Sinus bradycardia

Patient

84-year-old man participating in the LBBB-TAVI study.

Trace

Tracing 3a: episode of nocturnal bradycardia automatically recorded by the device;

sinus bradycardia with rate slightly above 40 beats/minute;
slight decrease in heart rate (< 40 beats/minute);
diagnosis of an episode of bradycardia by the device; the average heart rate over the previous 10 seconds is below the programmed threshold of 40 beats/minute.

Patient: 79-year-old man participating in the LBBB-TAVI study; lipothymia in the morning after breakfast; heat-type prodromes, vertigo followed by “malaise” without loss of consciousness; the patient did not use the assistant to trigger the recording.

Tracing 3b: episode of bradycardia contemporaneous with symptoms automatically recorded by the device;

on the tracing, stable rhythm initially at a rate close to 70 beats/minute;
a relatively sudden drop in rate leading to the diagnosis of bradycardia;
normalization of the rate;
the tracing confirms the presence of an initially stable sinus rhythm (difficulty in properly visualizing the P waves);
significant slowing of the heart rate with sinus bradycardia;
diagnosis of an episode of bradycardia by the device; the mean heart rate over the previous 10 seconds is below the programmed threshold of 40 beats/minute.

Comments

The first patient presented episodes of nocturnal sinus bradycardia. A so-called normal sinus rate corresponds by definition to a resting rate of between 50-60 and 100 beats/minute. The difference between physiological and pathological bradycardia is sometimes difficult to determine. It is indeed frequent and without pathological nature to observe during the day or more often at night, a slowing of the heart rate with sinus activity sometimes falling under 40 beats/minute. A vagal hypertonia frequently observed in athletic patients may explain a physiological bradycardia without the need for special investigation or treatment. A drug etiology is also frequently observed (beta-blocker, digoxin, amiodarone, calcium channel blocker, etc). It is common to define a sinus bradycardia as pathological when it causes the onset of symptoms. It was decided not to implant this asymptomatic patient presenting a perfectly normal daytime heart rate and a preserved chronotropic competence (normal acceleration of the heart rate during exercise).

The second patient presented with a paroxysmal sinus dysfunction occurring in a manifest vagal setting. When in presence of a pause or paroxysmal sinus bradycardia, it is imperative to search for a triggering factor (vagal context, violent pain, fear, stress, urination, etc) in order to differentiate patients presenting a true anatomic sinus (fibrosis, etc) or electrophysiological dysfunction (inability of sinus cells to spontaneously depolarize) and those patients with a reflex pause occurring in a vagal context (prolongation of the spontaneous depolarization slope of sinus cells or sinus activity conduction block in conjunction with a vagal brake), the therapeutic consequences of which differ completely. It was also decided not to implant this pauci-symptomatic patient in a vagal context in the absence of any significant pause.

The device automatically records an episode of bradycardia if the heart rate drops below a programmable value (between 30 and 80 beats/minute, nominal value 40 beats/minute) for a programmable duration (between 5 and 30 seconds, nominal value 10 seconds).

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