The intrinsic heart rate (IHR) was determined in 17 patients with symptomatic sinus bradycardia by administering atropine 0.04 mg/kg and propranolol 0.2 mg/kg, i.v. In this way, sick sinus (SSS) patients with intrinsic sinus node (SN) dysfunction could be distinguished from those patients with disturbed autonomic regulation of SN function. Sick sinus syndrome patients with normal corrected sinus node recovery time (SNRTC), adjusted for the magnitude and direction of autonomic chronotrophy, consistently had normal IHRs and therefore abnormalities of autonomic regulation. Sick sinus syndrome patients with abnormal adjusted SNRTC consistently had abnormal IHRs and therefore abnormalities of intrinsic SN function. We conclude that more than one pathophysiologic mechanism can produce the clinical manifestations of sick sinus syndrome and that abnormal prolongation of SNRTC is dependent upon the underlying mechanism of sinus node dysfunction.

Sinus node dysfunction is a common entity with significant clinical implications. Establishing a diagnosis may, on occasion, tax the skills of the clinician. Many causes have been cited, but no single factor appears to be established. Immunologic abnormalities may play a part in the etiologic process. Clinical invasive electrophysiology studies may be used to establish a diagnosis. In general, medical therapy must be integrated. Controversy exists regarding the best method of permanent pacing. Treatment may need to be individualized to the type of arrhythmia noted. Long-term prognosis is a large factor in choice of therapy, related to the underlying disease. Prevention of atrial fibrillation may occur with dual-chamber pacing; however, anticoagulation appears essential in this patient subgroup. The 5-year mortality rate in these patients is high and does not appear to be significantly improved with artificial pacing. Mortality is prominently influenced by the coexistence of cardiovascular and valvular heart disease. Patients who die do not differ substantially from survivors with regard to type of sinus dysfunction, occurrence of tachyarrhythmia, or distal conduction abnormalities. The survival rate in patients with sick sinus syndrome and congestive heart failure is significantly lower, and the incidence of embolic events remains high in patients with permanent pacing and the sick sinus syndrome. Thus, it has been proposed that all patients exhibiting the bradycardia-tachycardia syndrome be fully anticoagulated. The incidence of atrial fibrillation is significantly lower in patients with atrial demand pacing (22.3% versus 3.9%) than in patients with ventricular pacing and is accompanied by a decreased incidence of systemic embolization (13% versus 1.6%). Reports comparing survival with use of dual-chamber pacing versus ventricular pacing are encouraging in patients with congestive heart failure. At present, the natural history of the disease is unknown; furthermore, clinical risk factors for the development of symptoms have not been defined, and no electrophysiologic measure of sinus node function has been demonstrated to have reliable predictive value. Therefore, common practice has been to withhold pacemaker therapy in the asymptomatic patient.

Electrophysiologic studies were performed in 32 patients with angiographically documented coronary artery disease (CAD). Group I was composed of ten patients (31%) with severe stenosis (greater than or equal to 75%) proximal to the origin of the sinus node artery (SNA); group II was composed of five patients (16%) with moderate (50--75%) proximal stenosis; and group III was composed of 17 patients (53%) with insignificant (0--50%) proximal stenosis. The mean sinoatrial conduction time (SACT) for group I was 119 +/- 18 msec; group II was 84+/- 16 msec; and group III was 72 +/- 5 msec. The SACT was significantly longer in group I than in group III (P less than 0.005). In conclusion 1) in patients with CAD, SACT greater than 72 +/- 5 msec is abnormal; 2) the results suggest a pathogenetic role of CAD in the development of sinus node dysfunction; 3) the SACT is a more sensitive indicator of subtle sinus node dysfunction in CAD patients than is heart rate, sinus node response to artrial extrastimuli, or sinus node recovery time; and 4) the ability to diagnose sinus node dysfunction in its early stages and recognition that coronary artery disease is an etiologic factor may allow for the elucidation of the natural history of the sick sinus syndrome.

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