SUMMARY A 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we could assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node function studies revealed an underlying sick sinus syndrome.THE DIAGNOSIS of atrial arrhythmias is essentially based on the analysis of the configuration, timing, and rate of P waves on the surface ECG. However, recent studies in selected patients have demonstrated dissimilar atrial rhythms with direct intra-atrial recordings otherwise not discernible on the surface ECG."3 In this paper we report the electrophysiologic findings in a patient in whom the ECG revealed atrial flutter and intra-atrial recordings demonstrated the presence of sinus-like rhythm in and around the region of the sinus node, flutter and/or fibrillation of the remaining parts of the right atrium and fibrillation of the left atrium. We also assessed sinus node function, although a major part of the right and left atria were in flutter and/or fibrillation. Assessment of sinus node function revealed an underlying sick sinus syndrome.Case Report A 58-year-old man with hypertensive cardiovascular disease was admitted to the Medical Service of the Brooklyn Veteran's Administration Medical Center for uncontrolled hypertension, congestive heart failure and atrial flutter of recent onset. A 12-lead ECG suggested the presence of atrial flutter at a rate of 240 beats/min, with a ventricular response of 120 beats/min and poor R-wave progression from V1 to V3 ( fig. 1). Chest x-ray film showed cardiomegaly and pulmonary congestive changes. Echocardiogram revealed left atrial and left ventricular enlargement. The patient's hypertension and congestive heartfailure responded promptly to medical therapy. He was then referred to the cardiology service for elective electrical conversion of the atrial flutter after medical conversion with digitalis and quinidine had failed. Electrophysiologic StudiesThe patient underwent electrophysiologic studies to convert the atrial flutter by overdrive atrial stimulation. The procedure was explained to the patient, who gave signed consent. The electrophysiologic studies were performed after withholding digitalis and quinidine for 2 days. Serum digoxin level was 0.5 ng/ml on the day of the study. Two quadripolar #6FUSCI catheters with 10-mm interelectrode distance ...

The clinical, electrocardiographic and electrophysiologic determinants and effects of antiarrhythmic agents on sustained sinus node reentrant tachycardia remain poorly defined. Of 65 consecutive men undergoing electrophysiologic studies for symptomatic paroxysmal supraventricular tachycardia over a 4 year period, 11 (16.9%), who ranged in age from 39 to 76 years, demonstrated sustained sinus node reentrant tachycardia. On the surface electrocardiogram, before electrophysiologic studies, the following diagnoses were considered in the 11 patients: sinus node reentrant tachycardia on the basis of an RP'/P'R ratio of greater than 1 and P wave configuration similar to that of sinus P waves (7 patients); atrioventricular (AV) nodal reentrant tachycardia on the basis of an RP'/P'R ratio of less than 1 (3 patients); and paroxysmal atrial tachycardia with AV block (1 patient). All 11 patients had a history of recurrent palpitation, 4 had syncope, 2 had dizzy spells and 9 had organic heart disease. Sustained sinus node reentrant tachycardia could be reproducibly induced in all 11 patients during atrial pacing or premature atrial stimulation, or both, over a wide echo zone. The tachycardia could be terminated by carotid sinus massage, atrial pacing and premature atrial stimulation. Characteristics of tachycardia included: high-low activation sequence; cycle lengths of 250 to 590 ms with wide fluctuations of 20 to 180 ms in individual patients; RP'/P'R ratio of greater than 1 in 8 (73%) of the 11 patients and a ratio of less than 1 in 3 (27%). Induction of sustained sinus node reentrant tachycardia was prevented by intravenous ouabain (0.01 mg/kg body weight) in two of two patients, by intravenous verapamil (10 mg) in two of two patients and by intravenous amiodarone (5 mg/kg body weight) in four of four patients. In contrast, intravenous propranolol (0.1 mg/kg body weight) did not affect induction of sustained sinus node reentrant tachycardia in two of two patients. It is concluded that sustained sinus node reentrant tachycardia, seen in 16.9% of the study patients with paroxysmal supraventricular tachycardia, is not as benign as previously believed; it is frequently associated with organic heart disease; it demonstrates wide variations in cycle length, unlike other forms of paroxysmal supraventricular tachycardia; it can masquerade as AV nodal reentrant tachycardia and paroxysmal atrial tachycardia with AV block on the surface electrocardiogram in 36% of patients; and it is responsive to intravenous administration of ouabain, verapamil or amiodarone.

The significance and treatment of ventricular premature beats (VPBs) in patients without sustained ventricular tachycardia (VT), sudden death, or syncope remains unclear. We undertook a prospective study of programmed electrical stimulation (up to two extrastimuli and burst pacing) in 73 patients (age 60 ± 10 years) with high-grade VPBs who had no evidence of sustained VT, sudden death, or syncope as determined by 48 hr of monitoring in the cardiac care unit and 48 hr Holter monitoring. Fifty-six patients (76.7%) had atherosclerotic heart disease, 10 (13.7%) had cardiomyopathy or valvular heart disease, and seven (9.6%) had no evident heart disease. Thirty-seven patients (50.7%) had Lown grade IVB VPBs, 30 (41.1%) had Lown grade IVA VPBs, and six (8.2%) had Lown grade III VPBs. Programmed electrical stimulation identified two groups of subjects: group 1 comprised 20 patients (27%) in whom VT or ventricular fibrillation was induced, group 2 comprised 53 patients (73%) in whom no ventricular arrhythmia or only two to four repetitive ventricular responses were induced. There was a significant difference between the presence of atherosclerotic heart disease, old myocardial infarction, and ejection fraction of less than 40% in group 1 compared with group 2. However, there was no significant difference in the grade of VPBs between the two groups. Seventeen of 20 patients from group 1 were placed on antiarrhythmic therapy (defined by programmed electrical stimulation), whereas group 2 patients were randomly assigned to prophylactic antiarrhythmic therapy. A total of 70 patients were followed up for 30 + 15 months. The incidence of sustained VT and/or sudden death (31.5% vs 2%; p < .001) was significantly higher in group 1 compared with group 2. There was no difference in the occurrence of sudden or nonsudden cardiac death between the treated and untreated patients in group 2. The probability of surviving 1 year (0.75 vs 1.0) and 48 months (0.35 vs 0.67) was significantly lower (p < .0008) in group 1 than in group 2. In conclusion programmed electrical stimulation defines high-and low-risk subsets for sudden death among patients with highgrade VPBs. Patients in whom arrhythmias are not inducible and those with ejection fractions of greater than 40% have a low incidence of sudden death and an excellent 1 to 2 year survival; these patients do not need prophylactic antiarrhythmic therapy. Circulation 70, No. 1, [43][44][45][46][47][48][49][50][51] 1984 In the last few years programmed cardiac stimulation has been used in the diagnosis and management of patients with recurrent sustained ventricular tachycardia (VT) and in survivors of out-of-hospital cardiac arrest.'1-9 The results of these studies have demonstrated that programmed cardiac stimulation can induce the clinical ventricular arrhythmia in approximately 75% to 90% of these patients. Furthermore, these studies'-'9 have also shown that use of antiarrhythmic agents that prevent the induction of ventricu-

SUMMARY Sinus node electrograms (SNEs) were recorded in 44 patients using a standard quadripolar electrode catheter (USCI #6) with 10-mm interelectrode distance. In 23 patients, the catheter was positioned at the junction of the superior vena cava (SVC) and right atrial (RA) wall so that the concave curve of the catheter was facing the concave surface of the RA wall. The distal poles of the catheter were close to but not in direct contact with the RA endocardium underlying the anatomic location of the sinus node (method 1). In 21 patients, the catheter was looped in the RA and advanced to the junction of the SVC-RA wall so that the distal poles of the catheter were in direct contact with the RA endocardium underlying the area of the sinus node (method 2). Stable SNEs could be obtained in 10 of 23 patients (43%) by method 1 and in 18 of 21 (86%) by method 2. SNEs by both methods showed two negatively directed deflections (diastolic and upstroke slope of the sinus node) of low frequency and amplitude occurring after the deflections of the T and U waves but before the P wave and intraatrial electrograms from various atrial sites. Unlike method 1, atrial activation by method 2 was characterized by an atrial injury potential. SNEs by method 2 were more stable and less prone to baseline drifts.Carotid sinus massage performed in 10 patients resulted in prolongation of the onset of the upstroke slope to atrial activation. In one patient, it resulted in marked first-degree sinoatrial block. SNEs were recorded in one patient during and after a run of spontaneous atrial flutter. After termination of atrial flutter, sinoatrial conduction time (SACT) prolonged for the first postflutter sinus beat and normalized by the third sinus beat.Direct SACTwas assessed on the SNE in all 28 patients, 12 of whom had sick sinus syndrome (SSS). SACT was also estimated indirectly by continuous pacing in 28 patients and by premature stimulation in 20 patients. Direct SACT was significantly (p < 0.001) longer in patients with SSS (135 30 msec, mean SD) than in patients without SSS (87 12 msec). There was a good correlation between direct SACT and SACT by continuous pacing (r = 0.843, n = 28) and direct SACT and SACT by premature stimulation (r = 0.778, n = 18). However, in certain patients, there were appreciable differences and direct SACTwas longer than estimated SACT by continuous pacing or premature stimulation. We conclude that (1) the success rate of stable SNEs with no appreciable baseline drift is increased with direct contact of the catheter with atrial endocardium underlying the sinus node area (method 2); (2) carotid sinus massage results in depression of sinus node automaticity and prolongation of SACT; (3) direct SACT is significantly longer in patients with SSS and can separate most patients with from those without SSS; and (4) there is a good correlation between direct SACT and indirectly estimated SACT, although the latter underestimates the actual SACT.UNTIL RECENTLY, direct sinus node recordings were not possible in man. Thu...

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