Changes In Atrioventricular Conduction Research Articles

Atrioventricular Conduction in Mesial Temporal Lobe Seizures.

Purpose: Asymmetric cerebral representation of autonomic function could help to stratify cardiac complications in people with epilepsy, as some seizures are associated with potentially deleterious arrhythmias including bradycardia and atrioventricular (AV) conduction block. We investigated seizure-related changes in AV conduction and ascertained whether these alterations depend on the hemisphere in mesial temporal lobe epilepsy (mTLE).Methods: EEG and ECG data of people with pharmacoresistant mTLE undergoing pre-surgical video-EEG telemetry with seizures independently arising from both hippocampi, as determined by intracranial depths electrodes were reviewed. RR and PR intervals were measured using one-lead ECG. Statistics were done with paired student's t-tests and linear regression analysis. Data are given as mean ± SD.Results: Fifty-six seizures of 14 patients (5 men, age 34.7 ± 9.8 years) were included (2 seizures per hemisphere and patient). There were no differences of absolute PR intervals and HR before and during unilateral ictal activity between left- and right-sided hippocampal seizures. Peri-ictal modulation of AV conduction, however, appeared greater with left-sided seizures, as the slope of the PR/HR correlations was significantly steeper with seizures originating in the left hippocampus. PR lengthening >200 ms or full block did not occur in any seizure.Conclusions: Our data show that on average, PR intervals shortens with mesial temporal lobe seizures with more prominent effects in seizures with left-sided onset, supporting the notion of lateralized cerebral control of cardiac function. The clinical relevance of this subtle finding is unclear but may indicate a lateralized susceptibility to seizure-related AV node dysfunction in mTLE.

Chronotropic and dromotropic responses to localized glutamate microinjections in the rat nucleus ambiguus

The cardioinhibitory effects of cardiac vagal motoneurons (CVMs) are mediated by activation of postganglionic neurons in the epicardial ganglia which have been shown to exert functionally selective effects on heart rate and atrioventricular conduction in the rat. Here we investigate whether CVMs producing these responses may occupy different rostrocaudal positions within the nucleus ambiguus. Excitation of CVMs was attempted by microinjections of glutamate into the nucleus ambiguus of an arterially perfused preparation in a grid extending over 2mm in the rostrocaudal plane using the obex as a reference point. Microinjections were paired, one made during pacing to measure changes in atrioventricular conduction (P-R interval) independent of changes in heart rate and the other looking for changes in heart period (P-P interval) un-paced. Although evidence of a differential distribution was found in 7 cases, in the majority (13/20), sites producing maximal effects on both variables coincided. Maximal changes in atrioventricular conduction resulted from more rostral sites in 6 cases and from a more caudal site in only one. Overall, the ratio of the change in atrioventricular conduction to the change in heart rate for a given site was significantly greater 1mm rostral to the obex than at either end of the test grid. We conclude that while CVMs controlling atrioventricular conduction are distributed with a peak somewhat rostral to those controlling heart rate in a number of animals, there is a significant overlap and much greater variability in this distribution in the rat than in cats and dogs.

Cardiac responses to 24 hrs hyperoxia in Bmp2 and Bmp4 heterozygous mice

Background: Hyperoxia or clinical oxygen (O2) therapy is known to result in increased oxidative burden. Therefore, understanding susceptibility to hyperoxia exposure is clinically important. Bone morphogenetic proteins (BMPs) 2 and 4 are involved in cardiac development and may influence responses to hyperoxia.Methods. Bmp2+/−. Bmp4+/− and wild-type mice were exposed to hyperoxia (100% O2) for 24 hrs. Electrocardiograms (ECG) were recorded before and during exposure by radio-telemetry.Results: At baseline, a significantly higher low frequency (LF) and total power (TP) heart rate variability (HRV) were found in Bmp2+/− mice only (p < 0.05). Twenty-four hours hyperoxia-induced strain-independent reductions in heart rate, QTcB and ST-interval and increases in QRS, LF HRV and standard deviation of RR-intervals were observed. In Bmp4+/− mice only, increased PR-interval (PR-I) (24 hrs), P-wave duration (P-d; 18 and 21–24 hrs), PR-I minus P-d (PR – Pd; 24 hrs) and root of the mean squared differences of successive RR-intervals (24 hrs) were found during hyperoxia (p < 0.05).Discussion: Elevated baseline LF and TP HRV in Bmp2+/− mice suggests an altered autonomic nervous system regulation of cardiac function in these mice. However, this was not related to strain specific differences in responses to 24 hrs hyperoxia. During hyperoxia, Bmp4+/− mice were the most susceptible in terms of atrioventricular conduction changes and risk of atrial fibrillation, which may have important implications for patients treated with O2 who also harbor Bmp4 mutations. This study demonstrates significant ECG and HRV responses to 24 hrs hyperoxia in mice, which highlights the need to further work on the genetic mechanisms associated with cardiac susceptibility to hyperoxia.

192 Invasive assessment of atrioventricular conduction changes following transcatheter aortic valve implantation with self-expandable or balloon-expandable prosthesis

192 Invasive assessment of atrioventricular conduction changes following transcatheter aortic valve implantation with self-expandable or balloon-expandable prosthesis

Abstract 8171: Invasive Assessment of Atrioventricular Conduction Changes Following Transcatheter Aortic Valve Implantation with Self-expandable or Balloon-Expandable Prosthesis

Background: Atrio-ventricular block (AVB) is one of the complications after transcatheter aortic valve implantation (TAVI), and is more frequent after implantation of a Medtronic CoreValve (MCV) than after implantation of an Edwards Sapien prosthesis (ES). The aim of this prospective study was to quantify and compare by invasive measurement the exact influence of TAVI with MCV or ES valve on atrioventricular conduction. Methods: between February 2010 and March 2011, consecutive patients who underwent TAVI with a MCV or an ES valve were included in this prospective, single center study. The His-Ventricle (HV) interval was measured during an electrophysiology study (EPS) before and at least 4 days after the procedure. Patients with pre-existent permanent PM implanted for AVB were excluded Results: 60 patients were included. 25 (42%) were treated with a MCV, and 35 (58%) with an ES valve. Mean age was 83±6 years, 62% men with no significant difference of baseline clinical, ECG, echocardiographic data, Logistic EuroScore and STS Score between MCV and ES groups. There was no peri-procedural death. HV interval measurement was feasible in all patients. 19 patients (32%) needed implantation of a permanent PM. Indication was persistent complete AVB in 12 patients (20%) and transient high grade AVB in 4 patients (7%). PM implantation was required in 6 patients (17%) with ES valve and 13 patients (52%) with MCV (Odds Ratio: 6.8, [95% CI 1.9-24.8] p&lt;0.01). HV interval remained stable (increased duration ≤5ms) in 10 patients (30%) with ES valve and in 5 patients (20%) with MCV (p: 0. 15). HV interval was prolonged by 10ms or more after procedure in 12 patients (35%) with ES valve and in 17 patients (68%) with MCV (Odds Ratio: 5. [95% CI 1. 5-16.9] p&lt;0.01). Conclusion: This study supports the fact that atrioventricular and particularly infrahisian conductive tissue is frequently impaired after TAVI. This damage is more frequent and more severe with MCV compared with ES valve.

Changes in Atrioventricular Conduction and Predictors of Pacemaker Need After Percutaneous Implantation of the CoreValve ® Aortic Valve Prosthesis

Although changes in atrioventricular conduction frequently occur after percutaneous implantation of an aortic valve prosthesis, little is known about the mechanisms involved or how these changes progress. We investigated ECG abnormalities and predictors of pacemaker need after percutaneous implantation of the CoreValve® aortic valve prosthesis. Between April 2008 and October 2009, 65 patients with symptomatic severe aortic stenosis received a CoreValve® prosthesis. Clinical and ECG parameters were recorded and predictors of pacemaker need due to advanced atrioventricular block were investigated. The analysis excluded three patients because they had pacemakers and a fourth who died during the procedure. The patients' mean age was 79 ± 7.8 years and their logistic EuroSCORE was 20 ± 14%. Implantation was successful in 98.4%. After implantation, 47.5% had left bundle branch block and 21 patients (34.4%) required a permanent pacemaker. The need for a pacemaker was associated with a greater depth of prosthesis implantation in the left ventricular outflow tract (LVOT): 13 ± 2.5 mm vs. 8.8 ± 2.8 mm (P< .001). Moreover, depth was the only predictor: odds ratio 1.9, 95% confidence interval 1.19-3.05 (P< .007). A cutpoint of 11.1 mm for the prosthesis depth in the LVOT had a sensitivity of 81% and a specificity of 84.6% for predicting the need for a pacemaker. After CoreValve® aortic valve prosthesis implantation, a high percentage of patients needed a permanent pacemaker for advanced atrioventricular block. The only independent predictor was the depth of the prosthesis in the LVOT, which could serve as an early indicator of pacemaker need.

Chronotropic and dromotropic components of cardiac reflexes in rabbits.

The relationships between dromotropic and chronotropic components of five reflexes were studied in rabbits: intravenous and intraarterial blood injections, occlusion of the carotid arteries, Aschner maneuver, and stimulation of depressors. All these stimuli reduced heart rate (except carotid artery occlusion, which induced approximately equal number of tachi- and bradycardic responses). The former three stimuli also reduced atrioventricular (AV) conduction velocity, the changes in these two parameters were proportional. Changes in heart rate induced by Aschner maneuver were more pronounced than changes in AV conduction. Stimulation of depressor induced co-directed shifts in these parameters during the first seconds, but then AV conduction increased, while heart rate remained decreased; bradycardia and AV acceleration persisted for long time after termination of stimulation. Our findings attest to independent regulation of heart rate and AV conduction velocity and to the absence of a strict relationship between these two parameters.

What are the roles of substance p and neurokinin-1 receptors in the control of negative chronotropic or negative dromotropic vagal motoneurons? a physiological and ultrastructural analysis

Recent data indicate that there is a cardiotopic organization of negative chronotropic and negative dromotropic neurons in the nucleus ambiguus (NA). Negative dromotropic neurons are found in the rostral ventrolateral NA (rNA-VL), negative chronotropic neurons are found in the caudal ventrolateral NA (cNA-VL), and both types of neurons are found in an intermediate level of the ventrolateral NA (iNA-VL). Substance P (SP) immunoreactive nerve terminals synapse upon negative chronotropic vagal motoneurons in the iNA-VL, and SP microinjections in the NA cause bradycardia. In the present report we have attempted to: (1) define the type of tachykinin receptor which mediates the negative chronotropic effect of SP microinjections into the iNA-VL; (2) define the physiological effect of microinjections of a selective SP agonist into the rNA-VL on atrioventricular (AV) conduction; and (3) find ultrastructural evidence for synaptic interactions of SP-immunoreactive nerve terminals with negative dromotropic vagal motoneurons in the rNA-VL. Microinjections of the excitatory amino acid glutamate (Glu) into the iNA-VL to activate all local vagal preganglionic neurons caused both bradycardia and a decrease in the rate of AV conduction. Injections of the selective neurokinin-1 (NK-1) receptor agonist drug GR-73632 also caused bradycardia, however the rapid onset of agonist induced desensitization prevented an evaluation of potential effects on AV conduction in the iNA-VL. These data suggest that the SP-induced bradycardia which can be elicited from the NA is mediated, at least in part, by NK-1 receptors. Microinjections of Glu into the rNA-VL caused a decrease in AV conduction without an effect on cardiac rate. On the other hand, GR-73632 microinjections into rNA-VL did not affect AV conduction. Following injections of the β subunit of cholera toxin conjugated to horseradish peroxidase (CTB-HRP) into the left atrial fat pad ganglion which selectively mediates changes in AV conduction, retrogradely labeled neurons were histochemically visualized in the rNA-VL. These tissues were subsequently processed for the simultaneous immunocytochemical visualization of SP, and examined by electron microflapy. Histochemically labeled neurons were large, multipolar, with abundant cytoplasm containing large masses of rough endoplasmic reticulum, and exhibited distinctive dendritic and somatic spines. Unlabeled nerve terminals were noted to form either asymmetric or symmetric synapses with dendrites, dendritic spines, and perikarya of histochemically labeled neurons. SP-immunoreactive nerve terminals were also detected in the rNA-VL. SP terminals typically contained numerous small pleomorphic vesicles, multiple large dense core vesicles, and several mitochondria, and they synapsed upon unlabeled dendritic profiles. A total of 154 SP-immunoreactive nerve terminals were observed on photomicrographs of tissues which also contained histochemically labeled profiles. None made an identifiable synapse with a retrogradely labeled profile on the sections examined. In summary, both physiological and ultrastructural data indicate that SP terminals in the iNA-VL do modify the output of negative chronotropic vagal motoneurons. This effect is mediated by NK-1 receptors. On the other hand both physiological and ultrastructural data indicate that SP terminals in the rNA-VL do not modify the output of negative dromotropic vagal motoneurons. Therefore different mechanisms (neurotransmitters or receptors) mediate the central vagal control of cardiac rate and AV conduction.

Frequency-Dependent Effects of Adenosine and Verapamil on Atrioventricular Conduction of Isolated Guinea Pig Hearts

Frequency-dependent depressant effects of a drug on slow channels in the atrioventricular (AV) node are important in its efficacy against supraventricular tachycardias. Verapamil terminates reentrant supraventricular arrhythmias by depressing conduction through the AV node. Similar effects have been described for adenosine. We compared the use-dependent effects of both drugs on AV nodal conduction in isolated guinea pig hearts perfused by the method of Langendorff. Adenosine 3 microM and verapamil 0.01 microM caused a comparable prolongation of AV conduction time (AVCT) and reduction in sinus rate (SR). The time dependence of drug-induced changes in AV conduction was characterized after the atrial pacing rate was changed abruptly. The basic cycle length was shortened abruptly from 240 to 180 ms. The resulting time constant for adenosine (tau = 467 +/- 187 beats, mean +/- SD) was significantly (p < 0.05) longer than that for verapamil (tau = 264 +/- 121 beats). At a pacing cycle length of 180 ms, the rate-dependent conduction slowing tended to be more pronounced in the presence of adenosine than of verapamil. Adenosine had more pronounced frequency-dependent effects on AV conduction than did the calcium channel blocker verapamil. This may explain the higher clinical efficacy of adenosine in supraventricular tachycardias in which the AV node forms a part of the reentrant circuit.

Atrioventricular conduction in children of women with systemic lupus erythematosus

The neonatal lupus syndrome consists of transient cutaneous lupus lesions or permanent congenital complete heart block (or hepatic fibrosis), or both, in infants born to mothers with systemic lupus erythematosus (SLE). The frequency of conduction abnormalities was examined in 86 offspring of 53 women affected by SLE. Electrocardiograms from the offspring demonstrated normal sinus rhythm in 84 of 86 offspring. The PR interval was normal for age (<95th percentile) in 82 offspring and normal for heart rate in 81. Three children had a PR inter val >95th percentile (i.e., first-degree heart block) for both age and heart rate. The PR interval of the other 6 subjects with first-degree heart block for age or heart rate (≥95th percentile) was ≤0.18 second. In contrast, using a rank assignment of PR intervals in relation to heart rate and age derived from published standards, grouped data indicated that heart rate adjusted for age was greater and PR interval adjusted for heart rate longer in offspring of mothers who had the onset of SLE before or during pregnancy than in the normal population; this observation did not hold for offspring whose mothers developed SLE after the pregnancy. These findings indicate that offspring of mothers with SLE, even in the absence of an abnormal electrocardiogram, may have experienced a maternal internal environment that produces subclinical changes in atrioventricular conduction. However, newborns with a normal pulse rate are unlikely to have significant abnormalities in atrioventricular conduction and do not need screening electrocardiograms at birth.

Hemodynamic and electrophysiologic effects of amlodipine, a new calcium channel blocker

The effects of amlodpine (300 μg/kg administered intravenously), a new, long-acting, dhydropyridne class, calcium channel blocking drug, were studied in atrially paced (120 beats/min), autonomicaly blocked dogs. Hemodynmnic and electrophysiologic parameters were measured before and up to 3 hours after amlodpine. Coronary blood flow was significantly increased 10 and 30 minutes after drug administration, whereas cardiac output and mean arterial pressure were unaffected. Coronary vascular resistance was decreased but total systemic vascular resistance did not change. Atrioventricular (AV) nodal conduction was slightly prolonged, as reflected by increases in strial-His bundle and AV conduction times and PR interval, 30 minutes after administration. AN parameters returned toward their control values within 3 hours after drug administration. Comparison of coronary vascular resistance and AV conduction changes with those previously reported for other calcium channel blocking drugs where autonomic blockade existed suggests that at equivalent levels of coronary vasodilation, amlodipine's effects more closely resemble the effects of ditiazem or verapamil than other dihydropyrtdines.

Phasic influences of vagal stimulation on atrioventricular conduction.

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.

Theoretical Evaluation of the Rosenblueth Hypothesis

Rosenblueth's hypothesis states that atrioventricular (AV) nodal conduction delay and Wenckebach periodicity of AV transmission are not due to overall decremental conduction within the AV node but are due to a single step delay which is caused by a special element or layer of the AV nodal tissue. This paper discusses some theoretical considerations which allow detailed evaluation of the original hypothesis. Two artificial conduction structures which incorporate the Rosenblueth phenomenon are presented and tested by theoretical experiments that consider the potential of these structures to produce (a) basic pattern of Wenckebach periods, (b) decremental shortening of RR intervals during Wenckebach periods. These experiments are also employed to test whether or not the Rosenblueth concept can be used to explain (c) appropriate dependence of AV conduction changes on the prematurity of atrial depolarizations, and of (d) alternating cycle lengths such as may be seen with atrioventricular reentrant tachycardia. The results of the theoretical considerations show that the original concept of the Rosenblueth hypothesis is sufficient to explain (a) but it cannot be used for realization of (b), (c) and (d). A modification of the original concept complying with both (a) and (b) is proposed. This modified structure can also reproduce (c), but not simultaneously with (b). The experiments show that anisotropy of intra AV nodal conduction may create an electrophysiological mechanism of single-step delay. Different anisotropic conduction structures have to be considered to reproduce phenomenon (d).

Calcium reverses global and regional myocardial dysfunction caused by the combination of verapamil and halothane.

In order to evaluate the effects of the combination of halothane and verapamil on left ventricular function and coronary blood flow (CBF), six sheep were anaesthetized with halothane (1.2% inspired) and given increasing cumulative doses of intravenous verapamil. Regional myocardial function was assessed by sonomicrometry in the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (LC). Changes in global haemodynamics, atrioventricular conduction, LV relaxation and systolic shortening after 0.32 mg X kg-1 intravenous verapamil indicated impaired left ventricular function. Significant myocardial dysfunction (post-systolic shortening) occurred in the LAD territory, accompanied by a 64% decrease (42 +/- 6 to 15 +/- 3, P less than 0.01) in coronary perfusion pressure (CPP). Coronary blood flow in the LC segment decreased 83% (102 +/- 15 to 17 +/- 13, P less than 0.01) as coronary reserve was exhausted with the decrease in CPP. Calcium chloride reversed the impairment of global and regional myocardial function observed with verapamil, improved the impaired left ventricular relaxation, but did not significantly alter atrioventricular conduction. Thus the combination halothane-verapamil can cause significant left ventricular depression and myocardial dysfunction, possibly by inducing subendocardial ischaemia or by direct pharmacologic effect. Calcium chloride reverses this regional myocardial dysfunction as well as the deleterious global haemodynamic changes caused by halothane-verapamil; however, the changes in atrioventricular conduction are not corrected by calcium.

Beat-by-beat modulation of AV conduction. II. Autonomic neural mechanisms.

We examined the mechanism by which autonomic neural activity associated with respiration and blood pressure modulates atrioventricular (AV) conduction in conscious dogs. Mongrel dogs were anesthetized and instrumented under sterile conditions to record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded continuously, and heart rate and AV interval were plotted graphically as a function of time. To delineate the role(s) of sympathetic and parasympathetic activity, AV conduction was studied during abrupt and linear changes in heart rate after administration of atropine, propranolol, or both. In the basal state and after propranolol, AV interval oscillated with respiration both in the absence of atrial pacing and at pacing rates 10-100 beats/min above control. Following atropine, oscillations in AV interval associated with respiration were abolished; however, linear and abrupt heart rate increases resulted in AV conduction changes that were associated with fluctuations in blood pressure. In contrast, after both atropine and propranolol, alterations in blood pressure or respiration did not influence AV conduction and rate-dependent prolongation of AV conduction occurred. We conclude that in the basal state, AV conduction is influenced predominately by changes in parasympathetic activity which is the major determinant of respiratory-related AV interval oscillations; after atropine, sympathetic activity produces fluctuations in both AV conduction and blood pressure; and intrinsic rate-dependent properties of the AV node are modulated continually by both divisions of the autonomic nervous system.

Electrophysiologic and anatomic changes in the atrioventricular junction of dogs after direct-current shocks through tissue fixation catheters

Barb-tipped fixation electrode catheters were inserted under fluoroscopic control in the region of the atrioventricular (AV) node in 6 dogs. A series of direct-current shocks (20 to 240 J) were delivered from the electrode catheter to a back plate. Serial electrophysiologic studies were performed before and 2 to 3 weeks after delivery of the shocks. In general, low-energy shocks—20 to 180 J—resulted in predominant damage to the approaches to the AV node, the AV node and common bundle, whereas larger shocks created diffuse damage involving the His bundle and bundle branches. Despite histologic damage to the AV junction, only minimal changes in AV conduction were observed. Thus, there is a large safety margin for AV conduction.

Effects of hypokalemia on the various parts of the conduction system of the dog heart in situ.

The effects of hypokalemia were studied on the various parts of the conduction system by means of His bundle potential recording in the heart of vagotomized dogs. Plasma potassium concentration was lowered by extracorporeal dialysis, precautions being taken against the simultaneous impairment of other parameters, especially humoral. In order to make sure that the changes in atrioventricular conduction observed were due to hypokalemia, a control series of experiments was carried out, under strictly identical conditions except that the dialysis fluid was not devoid of potassium. The following alterations were observed during the lowering of potassium concentration from 3.2 to 1.6 mmol/l: atrioventricular node conduction time (AH interval) increased steadily up to 250% of control values; conduction time in atrial contractile tissue (SA interval) and His Purkinje system (HV interval) exhibited variations much later and much smaller; conduction time in ventricular contractile tissue was not significantly affected; effective refractory period (ERP) of atrial muscle, initially the longest in ERPs of conduction system in vagotomized animals, was shortened by about 20%. The mechanism of all these alterations is discussed.

The natural history of trifascicular disease following permanent pacemaker implantation. Significance of continuing changes in atrioventricular conduction.

Seventy-two patients with trifasicular disease were followed for an average of 40 months following permanent pacemaker insertion. The indications for pacemaker insertion were either electrocardiographic evidence of complete heart block with a wide QRS escape complex or a pattern of bifasicular block with either periods of Mobitz type II atrioventricular (A-V) block or a documented history of syncope. The patients were then divided into three groups depending on subsequent change in A-V conduction. There were 31 (43%) patients with no change in A-V conduction, 17 (24%) with increasing A-V block, and 24 (33%) with decreasing A-V block. The characteristics of these three groups, including age and sex distribution, were compared and found to be similar. The incidence of previous transmural myocardial infarction as determined by electrocardiographic criteria was higher in the group with decreasing block. Survival curves showed a significantly decreased probablity of surviving for those with decreasing block compared to both those with increasing block and those with no charge in conduction (P less than 0.03). We conclude that the probability of long-term survival was less in the group with decreasing block. This finding may be related to the greater prevalence of coronary heart disease in the patients.

Nonsinusal arrhythmias and atrioventricular conduction changes during hyperbaric oxygenation

Nonsinusal arrhythmias and atrioventricular conduction changes during hyperbaric oxygenation

Use of bundle of His potentials to assess changes in atrioventricular conduction produced by a series of beta-adrenergic blocking agents.

Use of bundle of His potentials to assess changes in atrioventricular conduction produced by a series of beta-adrenergic blocking agents.