically necessary guideline-directed therapy; Class IIa — tachy-brady syndrome where symptoms are attributable to bradycardia, and rate-responsive pacing for symptomatic chronotropic incompetence. Latest Updates and Current Practice Update (concise) 2023 HRS/APHRS/LAHRS guideline on cardiac physiologic pacing shifts emphasis from "which chamber" to "how physiological": conduction system pacing (His bundle or left bundle branch area) is preferred where a high ventricular pacing burden is anticipated, to avoid pacing-induced cardiomyopathy. Leadless pacemakers (Micra, Aveir) are now an established option for older patients with limited venous access, previous device infection or frailty, avoiding pocket and lead complications; dual-chamber and conduction-system leadless systems are in first-in-human evaluation (Heart Rhythm 2025). Practice point unchanged: the fundamental requirement remains symptom–rhythm correlation. Pacing an asymptomatic bradycardia produces no symptomatic benefit and exposes the patient to procedural risk.