Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

Association of sinus node dysfunction, atrioventricular node conduction abnormality and ventricular arrhythmia in patients with Kawasaki disease and coronary involvement.

BACKGROUND: This study was performed to investigate the incidence of arrhythmias in patients with Kawasaki disease (KD). METHODS AND RESULTS: Electrophysiologic studies (EPS) were performed in 40 patients (mean age: 10.3+/-5.1 years; 30 males, 10 females) with KD who had severe to moderate coronary artery disease. Clinical arrhythmias were documented in 4 patients (premature ventricular contractions, ventricular tachycardia, atrioventricular block, and ventricular fibrillation). Dual atrioventricular nodal pathways were demonstrated in 3 patients. Nonsustained atrial fibrillation was induced in 1 patient. The AH interval was prolonged in 2 patients. The Wenckebach rate was 164+/-37 beats/min, and 4 of the patients had a decreased Wenckebach rate. The maximum and corrected sinus node recovery times were 997+/-257 ms and 281+/-130 ms, respectively, and 7 patients were thought to be abnormal. The sino-atrial conduction time was 108+/-64 ms, and 2 patients had prolonged conduction times. CONCLUSIONS: Although there was no relationship between coronary stenosis or obstruction and the EPS parameters, the incidence of abnormal sinus node and atrioventricular node function is apparently higher in KD patients than in the normal population. These functional abnormalities may possibly be caused by myocarditis or an abnormal microcirculation in the sinus node and atrioventricular node artery. In some patients, myocardial ischemia may provoke malignant ventricular arrhythmia.     

Electrophysiological properties of the recipient atrial remnant after human orthotopic cardiac transplantation.

AIMS: The recipient atrial remnant has been used as a control in studies ofchronotropic response following orthotopic cardiac transplantation and as a trigger for the donor heart. It is not known, however, whether its function is normal. We investigated the electrophysiological properties of the recipient atrial remnant. METHODS AND RESULTS: Fifty patients were studied, mean age 49 years (range 20-63) and mean time post-orthotopic cardiac transplantation of 31 months (range 1-107). Recipient atrial rhythm, spontaneous cycle length and sinus node function were determined. Atrial fibrillation/flutter was identified in 10/50 (20%). Of those in sinus rhythm, significant bradycardia was present in 12/40 (30%). The mean spontaneous cycle length was 929+/-188 ms. Three patients demonstrated variable atrial electrocardiogram morphology and a further three patients had marked variations in resting cycle length. The sinus node function was abnormal in 2/34 (6%). CONCLUSIONS: Only 56% recipient atria had normal sinus rhythm, with 21% of these demonstrating features consistent with a wandering atrial pacemaker. The recipient atrial remnant is not normal in the majority of transplant recipients and should be used with caution in studies involving its use as a control or as a trigger for the donor heart.     

Hemodynamic influences on sinus node recovery time: effects of autonomic blockade

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 +/- 79 to 205 +/- 70 ms (p less than 0.04) and to 134 +/- 120 ms (p less than 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates. These findings suggest that hypotension during rapid atrial pacing activates autonomic reflexes that significantly shorten the corrected sinus node recovery time. Autonomic blockade negates this effect and the corrected sinus node recovery time prolongs with faster atrial pacing.     

The origins of the sinus node pacemaker complex in man: demonstration of dominant and subsidiary foci

To test the hypothesis that the human sinus node is capable of demonstrating multiple sites of impulse generation, we assessed spontaneous shifts in the sinus node pacemaker complex, and shifts after overdrive atrial pacing, premature atrial stimulation and carotid sinus massage. A total of 24 patients aged 59 +/- 15 years (mean +/- SD) in whom stable sinus node electrograms were obtained were selected for the study. Ten of the 24 patients had sick sinus syndrome, whereas 14 had no sinus node dysfunction. All 24 patients had atrial pacing at cycle lengths of 1,000 to 300 ms; 9 patients had premature atrial stimulation and 12 had carotid sinus massage. Shifts in the sinus node pacemaker complex occurred spontaneously in 4 (17%) of the 24 patients; after atrial pacing at cycle lengths of 800 to 300 ms (mean 387 +/- 92) in 15 (63%) of 24 patients; after premature atrial stimulation at one or more coupling intervals in 5 (56%) of 9 patients and during carotid sinus massage in 9 (75%) of 12 patients. Shifts in the sinus node pacemaker complex lasted one to six beats and returned to the original site within two to seven beats. Spontaneous shifts in the sinus node pacemaker complex occurred in 3 of 14 patients without sick sinus syndrome and were induced in 6 (60%) of 10 patients with sick sinus syndrome and 11 (79%) of 14 patients without sick sinus syndrome. Shifts in sinus node pacemaker complex were characterized by loss of primary negativity, change in P wave morphology, significant (p less than 0.001) prolongation of sinoatrial interval and sinus cycle length.     

Electrophysiologic findings after Fontan repair of functional single ventricle

Cardiac arrhythmias are well recognized sequelae of the Fontan operation for complex congenital anomalies. In this study the electrophysiologic effects of the Fontan procedure were evaluated in 30 patients who underwent cardiac catheterization with electrophysiologic study 1.9 +/- 1.3 years (mean +/- SD) after modified Fontan repair for functional single ventricle. Abnormalities of sinus node or ectopic pacemaker automaticity were detected in 50% (15 patients) by determination of a prolonged corrected sinus node or pacemaker recovery time. Total sinoatrial conduction time was prolonged in 50% of the patients with normal sinus rhythm. Sinus node or ectopic atrial pacemaker function was entirely normal in only 43% of patients. The predominant atrial rhythm was normal sinus in 70% and ectopic atrial or junctional in 30%. Abnormalities of atrial effective and functional refractory periods were noted in 43% of patients and were most pronounced at faster paced cycle lengths. Atrial endocardial catheter mapping revealed intraatrial conduction delays between adjacent sites in 76% of the patients tested and in eight of nine patients with inducible intraatrial reentry. Programmed atrial stimulation induced nonsustained supraventricular arrhythmias in 10% of the 30 patients and sustained arrhythmias in 27%. Intraatrial reentry was the most common inducible arrhythmia and was present in seven of the eight patients with sustained and two of the three patients with nonsustained atrial arrhythmias. Atrioventricular conduction abnormalities were noted in 10% (three patients). No patient had inducible ventricular arrhythmias with programmed ventricular stimulation. The electrophysiologic findings after Fontan repair include abnormal sinus node function, prolonged atrial refractoriness, delayed intraatrial conduction and inducible atrial arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.     

Developments, complications and limitations of catheter-mediated electrical ablation of posterior accessory atrioventricular pathways

Nineteen patients with posterior accessory pathways and disabling, refractory arrhythmias, underwent catheter ablation using standard defibrillator pulses at energy settings of 150 to 400 J. Accessory pathway ablation was successful in 13 of 19 (68%). Effective catheter ablation correlated with local ventriculoatrial (VA) intervals determined from the coronary sinus catheter at the site of earliest retrograde atrial activation during orthodromic reciprocating tachycardia. In 12 of the 13 successfully ablated patients, the local VA interval was less than 80 ms. In 4 of the 6 unsuccessfully treated patients, the local VA interval was greater than or equal to 80 ms, p less than 0.01. Transient abnormalities noted with the procedure included sinus bradycardia (3 patients), atrioventricular block (5), accelerated junctional rhythm (3), ectopic atrial tachycardia (2), myocardial depression (1), "ischemic" appearing T-wave inversions (10) and hemodynamically insignificant small pericardial effusions (5) Creatine kinase-MB increased from 3 +/- 2 U/liter to 26 +/- 18 U/liter (p less than 0.001), 4 to 8 hours after ablation. In addition, electrical shorts occurring during the ablation procedure in 2 patients were identified and corrected only with oscilloscopic monitoring of voltage and current waveforms. Significant adverse sequelae were seen in 4 patients. Three patients required sternotomy for control of cardiac tamponade secondary to a ruptured coronary sinus and 1 patient had a small posterior left ventricular infarction related to spasm of a right coronary artery extension branch. Coronary sinus rupture correlated with the ratio of catheter diameter to coronary sinus diameter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional changes of ventricular late potentials by provocation with increase of heart rate. Evaluation during atrial pacing.

BACKGROUND: Standard methods fail to reveal late potentials in 20 to 30% of patients with ventricular arrhythmias after myocardial infarction. However, these patients may develop transient delayed ventricular activation during increases in heart rate. METHODS AND RESULTS: Atrial pacing was performed, at the rates of 100 min-1 and 120 min-1, in 50 patients after myocardial infarction. Twenty-six patients had a history of documented, sustained ventricular tachycardia, 12 had a history of ventricular fibrillation and 12 no history of ventricular arrhythmias. The low-noise surface electrocardiogram was analysed before and during atrial pacing in the time and frequency domains. Fifteen of 26 patients with ventricular tachycardia, four of 12 with ventricular fibrillation and three of 12 without ventricular arrhythmias experienced late potentials during sinus rhythm. Atrial pacing led to a shift of 26 +/- 15 ms of preexistent late potentials into the ST segment, this being greater in patients with anterior infarctions and to an increase in magnitude in patients with inferior infarctions. In patients without late potentials during sinus rhythm, atrial pacing provoked late potentials in eight of 11 patients with ventricular tachycardia, in four of eight patients with ventricular fibrillation and in one of nine patients without ventricular arrhythmias. Low amplitude signals (LAS) were increased in patients after inferior and filtered QRS in patients after anterior infarction. In 10 patients without cardiac disease no late potentials were detectable in the time and frequency domain either at rest or during increased heart rate. CONCLUSIONS: Increase in heart rate may unmask late potentials in patients prone to malignant ventricular arrhythmias. Therefore, functional late potential analysis with non-invasive clinical stress tests, i.e. exercise tests, should be performed only with an adequate rate response. This might identify patients at risk of malignant ventricular arrhythmias otherwise not identified with conventional late potential analysis.     

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 510 to 900 ms (mean 743 +/- 141) and the longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,018 +/- 168). A long sinus or atrial pause occurring at the termination of tachycardia or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 +/- 1,674), was provoked by the administration of various drugs. These included an intravenous bolus injection of adenosine triphosphate (5 mg; one patient), intravenous bolus injection of verapamil (5 mg; one patient), a combination of a single oral dose of diltiazem (120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient). In five patients, low frequency deflections suggestive of sinus node activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing with a long arrest suggesting suppression of sinus automaticity was also noted in three of these five patients; the longest sinus arrest in these three patients was 4,160, 4,800 and greater than 4,910 ms, respectively. The remaining patient with a pause of 6,840 ms had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Syncope in patients with normal EKG and without cardiac disease: value of ambulatory esophageal electrophysiology in determining etiology

The aim of this study was to determine whether ambulatory oesophageal electrophysiological recordings are valuable in identifying the cause of syncope in patients with a normal ECG and without cardiac disease. One hundred and forty-five patients aged 16 to 88 years of age, without cardiac disease, and with a normal ECG without a documented arrhythmia, were examined for unexplained syncope: 55 patients complained of palpitations at the time of syncope. The electrophysiological study was carried out in the clinic with oesophageal recordings using a classical protocol: Wenckebach point and sinus node recovery time were determined; programmed atrial stimulation was used with delivery of 1 and 2 extra-stimuli on the basal rhythm and with 20/30 micrograms infusion of isoprenaline; blood pressure was monitored. The study was negative in 41 patients (28%). Sinus node dysfunction was observed in 9 patients (6%). A vaso-vagal reaction reproducing the symptoms was induced by isoprenaline in 21 patients (14.5%); a conduction defect was revealed in 2 cases (1%). Atrial fibrillation or tachycardia > 1 minute was induced in 22 patients (15%). Paroxysmal junctional tachycardia was induced in 50 patients (35%). Patients with a negative study were younger than those with sinus node dysfunction or atrial fibrillation (44 +/- 21, 71 +/- 9 and 63 +/- 14 years respectively). Treatment was guided by these results: cardiac pacing, antiarrhythmic therapy or radiofrequency ablation of the reentrant pathway were indicated and suppressed syncope in all but two patients. The authors conclude that electrophysiological studies in the out-patient clinic with oesophageal recordings is a safe, rapid and economic method of detecting arrhythmias (sinus node dysfunction or supraventricular tachycardia) in 60% of patients with syncope, especially if they have symptoms of palpitations.     

Short-term rapid atrial pacing produces electrical remodeling of sinus node function in humans

INTRODUCTION: Depression of sinus node function occurs in dogs and in patients after cessation of atrial flutter and fibrillation. We tested whether transient atrial pacing might produce similar changes in humans. METHODS AND RESULTS: We studied the impact of short-term rapid atrial pacing, simulating atrial tachyarrhythmias, on sinoatrial conduction time (SACT) and corrected sinus node recovery time (CS-NRT) in 10 patients undergoing electrophysiologic study. None had recognizable structural heart disease, history of atrial fibrillation or flutter, autonomic dysfunction, or any tachycardia for at least 24 hours before study. All cardiac drugs were discontinued >5 half-lives prior to study. No patient had significant hypotension during atrial stimulation. SACT and CSNRT were measured at baseline, and sinus node reset zone was determined. Right atrial pacing was performed for 10 to 15 minutes, after which SACT and CSNRT were measured again. Both parameters increased significantly, from 423+/-208 msec to 491+/-214 msec and from 80+/-50 msec to 96+/-53 msec, respectively (P = 0.02 and P < 0.001, respectively). CONCLUSION: Rapid atrial pacing for only 10 to 15 minutes, simulating transient atrial tachyarrhythmias, alters sinus node function in humans. Additional studies are needed to evaluate the mechanism, but the clinical implication is that even transient episodes of atrial tachyarrhythmias can cause sinus node remodeling in patients.     

Surgical therapy for atrial tachycardia in adults

Eighteen adult patients with atrial tachycardia refractory to treatment with a mean of four drugs underwent attempted surgical cure. Atrial tachycardia originated in the right atrium in 17 patients and the left atrium in 1 patient. Tachycardia could be reproducibly induced and terminated by atrial extrastimuli or atrial pacing in 8 patients (44%). Resection of the arrhythmogenic area was performed in 16 patients (89%), and an isolation procedure was performed in 1 patient. In seven cases (39%), the area of isolation or excision included the sinoatrial node. One patient underwent His bundle section because the arrhythmogenic region was too close to the atrioventricular (AV) conduction system to enable resection. The mean duration of clinical follow-up was 56 +/- 34 months. Clinical tachycardia recurred in five patients (28%), but in two patients it did not recur until greater than 1 year after surgery. A permanent pacemaker was implanted in 3 (18%) of the 17 patients whose His-Purkinje system was left intact. One other patient had required permanent pacing before surgery. Only one of the seven patients undergoing sinoatrial node resection or isolation required permanent pacing for symptomatic bradycardia. Apart from the requirement for permanent pacing, no significant complications occurred. Surgical therapy for atrial tachycardia is a safe procedure, but the rate of cure appears to be less than that of supraventricular tachycardias associated with accessory AV connections. Excision or isolation of the sinoatrial node does not necessitate permanent pacing in most patients.     

Functional abnormalities of the conduction system in children with an atrial septal defect

We performed an electrophysiologic study in 40 children with an atrial septal defect and analyzed their pre- and postoperative electrocardiograms and 24-hour Holter recordings. The electrophysiologic study showed a prolonged corrected sinus node recovery time in 83% and an abnormal sinuatrial conduction time in 25% of the children. An early Wenckebach response to atrial pacing was seen in 18%. Sixteen percent had a prolonged atrial conduction time. The atrial functional refractory period was abnormal in 35%. Two children developed nonsustained supraventricular tachycardia during the electrophysiologic study. The preoperative electrocardiogram showed first-degree atrioventricular block in 15% of the children; prolonged periods of accelerated atrial rhythm were found in 35% of the preoperative 24-hour Holter recordings. The incidence of first-degree atrioventricular block and accelerated atrial rhythm decreased postoperatively. We could not find a significant correlation between age or shunt size and the presence of electrophysiologic abnormalities or arrhythmias. These results indicate that the sinus node, atrioventricular node and atrial myocardium show some degree of dysfunction in patients with an atrial septal defect. An early operation may prevent further progression of electrophysiologic abnormalities and the development of symptomatic arrhythmias.     

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.     

Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents

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.     

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.     

Clinical study of double-chamber stimulation. Apropos of 50 cases followed-up for 1 to 5 years

The authors report their experience of dual chamber pacing in 29 men and 21 women of mean age 71 +/- 4 years. 35 had sinus node dysfunction associated with node-His bundle conduction disorders; 31 presented with neurological symptoms and 4 with heart failure (due to pacemaker syndrome in 1 case). Sinus node dysfunction was diagnosed by surface ECG in 25 cases and after electrophysiological studied in only 10 cases. Fifteen patients had atrioventricular block without sinus node dysfunction: 2 of them were young subjects, 1 had pacemaker syndrome and 12 were actual or potential heart failure patients for whom preservation of the atrial systole was justified. Nine patients presented with neurological symptoms. 43 (86%) had cardiac or arterial disease associated with cardiac rhythm and conduction disorders. The percutaneous single subclavian vein approach was used in 36 cases (78%). 41 active and 9 passive fixation electrodes were utilized. The mean follow-up period was 25 months (12 to 70 months), with a cumulative figure of 1,253 months/patients. Two late re-operations for displacement of the atrial electrode were performed. Dual chamber pacing was abandoned, 14 months on average after implantation, in 9 patients (18%), on account of arrhythmias in 4 of them. Three cases of tachycardia from "electronic re-entry" and 6 cases of supraventricular arrhythmia transferred to the ventricle by the pacemaker were observed. Sixteen patients (32%) died 12 +/- 4 months on average after surgery: 12 (33%) had sinus node dysfunction and 4 (26%) had AV block. Death was caused by a cardiovascular disease in 12 cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rhythm profile in patients with psoriatic arthritis

OBJECTIVE: To analyze the rhythmic profile in patients with psoriatic arthritis (PA). DESIGN: In order to evaluate the rhythmic profile of patients with PA, we have carried out ambulatory 24 hour ECG recordings in 22 patients presented consecutively to the Holter ECG laboratory. SETTING: Patients followed in a specialised rheumatology consultation, in Santa Maria Hospital. PATIENTS: We have studied 22 patients (pts), 10 male and 12 female, aged 49.8 +/- 8.4 years, presenting PA diagnosed in average 12.9 years before. A group of 36 individuals, 25 male and 11 female, aged 37 +/- 8 years and without disease, were used as control. RESULTS: All patients were in sinus rhythm with a mean heart rate of 71 +/- 6 (min - 51.5 +/- 7.0 and max - 130.3 +/- 15.0). In 8 (36.6%) there were sinus bradycardia less than 50/min and sinus tachycardia (greater than 120/min) in 15 patients (68.1%). Two patients (9%) presented supraventricular tachycardia and one had AV block. There were premature atrial systoles in 14 pts (63.6%), and ventricular arrhythmias in 9 (40.9%). In control group, there were sinus bradycardia in 16.6%, sinus tachycardia in 33.3%, premature atrial systoles in 33.3% and ventricular arrhythmias in 25% of them; in 11% there were conduction disturbances. CONCLUSIONS: a) Premature atrial systoles were the rhythm disturbance more prevalent. b) Patients with PA presented a significant higher incidence of sinus bradycardia and sinus tachycardia. c) Cardiac conduction disturbances were not frequent. d) Our results may suggest the presence of a subtle autonomic dysfunction in patients with psoriatic arthritis.