Reliability of Transesophageal Pacing in the Assessment of Sinus Node Function in Patients with Sick Sinus Syndrome

The purpose of this study was to find out whether transesophageal pacing could be utilized for assessment of sinus node function in patients with sick sinus syndrome (SSS). In 17 patients with SSS (study group) we compared the results of sinus node tests obtained both in the basal state and after pharmacological autonomic blockade by endocavitary stimulation and, 24 hours later, by transesophageal pacing. In another group of 17 patients with SSS (control group), we compared the results obtained by two endocavitary studies. In "study group", sinus cycle length (SCL) and corrected sinus node recovery time (CSRT) did not show significant differences between the two studies both in the basal state and after autonomic blockade, whereas sinoatrial conduction time (SACT) was more prolonged during esophageal pacing (P less than 0.01). In "control group", sinus node measures did not show significant differences between the two studies. In the "study group," the following coefficients of correlation were obtained in the basal state; SCL, r = 0.65, CSRT, r = 0.57, SACT, r = 0.52 and after autonomic blockade: SCL, r = 0.95, CSRT, r = 0.62 and SACT, r = 0.53. In the basal state, the correlation for SCL and CSRT between the two studies was lower in the "study group" than in the "control group" (P less than 0.05), whereas after autonomic blockade the correlation for sinus node measures did not show significant differences between the two groups of patients. These data suggest that transesophageal study influences the autonomic tone regulating the sinus node; however, it is not responsible for important variations in sinus node measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Effect of Exogenous Adenosine in Patients with Neurally-Mediated Syncope and Sick Sinus Syndrome

The effects of a 20-mg IV, bolus of adenosine 5'triphosphate (ATP) on the heart rhythm was studied in 79 patients affected by neurally-mediated syncope (26 cases) or sick sinus syndrome (22 cases) or both syndromes (31 cases) and in 31 healthy control subjects in order to examine the sensitivity of cardiac purinoceptors in such circumstances. During ATP infusion, the sinus cycle lengthened to > 2 seconds in no control, in 1 (4%) patient with neurally-mediated syncope, in 5 (23%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated and sick sinus syndromes (P = 0.01). Atrioventricular block occurred in 14 (45%) of controls, in 10 (38%) patients with neurally-mediated syncope, in 4 (18%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated syncope and sick sinus syndrome (n.s.). Thus, exogenous ATP exerts different effects on patients with neurally-mediated syncope and patients with sick sinus syndrome. In fact, intrisic disease of the sinus node is necessary to modulate an abnormal adenosine-mediated sinus arrest, whereas patients affected by neurally-mediated syncope alone show a normal sensitivity to the drug administration. The effect of ATP on atrioventricular conduction is greater than that on sinus node and is of similar magnitude in patients and controls; thus the clinical meaning of ATP induced atrioventricular block remains uncertain.     

Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block

Thirty-four patients with a prolonged A-H interval (group I)and 26 with A-V nodal Wenckebach block (group II) were studiedin the basal state and after autonomic blockade (propranolol0.2mg kg^–1 and atropine 0.04 mg kg^–1 in order toassess the role of autonomic system in A-V nodal conductiondisturbances. In group I, the A-H intervals did not change significantlyafter autonomic blockade, whereas pacing cycle length for Wenckebachblock, effective and functional refractory periods of the A-Vnode decreased significantly (P<005). In the 22 patientswith organic heart disease these variables did not change significantlyafter autonomic blockade, whereas in the 12 without underlyingheart disease, they decreased in all cases (P< 0001). Inthe former, the variables of intrinsic A-V nodal conductionwere normal in only 6% of patients, whereas in the latter theywere normal in 66%. Also in group II, the intrinsic A-H intervalswere normal in only 6% of patients with cardiac disease butwere normal in 63% without underlying heart disease. These datasuggest that in the patients with first and second degree A-Vnodal block and organic heart disease, the conduction disturbanceis predominantly related to intrinsic involvement of A-V node,whereas in the subjects without underlying heart disease theA-V nodal blocks appear mainly related to autonomic alterations.     

Relationship between the most proximal His bundle and the morphology of intracavitary pressure curves

A precise localization of the most proximal His bundle (HB)is useful both for diagnostic and for therapeutic purposes,allowing the modification of atrioventricular (AV) nodal conduction.For selective diagnosis a bipolar lead is utilized; for therapy,a unipolar lead. The aim of the present study was to determinethe relationship between the most proximal HB and the morphologyof intracavitary pressure curves. In 15 patients (aged 64 ± 10 years), both bipolar andunipolar H-V intervals were continuously recorded while graduallywithdrawing the catheter, which detected the pressure at itstip, from the right ventricle to the atrium. The longest bipolarH—V was 55.5±13 ms and the shortest 44.5±11ms (P<0.001); the longest unipolar H—V was 56.5 ±14 ms and the shortest 46.2±11 ms (P<0.001). During unipolar recording, H deflection was present in all patientsat the same time as ventricular, transvalvular and atrial pressurecurves; during bipolar recording, the H electrogram was notpresent in only one patient concomitantly with the atrial curve.During bipolar recording, the atrial H—V interval wasgreater than transvalvular H—V in nine patients (meandifferences: 6 ± 2 ms) and they were equal in five; withunipolar recording the atrial H—V interval was greaterthan transvalvular H—V in 13 patients (mean difference:8 ± 6 ms) and they were equal in two. In all patients,the H wave amplitude diminished from the transvalvular areato the atrial one. These data suggest that the values of the H—V intervalrecorded in the past have been underestimated. Furthermore,in order to modify AV nodal conduction selectively without damagingthe HB it might be useful to record, in addition to the H deflection,the intracavitary pressure curves so as to deliver energy onlywhen the tip of the catheter picks up an atrial curve.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Electrophysiological effects and mechanism of action of oral quinidine in patients with sinus bradycardia and first degree A-V nodal block

The effects of quinidine on sinus nodal and A–V nodalfunction were assessed in 20 patients (age: 60±7 years)with sinus bradycardia and a prolonged A–H interval. Electrophysiologicalstudies were performed twice in each patient. In the first study,the measurements of sinus and A–V node function were evaluatedboth in the basal state and after autonomic blockade (propranolol0.2 mg kg^-1 and atropine 0.04 mg kg^-1). Oral quinidine was administeredfor 3–4 days (1200 mg day^-1) and the study was then repeatedusing the same methods. Comparison of data obtained in the twostudies in the basal state allowed us to evaluate the overalleffect of quinidine. Comparing the results obtained followingautonomic blockade, the direct action of the drug could be assessed.Inthe basal state quinidine did not significantly change the functionof either node. In contrast, after autonomic blockade, significantchanges were noted after quinidine. In 3 patients with sinusrate <50 beats min^-1 and an abnormal intrinsic heart rate,quinidine induced marked depression of sinus automaticity.Thesedata suggest that: (1) in patients with sinus bradycardia andprolongation of the A–H interval, oral quinidine has adirect depressant effect on sinus and A–V nodal function,but this effect is counteracted by autonomically mediated actions;(2) in patients with moderate or severe bradycardia and an abnormalintrinsic heart rate, the drug can induce marked depressionof sinus automaticity.     

Hemodynamics of Idiopathic Paroxysmal Atrial Fibrillation

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 ± 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 ± 11 to 128 ± 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 ± 11 vs 89 ± 12 mmHg, P < 0.01). Left ventricular enddiastolic pressure decreased during AF (9 ± 3 vs 6 ± 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 ± 2 vs 12 ± 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 ± 2 vs 3.8 ± 2 mmHg, P < 0.01 j, whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O₂ difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamicaily, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.     

Dromotropic effects of oral theophylline in patients with atrial fibrillation and a slow ventricular response

Theophylline increases sinus rate, but as yet its use has notbeen investigated in patients with chronic atrio ventricularconduction disturbances. Resting electrocardiogram, 24-h Holterrecording and treadmill test were performed in 17 patients withchronic atrialfibrillation and a slow ventricular response notrelated to drugs (age: 75±8 years). Then slow-releasetheophylline was administered (700mg daily) and after 5 daysthese investigations were repeated with the same methods. Theophyllineincreased mean resting heart rate (51±6 versus 67±13beats.min^–1, P<0·01 mean 24-h heart rate (51±6versus 68±14 beats.min^–1, P<0·01 andminimal 24-h heart rate (32±6 versus 42±11 beats.min^–1,P<0·01 Cardiac pauses >2·5 s were presentin 13 patients during control recording; after theophyllinethey disappeared in 11 and markedly decreased in the remainingtwo. The longest R-R interval decreased in all patients (3218±943versus 2121±518ms, P<0·01). The daily numberof wide QRS complexes increased in 16 out of 17 patients (428±752versus 1146±1464 ms, P<0·01). Exercise heartrate, evaluated at the end offirsi andsecondstage, was higherafter theophylline than during control test (P<0·01). These data suggest that oral theophylline can represent a validtherapy in most patients with atrialfibrillation and a slowventricular response.     

Electrophysiological effects and mechanism of action of oral quinidine in patients with sinus bradycardia and first degree A-V nodal block

The effects of quinidine on sinus nodal and A–V nodalfunction were assessed in 20 patients (age: 60±7 years)with sinus bradycardia and a prolonged A–H interval. Electrophysiologicalstudies were performed twice in each patient. In the first study,the measurements of sinus and A–V node function were evaluatedboth in the basal state and after autonomic blockade (propranolol0.2 mg kg^-1 and atropine 0.04 mg kg^-1). Oral quinidine was administeredfor 3–4 days (1200 mg day^-1) and the study was then repeatedusing the same methods. Comparison of data obtained in the twostudies in the basal state allowed us to evaluate the overalleffect of quinidine. Comparing the results obtained followingautonomic blockade, the direct action of the drug could be assessed.Inthe basal state quinidine did not significantly change the functionof either node. In contrast, after autonomic blockade, significantchanges were noted after quinidine. In 3 patients with sinusrate <50 beats min^-1 and an abnormal intrinsic heart rate,quinidine induced marked depression of sinus automaticity.Thesedata suggest that: (1) in patients with sinus bradycardia andprolongation of the A–H interval, oral quinidine has adirect depressant effect on sinus and A–V nodal function,but this effect is counteracted by autonomically mediated actions;(2) in patients with moderate or severe bradycardia and an abnormalintrinsic heart rate, the drug can induce marked depressionof sinus automaticity.     

Different electrophysiological modes of action of oral quinidine in man

The purpose of this study was to evaluate the effects of oralquinidine on the normal sinus node (SN) and A- V node and todetermine if the drug exerts in man the same effects observedin cardiac tissue preparations (i.e. both direct and vagolyticaction). Electrophysiological studies were performed twice in each of16 patients (mean age: 57.7± 12 years) with normal restingand intrinsic heart rates and normal A-H intervals. In the firststudy, the parameters of SN and A-V node were evaluated bothin the basal state and following pharmacological autonomic blockade(AB), (propranolol 0.2 mg kg 1 and atropine 0.04 mg kg1), Oralquinidine was administered for 3–4 days (1200 mg day1)and the electrophysiological study was then repeated using thesame methods. From the comparison of data obtained in the twostudies in the basal state the overall effect of quinidine wasevaluated, and by comparing those obtained following ABthe directaction of the drug was assessed. The overall effect of quinidine on SN and A-V nodal functionswas very slight since sinus cycle length, corrected SN recoverytime, sino-atrial conduction time, A-H interval, Aj-Hj intervalat a cycle length of 600 ms and Wenckebach periods did not changesignificantly after the drug. On the contrary, following ABthese measures increased significantly (P0.01). These results provide evidence of dual effects of oral quinidinein man: a direct depressant action and an autonomically mediatedopposing action, very probably vagolytic. The overall effectof the drug is very slight.