Tachycardia-bradycardia syndrome (so-called "sick sinus syndrome"). Pathology, mechanisms and treatment

The tachycardia-bradycardia syndrome consists of paroxysmal atrial fibrillation, flutter or tachycardia followed by sinoatrial block or sinus arrest resulting in Stokes-Adams attacks. Detailed histologie findings of the conduction system of 2 patients with this entity correlated well with the clinical observation of cardiac rhythm disturbances in the sinus node, atria and atrioventricular (A-V) junction. Eight other patients with the syndrome were studied clinically. The mechanisms (as revealed by the electrocardiogram) producing the bradycardia phase include depression of pacemaker function (arrest) or of conduction (exit block) of the sinus impulse, or both, plus depression of A-V junctional impulse formation. Proper therapy usually requires electrical pacing in conjunction with administration of digitalis or propranolol, or both. Our findings suggest that the term “sick sinus syndrome” is an inaccurate and inappropriate synonym for the tachycardia-bradycardia syndrome.     

Unusual manifestations of severe sick sinus syndrome

An extremely athletic 56-year-old male physician was found to have profound sinus bradycardia. His only symptom was markedly increased alertness while actively exercising. During pacemaker insertion he had an episode of prolonged sinus arrest terminated by a precordial thump. This case suggests that exercise can alter autonomic tone and increase cardiac output in sick sinus syndrome, causing improvement in possibly unrecognized, subtle, cerebral symptoms. It also appears that patients with profound sinus bradycardia should be given a substantial dose of atropine prior to pacemaker insertion in an effort to prevent prolonged sinus arrest.     

Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.     

"Paradoxical" prolongation of sinus nodal recovery time after atropine in the sick sinus syndrome.

A case of symptomatic sick sinus syndrome is presented with confirmation of sinus nodal dysfunction established by functional testing. The validity of such provocative testing and the criteria for abnormality are discussed. A newly recognized, seemingly "paradoxical" and potentially detrimental effect of atropine noted in this patient is examined. Despite an increase in sinus rate and an improvement in sinoatrial conduction time after administration of atropine, a markedly prolonged sinus recovery time after rapid atrial pacing occurred, and atrial quiescence for more than 10 seconds was seen. Possible electrophysiologic mechanisms for this phenomenon, such as decreased atriosinus entrance block, concealed sinoatrial reentry or enhanced intranodal depolarization, are discussed and potential clinic correlates are made.     

Atrial pacing for sick sinus syndrome

Atrial pacing is the most physiological way to pace patients with sinus node disease, as it provides both AV synchrony and a normal ventricular activation pattern. Long-term studies comparing atrial and ventricular pacing imply that atrial pacing results in fewer cardiac complications and, possibly, reduced mortality. Ventricular pacing should thus, if possible, be avoided in patients with sinus node disease. The potential risk of impending high-grade AV block during atrial pacing is low, with an annual incidence around 1% if patients are selected appropriately. Approximately 40-50% of patients with sinus node disease show signs of chronotropic incompetence during physical exercise, and are thus candidates for atrial rate responsive pacing. A preoperative evaluation of candidates for atrial pacing should include long-term Holter/telemetry, exercise test, carotid sinus stimulation, and an electrophysiological study excluding significant AV conduction disturbances.     

Stroke complicating congenital sick sinus syndrome

We report the case of a patient with congenital sick sinus syndrome complicated by atrial fibrillation and embolic stroke 23 years after the initial diagnosis, at the age of 34 years. Treatment with a dual-chamber pacemaker and oral anticoagulation were initiated; further follow-up was uneventful but pacemaker diagnostics constantly documented asymptomatic recurrences of paroxysmal atrial fibrillation.     

Single coronary artery and sick sinus syndrome

We report 2 patients with recurrent syncope and dizziness, later noted to have single coronary arteries. Both had right heart strain, one having pulmonary hypertension and the other having right ventricular outflow obstruction, which resulted in sinus node dysfunction. Patients were refractory to medical therapy and improved after pacemaker implantation.     

Junctional escape rhythm in the sick sinus syndrome

In 21 patients with and 31 without junctional escape beats, a comparison of the symptoms, revealed that there were no significant differences (p greater than 0.05) in the symptoms between these two groups manifesting a sick sinus syndrome. Thus, the occurrence of junctional escape beats did not provide the anticipated shortening of the asystolic pauses to prevent the occurrence of symptoms related to the period of electrical silence. In 7 patients with an escape junctional rhythm, the long pause was interrupted by the occurrence of a regular junctional rhythm. The pause was not preceded by a supraventricular tachycardia, ruling out physiologic overdrive suppression of the junctional pacemaker. The period of asystole preceding the junctional rhythm was not multiple of the R-R interval of the junctional rhythm. 4 additional patients demonstrated long periods of asystole, uninterrupted by junctional escape beats and at other times exhibited shorter pauses which were terminated by junctional escape beats. These findings can be explained by the presence of a 'junctional arrest' which is analogous to sinoatrial arrest. The phenomenon of 'junctional arrest' may be one tenable explanation to account for the lack of protection by junctional escape activity against the symptoms associated with the sick sinus syndrome.