PA Intervals Research Articles

Prolonged atrial refractoriness to predict the onset of atrial fibrillation after transcatheter aortic valve implantation.

Atrial fibrillation (AF) is the most common atrial arrhythmia after transcatheter aortic valve implantation (TAVI) and is associated with high mortality. Although some clinical and echocardiographic variables have been defined to predict new-onset atrial fibrillation (NOAF), electrophysiologic (EP) parameters have not been identified yet. We aimed to investigate the impact of atrial refractoriness on NOAF after TAVI. Seventy-nine consecutive patients who underwent TAVI were enrolled in this trial. All patients undergoing TAVI were screened for AF. Fifteen (19%) had AF during the follow-up period. Patients with NOAF were older and had a higher BMI and STS. Left atrial diameter (LAD) was higher, left ventricular ejection fraction (LVEF) was lower, and preprocedural LVEDP was higher in patients with NOAF. As electrophysiologic (EP) parameters, atrial effective refractory periods (AERP) (in high right atrium [AERP<inf>HRA</inf>], in right posterolateral atrium [AERP<inf>RPL</inf>], and in distal coronary sinus [AERP<inf>DCS</inf>]) were lower, difference between atrial effective refractory periods (AERP<inf>DISP</inf>) and PA intervals were higher in patients with AF than those without AF. The only independent parameter that influenced the development of AF after TAVI was AERP<inf>DISP</inf>. The Receiver Operating Characteristic (ROC) analysis showed that an AERP<inf>DISP</inf>>46 msec significantly separated those with AF and those without AF with a sensitivity of 85% and a specificity of 97%. The current study demonstrates that the only independent variable predicting NOAF is AERPDISP. Therefore, increased AERPDISP values may help predict patients with high risk for NOAF and needing specific therapies.

Atrial refractoriness early after transcatheter aortic valve implantation TAVI in patients with severe aortic stenosis and sinus rhythm.

Aortic valve stenosis (AS) is a common valvular heart disease, especially in the elderly, and is associated with a high prevalence of atrial fibrillation. Although the risk of atrial fibrillation is expected to decrease after the intervention, atrial fibrillation develops in many patients undergoing surgical or percutaneous transaortic valve implantation. We aimed to evaluate atrial refractoriness since it may play a key role in the occurrence of atrial fibrillation after transaortic valve implantation. Seventy-nine consecutive patients who underwent TAVI between October 2021 and May 2023 were enrolled in this trial. Sixty-seven patients underwent electrophysiology study before and after TAVI. We evaluated the changes in PA and AH intervals, as well as atrial effective refractory periods. Besides the hemodynamic changes, atrial effective refractory periods increased, and atrial effective refractory period dispersion (39.8±21.6 vs. 31.1±18.0) decreased significantly after TAVI. The change in atrial effective refractory period dispersion after TAVI was correlated only with the changes in left ventricular end-diastolic pressure (r=0.77, P=0.001) and the changes in aortic gradient (r=0.4, P=0.001). The independent variables affecting the changes in atrial effective refractory period dispersion were basal pro-BNP levels, besides the changes in left ventricular end-diastolic pressure and aortic gradient after transaortic valve implantation. Our results show an acute improvement in atrial refractoriness after TAVI, though high atrial fibrillation rates are reported in the literature. The timing of aortic valve replacement is important, as irreversible maladaptive changes might have already developed by the time of intervention.

Atrial conduction time associated predictors of recurrent atrial fibrillation.

Identifying patients at high risk of atrial fibrillation (AF) recurrence remains challenging. This study aimed to evaluate total atrial conduction time (TACT) and left atrial (LA) asynchrony as predictors of AF recurrence. Consecutive patients after the first AF episode, terminated either spontaneously or with cardioversion, underwent transthoracic echocardiography. TACT, estimated by the time delay between the onset of P-wave and the peak A'-wave on the Tissue Doppler Imaging (PA-TDI duration), atrial volumetric and functional parameters, and biatrial strain were assessed. We calculated mean PA-TDI-the average of PA-TDI measurements in all left atrial (LA) walls-and the difference between the longest and the shortest PA interval (DLS) and the standard deviation of 4 PA intervals (SD4) to assess the LA global remodeling and asynchrony, respectively. The primary endpoint was AF recurrence. Patients with recurrent AF had significantly prolonged PA-TDI intervals in each LA wall-and thus mean PA-TDI-than those without recurrence (mean PA-TDI: 157.4 ± 17.9 vs. 110.2 ± 7.7ms, p < 0.001). At univariate analysis, LA maximum volume index, total LA emptying fraction, right atrial maximum volume index, PA-TDI, DLS, and SD4 were predictors of AF recurrence. At multivariable analysis, PA-TDI intervals in all LA walls remained strong predictors with mean PA-TDI (odds ratio 1.04; 95% confidence interval 1.03-1.06) having an optimal cutoff of 125.8ms in receiver operator characteristics curve analysis providing 98% sensitivity and 100% specificity for AF recurrence (area under the curve = 0.989). PA-TDI was an independent predictor of AF recurrence and outperformed established echocardiographic parameters.

Surface electrocardiogram: Could atrioventricular nodal and His bundle potentials be recorded beat by beat on "Saah electrocardiogram"?

Objective:The P-QRS-T wave on surface electrocardiogram (ECG) reflects the changes in atrial and ventricular electrical properties. However, the atrioventricular conduction system potentials cannot be recorded to date. This study aimed to explore the possibility of micropotential of the atrioventricular conduction system recorded by surface “SAN-Atrial-AVN-His (Saah) ECG.”Methods:We randomized 100 healthy volunteers (50 females and 50 males; mean age 25.12±1.62 years) to receive “conventional 12-lead ECG” and “Saah ECG,” which were recorded by the “Saah ECG” machine. We recorded and further analyzed “conventional 12-lead ECG” and “Saah ECG.” According to the microwavelets before the QRS complex, the PR interval was the sum of three intervals: PAs interval (PA interval recorded on surface ECG), AHs interval (AH interval recorded on surface ECG), and HVs interval (HV interval recorded on surface ECG). The PR interval, PAs interval, AHs interval, and HVs interval were measured.Results:Not only the P-QRS-T waves but also the microwavelets before the P wave, before the QRS complex, and after the QRS complex were recorded in 100 healthy volunteers. The PAs interval, AHs interval, and HVs interval were 22–37 (31.23±2.93) ms, 60–103 (76.07±13.43) ms, and 39–55 (49.29±4.44) ms, respectively. The PAs interval, AHs interval, and HVs interval were consistent with the intracardiac measurements (PA, AH, and HV intervals) obtained in previous studies. Compared with female volunteers, male volunteers had a longer AHs interval (p<0.05).Conclusion:Not only the P-QRS-T waves but also the microwavelets before the P wave, before the QRS complex, and after the QRS complex were recorded on surface ECG. The wavelets before the QRS complex may be related to atrioventricular nodal, His bundle (bundle branch) potentials.

Normal Values for Heart Electrophysiology Parameters of Healthy Swine Determined on Electrophysiology Study.

Swine are a well-recognized animal model for human cardiovascular diseases. Despite the widespread use of porcine model in experimental electrophysiology, still no reference values for intracardiac electrical activity and conduction parameters determined during an invasive electrophysiology study (EPS) have been developed in this species thus far. The aim of the study was to develop a set of normal values for intracardiac electrical activity and conduction parameters determined during an invasive EPS of swine. The study included 36 healthy domestic swine (24-40 kg body weight). EPS was performed under a general anesthesia with midazolam, propofol and isoflurane. The reference values for intracardiac electrical activity and conduction parameters were calculated as arithmetic means ± 2 standard deviations. The reference values were determined for AH, HV and PA intervals, interatrial conduction time at its own and imposed rhythm, sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), anterograde and retrograde Wenckebach points, atrial, atrioventricular node and ventricular refractory periods. No significant correlations were found between body weight and heart rate of the examined pigs and their electrophysiological parameters. The hereby presented reference values can be helpful in comparing the results of various studies, as well as in more accurately estimating the values of electrophysiological parameters that can be expected in a given experiment.

Abstract T P158: Prolonged Atrial Electrical Mechanical Delay on Echocardiography in Patients With Cryptogenic Stroke

Backgrounds and Purpose: One quarter of strokes are cryptogenic, and subclinical atrial fibrillation may be a common etiologic factor. Prolonged atrial electrical-mechanical delay was known as a predictor of paroxysmal atrial fibrillation (AF). We evaluated whether the prevalence of prolonged atrial electrical-mechanical delay suggesting the presence of atrial substrates for paroxysmal AF may be higher in patients with cryptogenic stroke. Methods: We retrospectively reviewed data from patients with ischemic stroke who were admitted to our hospital between January 2011 and December 2012, and selected patients with cryptogenic stroke who underwent echocardiography. Patients who underwent echocardiography for health care examination were enrolled in control group. Age, sex and underlying risk factors were matched in two groups. Atrial electrical-mechanical delay (PA interval) was defined as the time interval (msec) from the initiation of P wave on surface electrocardiogram to the initiation of trans-mitral inflow on pulse wave Doppler echocardiogram during late diastole. Clinical significance of PA interval was evaluated. Results: Total 130 patients in cryptogenic stroke group and 130 persons in control group were enrolled. Mean age was 63 ± 11 years and 176 (68%) were male. The PR interval (178 ± 27 vs. 165 ± 27 msec, p &lt; 0.0001) and PA interval (74 ± 15 vs. 61 ± 13 msec, p &lt; 0.0001) were longer in cryptogenic stroke patients. The body mass index (23 ± 3 vs. 24 ± 3, p = 0.043) was lower and mitral E/E’ ratio (8.8 ± 3.0 vs. 8.0 ± 2.6 msec, p &lt; 0.0001) was higher in cryptogenic stroke group. Prolonged PR (OR: 1.019, CI: 1.009 - 1.029, p &lt; 0.0001) and PA (OR: 1.068, CI: 1.045 - 1.093, p &lt; 0.0001) intervals, and lower body mass index (OR: 0.919, CI: 0.846 - 0.998) were risk factors for cryptogenic stroke in univariate logistic regression analysis. Prolonged PA (OR: 1.060, CI: 1.035 - 1.086, p &lt; 0.0001) and PR (OR: 1.019, CI: 1.004 - 1.034, p = 0.011) intervals, and lower body mass index (OR: 0.845, CI: 0.764 - 0.935, p = 0.001) were risk factors for cryptogenic stroke in multivariate logistic regression analysis. Conclusion: The prevalence of prolonged atrial electrical-mechanical delay suggesting atrial substrates for paroxysmal AF was higher in patients with cryptogenic stroke.

Electrophysiological study in a patient with Fabry disease and a short PQ interval

A short PQ interval is a common finding in patients with Fabry disease. However, there have been few electrophysiological studies in Fabry disease, and it is not clear whether the short PQ interval that is present in this disease results from preexcitation or enhanced atrioventricular nodal conduction. We present a case of a 43-year-old man with syncope, sick sinus syndrome, a PQ interval of 80 ms, and palpitations. Electrophysiological study showed PA, AH, and HV intervals of 24, 32, and 34 ms, respectively, and features of enhanced atrioventricular nodal conduction. The presence of an atrioventricular accessory pathway was excluded. We conclude that the short PQ interval in Fabry disease can result from accelerated conduction in the atrioventricular node.

Clinical and Electrophysiological Characteristics of Binodal Disease

Although coexistence of atrioventricular conduction disturbances with sick sinus syndrome (SSS), so-called binodal disease (BND), is a frequently encountered disorder, its clinical significance and electrophysiological characteristics remain unknown. One hundred and seven patients with SSS were divided into BND (n=30) and N-BND groups (n=77). Sinus cycle length, sinus node recovery time (SRT), sino-atrial conduction time (SACT), the number of isolated sinus node electrograms, atrio-His (AH) interval, His-ventricular (HV) interval, intra-atrial conduction time (PA intervals) and QRS width were measured. In addition, the prevalence of bundle-branch block was obtained. The parameters of sino-atrial and intra-atrial conduction were significantly longer in the BND group: SRT (5,070+/-2,628 vs 3,122+/-1,856 ms, p<0.05), SACT (115+/-30 vs 87+/-21 ms, p<0.05), PA intervals (56+/-13 vs 41+/-8 ms, p<0.05). The BND group was more likely to have atrial fibrillation than the N-BND group (83.3% vs 53.2%, p<0.01). HV interval, QRS width and the prevalence of associated bundle-branch block did not differ between the 2 groups. BND patients not only had sino-atrial and atrioventricular node dysfunction, but also widespread atrial conduction disturbances. Thus, in the clinical setting BND should be categorized as severe SSS.

Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts.

To characterize the cardiac electrophysiologic effects of cocaine. In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/kg/min for 25 minutes). Cocaine plasma levels (n=5) rose to 6.73 +/- 0.56 mg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54 +/- 6 vs 73 +/- 4 ms, P<0.001), PR interval (115 +/- 17 vs 164 +/- 15 ms, P<0.001), QRS duration (62 +/- 10 vs 88 +/- 14 ms, P<0.001), and QTc interval (344 +/- 28 vs 403 +/- 62 ms, P=0.03) but not JT interval (193 +/- 35 vs 226 +/- 53 ms, NS). Cocaine prolonged PA (9 +/- 6 vs 23 +/- 8 ms, P<0.001), AH (73 +/- 16 vs 92 +/- 15 ms; P=0.03), and HV (35 +/- 5 vs 45 +/- 3 ms; P<0.001) intervals and Wenckebach point (247 +/- 26 vs 280 +/- 28 ms, P=0.04). An increase occurred in atrial (138 +/- 8 vs 184 +/- 20 ms; P<0.001) and ventricular (160 +/- 15 vs 187 +/- 25 ms; P=0.03) refractoriness at a cycle length of 300 ms. Atrial arrhythmias were not induced in any dog. Ventricular fibrillation (VF) was induced in 2/8 dogs at baseline and 4/8 dogs after cocaine. High doses of cocaine exert significant class I effects and seem to enhance inducibility of VF but not of atrial arrhythmias.

Electrophysiological effects of MS-551 in humans: a class III antiarrhythmic agent.

To investigate the clinical effects of MS-551, a Class III antiarrhythmic agent, 11 patients underwent electrophysiological study. MS-551 was given intravenously as an initial dose of 0.2 or 0.3 mg/kg for 5 minutes followed by the continuous infusion at 0.2 or 0.3 mg/kg for 30 minutes, respectively, in all patients. The rate corrected QT interval increased significantly from 3 minutes after the beginning of MS-551 infusion. The sinus heart rate decreased significantly by 8% at 10 minutes after the drug administration (P < 0.025). Mean PR and QRS intervals, and blood pressure were not significantly affected by the drug. Mean PA, AH, and HV intervals during sinus rhythm were also not affected. The effective refractory periods (ERPs) of the atrium and ventricle were significantly prolonged by 13% from 202 +/- 24 ms to 231 +/- 26 ms (P < 0.0005), and by 7% from 238 +/- 11 ms to 257 +/- 13 ms (P < 0.002), respectively, by MS-551. The ERP of the atrioventricular node and sinoatrial nodal recovery time were not changed significantly by the drug. This is a report of the effects of MS-551 in humans. This agent could be useful for treatment of tachyarrhythmias by prolongation of ERPs of the atrium and ventricle without significant variations of blood pressure and intracardiac conduction times. It is noteworthy that MS-551 slightly but significantly decreased heart rate.

Epicardial his bundle recordings in the guinea pig in vivo

In small animals, His bundle activity is commonly registered using intracavitary electrodes in Langendorff-perfused hearts. The present study evaluates the feasibility of epicardial registration of His bundle activity in 30 guinea pig in vivo, anesthetized with 60 mg/kg sodium pentobarbital i.p. Following median sternotomy, a bipolar electrode, mounted on a flexible stand, was placed into the aortic-right atrial groove. His bundle activity was easily detected in all animals. Mean PA, AH, and HV intervals were 16.7 ± 1.4 msec (range: 6.0–34.0 ms), 36.4 ± 1.5 ms (range: 22.0–54.0 msec and 14.4 ± 0.4 msec (range: 9.0–20 msec), respectively. Administration of verapamil and vagal stimulation induced significant prolongations of AH intervals without affecting HV intervals; lidocaine prolonged both AH and HV intervals. Both at baseline and following drug administration there was excellent agreement between the AH and HV intervals assessed from simultaneously registered epicardial and endocardial His bundle electrograms ( n = 12). The presented model provides reproducible values for atrioventricular (AV) nodal and His-to-ventricular conduction intervals in the guinea-pig in vivo and will, thus, be a valuable tool in electrophysiologi drug evaluation.

Clinical and electrophysiologic effects of intravenous dofetilide (UK-68,798), a new class III antiarrhythmic drug, in patients with angina pectoris

Dofetilide (UK-68,798) is a new class III antiarrhythmic agent. In animal experiments it selectively prolongs the refractory periods parallel to the action potential duration without any influence on upstroke velocity or conduction parameters. The present double-blind, placebo-controlled study was designed to show the effect of dofetilide on basic electrophysiologic parameters in patients with coronary artery disease. Eighteen patients (aged 31 to 64 years) with symptoms of stable angina pectoris admitted for routine coronary angiography were recruited. They were randomly allocated to receive either placebo or 1 of 2 dose levels of dofetilide intravenously with 6 patients in each group. Paired electrophysiologic variables were compared before and after administration of dofetilide. Both active dose levels produced significant prolongations (p < 0.05) of 10 to 23% in atrial effective refractory period, 6 to 16% in ventricular effective refractory period and 11 to 15% in ventricular functional refractory period. Atrial functional refractory period was prolonged by 14 to 22% at the high-dose level (p < 0.05). No effect was observed on conduction parameters (PA, AH, HV, PR or QRS intervals), sinus cycle length or sinus node recovery. The selective prolongation of the refractory periods in both atrium and ventricle, combined with a lack of effect on cardiac conduction parameters, indicates that this drug could be useful in the treatment of both atrial and ventricular reentrant tachyarrhythmias and fibrillation.

Electrophysiological effects of intravenous rilmenidine in man

Ten patients (44 y), 6 with the Wolff-Parkinson-White syndrome, and none with hypertensive disease, underwent electrophysiological studies before and after intravenous infusion of a single dose of 1 mg rilmenidine administered over 15 min. The regimen produced a mean plasma rilmenidine concentration of 3.16 ng.ml-1 at the end of the infusion. There was no significant change in sinus cycle length, PR interval, QRS, QT duration or in PA, AH and HV intervals. Estimated sinoatrial conduction time and corrected sinus node recovery time did not significantly change. In one patient, however, an abnormal pause was noted after termination of rapid atrial pacing. The right atrial effective refractory period decreased from 209 to 194 ms. There was no significant change in the anterograde and retrograde block cycle length or in the refractoriness of the nodal, ventricular and accessory pathways. The cycle length of induced reciprocating tachycardia decreased slightly from 374 to 351 ms. No patient exhibited an abnormal response to the carotid sinus massage. The findings indicate that intravenous administration of 1 mg rilmenidine exerts modest effects on the electrophysiological parameters of the human heart.

Electrophysiologic effects and clinical hazards of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system

Carbamazepine, a first-line drug for the treatment of epilepsy and neuralgia, may exert hazardous effects on the cardiac conduction system. Standard ECG and long-term ECG monitoring and invasive electrophysiologic testing were carried out in 10 patients who required this drug for neurologic disorders, but in whom its safe use had been questioned because of symptoms or ECG abnormalities. We observed depression of sinus node function and an atrioventricular conduction delay with a significant prolongation of the PQ interval of 16 msec (9%; 95% confidence interval: 1.9% to 16.5%; p < 0.05), of which the HV interval was significantly prolonged but not the PA and AH intervals. These effects are in accordance with previously shown class 1A properties. However, the lack of effects on QRS, JT, and QT intervals at normal heart rates is a class 1B characteristic. Thus carbamazepine seems to have composite electropharmacologic actions. A cause effect relationship between carbamazepine treatment and significant arrhythmias was established in five patients. Thus the negative chronotropic and dromotropic effects of carbamazepine may, at least in predisposed patients, induce symptoms confusingly similar to the epileptic seizures it is used to prevent.

Acute electrophysiologic effects of an HT2-serotonin antagonist, ketanserin, in humans

The acute electrophysiologic effects of an intravenous bolus of ketanserin, a 5HT2 serotonin blocker, were studied in ten patients (four females, six males) during invasive electrophysiology. Following baseline electrophysiologic measurements during sinus rhythm and fixed-rate atrial pacing at 600 ms, a bolus of 0.2 mg/kg ketanserin was given over a 3-minute period. After 30 minutes all measurements were repeated. Systemic blood pressure was measured at regular intervals throughout. During sinus rhythm, there was no significant change in the basic cycle length or in the PA, AH, HV, QRS, QT, and QTc intervals. During atrial pacing there was a nonsignificant increase in the QT interval, from 342 +/- 13 ms to 366 +/- 16 ms, and a significant increase in the QTc interval, from 422 +/- 27 ms to 449 +/- 29 ms (p less than 0.05). There was no reduction in blood pressure. Thus ketanserin produced a significant prolongation of the QTc interval, in the absence of hypokalemia, in humans.

In-vitro and in-vivo electrophysiologic effects of encainide

The intracellular electrophysiologic effects of encainide (E) and its main metabolite, O-desmethyl-encainide (ODE), were studied in guinea-pig papillary muscle preparations and related to the in-vivo electrophysiologic effects observed after intravenous (IV) infusion of E in 11 patients undergoing electrophysiologic study (EPS). At equipotent concentrations of E and ODE, frequency-dependent reductions in Vmax studied at pacing rates of 30-180 beats/min ranged from -11.5% to -53%, with maximum reductions of -53% and -47%, respectively at the highest frequency. The kinetics of onset of use-dependent Vmax reduction were slower for ODE than for E at each studied pacing rate. The kinetics of total recovery from use-dependent block were still slower (120 seconds for E and 300 seconds for ODE at a 90 beats/min pacing rate). These in-vitro electrophysiologic data could explain the marked alterations in intraventricular and atrioventricular conduction observed in humans 60 minutes after IV administration of 1 mg/kg of E over a 15-minute period. The QRS, PA, AH, and HV intervals were significantly increased (p less than 0.01) and the Wenckebach cycle length was increased by 8% (p less than 0.05). Blood pressure, RR, QT, CSNRT, ESACT, ERP, and FRP did not vary significantly. The HV interval was already increased 2 minutes after drug administration, while AH was not increased until 15 minutes after drug administration. There was a positive correlation between the increase of the AH interval and the blood level of ODE.

Efficacy, safety, and tolerance of d-sotalol in patients with refractory supraventricular tachyarrhythmias

The efficacy, safety, and electrophysiologic effects of intravenous and oral d-sotalol, an investigational class III antiarrhythmic agent, are not yet well characterized. We evaluated the electrophysiologic, antiarrhythmic, and hemodynamic effects of d-sotalol infusion (1.5 to 2.75 mg/kg) and of chronic oral therapy (200 to 400 mg bid) in 10 patients with chronic, paroxysmal supraventricular tachyarrhythmias refractory to 5 ± 2 standard agents. Four patients had paroxysmal supraventricular tachycardia (PSVT), four had paroxysmal atrial fibrillation, two had atrial flutter, and one had nonparoxysmal reciprocating junctional tachycardia (NPRJT). PSVT was inducible or spontaneously present in 4 of 4 before d-sotalol. After intravenous d-sotalol PSVT was noninducible in three patients and slowed by 40% in one. Atrial fibrillation was inducible or spontaneously present in 4 of 4 before therapy. After intravenous d-sotalol, one became noninducible, and three achieved rate-slowing (the mean falling from 69 to 61 bpm). In one patient, atrial flutter became noninducible; in another, d-sotalol slowed the rate of atrial flutter by 28%. D-sotalol restored sinus rhythm in the patient with NPRJT. Intravenous d-sotalol increased the sinus cycle length; the QTc, PR, and AH intervals; and the AV nodal functional refractory period, the AV nodal effective refractory period; and the right ventricular effective refractory period significantly. The atrial effective refractory period, sinoatrial conduction time, and corrected sinus recovery time tended to increase, but did not reach statistical significance. The QRS, PA, and HV intervals did not change. Mean BP fell 13.4 ± 9.2% after intravenous d-sotalol, but no adverse symptoms developed. Oral d-sotalol caused hypotension (predrug 120/80, post-sotalol 80/60) and had to be discontinued in one patient. Sustained benefit during chronic therapy was noted in 9 of 10 patients (mean followup, 7.4 ± 5.1 months), with no adverse effects other than mild light intolerance in one patient and fatigue (which responded to dose reduction) in another. The electrocardiogram and electrophysiologic parameters measured an oral d-sotalol were not different than those produced by intravenous d-sotalol. Thus, d-sotalol is usually effective and well-tolerated in patients with refractory PSVT. Also, intravenous testing appears predictive of chronic oral efficacy.

Electrophysiological effects of propranolol in patients with sinus node dysfunction.

The electrophysiological effects of intravenous propranolol (0.15 mg/kg) were studied in 26 patients with sinus node dysfunction (SND group) and 9 patients with normal sinus node function (control group). Spontaneous cycle length and AH interval were significantly increased in the control and SND groups after propranolol. PA and HV intervals, calculated sinoatrial conduction time and refractory periods of the atrium, AV node and ventricle were not significantly changed in either group. Maximum corrected sinus node recovery time (max CSRT) was not changed in the control group, but it was significantly prolonged in the SND group. These results of the overdrive suppression test were in disagreement with those of previous studies. Propranolol lengthened spontaneous cycle length (by more than 200 msec) and/or max CSRT (by more than 1000 msec) in 8 of 26 patients with SND. Thus, it is suggested that propranolol should be used with caution in patients with SND.

Electrophysiologic effects of ethmozin on sinus node function in patients with and without sinus node dysfunction.

To compare the effects of ethmozin on sinus node (SN) function in the presence (9 patients) and absence (17 patients) of SN dysfunction, sinus cycle length (SCL), maximal corrected sinus recovery time (CSRT), paced cycle length yielding peak SN suppression, and indirect sinoatrial SA conduction time (SACT) were determined before and after intravenous administration of ethmozin in the dose 2 mg/kg. The mean +/- SD SCL were significantly shortened in patients with normal SN and were not changed in patients with SN dysfunction after ethmozin administration. The mean maximal CSRT was 252 +/- 72 before and 284 +/- 86 ms after ethmozin administration in patients with normal SN function (p less than 0.05). In patients with SN dysfunction (p less than 0.1) the mean maximal CSRT was found to be 1016 +/- 434 before and 2170 +/- 1756 ms after ethmozin administration. The mean SACT was 158 +/- 41 before and 174 +/- 51 ms after drug administration in patients with normal SN (p less than 0.05). Four out of nine patients with SN dysfunction developed second degree SA exit block after ethmozin administration, whereas SACT increased significantly in the remaining group of patients (180 +/- 35 to 210 +/- 32 ms; p less than 0.05). The PR, PA, AH, and HV intervals significantly lengthened and the valves of QRS and QT were not changed after ethmozin administration in either group. The conclusion is drawn that ethmozin should be administered cautiously to patients with SN dysfunction, particularly to patients with SA exit block, sinus pauses, or secondary pauses (in particular, with bradycardia-tachycardia syndrome).

Electrophysiological effects of diphenylhydantoin in patients with sinus node dysfunction.

The electrophysiological effects of intravenous administration of diphenylhydantoin (DPH) (5 mg/Kg, maximum 250 mg) were studied in 20 patients with sinus node dysfunction (SND). DPH shortened spontaneous cycle length (SCL) in 3 patients and lengthened it in 3. Maximum corrected sinus node recovery time (max CSRT) was prolonged in 7 patients and shortened in 3. Estimated sinoatrial conduction time was prolonged in 3 patients and shortened in 2 of 10 patients in whom this measurement was possible. However, these changes were not statistically significant. Neither were there any significant changes in PA, AH and HV intervals nor refractory periods of the atrium, the AV node and the ventricle. DPH prolonged SCL and/or max CSRT in 9 of 20 patients with SND, and it was suggested that DPH has depressant effects on the sinus node in some patients with SND. Thus, this drug should be used with caution in the treatment of ventricular arrhythmias accompanied by sinus node dysfunction.