Sinus Node Dysfunction In Patients Research Articles

Sinus node dysfunction in acute inferior myocardial infarction. Role of sinus node artery and clinical course in patients with one-vessel coronary artery disease.

To determine the role of the sinus node artery and the clinical course in postmyocardial infarction sinus node dysfunction, 27 patients with acute inferior myocardial infarction and single-vessel coronary artery disease were studied. In 13 patients (group 1) the infarct-related coronary artery was occluded proximally and in 14 (group 2) distally to the site of origin of the sinus node artery. At electrophysiology, performed 10 +/- 3 days from the acute event, basal and intrinsic heart rate were lower in group 1 compared to group 2 patients (54 +/- 4.8 vs. 69 +/- 7 beats/min, p = 0.001, and 66 +/- 7 vs. 76 +/- 8 beats/min, p = 0.006, respectively) while basal and intrinsic corrected sinus node recovery times were prolonged in group 1 compared to group 2 patients (585 +/- 49.3 vs. 324 +/- 61.3 ms, p = 0.0001, and 601 +/- 39.1 vs. 335 +/- 73 ms, p = 0.0001). During a 6-month follow-up no episodes of dizziness, syncope or angina were reported. Moreover, at the end of follow-up resting heart rate (70 +/- 11 vs. 73 +/- 7 beats/min, nonsignificant), maximal exercise heart rate (166 +/- 19 vs. 170 +/- 23 beats/min, nonsignificant), and exercise time (491 +/- 120 vs. 480 +/- 155 s, nonsignificant) were similar between the two groups and no exercise-induced ischemic ST segment depression was observed. Sinus node dysfunction in patients with inferior myocardial infarction and one-vessel disease is related to the occlusion of the infarct-related coronary artery proximal to the site of origin of the sinus node artery and is not associated with increased cardiovascular morbidity in the first 6 months from the acute event.

Transvenous Atrial Pacing in the Management of Sick Sinus Syndrome Following Surgical Treatment of the Univentricular Heart: Case Report and Review

An 11-year-old boy with univentricular heart type A-III underwent surgical treatment at age 10 with a modified Fontan operation. Six months postoperatively he developed intermittent periods of cyanosis and fatigue associated with profound sinus bradycardia and nodal escape. After demonstrating normal atrioventricular conduction, a transvenous atrial pacemaker was implanted. This produced a marked clinical improvement. Transvenous atrial pacing is a satisfactory method of treating sinus node dysfunction in patients with univentricular heart following the Fontan operation provided that there is normal AV conduction.

Preoperative secundum atrial septal defect with coexisting sinus node and atrioventricular node dysfunction.

Sinus node dysfunction in patients after repair of the secundum atrial septal defect has been ascribed to surgical damage. We studied 15 consecutive patients with secundum atrial septal defect before operative intervention. Noninvasive testing included 34-hour electrocardiographic monitoring and a standard 13-lead ECG. Intracardiac electrophysiologic techniques included corrected sinus node recovery time, sinoatrial conduction time, His bundle recording to measure AH and HV intervals, the atrial pacing rate at which atrioventricular node Wenckebach occurred, and atrioventricular nodal refractory period. The ECG revealed an ectopic atrial rhythm in two patients. Intracardiac electrophysiology showed an abnormal corrected sinus node recovery time (range -40 to 800 msec) in 10 patients. Five patients had evidence of atrioventricular nodal dysfunction with prolonged AH interval or abnormal atrial pacing rate at which atrioventricular Wenckebach occurred. These data indicate that sinus node dysfunction or atrioventricular node dysfunction were present before surgical intervention.

Sinus node dysfunction in spinal cord injury with quadriplegia

Patients with recent spinal cord injury and quadriplegia often demonstrate sinus bradycardia (SB), sinus arrest (SA), AV block, and hypersensitivity to vagotonic maneuvers. The presumed mechanism is interruption of the sympathetic nerves to the heart, with a relative increase in parasympathetic tone. To determine the need for permanent pacing, we examined seven patients with recent spinal cord injury and quadriplegia prospectively, 1 to 2 weeks after injury. All patients had transient SB (35-60) and SA (2-8 set). These episodes often occurred with nasotracheal suctioning, despite prior treatment with atropine and hyperventilation. In 5 of 7 patients, His-Bundle Ek!CtFogramS and sinus node recovery times (SNRT)were determined and found to be normal (A-~=10&20 msec, H-V=443 msec, SNRT=llO??lO% of resting cycle length). In 4 of 5 patients there was no disturbance in sinus node function with carotid sinus pressure, during nasotracheal suctioning or with hypoxemia. One patient had SA (4-6 set) with carotid sinus pressure and during suctioning. 6 of 7 patients had later episodes of SA and SB requiring permanent pacemakers. We conclude that there is marked temporal variability in sinus node dysfunction in patients with recent spinal cord injury and quadriplegia. A normal response to sinus node testing does not assure continued normal function. We, therefore, recommend permanent pacemaker insertion in patients with recent spinal cord injury with quadriplegia who have had significant SA or SB.

Procainamide-Induced Sinus Node Dysfunction in Patients with Chronic Renal Failure

Two patients with chronic renal failure developed transient sinus node dysfunction requiring insertion of a temporary pacemaker while receiving procainamide to control ventricular arrhythmias. Blood levels of procainamide were found to be elevated, although at these levels, sinus node dysfunction has not previously been reported. Following discontinuance of procainamide, sinus rhythm returned. A combination of factors, including elevated levels of N-acetyl procainamide, the metabolite of procainamide with anti-arrhythmic properties, are suggested as possible contributory causes for the ECG findings. Thus, procainamide may produce electrophysiologic features of "sick sinus syndrome" in patients with chronic renal failure even when blood levels of this substance are being monitored.

Syncope Caused by Lithium Treatment

Lithium salts have been widely used for several years in the treatment of manic-depressive psychosis. Various side-effects of lithium salts have been described. The present case report present two patients in whom sinus node dysfunction leading to syncope was caused by lithium. One of the cases showed signs of depressed sinus node function even when not on lithium, but no symptoms arose until lithium treatment was commenced. The second case showed no signs of depressed sinus node function when lithium was withdrawn. To study the prevalence of sinus node dysfunction in patients on lithium therapy, 97 consecutive patients on lithium were examined. The examination included case history, ECG and carotid massage. In two patients lithium could not be ruled out as being responsible for sinus node depression and in one patient the same was true for the atrioventricular node. None of these patients had any symptoms. It is concluded that lithium treatment may result in sinus node dysfunction. This side-effect is, however, not common. Lithium treatment can obviously be instituted in all patients without a history suggesting sinus node dysfunction. Patients with a history of dizziness and/or syncope should not be given lithium until thorough cardiological examination has been carried out. Likewise, a cardiological examination should be performed if patients on lithium develop symptoms of this type.

Sinoatrial disease in acute myocardial infarction. Long-term prognosis.

Of 32 patients with acute myocardial infarction complicated by sinoatrial disease, 23 survived. All 23 had inferior infarction. During follow-up lasting 4 to 6 years only one patient developed severe chronic sinoatrial disease (sick sinus syndrome) necessitating permanent pacemaker treatment; twelve others died during this time. In 2 of them death was sudden 5 and 6 months after infarction. Atrial pacing studies in 7 of the 11 patients still alive showed no gross abnormalities. A review of 71 patients with chronic sinoatrial disease treated with a permanent pacemaker revealed only 5 with previous documented infarction. The present data suggest that sinus node dysfunction in patients surviving acute infarction is most often only temporary as is atrioventricular block. Occasionally, however, severe chronic sinoatrial disease requiring a permanent pacemaker may develop later, and this course of events is most likely to occur in those patients who had additional complications during the acute infarct.