Sinus Node Recovery Time Research Articles

High-Dose Remifentanil Suppresses Sinoatrial Conduction and Sinus Node Automaticity in Pediatric Patients Under Propofol-Based Anesthesia

We sought to determine the effect of remifentanil on sinus node function and the atrial-His (AH) interval in pediatric patients undergoing radiofrequency catheter ablation. Sixty pediatric patients with Wolff-Parkinson-White syndrome were prospectively enrolled in this study. General anesthesia was induced and maintained with a continuous infusion of propofol. We recorded the calculated sinoatrial conduction time (CSACT), corrected sinus node recovery time (CSNRT), and AH interval when the patients were in a stable anesthetic state and compared the values before and during remifentanil administration at a moderate dose (0.2 μg · kg(-1) · min(-1)) or a high dose (0.4 μg · kg(-1) · min(-1)). Data are expressed as mean (95% confidence interval). At the moderate dose, remifentanil prolonged CSNRT (from 177 [117-237] milliseconds to 245 [167-322] milliseconds after administration; P=0.016), but had no effect on either CSACT (P=0.59) or AH interval (P=0.11). However, high-dose remifentanil prolonged both CSNRT (from 201 [144-260] milliseconds to 307 [232-382] milliseconds after administration; P=0.019) and CSACT (from 48 [31-65] milliseconds to 78 [59-96] milliseconds after administration; P=0.038), but had no effect on the AH interval (P=0.058). The interaction in CSNRT between remifentanil administration and its dose was not different (P=0.44). Remifentanil may inhibit both intraatrial conduction and sinus node automaticity, but it has no effect on conduction through the atrioventricular node. Dose dependency was not observed within the range of 0.2 to 0.4 μg · kg(-1) · min(-1) of remifentanil.

Acute effects of ganglionated plexi ablation on sinoatrial nodal and atrioventricular nodal functions

Ganglionated plexus (GP) ablation has been shown effective for eliminating atrial fibrillation (AF), the most common clinical tachyarrhythmia. However, the safety of destroying the main cardiac autonomic structures remains unclear. This study investigated the acute effects of GP ablation on the sinoatrial nodal (SAN) and atrioventricular nodal (AVN) functions in a canine model. In 10 open-chest dogs, multiple electrode catheters were sutured at both atria for recording and pacing. SAN and AVN function were evaluated. GP ablation caused no significant change of sinus rate immediately after GP ablation compared with the baseline state. After GP ablation, the sinus node recovery time (SNRT) and corrected SNRT did not show significant changes at long pacing cycle lengths (CLs), and only showed significant decrease at shorter pacing CLs. The AH interval at different pacing CLs, the Wenckebach atrioventricular block (AVB) CL, 2:1 AVB CL or the ventricular rate during AF were not significantly altered by GP ablations. Vagal suppression of SAN and AVN functions was eliminated by GP ablation. GP staining showed abundant choline acetyl transferase or tyrosine hydroxylase positive neurons. These findings suggest the functions of the SAN and AVN are mainly retained after GP ablation. These results may be partially related to destroying both parasympathetic and sympathetic elements in the GP by ablation.

Electrophysiological features in patients with sinus node dysfunction and vasovagal syncope

IntroductionSyncope is a common presentation of sinus node dysfunction (SND). Some patients who receive a permanent pacemaker due to SND do not benefit from it and further diagnostic workup leads to the diagnosis of vasovagal syncope (VVS). The aim of the study was to identify electrophysiological criteria that can be used for identification of patients with SND and concurrent VVS.Material and methodsTransoesophageal atrial pacing (TAP) was performed in 100 patients divided into four groups depending on symptoms and TAP results. Standard electrophysiological parameters of sinus node function and their variability were obtained in the basal state and after pharmacological autonomic blockade (AB).ResultsPatients with concurrent SND and VVS had a greater variability of sinoatrial conduction time assessed by Strauss’ method than patients without incidents of syncope (83.2 ±53.9 vs. 34.1 ±19.6, 47.8 ±33.6 and 32.1 ±22.99). Apart from abnormal sinus node recovery time and second pause, patients with SND had bigger basal state variability of these parameters. In patients with SND and concurrent vasovagal syncope the variability of sinus node recovery time (SNRT), corrected SNRT (cSNRT) and second pause (IIP) decreased after autonomic blockade.ConclusionsPatients with concurrent SND and VVS have distinct electrophysiological features – greater sinoatrial conduction time (SACT) variability and the decrease of SNRT, cSNRT and IIP variability after AB. However, further studies in larger study groups are needed to validate our findings. Transoesophageal atrial pacing is a useful procedure in patients with syncope, especially when the coexistence of more than one cardiac cause is suspected.

Longitudinal Change of Electrophysiological Characteristics in Patients with Sick Sinus Syndrome

Introduction: Previous studies have showed stable AV conduction in patients with sick sinus syndrome (SSS) during long-term follow-up. However, detailed electrophysiological (EP) data is not clearly enucleated. Methods: Fifty-six patients (30 males, mean age: 68±10 years) with SSS were enrolled. EP study was performed at the time of pacemaker implantation and replacement. Mean followed-up duration was 8.5±2.3 years. Results: Sinus node recovery time (SRNT) (2431±1630 vs. 3390±2368 ms), 1:1 AV conduction (484±160 vs. 548±161 ms), point of AV block (AVB) (453±153 vs. 502±152 ms) and ventricular effective refractory period (265±27 vs. 296±50 ms) were significant prolonged (p 800 ms). Six of 45 patients (13%) with intact AVN function developed new onset AVN dysfunction but none has advanced AVB. Conclusion: Panconduction system was degenerated in the SSS patients during long-term followed-up. AV conduction was relative stable but advanced AVB would occur in the patients with initial AVN dysfunction. Pre-implantation EPS may be useful to predict the risk of advanced AVB.

The Relationship between Internal Cardioversion Threshold or Post-Cardioversion Sinus Node Recovery Time and Atrial Structural or Autonomic Neural Remodeling in Persistent Atrial Fibrillation

Background: We hypothesized that cardioversion (CV) threshold and post-CV sinus node recovery time (PC-SNRT) are related with cardiac autonomic nerve function or atrial structural remodeling in persistent atrial fibrillation (PeAF). Methods: We included 74 patients with PeAF (62 males, 54.8±10.5 years old) who underwent radiofrequency catheter ablation (RFCA) and maintained sinus rhythm at the time of 3rd month Holter without taking any anti-arrhythmic drug or beta-blocker. At the beginning of RFCA, we delivered internal CV 2, 3, 5, 7, and 10 J serially, and measured CV threshold and PC-SNRT. Results: 1. The patients with CHADS2 score >=1 showed higher CV threshold than those with 0 (8.3±2.1 J vs. 6.2±2.5 J, p=0.034). 2. CV threshold of the patients with left atrial (LA) volume >=120 mL was significantly higher than those of patients with =45 mm) by echocardiography were significantly longer than that of the patients with <45 mm (1422.2±1031.7 ms vs. 1060.2±448.2 ms, p=0.05). 4. PC-SNRT was correlated with 3rd month heart rate variability (HRV) including SDNN (R=0.400, p=0.005), HF (R=0.480, p=0.001), but not related with clinical recurrence of AF after RFCA. Conclusion: Both CV threshold and PC-SNRT were significantly greater in patients with atrial structural remodeling, but were not related with clinical outcome of RFCA in PeAF.

Bradycardia Due To Sick Sinus Syndrome Induced Torsades de Pointes in a Patient with Takotsubo Cardiomyopathy and QT Prolongation

A 62-year-old female experiencing syncope following emotional stress was seen in our emergency room. She had a history of pre-syncope. ECG showed first-degree atrioventricular block with a ventricular rate of 52 bpm and mild QT interval prolongation (QTc 517 msec). Two days later, her ECG showed ventricular bigeminy and torsade de pointes. After her emergency admission, the torsade de pointes was eliminated with an injection of intravenous magnesium sulfate. The ECG after the administration of the magnesium sulfate showed junctional rhythm with a ventricular rate of 43 bpm and excessive QT interval prolongation (QTc 761 msec). An emergency coronary angiogram revealed no significant coronary artery disease, but the left ventriculography showed akinesis of the mid- to distal portion of the left ventricular chamber (ejection fraction of 38%). She was diagnosed with takotsubo cardiomyopathy. Temporary ventricular pacing, which was performed at a rate of 70 bpm, prevented the recurrence of torsade de pointes. One month after her admission, an electrophysiological study showed that the sinus node recovery time was extended to 5.5 sec. She was diagnosed with sick sinus syndrome. She received a dual-chamber pacemaker during her admission. We experienced a case of torsade de pointes associated with sick sinus syndrome and takotsubo cardiomyopathy.

A Case Report of Uncommon Atrial Flutter (AFL) with Coexistence of Sick Sinus Syndrome and Atrioventricular Conduction Disturbance Who Underwent Radiofrequency Catheter Ablation and Pacemaker Implantation

A 82-year-old male who had near syncope was admitted to our hospital. His heart rate monitoring had been demonstrating uncommon AFL with heart rate 30–45/minute (F-F interval: 210 milliseconds) because of atrioventricular conduction disturbance. Activation map recorded by the CARTO system during tachycardia showed reverse common AFL. We confirmed that the circuit of AFL existed in tricuspid valve annulus by post pacing interval mapping. We could also induce common AFL. We performed linear ablation at anatomical isthmus between tricuspid annulus and inferior vena cava by radiofrequency catheter ablation during AFL, which resulted in termination. We confirmed bidirectional conduction block at anatomical isthmus after the procedure. Atrial fibrillation (AF) instead of AFL was induced by burst pacing, which could not be terminated by 70 mg of Pilsicainide injection. Sinus arrest for five seconds was recorded just after the DC therapy for AF, although sinus node recovery time was within normal limits without any anti-arrhythmic drugs. We diagnosed so-called binodal disease, which became clinically evident by Pilsicainide. It is suggested that we had better pay attention to binodal disease when we encounter the atrioventricular conduction disturbance.

Up to 6-year follow-up after pulmonary vein isolation for persistent/permanent atrial fibrillation: Importance of sinus node function

Sinus node dysfunction is commonly associated with atrial fibrillation. There is little information about the long-term results of pulmonary vein isolation in relation to sinus node function. The present study was conducted to investigate whether sinus node dysfunction affects the late outcome of pulmonary vein isolation in patients with persistent/permanent atrial fibrillation. Among 76 consecutive patients with persistent/permanent atrial fibrillation who had undergone cut-and-sew pulmonary vein isolation, 66 patients without evidence of intra-atrial thrombus by transesophageal echography, and who were able to tolerate cardioversion, were enrolled. Sinus node recovery time after cardioversion was examined intraoperatively. All of the patients underwent valvular surgery concomitantly (mitral in 62). Sinus node dysfunction was detected in 18 patients. These patients had a significantly lower f wave voltage in V(1) of the electrocardiogram and a larger cardiothoracic ratio than patients with normal sinus node function. Hospital mortality was 3%, and 3 late deaths were observed. Follow-up was conducted for up to 72 months (mean 30 months), with a 100% complete follow-up rate. There were no significant differences in actuarial survival and freedom from cardiac events between patients with normal and abnormal sinus node function. No thromboembolic events occurred. A significantly higher proportion of patients with normal sinus node function (82%) were free of atrial fibrillation at 4 years than patients with sinus node dysfunction (25%; P<.0001). The atrial fibrillation cure rate after pulmonary vein isolation may be influenced by sinus node function in both the early and late stages. Although further examinations are required, pulmonary vein isolation may be an adequate treatment for persistent/permanent atrial fibrillation in patients with normal sinus node function.

Cardiac conduction disturbances and differential effects on atrial and ventricular electrophysiological properties in desmin deficient mice

Desmin mutations in humans cause desmin-related cardiomyopathy, resulting in heart failure, atrial and ventricular arrhythmias, and sudden cardiac death. The intermediate filament desmin is strongly expressed in striated muscle cells and in Purkinje fibers of the ventricular conduction system. The aim of the present study was to characterize electrophysiological cardiac properties in a desmin-deficient mouse model. The impact of desmin deficiency on cardiac electrophysiological characteristics was examined in the present study. In vivo electrophysiological studies were carried out in 29 adult desmin deficient (Des-/-) and 19 wild-type (Des+/+) mice. Additionally, epicardial activation mapping was performed in Langendorff-perfused hearts. Intracardiac electrograms showed no significant differences in AV, AH, and HV intervals. Functional testing revealed equal AV-nodal refractory periods, sinus-node recovery times, and Wenckebach points. However, compared to the wild-type situation, Des-/- mice were found to have a significantly reduced atrial (23.6+/-10.3 ms vs. 31.8+/-12.5 ms; p=0.045), but prolonged ventricular refractory period (33.0+/-8.7 ms vs. 26.7+/-6.5 ms; p=0.009). The probability of induction of atrial fibrillation was significantly higher in Des-/- mice (Des-/-: 38% vs. Des+/+: 27%; p=0.0255), while ventricular tachycardias significantly were reduced (Des-/-: 7% vs. Des+/+: 21%; p<0.0001). Epicardial activation mapping showed slowing of conduction in the ventricles of Des-/- mice. Des-/- mice exhibit reduced atrial but prolonged ventricular refractory periods and ventricular conduction slowing, accompanied by enhanced inducibility of atrial fibrillation and diminished susceptibility to ventricular arrhythmias. Desmin deficiency does not result in electrophysiological changes present in human desminopathies, suggesting that functional alterations rather than loss of desmin cause the cardiac alterations in these patients.

Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties.

AimIn contrast to extensive reports on the roles of Nav1.5 α-subunits, there have been few studies associating the β-subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b−/− mice.MethodsThe following properties were compared in the hearts of wild-type (WT) and Scn3b−/− mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the β3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts.ResultsScn3b mRNA was expressed in the atria of WT but not Scn3b−/− hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the β3 protein was expressed in WT and absent in Scn3b−/− cardiac myocytes. Lead I electrocardiograms from Scn3b−/− mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b−/− hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b−/− but hardly any WT hearts. Scn3b−/− hearts also demonstrated significantly longer sinus node recovery times than WT hearts.ConclusionThese findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion.

Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model

Remifentanil has been implicated as causing intraoperative bradyarrhythmias, but little information is available regarding its cardiac electrophysiological effects. Thus, we evaluated the cardiac electrophysiological properties before and after remifentanil in a closed-chest porcine model. Eighteen Landrace-Large pigs were premedicated with ketamine and anaesthetized with propofol (4.5 mg kg(-1) bolus followed by 13 mg kg(-1) h(-1)). After instrumentation, an electrophysiological evaluation was performed under propofol and repeated after remifentanil (bolus of 1 microg kg(-1), followed by an infusion of 0.5 microg kg(-1) min(-1)). We evaluated sinus node function [sinus node recovery time (SNRT) and sinoatrial conduction time (SACT)], atrioventricular (AV) nodal function [AH intervals during sinus rhythm (SR) and atrial pacing, Wenckebach cycle length (WCL), and effective refractory periods (ERP)], atrial, His-Purkinje, and ventricular conduction and refractoriness. Significant changes between 'propofol protocol' and 'propofol+remifentanil protocol' were evaluated. Remifentanil caused a significant increase in sinus cycle length (21%, P=0.001) and a significant prolongation of SNRT (43%, P=0.001), corrected SNRT (136%, P=0.003), SACT (40%, P=0.005), AH interval during SR (17%, P=0.02), AH interval during atrial pacing (25%, P=0.01), and ventricular ERP (12%, P=0.004). There was a tendency towards a prolongation of WCL and AV nodal refractoriness. Similar significant changes were observed in a reference group of seven animals in which sevoflurane was used instead of propofol. No significant changes were observed in atrial parameters, His-Purkinje function, parameters of intraventricular conduction, and QT intervals. Remifentanil depresses sinus node function and most parameters of AV nodal function. This contributes to an explanation for clinical observations of remifentanil-related severe bradyarrhythmias.

Evaluation of Sinus and Atrioventricular Nodes Function in Patients with Vasovagal Syncope

Evaluation of sinus and atrioventricular nodes function as a potential factor responsible for prolonged bradycardia, asystole, or both in patients with cardioinhibitory and non-cardioinhibitory vasovagal syncope (VVS). The study included 258 patients (mean age = 47.7 +/- 17.2 years; range 18-62; 147 females) with a history of VVS. They were divided among four groups, according to results of head-up tilt test (HUTT). All patients underwent standard HUTT, carotid sinus massage (CSM), and rapid transesophageal atrial pacing for evaluation of total sinus node recovery time (SNRT), and corrected sinus node recovery time (CNRT), resting and intrinsic heart rate (IHR), and Wenckebach point (WP). Values of SNRT > 1,500 ms, CNRT > 525 ms, WP < 130 bpm, and CSM-induced pause >3 seconds were considered abnormal. SNRT, CNRT, and WP before and after pharmacological blockade, resting heart rate, and IHR did not differ significantly among the study groups. The prevalence of mild sinus node dysfunction (SND), decreased value of WP, and cardioinhibitory carotid sinus hypersensitivity was similar among all study groups. The prevalence of mild SND, abnormal atrioventricular conduction, and carotid sinus hypersensitivity (CSH) was similar among patients with VVS regardless of the type of vasovagal reaction. SND and CSH do not seem to play an important role in the pathogenesis of cardioinhibitory vasovagal reaction.

Fentanyl Added to Propofol Anesthesia Elongates Sinus Node Recovery Time in Pediatric Patients with Paroxysmal Supraventricular Tachycardia

In some types of pediatric supraventricular tachycardia, reentrant mechanisms are sensitive to enhanced vagal tone. Propofol is a feasible anesthetic for pediatric electrophysiological study and radiofrequency catheter ablation. Although fentanyl and propofol infusions both enhance cardiac vagal tone, it is unclear whether the combination of propofol and fentanyl has a potential to enhance it. In this study, we evaluated the hypothesis that fentanyl combined with propofol could alter cardiac electrophysiological activities in pediatric patients undergoing electrophysiological study and radiofrequency catheter ablation. Twenty-seven pediatric patients (9 Wolff-Parkinson-White syndrome, 7 concealed accessory pathway and 11 atrioventricular nodal reentry tachycardia) were enrolled in this study. Anesthesia was induced with propofol 2.0 mg/kg and was maintained with a continuous infusion of propofol at a rate of 100-167 microg x kg(-1) x min(-1). During a stable anesthetic state, the calculated sinoatrial conduction time and corrected sinus node recovery time (CSNRT) were measured before and after fentanyl administration. The fentanyl dose consisted of an initial 2.0 microg/kg IV bolus and subsequent continuous infusion of 0.075 microg x kg(-1) x min(-1). Bispectral Index scores and systemic blood pressure remained unchanged throughout the examinations. Fentanyl administration significantly prolonged CSNRT (P = 0.005) but not calculated sinoatrial conduction time (P = 0.35). Since an enhanced cardiac vagal tone is one of the causative factors for prolonged CSNRT, our findings greatly support the hypothesis that fentanyl combined with propofol has a potential to enhance cardiac vagal tone.

Sinus node dysfunction in ATX-II-induced in-vitro murine model of long QT3 syndrome and rescue effect of ranolazine

The aim of this study was to characterize the role of the late Na+ current (INa,L) as a mechanism for induction of both tachy and bradyarrhythmias in murine heart and sino-atrial node tissue. The sea anemone toxin ATX-II and ranolazine were used to increase and inhibit, respectively, INa,L. In sixteen hearts studied, exposure to 1–10nM ATX-II caused a slowing of intrinsic heart rate and prolongations of the P–R and QT intervals, the duration of the monophasic action potential, and the sinus node recovery time, accompanied by frequent occurrences of early afterdepolarisations, delayed afterdepolarisations and rapid, repetitive ventricular tachy and sino-atrial bradyarrhythmias. ATX-II also slowed sinus node pacemaking, and induced bradycardic arrhythmias in isolated sino-atrial preparations (n=5). The ATX-II-induced alteration of electrophysiological properties and occurrence of arrhythmic events were significantly attenuated by 10μM ranolazine in intact hearts (n=11) and isolated sino-atrial preparations (n=5). In conclusion, the INa,L enhancer ATX-II causes both tachy and bradyarrhythmias in the murine heart, and these arrhythmias are markedly attenuated by the INa,L blocker, ranolazine (10μM). The results suggest that INa,L blockade may be the mechanism underlying the reductions of both brady and tachyarrhythmias by ranolazine that were observed during the MERLIN-TIMI clinical outcomes trial.

Recurrent Syncope Due to Carotid Sinus Hypersensitivity and Sick Sinus Syndrome

Syncope is a sudden and brief loss of consciousness with postural tone. Its recovery is usually spontaneous. There are various causes of syncope including cardiac, vascular, neurologic, metabolic and miscellaneous origins. The tracing is usually time-consuming and costly. The diagnosis of carotid sinus syncope may sometimes be difficult since the symptoms are nonspecific, especially in older persons. Here, we report the case of a 72-year-old woman who sought medical attention at our hospital due to repeated syncope episodes over the previous 5 years. Neurologic examinations showed negative results (including brain computed tomography). Twenty-four-hour ambulatory electrocardiogram monitoring showed atrial and ventricular premature contractions only. Electrophysiologic study disclosed prolonged corrected sinus node recovery time (1,737 ms) with poor atrioventricular conduction. Drop of blood pressure together with sinus bradycardia developed after left side carotid sinus massage. Both carotid sinus hypersensitivity with sick sinus syndrome contributed to this patient's syncope, and after pacemaker placement together with selective serotonin reuptake inhibitor treatment, she was free from syncope thereafter.

Effect of Qiangxin Fumai Granule (强心复脉颗粒) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion of the right coronary artery in rabbits

To study the effect of the Chinese medicine Qiangxin Fumai Granule (, QFG) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion (IR) of the right coronary artery in rabbits. The right coronary artery IR model in rabbits was adopted. The modeled rabbits were randomly divided into 4 groups: the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, with 8 animals in each group. In addition, twelve rabbits were selected for the sham-operative group. The drugs were administered once via duodenal perfusion after modeling had been stabilized for 10 min. The changes in AA interval, the sinoatrial conduction time (SACT), the sinus node recovery time (SNRT), the corrected sinus node recovery time (CSNRT) and the index of sinus node recovery time (ISNRT) at different time points during ischemia and reperfusion were measured. The AA interval was prolonged for more than 40 ms in the model group during ischemia. Compared with the model group, the four electrophysiological parameters abovementioned in the high-dose QFG group and the low-dose QFG group were decreased to different extents at each time point (P<0.01 or P<0.05), and no statistically significant differences were found between the QFG groups and the atropine group (P>0.05). QFG is beneficial for accelerating the recovery of sinus node autorhythmicity and conduction function, so as to protect electrophysiological functions of the sinoatrial node. Accelerating the recovery of autorhythmicity and conduction function in the sinus node is considered its electrophysiological mechanism in the treatment of sinoatrial node injury induced by ischemia.

Expecting the Unexpected

Expecting the Unexpected

Clinidine-induced bradycardia: studies of the effect on the human sinus node (author's transl)

Heart rate, atrioventricular conduction, sinus-node recovery time and effectiveness of carotid-sinus massage on heart rate were measured before and every five minutes after intravenous injection of 0.15 mg clonidine (Catapresan) in 11 patients (averaged age 60 years) with symptomatic bradycardia (dizzy spells, syncope, palpitations). Th results indicated the following significant (P less than 0.05) mean maximal effects: heart rate fell by 12% (from 59 to 52/min), capacity of atrioventricular conduction by 9% (from 132 to 121/min), while maximal sinus-node recovery time ("over-drive suppression") doubled (from 1704 to 3562 ms), heart rates of 120, 150 and 200/min being used for diagnostic atrial overdrive stimulation at each five-minute period after clonidine. During clonidine administration three patients developed a so-called hypersensitive carotid sinus reflex, in two patients the effectiveness of carotid sinus massage decreased, in three if increased, while in three it remained normal. It is concluded that (1) during bradycardia, initiated or increased by sympatholytic drugs, tests should be undertaken to exclude latent sinus-node syndrome and (or) hypertensive carotid-sinus reflex; (2) clonidine should not be used in patients with signs of sinus-node dysfunction.

Functional autonomic blockade in the diagnosis of functional sinus node disorders

The influence of the autonomic nervous system on sinus node automatism was assessed in 61 patients with suspect sinus node dysfunction. Cardiac frequency and corrected sinus node recovery time (CSNRT) were determined before and after functional autonomic blockade with intravenously administered propranolol (0,2 mg/kg) and atropine (0,04 mg/kg). A pathologic CSNRT was found in 59% of patients before and in 54% after autonomic blockade. In 44% pathologic CSNRT occurred during both conditions. In these patients intrinsic sinus node disease can be assumed. In 15% of patients an initially pathologic CSNRT became normal after blockade. In these patients sinus node dysfunction is caused by autonomic dysregulation. In 10% of patients pathologic CSNRT was seen for the first time after blockade. In such patients an altered autonomic balance seems to camouflage the primary intrinsic sinus node disease. Abnormal intrinsic cardiac frequency (cardiac frequency after autonomic blockade) was observed in pathologic prolongation of CSNRT after blockade, however not in normal CSNRT. On the other hand only 39% of patients with prolonged CSNRT after blockade had at the same time an abnormal intrinsic cardiac frequency. Autonomic blockade improves the diagnosis of the sick sinus node syndrome. Demonstration of abnormal intrinsic cardiac frequency is highly specific of intrinsic sinus node disease. Normal intrinsic cardiac frequency does, however, not exclude intrinsic sinus node disease.

Intravenous magnesium for cardiac arrhythmias: jack of all trades.

Intravenous magnesium has been used to prevent and treat many different types of cardiac arrhythmia. It has diverse electrophysiological actions on the conduction system of the heart; including prolonging sinus node recovery time, and reducing automaticity, atrioventricular nodal conduction, antegrade and retrograde conduction over an accessory pathway, and His-ventricular conduction. Intravenous magnesium can also homogenise transmural ventricular repolarisation. Because of its unique and diverse electrophysiological actions, intravenous magnesium has been reported to be useful in preventing atrial fibrillation and ventricular arrhythmias after cardiac and thoracic surgery; in reducing the ventricular response in acute onset atrial fibrillation, including for patients with Wolff-Parkinson-White syndrome; in the treatment of digoxin induced supraventricular and ventricular arrhythmias, multifocal atrial tachycardia, and polymorphic ventricular tachycardia or ventricular fibrillation from drug overdoses. Intravenous magnesium is, however, not useful in monomorphic ventricular tachycardia and shock-resistant ventricular fibrillation. Large randomised controlled studies are needed to confirm whether intravenous magnesium can improve patient centre outcomes in different cardiac arrhythmias.