PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Atrial conduction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMedDate not supplied

[Familial occurrence of Wolff-Parkinson-White syndrome. Report of a family group and review of the literature].

A family group of nine members was studied, two of which had W-P-W syndrome; the father type A; and the son type B. These two patients were studied from the clinical electrocardiographic and vectocardiographic point of view; and they were subject to hisian electrogram recordings. The atrial-ventricular conduction under basal conditions and during atrial stimulation is analyzed. In the first case, potential H is registered after the beginning of delta wave of the ventricular complexes in lead II. In th second case, atrial-ventricular conduction can only occur through the abnormal via (no H potential and register of delta wave in the periferial simultaneous lead), or only through the normal via (evidence of potential H with a normal H-V interval and no delta wave in the periferial line of control). The bibliography of the observation that in most family groups described up until now, there is a good correlation concerning sex. This gives the impression to be a genetic disorder linked to sex.

Adult↗
PubMed1999

Characterization of atrioventricular nodal reentry with continuous atrioventricular node conduction curve by double atrial extrastimulation.

BACKGROUND: Characterization of typical atrioventricular nodal reentrant tachycardia (AVNRT) with continuous AVN conduction (A1A2/A2H2) curves by double atrial extrastimulation (A1A2A3) has never been systematically studied. METHODS AND RESULTS: This study was composed of 33 patients with typical AVNRT and continuous AVN conduction curves (group 1) and 103 patients with AVNRT and discontinuous AVN conduction curves (group 2). Using A1A2A3 with predefined fast pathway-conducted A2, we examined the effects of slow pathway ablation on the A2A3/A3H3 curves in both groups. In group 1, anterograde AVN effective refractory period (272+/-33 versus 277+/-47 ms, P>0.05) and AVN Wenckebach block cycle length (320+/-45 versus 343+/-59 ms, P>0.05) remained unchanged after ablation. A2H2max was shorter in group 1 than group 2 (237+/-89 versus 395+/-72 ms, P<0.05) at baseline. It shortened in group 2 (395+/-72 versus 221+/-78 ms, P<0.001) but remained unchanged in group 1 (237+/-89 versus 214+/-59 ms, P>0.05) after ablation. A1A2A3 could further disclose discontinuous A2A3/A3H3 curves in 29 patients of group 1. A3H3max shortened in both groups (375+/-81 versus 238+/-82 ms, P<0.001, and 419+/-104 versus 220+/-78 ms, P<0.001, respectively) in a similar fashion. Successful ablation resulted in loss of the left portion of the A2A3/A3H3 curves in the 4 patients of group 1 with continuous A2A3/A3H3 curves. CONCLUSIONS: Use of A1A2A3 could expose discontinuous A2A3/A3H3 curves in most patients with continuous A1A2/A2H2 curves. Significant shortening of A3H3max after ablation may be indicative of successful elimination of AVNRT.

Catheter Ablation↗
PubMed2006

Characterization of conduction recovery across left atrial linear lesions in patients with paroxysmal and persistent atrial fibrillation.

BACKGROUND: Left atrial (LA) linear lesions are effective in substrate modification for atrial fibrillation (AF). However, achievement of complete conduction block remains challenging and conduction recovery is commonly observed. The aim of the study was to investigate the localization of gap sites of recovered LA linear lesions. METHODS AND RESULTS: Forty-eight patients with paroxysmal (n = 26) and persistent/permanent (n = 22) AF underwent repeat ablation after pulmonary vein (PV) isolation and LA linear ablation at the LA roof and/or mitral isthmus due to recurrences of AF or flutter. In 35 patients, conduction through the mitral isthmus line (ML) had recovered whereas roof-line recovery was observed in 30 patients. The gaps within the ML were distributed to the junction between left inferior PV and left atrial appendage in 66%, the middle part of the ML in 20%, and in 8% to the endocardial aspect of the ML while only 6% of lines showed an epicardial site of recovery. The RL predominantly recovered close to the right superior PV (54%) and less frequently in the mid roof or close to the left PV (both 23%). Reablation of lines required significantly shorter RF durations (ML: 7.24 +/- 5.55 minutes vs 24.08 +/- 9.38 minutes, RL: 4.24 +/- 2.34 minutes vs 11.54 +/- 6.49 minutes; P = 0.0001). Patients with persistent/permanent AF demonstrated a significantly longer conduction delay circumventing the complete lines than patients with paroxysmal AF (228 +/- 77 ms vs 164 +/- 36 ms, P = 0.001). CONCLUSIONS: Gaps in recovered LA lines were predominantly located close to the PVs where catheter stability is often difficult to achieve. Shorter RF durations are required for reablation of recovered linear lesions. Conduction times around complete LA lines are significantly longer in patients with persistent/permanent AF as compared to patients with paroxysmal AF.

Atrial Fibrillation↗
PubMed2001

Effect of different pacing protocols on the induction of atrial fibrillation in a transvenously paced sheep model.

In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 +/- 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., > 1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 +/- 5 ms in the continuously paced group and 107 +/- 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 +/- 4 ms in this group versus 116 +/- 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 +/- 0.1 cm2 at baseline to 4.2 +/- 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 +/- 0.1 to 2.8 +/- 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions.

Animals↗
PubMed2002

[Atrial flutter with 1/1 nodo-ventricular conduction with amiodarone. From physiopathology to diagnosis].

Atrial flutter with 1/1 nodo-ventricular conduction is a classical complication of Vaughan-Williams's Class I antiarrhythmic drugs. The increase of the flutter cycle and weak action of the antiarrhythmic on the atrioventricular node leads to 1/1 conduction of atrial depolarisation to the ventricles. In view of their marked action on the atrioventricular node, this type of pro-arrhythmic effect is very unexpected with Class III antiarrhythmics. The authors report 7 cases of 1/1 atrial flutter with oral amiodarone observed between 1994 and 2001. The patients were 6 men and 1 woman with an average age of 58 +/- 14 years. Four of them had underlying cardiac disease; none were hyperthyroid. The initial arrhythmia was 2/1 atrial flutter (n = 4), 1/1 atrial flutter (n = 2) and atrial fibrillation (n = 1). Treatment was preventive with doses of 400 mg/day associated with carvedilol in one patient and 200 mg/day in another. The other five patients all received loading doses of 9200 +/- 2400 mg over 10 +/- 4 days. The symptoms were palpitations (n = 2) associated in one patient with hypotension, one syncope, one near syncope and one cardiogenic shock. The ventricular cycle of the 1/1 flutter was 287 +/- 33 ms. The QRS duration was 136 +/- 35 ms with ventricular tachycardia-like appearances in 3 cases. An adrenergic trigger factor was noted in 5 patients. One patient required emergency cardioversion. The authors discuss the physiopathology of 1/1 flutter and theoretical diagnostic methods are proposed. In conclusion, amiodarone does not always prevent the occurrence of 1/1 nodo-ventricular conduction in atrial flutter.

Administration, Oral↗
PubMed2001

Apparent bradycardia-dependent right bundle branch block associated with atrial fibrillation: concealed electrotonic conduction as a possible mechanism.

A 79-year-old woman with atrial fibrillation was reported in whom apparent bradycardia-dependent right bundle branch block was suggested. When a conducted supraventricular impulse occurred within a critical period after the preceding conducted impulse, the impulse was blocked in the right bundle branch except when it fell in the supernormal period of the right bundle branch. When the conducted impulse occurred between the critical period and another longer period, it was conducted without bundle branch block. When the impulse occurred beyond that longer period, it was usually blocked in the bundle branch again. However, when the impulse occurred beyond a still longer period, it was conducted without bundle branch block again. These findings suggest that when impulses fell in the right bundle branch shortly after the preceding conducted impulses, they were blocked in both bundle branches; however, it seemed that concealed electrotonic conduction of the blocked impulses affected conduction of the subsequent impulses.

Aged↗
PubMed2003

Right atrial modification of maze surgery does not affect refractoriness and conduction patterns of human lone atrial fibrillation.

BACKGROUND: Tissue mass and structure are relevant for initiation and persistence of fibrillation. Modification of the right atrium during maze surgery may change the arrhythmogenic substrate of atrial fibrillation (AF). METHODS AND RESULTS: Epicardial mapping was performed in 9 patients undergoing unmodified maze III surgery for lone paroxysmal AF. Simultaneous recording of AF on the right and left atrium was carried out with two spoon-electrodes each harbouring 64 terminals. Activation maps of AF were made to study AF wavelet organization. The recording position on right and left atria was outside the surgical field and remained unchanged before and after surgery. Before surgery, mean right and left fibrillatory intervals were 174+/-23 ms, and 175+/-26 ms, respectively, and did not differ. After completed right atrial surgery, these fibrillary intervals remained unchanged. Mean right and left atrial dispersion of refractoriness (expressed as the coefficient of variation) were 4.2+/-0.8 and 5.2+/-3.8 ms. Only right atrial dispersion of refractoriness increased significantly after right-sided surgery. Prior to surgery, activation patterns of the left atrium were more complex than that of the right atrium. The left activation patterns became less complex afterwards; the right atrial activation patterns did not change. CONCLUSION: The right atrial modification of maze III surgery neither affects atrial refractoriness during human lone AF nor changes AF wavelet organization. Thus, right atrial surgery does not modify the arrhythmogenic substrate of AF. These findings may imply that maze surgery can be restricted to the left atrium.

Atrial Fibrillation↗
PubMed1985

Electrocardiographic and vectorcardiographic study of interatrial conduction disturbances with left atrial retrograde activation.

From 81,000 ECGs we collected 83 cases that fulfilled the criteria of Interatrial Conduction Disturbances with Left Atrial Retrograde Activation (IACD-LARA) (P +/- in II, III and VF with P width greater than or equal to 120 msec.). We present the detailed study of 35 cases with surface ECG and VCG and 29 cases with orthogonal ECG leads. The results are then compared against two control groups: with cardiopathy (30 cases) and without cardiopathy (25 cases). The prevalence of IACD-LARA was nearly 1% globally, and 2% among patients with valvular heart disease. The diagnostic criteria for IACD-LARA are: 1) ECG: P +/- in II, III and VF with P greater than or equal to 120 msec. with open angle (usually greater than 90 degrees) between the first and the second part of the P.2) Orthogonal ECG: P +/- in Y lead with a negative mode greater than 40 msec. 3) VCG: More than 50 msec. above the X or Z axis, duration of the P loop greater than or equal to 110 msec., open angle between the two parts of the P loop in both frontal (131.3 degrees +/- 32.3) and right sagital planes (171.2 degrees +/- 15.1), and presence of notches and slurrings in the last part of the P loop.

Adult↗
PubMed1988

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.

Adolescent↗
PubMed1995

[Modulation of atrioventricular conduction in patients with atrial fibrillation or flutter. Immediate and long-term results].

The modulation of atrioventricular (AV) conduction by radiofrequency catheter ablation of the "slow" AV node pathway reduces the ventricular rate during atrial flutter (AFL) or fibrillation (AF), without affecting AV conduction during sinus rhythm. In this study the acute and long-term effects of AV node modulation in 41 patients with AFL-AF are presented. The arrhythmia was paroxysmal in 34 and chronic in 7 patients, and was responsible in all patients for severe symptoms of heart failure. The procedure was performed during sinus rhythm in 23, AFL in 8, AF in 10 patients, and caused respectively an increase in Wenckebach cycle from 330 +/- 64 to 452 +/- 91 ms (p < 0.001), and a reduction in ventricular rate from 182 +/- 53 to 95 +/- 40 b/min (p < 0.001) and from 170 +/- 40 to 90 +/- 27 b/min (p < 0.001). The arbitrary endpoint of the procedure (Wenckebach cycle > 500 ms during sinus rhythm, maximum heart rate < 100 b/min during AFL-AF) was achieved in 19/41 patients; permanent complete AV block was induced in 6 "non-responder" patients (15%). At a mean follow-up of 15 +/- 7 months (range 1-31) all patients reported a substantial subjective improvement and a better exercise tolerance--as documented by a quantitative questionnaire concerning quality of life--without any recurrence of acute pulmonary edema, syncope or severe hypotension. In 5 patients during paroxysmal AFL-AF, and in 1 patient with chronic AF, a heart rate higher than 120 b/min was documented, and in 3 cases it was associated with severe palpitations. No late AV block occurred. The mean number of hospital-emergency room admissions per patient per year decreased from 3.9 before to 0.2 after the modulation. Considering complete AV block (6 patients, 15%) and clinical failures (6 patients, 15%), the success of the procedure was 70%, and was independent of the rhythm at the time of the procedure; the percentage of AV block was nevertheless higher during AFL-AF (22 vs 9%). Both endpoints of the procedure (Wenckebach cycle > 500 ms; heart rate < 100 b/min) were confirmed to be good predictors of long-term efficacy; on the other hand, a Wenckebach cycle < 430 ms was demonstrated to represent a specific marker of late failure. In conclusion, the study confirms that modulation of AV conduction is feasible in 70% of patients with AFL-AF: in these patients the procedure allows the long-term control of ventricular rate and a substantial improvement in quality of life, avoiding the need for His ablation and pacemaker implantation. "Non-responder" patients can be acutely identified and should be therefore considered condidates for His ablation during the same session.

Adolescent↗
PubMed2002

Conduction properties of the crista terminalis and its influence on the right atrial activation sequence in patients with typical atrial flutter.

The conduction properties of the crista terminalis (CT) and its influence on the right atrial activation sequence were analyzed in 14 patients with typical atrial flutter (AF). Atrial mapping was performed with 35 points of the right atrium during typical AF and during atrial pacing performed after linear ablation of inferior vena cava-tricuspid annulus (IVC-TA) isthmus. Atrial pacing was delivered from the septal isthmus at cycle lengths of 600 ms and the tachycardia cycle length (TCL). The right atrial activation sequence and the conduction interval (CI) from the septal to lateral portion of the IVC-TA isthmus were analyzed. During AF, the conduction block line (CBL) (detected by the appearance of double potentials along the CT and craniocaudal activation on the side anterior to CT) was observed along the CT in all patients. The TCL and CI during AF were 254 +/- 19 and 207 +/- 14 ms, respectively. During pacing at a cycle length of 600 ms, the CBL was observed along the CT in four patients, however, a short-circuiting activation across the CT was observed in the remaining ten patients. The CI during pacing at 600 ms was 134 +/- 38 ms, shorter than that during AF (P < .0001). During pacing at the TCL, the CBL was observed along the CT in all patients. The presence of the CBL along the CT prevented a short-circuiting activation across the CT and resulted in the same right atrial activation as observed during AF. With the formation of the CBL, the CI significantly increased to 206 +/- 17 ms and was not different from that during AF. These data suggest that the conduction block along the CT is functional. It was presumed that presence of conduction block at the CT has some relevance to the initiation of typical AF though it was not confirmed.

Aged↗
PubMed2002

Prevention of atrial fibrillation by inter-atrial septum pacing guided by electrophysiological testing, in patients with delayed interatrial conduction.

AIMS: Interatrial septum (IAS) pacing seems efficient in synchronizing atrial depolarization in patients (pts) with delayed inter-atrial conduction, but its clinical role in preventing atrial tachyarrhythmias is still debated. This study was conducted in order to evaluate the clinical efficacy of IAS pacing guided by pace mapping of the IAS, as an alternative treatment modality in pts with drug refractory paroxysmal atrial fibrillation (PAF). METHODS AND RESULTS: We evaluated 29 pts (13 male, 16 female, 60 +/- 11 years), with drug refractory PAF, normal sinus node function and prolonged inter-atrial conduction time (P wave 142 +/- 10 ms). Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle and distal coronary sinus (CS) were recorded. The IAS was paced from multiple sites. The site of IAS where the timing between HRA and distal CS was <20 ms was considered the most suitable for synchronizing the atria. This site was found to be superior to the CS os. near the fossa ovalis in all pts. An active fixation atrial lead was positioned at this site and a standard lead was placed in the right ventricle. During IAS pacing, the P wave duration decreased significantly to 107 +/- 15 ms (P<0.001). At implant, the atrial sensing was 2.3 +/- 0.7 mV, the atrial pacing threshold was 0.95 +/- 0.15 V (0.5 ms) and the impedance was 760 +/- 80 Ohm. We evaluated the pts during four periods of 3 months duration each. The first period (control) was before pacemaker implantation, while the pts were under antiarrhythmic treatment. During the subsequent two periods, we evaluated the clinical efficacy of IAS pacing to prevent PAF recurrences, in AAT (75 bpm) and AAIR (75-140 bpm) mode, with random selection of the order and after discontinuation of antiarrhythmic treatment. During the fourth period, the same AAIR mode was assessed, but antiarrhythmic drugs were also administered. We compared the arrhythmia free interval among the four periods. The proportion of atrial paced beats in AAIR pacing mode plus antiarrhythmics was significantly higher compared with the drug-free period in AAIR mode (57 +/- 9% and 49 +/- 9% respectively, P=0017) and with AAT pacing mode (44 +/- 10%,(, P<0.001). In AAT mode, the arrhythmia free interval was 24.2 +/- 5.1 days, while it was 26.2 +/- 5.7 days in AAIR mode. These intervals did not differ significantly from the pre-implantation period (24.1 +/- 6.3 days). The arrhythmia free interval in AAIR pacing in combination with antiarrhythmic drug therapy was 38.7 +/- 8.1 days and this was significantly longer than the previous periods (P<0.05). CONCLUSION: Atrial septal pacing in combination with antiarrhythmic drug therapy reduced the incidence of PAF in pts with prolonged inter-atrial conduction times. Pace mapping of the IAS is an attractive technique to assess the shortest atrial activation time between HRA and distal CS. Whether placement of the atrial lead based on the shortest HRA--distal CS time is the best place in the IAS to prevent PAF still remains to be proven.

Aged↗
PubMed1978

Electrophysiological studies in four patients with atrial flutter with 1:1 atrioventricular conduction.

Electrophysiological studies of atrioventricular conduction during rapid atrial overdrive pacing and during programmed premature atrial stimulation are reported in four patients with an unusually rapid 1:1 ventricular response to atrial flutter (ventricular rates 240 to 310 per minute). Second-degree AV block development during atrial overdrive pacing at rates well below those during spontaneous atrial flutter. Although none of the four patients showed evidence of pre-excitation on the standard 12-lead electrocardiogram, evidence suggesting a partial AV nodal bypass was demonstrated at electrophysiological study in one case. It is postulated that the profile of the atrial wavefront presented to the normal AV node by atrial flutter differs from that during high right atrial pacing and may account for the lower ventricular rates achieved during high right atrial overdrive pacing than during spontaneous atrial flutter in the remaining three cases.

Adult↗
PubMed1988

Effects of N-acetylprocainamide and recainam in the pharmacologic conversion and suppression of experimental canine atrial flutter: significance of changes in refractoriness and conduction.

The electrophysiologic determinants of the pharmacologic conversion and the prevention of atrial flutter are poorly defined. This study investigated the effects of pharmacologically induced changes in atrial conduction velocity and refractoriness, in the conversion and suppression of atrial flutter induced in the open-chest anesthetized dog by intercaval crush and rapid atrial pacing. The effects of an intravenous infusion of the new class III antiarrhythmic drug N-acetylprocainamide (30 mg/kg over 15 min) and the class Ic antiarrhythmic drug recainam (10 mg/kg over 20 min followed by 10 mg/kg/h) were evaluated. N-acetylprocainamide restored sinus rhythm in 10 of 15 (66%) dogs, while recainam converted only 2 of 10 (20%). N-acetylprocainamide prevented reinduction in 3 (20%), while recainam was effective in none. In the atria, N-acetylprocainamide induced significant increases in effective refractory period (+27%, p less than 0.01), functional refractory period (+22%, p less than 0.01), and in atrial flutter cycle length (+13%, p less than 0.01). Recainam increased effective refractory period (+28%, p less than 0.01), functional refractory period (+20%, p less than 0.01), conduction time at atrial paced cycle length of 150 msec (+70%, p less than 0.01) and atrial flutter cycle length (+56%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1988

[Contribution of specific potential monitoring in the expression of accessory pathways].

The electrocardiographic expression of preexcitation results from the electrophysiological behaviour of the 2 conduction pathways: the normal pathway and the accessory pathway (AP). Its interpretation can only be deductive since the electrical activities of these 2 pathways are not recorded simultaneously. The validation of a K potential likely to represent Kent's bundle activation is based on criteria of exclusion of other origins (atrium, His bundle, ventricle). The K potential could be obtained in 16 of 32 consecutive studies. In 2 cases the unusual behaviour of the AP could be reliably studied owing to recording of the K potential. In case n. 1 a 35 ms increment in conduction was reproducibly observed by atrial extrastimulation at the atrium-Kent's bundle interface. In case n. 2 preexcitation was expressed on ECG only when the atrial rate was 70 to 100/mn. With lower atrial rates conduction in the AP was impaired by a 1st degree block with an atrium-Kent's bundle delay of 100 ms. Atrial acceleration reduced this delay to 40 ms, showing that this improvement in conduction reflected an initial block on the AP in phase IV. With higher atrial rates a block was observed on the AP in phase III either as an abrupt rupture of the atrium-Kent's bundle conduction, or as a block following progressive increment of the Luciani-Wenckebach type. Injection of ATP 20 mg produced and anterograde block on the AP at the atrium-Kent's bundle interface. Retrograde conduction seemed to be lacking in the AP since atrial activity was completely dissociated from induced ventriculograms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Electrophysiologic evaluation of intravenous nicardipine in man.

The acute electrophysiological effects of intravenous nicardipine (0.014 mg/kg per min for 5 minutes) were studied in 12 subjects with estimated normal sinus node functions and atrioventricular conduction parameters. The most important effects were sinus cycle length shortening, increase of corrected sinus node recovery time and reduction of effective and functional refractory period of the atrioventricular node. Sinuatrial conduction time, atrial refractory periods, intranodal conduction, bundle branch refractoriness and ventricular refractoriness were unchanged. Systolic and diastolic blood pressure was reduced. The clinical implications of these properties of the drug are discussed and compared with those of verapamil, diltiazem and nifedipine.

Blood Pressure↗
PubMed1991

Electrophysiologic evaluation of intravenous L-propionylcarnitine in man.

L-propionylcarnitine, a short-chain acylcarnitine, has been shown in experimental studies to induce, during acidic and hypoxic conditions, some electrophysiological changes such as an increase of duration of the action potential and of the effective refractory period. In this study, the acute electrophysiological effects of intravenous L-propionylcarnitine (30 mg/kg in 3 min) were studied in 12 subjects with estimated normal function of the sinus node and normal parameters for atrioventricular conduction. Statistically significant changes were observed 2 min after infusion. The sinus cycle length shortened (866 +/- 138 vs 818 +/- 124 msec, P less than 0.05) while refractory periods of the atrioventricular node increased (effective by 30-50 msec in four cases; functional from 425 +/- 52 to 436 +/- 55 msec, P less than 0.05). Sinuatrial conduction time, atrial refractory periods, infranodal conduction, bundle branch, His-Purkinje system and ventricular refractoriness were unchanged. Systolic and diastolic blood pressure were also unchanged. Because of the limited effects on electrophysiological parameters, L-propionylcarnitine should be used as a metabolic drug even in patients with mild disturbances of conduction.

Blood Pressure↗