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The electrophysiological effects of flosequinan.

We have evaluated the acute electrophysiological effects of flosequinan in 18 patients with normal ventricular function. Following intravenous infusion of flosequinan 100 mg over 1 h, mean (SD) systolic blood pressure fell from 131 +/- 19 to 120 +/- 22 mmHg (P less than 0.02) and there was significant shortening of sinus cycle length (732 +/- 151 to 575 +/- 93 ms, P less than 0.001), AH interval (110 +/- 45 to 71 +/- 19 ms, P less than 0.01), QRS duration (98 +/- 28 to 91 +/- 26 ms, P less than 0.02) and QT interval (373 +/- 47 to 337 +/- 35 ms, P less than 0.001), but no change in sinus node recovery time, intra-atrial conduction time, HV interval or the corrected QTc interval. There was a reduction in both anterograde atrioventricular Wenckebach cycle length (299 +/- 53 to 259 +/- 52 ms, P less than 0.01) and retrograde ventriculoatrial Wenckebach cycle length (375 +/- 77 to 300 +/- 56 ms, P less than 0.01). There was no change in atrial or ventricular effective refractory period (ERP) but atrial functional refractory period (FRP) shortened (233 +/- 31 to 212 +/- 24 ms, P = 0.07) as did ventricular FRP (249 +/- 24 to 234 +/- 21 ms, P less than 0.01). Patients received an oral dose of flosequinan 50 mg 12 h later. By 24 h, sinus cycle length, QRS duration and the QT interval had all returned towards baseline values, but ventricular ERP had lengthened (199 +/- 22 to 215 +/- 26 ms, P less than 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of digoxin on atioventricular conduction. Studies in patients with and without cardiac autonomic innervation.

The effect of digoxin on atrioventricular (a-v) conduction was compared in five patients with an intact cardiac autonomic nervous system (Group I) and seven patients who had undergone cardiac transplantation (Group II), in whom we have previously shown the transplanted heart to be completely denervated. Small decreases in the atrial effective refractory period (ERP) (from 262 plus or minus 12 to 254 plus or minus 11 msec) and atrial functional refractory period (FRP) (from 304 plus or minus 12 msec) were observed in Group I patients after digoxin, but these changes were not significant. However, significant increases in the A-V nodal ERP (from 315 plus or minus 18 msec to 351 plus or minus 17 msec, P less than 0.05), and A-V nodal FRP (from 426 plus or minus 42 to 460 plus or minus 46 msec, P less than 0.01) were produced by digoxin and were unrelated to changes in cycle length. In Group II patients with denervated hearts, changes in atrial ERP (from 246 plus or minus 4 to 243 plus or minus 6 during spontaneous sinus rhythm; from 204 plus or minus 10 to 216 plus or minus 8 msec during atrial pacing) and atrial FRP (from 311 plus or minus 12 to 316 plus or minus 11 msec during spontaneous sinus rhythm; from 254 plus or minus 12 to 260 plus or minus 10 msec during atrial pacing) were not significant. However, in contrast to the Group I patients, the digoxin-induced changes in A-V nodal ERP (from 280 plus or minus 22 to 297 plus or minus 18 msec during atrial pacing) and FRP (from 368 plus or minus 18 to 377 plus or minus 18 msec during spontaneous sinus rhythm; from 334 plus or minus 13 to 346 plus or minus 16 msec during atrial pacing) were also statistically insignificant. Our results demonstrate that the electrophysiologic effects of digoxin on atrioventricular conduction in man are most marked in the atrioventricular node and are dependent on cardiac innervation

Adult↗

Rat hippocampal muscarinic autoreceptors are similar to the M2 (cardiac) subtype: comparison with hippocampal M1, atrial M2 and ileal M3 receptors.

1. Affinity constants for 15 non-selective or putatively selective muscarinic antagonists were determined at muscarinic autoreceptors and postsynaptic receptors (linked to phosphatidylinositol (PI) hydrolysis) in rat hippocampal slices, at muscarinic receptors mediating contractility in guinea-pig atria or ileal smooth muscle and at binding sites in rat cerebral cortical membranes labelled with [3H]-1-quinuclidinyl benzilate or [3H]-pirenzepine. 2. Comparison of the affinities of these antagonists at central M1 receptors (inositol-monophosphate formation in rat hippocampal slices) with their affinities at peripheral M1 receptors (inhibition by McN-A-343 of electrically stimulated twitches in rabbit vas deferens) provides support for the suggestion that these receptors may differ pharmacologically. 3. Comparison of affinity constants obtained by displacement of specifically bound [3H]-pirenzepine from rat cerebral cortical membranes with those obtained in functional tests showed poor correlations between affinities for binding sites and for functional atrial receptors or for hippocampal autoreceptors. A significant correlation was found between affinities for [3H]-pirenzepine binding and those determined at muscarinic receptors linked to PI turnover in rat hippocampus. A significant correlation was also obtained between the affinities for specific [3H]-pirenzepine binding sites in cortical membranes and the affinities at ileal receptors. 4. Comparison of the affinity values for muscarinic autoreceptors in rat hippocampus with affinity values obtained from in vitro models of muscarinic receptor subtypes showed no significant correlations between these autoreceptors and either M1 or M3 receptors. A significant correlation was found between antagonist affinities for hippocampal autoreceptors and muscarinic receptors in the heart. Therefore, muscarinic autoreceptors in rat hippocampus are pharmacologically similar to the M2 (cardiac) muscarinic receptor subtype.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

[Treatment of atrial fibrillation using intravenous infusion of quinidine].

Quinidine gluconate was administered slowly by intravenous infusion to 20 patients with atrial fibrillation. Nineteen of them had rheumatic heart disease and the other one had Ebstein's disease. The first ten patients received 0.027 mg/kg/min during 6 hs or less if they returned to normal sinus rhythm (SR). The other ten received 0.041 mg/kg/min with the same protocol. Plasma quinidine concentrations were determined in all patients. Atrial functional refractory period was measured in five of the patients returning to normal sinus rhythm. Six patients in the first group were returned to SR. The required time of infusion was 4.2 hs. The maximal quinidine plasma level was 1.91 ug/ml. In the Second group; five patients returned to normal sinus rhythm, four of them in a mean time of 4.75 hs ofinfusion and the other one spontaneously 11 hs after the infusion was finished. The maximal quinidine plasma level in this group was 4.7 ug/ml. Side effects were observed in five patients. Diarrhea in one, vomiting in one, hypotension in two atrial flutter with 1: 1 A-V conduction in one.

Adolescent↗

In-vivo electrophysiological study in mice with chronic anterior myocardial infarction.

INTRODUCTION: An increasing number of genetically altered mice with specific molecular cardiac defects are being assessed by electrophysiological studies and ECG monitoring. This approach should allow for the identification of critical genes involved in the arrhythmogenesis in myocardial infarction. Therefore it was the aim of this study to establish a standard for the in-vivo electrophysiological characteristics in the mouse model of chronic anterior myocardial infarction. METHODS AND RESULTS: Using a minimized, invasive, in-vivo electrophysiological study, surface ECG parameters, sinus node function, atrial, atrio-ventricular and ventricular conduction and ventricular repolarization, and enhanced vulnerability to atrial and ventricular arrhythmia were studied in 20 wild-type C57BL/6 mice either under control or 11 weeks after large anterior myocardial infarction induced by ligation of the left anterior descending coronary artery. Telemetric ECG recording was performed in the same animals at baseline unrestrained, conscious condition to study surface ECG parameters, heart rate variability and the prevalence of supraventricular and ventricular arrhythmia. During electrophysiological study, infarcted mice showed an 81% increase of the angle of the QRS axis (p < 0.001) and a prolongation of the P wave by 23% (p = 0.01), the QRS complex by 39% (p = 0.001), the QT interval by 23% (p<0.05), the QT(c) interval by 30% (p < 0.005) and the JT(c) interval by 31% (p < 0.05) in comparison to control animals. Furthermore, there was a prolongation of the atrio-ventricular interval by 28% (p < 0.0005) and the atrio-ventricular functional refractory period by 26% in infarcted animals (p < 0.05), and inducibility of ventricular tachycardia in 4 of 6 infarcted versus in none of control animals (0 < 0.01). During telemetric ECG recording, there was a marked increase in ventricular ectopic activity in infarcted mice in comparison to controls (p < 0.05). Heart rate and time- and frequency-domain of heart rate variability were not significantly different in both groups (p > 0.05, respectively). CONCLUSIONS: The mouse model of chronic anterior myocardial infarction is associated with significant atrial and ventricular conduction disturbances and vulnerability to ventricular arrhythmia and thus may provide a highly valuable tool to study molecular determinants of arrhythmogenesis in myocardial infarction.

Animals↗

Frequency and implications of resetting and entrainment with right atrial stimulation in atrial flutter.

Thirty-three patients (24 with typical and 9 with atypical flutter-wave morphology) were studied to evaluate the incidence and implications of resetting and entrainment of atrial flutter with right atrial stimulation. Resetting with single extrastimulus was present in 23 cases (group A) and absent in 10 (group B). Most cases of reset flutter were typical (20 of 23). Fixed fusion indicative of entrainment was observed in all 29 cases with pacing trains. Groups A and B did not differ significantly in flutter cycle length (230 +/- 20 vs 223 +/- 19 ms), atrial functional refractory period (165 +/- 18 vs 167 +/- 22 ms) or longest paced cycle length producing entrainment (213 +/- 19 vs 210 +/- 19 ms). In contrast, the return cycle after the longest paced cycle length producing entrainment was significantly shorter in group A (228 +/- 27 vs 284 +/- 56 ms; p = 0.001). The return cycle in group A was virtually identical to the flutter cycle length, whereas in group B it was greater (p = 0.002 compared with group A). Resetting was more frequent in typical than atypical flutter (20 of 24 vs 3 of 9; p = 0.01). Both typical and atypical flutter can be transiently entrained by right atrial pacing. Lack of resetting and longer return cycle, suggesting a longer conduction time between the reentrant circuit and the stimulation site, were mostly observed in atypical flutter. The data suggest a different location for both types of flutter, and may have implications for ablation techniques. A more cautious approach, with more extensive mapping, appears appropriate for ablation attempts of atypical flutter.

Adult↗

Effects of pretreatment with intravenous flecainide on efficacy of external cardioversion of persistent atrial fibrillation.

Electrical cardioversion is the most effective and safe method to restore sinus rhythm in patients with persistent AF. However, at least 25% of electrical cardioversions are unsuccessful. The aim of the present study was to evaluate, in a prospective, randomized and double-blind study, the efficacy of a pretreatment with intravenous flecainide in patients who underwent electrical cardioversion. Fifty-four consecutive patients with persistent AF, mean arrhythmia duration 8 (mean 3-18) weeks, were randomized in two groups. In the first group (n = 26), patients received flecainide (2 mg/kg as a 30-minute IV infusion) before electrical cardioversion. In the second group (n = 28), 100 mL IV infusion of 5% glucose was administered 30 minutes before electrical cardioversion. The study evaluated the (1). acute efficacy of electrical cardioversion, (2). mean and maximal energy required, (3). mean number of shocks needed, and (4). incidence of complications. The two groups were similar in terms of age, sex, mean AF duration, left ventricular systolic function, atrial dimension, and cardiovascular risk factors. Seventy-seven percent of patients recovered sinus rhythm with electrical cardioversion. No statistical difference was noted between the two groups: flecainide 19/26 (73%) versus placebo 23/28 (82%). No significant differences were found concerning mean or maximal energy and number of shocks required. No major complications were observed. After a 30-day follow-up, 54% of patients maintained sinus rhythm with no difference between the two groups. Pretreatment with intravenous flecainide before electrical cardioversion is not useful in reducing technical failure of cardioversion, however, flecainide does not diminish the effectiveness of electrical cardioversion.

Aged↗

Left atrial ultrastructure in mitral valvular disease.

Light microscopic and ultrastructural observations were made on left atrial tissues obtained from 14 patients at the time of operation for correction of mitral valvular disease. Cardiac muscle cells varied in size but most frequently were hypertrophied. In fibrotic areas, present in all left atria, the muscle cells tended to be isolated from adjacent cells and exhibited degenerative changes of varying severity. These changes consisted or proliferation of Z-band material and cytoskeletal filaments, myofibrillar loss, proliferation of elements of free and extended junctional sarcoplasmic reticulum, variations in size and number of mitochondria, occurrence of abnormal mitochondria, dissociation of intercellular junctions, formation of spherical microparticles, and accumulation of lysosomal degradation products. Hypertrophy was considered to lead to cellular degeneration, with decrease or loss of contractile function. Atrial fibrillation was associated with severe cellular degeneration. The severity of degeneration was greater in patients with mitral regurgitation, with or without associated mitral stenosis, than in patients with pure mitral stenosis.

Adult↗

Production of narrow but deep lesions suitable for ablation of atrial fibrillation using a saline-cooled narrow beam Nd:YAG laser catheter.

BACKGROUND AND OBJECTIVE: Lines of radiofrequency ablation for cure of atrial fibrillation are broad, and the consequent loss of atrial mass may impair atrial function and contribute to the risk of stroke. We studied whether Nd:YAG laser could produce deep but narrower lesions. STUDY DESIGN/MATERIALS AND METHODS: Laser lesions were made in ventricular myocardium of nonperfused ovine hearts and at thoracotomy in dogs. RESULTS: Lesions were well demarcated, deep, and narrow. Saline irrigation prevented crater formation for energy levels below 200 J. Lesion depth increased with increasing duration of ablation (maximum 5.3 +/- 0.8mm, P < 0.01). The depth to width ratio was >1 in all cases (maximum 2.5 +/- 1.6). The narrowest lesions were made by using high power, short duration of exposure, and intermittent delivery. CONCLUSIONS: Irrigated Nd:YAG laser can be used to make deep narrow myocardial lesions without crater formation. Laser ablation may be more suitable than radiofrequency ablation for intraoperative or catheter-based cure of atrial fibrillation.

Animals↗

Left atrial systolic and diastolic function after cessation of pacing in tachycardia-induced heart failure.

Studies in the rapid-pacing model of heart failure have shown that left ventricular (LV) systolic function normalizes on cessation of pacing and LV diastolic dysfunction persists, but there is no information regarding atrial function under these conditions. To determine the effects of cessation of pacing on left atrial (LA) systolic and diastolic function, ten dogs with rapid pacing-induced heart failure (250 beats/min for 3-4 wk), six dogs with regression of heart failure (4 wk after cessation of rapid pacing), and seven control dogs were instrumented with LA sonomicrometers and micromanometers. At matched LA pressure, LA ejection (10.2 +/- 3.0 vs. 17.4 +/- 5.5%), reservoir volume fractions (19 +/- 8 vs. 35 +/- 11%), and heart rate-corrected mean normalized systolic ejection rate (1.25 +/- 0.33 vs. 1.60 +/- 0.44 EF/s) were significantly less, and the volume-normalized diastolic stiffness constant (4.9 +/- 0.8 vs. 3.2 +/- 1.1) was significantly greater, in regression versus control dogs; these changes were associated with incomplete regression of LA hypertrophy and a persistent 77.4% increase in beta-myosin heavy chain (beta-MHC) in the LA body. LV systolic function and weight were not significantly different, whereas the time constant of LV relaxation was longer (52.5 +/- 4.4 vs. 40.8 +/- 7.6 ms; P < 0.05) and LV end-diastolic pressure was greater (12.2 +/- 1.8 vs. 7.1 +/- 2.0 mmHg; P < 0.05) in regression compared with control dogs. Thus, unlike the normalization of LV systolic function observed with cessation of rapid pacing, LA systolic function is persistently abnormal, owing in part to persistent LV diastolic dysfunction, residual LA hypertrophy, and MHC isoform switches.

Animals↗

Abnormal maternal cardiac function and morphology in pregnancies complicated by intrauterine fetal growth restriction.

OBJECTIVE: To explore maternal cardiac function through an echocardiographic evaluation, in a group of nulliparous patients with intrauterine fetal growth restriction during the third trimester of pregnancy. METHODS: Twenty-one consecutive nulliparous pregnant women who had fetuses with intrauterine growth restriction (IUGR) and abnormal umbilical artery Doppler pulsatility index (PI) underwent maternal echocardiographic examination during the third trimester of gestation. The data were then compared with those obtained from 21 normal nulliparous women who had fetuses with an estimated fetal weight > 10th percentile and a normal umbilical artery Doppler PI who were considered as the control group. RESULTS: Heart rate was slightly lower in the IUGR group, whereas blood pressure and total vascular resistance were higher compared with the control subjects. End-diastolic volume, stroke volume and cardiac output were lower in the IUGR patients compared with normal patients. The IUGR group had smaller left atrial maximal dimensions and greater left atrial minimal areas compared with the control subjects. Left atrial function was depressed in the IUGR group. A smaller left ventricular mass was present in the IUGR patients compared with the control subjects. Isovolumetric relaxation time (IVRT) was prolonged in the IUGR patients compared with the controls. CONCLUSIONS: The absence of a 'correct' maternal cardiovascular compensatory response to abnormal trophoblastic invasion, might be one of the factors that slowly determine the conditions of reduced placental perfusion and eventually of the development of fetal growth restriction.

Adult↗

Atrial natriuretic peptide reduces the basal level of cytosolic free Ca2+ in guinea pig cardiac myocytes.

The cytosolic free Ca2+ concentration ([Ca2+]i) was monitored in quiescent atrial and ventricular myocytes isolated from guinea-pig hearts by the fura-2 fluorescence ratio technique. Recombinant human atrial natriuretic peptide (ANP) was found to reduce their basal [Ca2+]i level in a dose-dependent manner. Dibutyryl-cGMP mimicked the effect of ANP. Neither the prior application of caffeine nor removal of extracellular Na+ impaired the ANP effect. ANP had no inhibitory effect on voltage-gated Ca2+ currents measured by a whole-cell patch clamp technique. The ANP-induced [Ca2+]i decrease was abolished by orthovanadate. Thus, it is concluded that ANP reduces the basal [Ca2+]i presumably through the cGMP-mediated activation of the plasma membrane Ca2(+)-pump in cardiac myocytes.

Animals↗

Assessment of left ventricular function in secundum atrial septal defect by computer analysis of the M-mode echocardiogram.

Left ventricular function in 53 patients with secundum atrial septal defect was assessed by computer-assisted analysis of the left ventricular echocardiogram and by cardiac catheterization. The patients were divided into two groups, those younger and those older than 60 years, to investigate the effect of aging on left ventricular function. Cavity size was significantly smaller than normal (p less than 0.01) and septal motion was abnormal in 86%, but values for cardiac index, left ventricular end-diastolic pressure, velocity of circumferential fiber shortening, left ventricular filling rate, and duration of rapid filling were normal in both groups. Regional dynamics assessed in terms of peak rates of systolic thickening and diastolic thinning of the septum and posterior wall were also normal in both groups. We concluded that, although left ventricular minor dimensions are small, and septal motion is reversed in the majority of patients with atrial septal defect, left ventricular function is normal, and it does not appear to deteriorate with increased age, pulmonary hypertension, or the presence of right ventricular failure. The abnormal septal motion appears to be compensated for by enhanced septal and posterior wall percentage thickening.

Adolescent↗

Cardionatrin causes vasodilation in vitro which is not dependent on the presence of endothelial cells.

Vasodilation, in vitro, evoked by atrial extracts (cardionatrin) was compared with the relaxation due to acetylcholine and papaverine in rat precontracted aortae with and without endothelium. Ventricular extracts were tested as controls. Atrial extracts and papaverine caused a similar concentration-dependent relaxation of both preparations whereas acetylcholine failed to relax preparations without endothelium. Ventricular extracts were ineffective on both preparations. It is concluded that the response of the preparations to atrial extracts (cardionatrin) is not dependent on the presence of the endothelial cells. Some pathophysiological implications are discussed.

Acetylcholine↗

[Heart transplantation--state of the art today].

In spite of pharmacological progress, end stage congestive heart failure is still associated with a decrease in quality and expectation of life. Heart transplantation remains the last therapeutic option for these patients. While the one year survival rate has increased over the last few years up to 84%, a major problem remains the significant lack of donors. Therefore, the criteria for the selection of candidates for cardiac transplantation have to be kept quite tight: Evidence of poor outcome without transplantation is associated with ejection fractions below 20 to 25%, cardiac indices less than 2.01/min/m2, left ventricular filling pressure above 20 mm Hg and a enddiastolic diameter of > 80 mm. There are, however, also quite important functional parameters indicating the need for heart transplantation, e.g. the maximal oxygene uptake being less than 10 ml/kg/min or below 50% of the age-appropriate value. Elevated pulmonary vascular resistance above 4 to 5 Wood units without a significant decrease during application of prostaglandin derivatives or inhalation of NO represents a contraindication for orthotopic heart transplantation; alternatively, a heterotopic transplantation can be considered. Since there is a significant shortage of suitable donor organs, the donor criteria have been broadened, e. g. the accepted donor age was increased to 60 years. Based on these extended criteria, a careful donor evaluation including cardiac history, cardiac examination, ECG and echocardiogram has to be performed. Coronary angiography in older donors is suggested, but in many cases not possible due to circumstances. Further precondition for a good graft function is a sophisticated donor management until the time of explantation. Hypovolemia and hypocalemia, hypothermia, hypoxia and rapid lost of circulating triiodothyronine (T3) have to be detected and balanced. The cardioplegic solution used might not only have an impact on the immediate postoperative performance of the graft, but also on the long term outcome, particularly with regard to graft vessel disease. There are generally two types of solutions: Those with intracellular and those with extracellular electrolyte concentrations. In addition, the potassium concentration might be of some importance. Potassium seems to damage endothelial cells and trigger subsequent immunological reactions. Therefore, high potassium concentrations in the cardioplegic solution might correlate with the incidence of graft vessel disease during the long term follow-up. The surgical technique for orthotopic heart transplantation developed at the beginning of the sixties by Lower and Shumway has been used unchanged for the last 30 years. The only alteration recently introduced is the separate direct anastomosis of the pulmonary and systemic veins in order to improve the atrial function. Until recently the commonly employed immunosuppressive strategy after heart transplantation consisted of the standard drugs cyclosporin, azathioprin and prednisolon. Some transplant-units use additionally induction therapy with antibody preparations. Many centers, however, abolished this regimen due to significant short and long term side effects. Promising new, more specific antibodies (which are chimerized or humanised) could revive the induction concept. The most thoroughly tested novel immunosuppressive agent is tacrolimus (FK506). It has been demonstrated to be 10 to 100 times more potent than cyclosporin A in in vitro and in vivo models. It binds to a different binding protein (FK-binding-protein) than cyclosporin (cyclophilin), but has a similar mechanism of action inhibiting the expression of T-cell-activator genes for certain cytokines. First non-randomised studies after heart transplantation performed at the University of Pittsburgh revealed that significantly more tacrolimus than cyclosporin patients were free of rejection. In order to confirm these observations, we performed a prospective randomised controlled clin

Clinical Trials as Topic↗

Cytosolic Ca2+ during atrial natriuretic peptide secretion from cultured neonatal cardiomyocytes.

Mechanisms of atrial natriuretic peptide (ANP) release were studied in neonatal rat heart atrial and ventricular myocytes cultured on Cytodex 3 microcarriers. For simultaneous observations of cytosolic free calcium concentration ([Ca2+]f) and ANP secretion, the culture was packed in a chromatography column, inserted into the cell holder of a spectrofluorometer was perifused with a buffer solution. [Ca2+]f was measured by the fluorescent calcium indicator Fura-2 and ANP in the effluent perfusate by radioimmunoassay. No cell damage was observed and the basal ANP secretion rate and [Ca2+]f were comparable with values obtained by other methods. K(+)-induced depolarization raised [Ca2+]f by 50%, but it rapidly declined again to a steady level 10-20% above the baseline. The calcium channel agonist Bay k8644 elicited a similar temporal pattern of [Ca2+]f changes and 1 microM ionomycin induced a 100-fold increase in [Ca2+]f with a slow re-establishment of the original baseline. None of these stimuli increased the ANP secretion rate of the atrial or ventricular myocytes. Protein kinase C activation by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) stimulated ANP secretion from the atrial myocytes, while the ventricular myocytes were unresponsive to TPA. It is concluded that Ca2+ is not the main mediator in the regulation of ANP release in cultured neonatal heart cells.

Animals↗

Atrial pacing stimulates secretion of atrial natriuretic polypeptide without elevation of atrial pressure in awake dogs with experimental complete atrioventricular block.

To clarify whether or not tachycardia stimulates the secretion of atrial natriuretic polypeptide (ANP) without elevation of atrial pressure, we examined the effects of atrial pacing on ANP secretion in awake dogs with normal sinus rhythm and with complete atrioventricular block (CAVB), which was produced surgically by heat cauterization of His' bundle. In four dogs with normal sinus rhythm, atrial pacing increased the atrial rate from 146 +/- 20 to 260 +/- 10 beats/min, with marked elevation of right atrial pressure (from 0.2 +/- 0.1 to 3.9 +/- 0.8 mm Hg) and left atrial pressure (from 0.2 +/- 0.1 to 8.6 +/- 2.8 mm Hg). Along with the hemodynamic changes, the ANP level in plasma obtained from the coronary sinus was increased from 405 +/- 99 to 849 +/- 199 pg/ml (p less than 0.01). In five dogs with CAVB, the ANP level was also significantly increased from 730 +/- 82 to 1,137 +/- 35 pg/ml (p less than 0.01) by rapid atrial pacing (from 164 +/- 20 to 317 +/- 30 beats/min) in spite of the lack of any appreciable changes in either left or right atrial pressure. Furthermore, in the CAVB group, while the ventricular rate was increased by ventricular pacing from 52 +/- 5 to 146 +/- 16 beats/min, atrial pacing was performed simultaneously without atrioventricular (A-V) sequential form. Even under this condition, the ANP level was increased from 480 +/- 172 to 626 +/- 223 pg/ml (p less than 0.05) without any substantial changes in atrial pressure. Such effects of rapid atrial pacing on ANP secretion were suppressed after infusion of autonomic blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiodynamic and neurohormonal importance of atrial contribution in rate-responsive pacing.

To elucidate the physiologic importance of atrial contribution in recently developed rate-responsive pacing, changes in cardiodynamics and neurohormonal factors were analyzed during exercise in patients with respiratory rate-dependent, rate-responsive atrial (AAIR; n = 6) and ventricular (VVIR; n = 9) demand mode pacemakers implanted for sick sinus syndrome. With increasing pacing rate during bicycle ergometer exercise, the AAIR group had significant increases in cardiac index (p < 0.05), left ventricular ejection fraction (p < 0.05), and ejection (p < 0.05) and peak filling (p < 0.05) rates; however, the VVIR group had a significant decrease in ejection fraction (p < 0.05), and an increase in cardiac index (p < 0.05) that was significantly less than in the AAIR group. At rest, the mean plasma concentrations of atrial natriuretic peptide (p < 0.005) and cyclic guanosine monophosphate (p < 0.05) were significantly greater in the VVIR group than in the AAIR group and normal subjects (n = 8). Atrial natriuretic peptide, norepinephrine, and cyclic adenosine and guanosine monophosphates were significantly greater (p < 0.05) during exercise, and atrial natriuretic peptide was significantly greater in the VVIR group (207.5 +/- 8.3 pg/ml) than in the AAIR group (116.4 +/- 51.5) and normal subjects (30.8 +/- 19.2; p < 0.05); this suggested a further increase in the nonphysiologic atrial overload with VVIR pacing. The data show both the neurohormonal and cardiodynamic importance of atrioventricular synchrony in rate-responsive pacing.

Aged↗