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Electrophysiologic effects and pharmacokinetics of intravenous penticainide (CM 7857).

Penticainide is a new class I antiarrhythmic agent. Its electrophysiological effects and pharmacokinetic properties were studied in 28 patients undergoing endocavitary exploration for paroxysmal supraventricular tachycardia (10 cases), WPW syndrome involving an accessory pathway (5 cases), and unexplained dizziness (13 cases). Increasing doses of penticainide were infused in the first 18 patients (0.12 up to 3.5 mg kg-1). The next ten patients received 4 mg kg-1 over a 30 minute period. Penticainide shortened the sinus cycle length and increased the transnodal conduction time. The ventricular conduction time tended to increase. Atrial functional refractory period increased when atrioventricular nodal and ventricular refractory periods remained unchanged. In patients with previous supraventricular tachycardias all triggered arrhythmias were prevented with dosages higher than 2 mg kg-1 and related blood levels higher than 3 mg l-1. A dose-dependency of plasma and renal clearance was documented. Average Cmax values after 4 mg kg-1 was 7.37 +/- 1.28 mg l-1. No adverse events occurred during the trial and penticainide proved to be well tolerated.

Adult↗

Atrial natriuretic peptide decrease during spontaneous breathing with continuous positive airway pressure in volume-expanded healthy volunteers.

We examined the effect of spontaneous breathing with continuous positive airway pressure (CPAP) on the plasma concentrations of immunoreactive (ir) alpha-atrial natriuretic peptide (ANP). In three experiments, each of 11 healthy male volunteers performed CPAP at 20, 10 and 0 cm H2O for 2 h during continuous volume loading. Samples were drawn from a peripheral vein. Plasma concentrations of irANP were determined by a sensitive radioimmunoassay. Significantly lower concentrations of irANP were observed during 20 cm H2O CPAP than at 10 and 0 cm H2O. The concentrations of irANP did not differ significantly when individuals breathing with CPAP at 10 and at 0 cm H2O were compared. Our data suggest that CPAP at 20 cm H2O lowers the release of ANP in volume-expanded subjects. We hypothesize that this phenomenon may contribute to the fluid retention and renal dysfunction observed frequently during high CPAP levels. The decline in plasma concentrations of irANP may be the result of atrial compression by the distended lungs and of reduced venous return to the heart during CPAP.

Adult↗

Reduction volume dependence of immunoreactive atrial natriuretic peptide secretion in isolated perfused rabbit atria.

A new technique to permit gradual changes in atrial distension has been developed in an isolated perfused rabbit atrium preparation. Graded volume reduction in the atrium was induced by changing the elevation of the outflow catheter tip. Pressure reduction from 6 cm H2O atrial distension resulted in a decrease in atrial distension volume. Atrial distension by 6 cmH2O did not change the release of immunoreactive atrial natriuretic peptide (irANP). The graded reduction in atrial distension from 0.11 +/- 0.03 (1.5 cm H2O) to 1.36 +/- 0.19 microliters/mg wet weight (6.0 cm H2O) resulted in 1.7 (6.76 +/- 2.05 versus 3.83 +/- 1.18 pg/mg per min, n = 9, P less than 0.025) to 40.1-fold (77.66 +/- 17.82 versus 3.0 +/- 1.14 pg/mg per min, n = 11, P less than 0.025) increases in irANP release. IrANP release in response to the reduction of atrial distension was volume dependent. The relation of percentage increase in irANP release with the percentage reduction of atrial distension was exponential. The data suggest that the atrial muscle shortening, but not stretch per se, may be a potent direct stimulus for the regulation of irANP secretion.

Animals↗

Defective stretch-induced release of atrial natriuretic peptide from aging hypertensive rat heart: possible role of phosphatidylinositol pathway.

Because the phosphatidylinositol pathway may be part of the signaling system associated with stretch-induced release of atrial natriuretic peptide (ANP), we tested the hypothesis that formation of the intermediate inositol-1,4,5-trisphosphate (IP3) is impaired when ANP release is decreased in response to atrial stretch in hearts from aging genetically hypertensive (GH) rats. Immunoreactive ANP release into the coronary effluent and IP3 levels were studied in cardiac tissues of isolated perfused hearts from normotensive control (WAG) or GH rats aged 4, 11, or 16 months. Left atria were repeatedly distended and released with a latex balloon. ANP was measured in coronary effluent, and IP3 was measured in cardiac tissues. In all age groups, stretch and relief of stretch evoked considerably less ANP release in spontaneously beating hearts from GH than from WAG rats. Hearts from GH rats aged 16 months released no ANP, but electrical pacing restored some stretch-induced ANP secretion. With repeated stretch and release of stretch of the left atrium for 2 min, IP3 levels increased in left atrial tissue in WAG but not in GH hearts of all age groups. IP3 levels in (unstretched) left ventricles were much lower than in left atria and were unaltered by atrial stretch. In aging GH rats, the capacity to release ANP on atrial stretch is largely lost, in association with complete suppression of stimulus-induced increase in IP3 levels. These data support a role for IP3 in stretch-mediated atrial ANP secretion and suggest a progressive uncoupling of this signaling pathway in aging hypertensive rats.

Aging↗

Difficult cases in heart failure. Percutaneous transluminal septal myocardial ablation in the management of hypertrophic obstructive cardiomyopathy.

Hypertrophic cardiomyopathy is a complex genetic condition with a heterogeneous clinical course. Some patients remain asymptomatic throughout life while others develop one or more of the adverse clinical consequences including symptoms of congestive heart failure with exertional dyspnea and functional disability (usually with preserved left ventricular systolic function), atrial fibrillation, or sudden cardiac death. Because of this heterogenicity in the clinical presentations, management of patients with hypertrophic cardiomyopathy includes a wide range of pharmacologic therapies as well as invasive approaches. In recent years, nonsurgical catheter-based treatment of hypertrophic cardiomyopathy has been increasingly used in the management of a subset of these patients. The authors present a case of percutaneous transluminal septal myocardial ablation in a patient with hypertrophic cardiomyopathy who was symptomatic despite maximal medical treatment.

Atrial Fibrillation↗

Intrapatient comparison between chronic VVIR and DDD pacing in patients affected by high degree AV block without heart failure.

In patients affected by high degree AV block without preexisting congestive heart failure there is no definite demonstration that DDD pacing gives real clinical advantages in respect to VVIR pacing. We performed an intrapatient, long-term study between the two pacing modes in 14 high degree AV block patients, using the Medtronic Synergyst 7027 dual chamber pacemaker, who could be programmed alternatively in DDD or VVIR mode. After a 4-week run-in period following the pacemaker implant, patients completed a randomized, double-blind, cross-over study to compare the effect of 6-week period VVIR and DDD pacing on symptoms and cardiovascular parameters. A semiquantitative score scale was used to quantify the symptoms of general well-being, palpitations, dizziness, pulsating sensation in the neck or abdomen, shortness of breath at rest and during effort, chest pain, and NYHA classification. The sum of symptom scores was 10.4 +/- 6.7 in VVIR period and 4.6 +/- 2.7 in DDD period (P less than 0.001); five patients (36%) crossed over early from VVIR to DDD because of intolerable symptoms; overall, eight patients preferred the DDD mode and no one preferred the VVIR. Cardiac output at rest (echo-Doppler method) was 4.7 +/- 1.4 versus 5.7 +/- 1.6 liter/min (P less than 0.01), body weight was 65.9 +/- 6.6 versus 64.9 +/- 6.1 kg (P less than 0.02), atrial natriuretic peptide was 236 +/- 112 versus 198 +/- 110 pg/mL (P less than 0.01), respectively, during VVIR and DDD modes. Effort tolerance was similar with the two modes of pacing (68 +/- 15 vs 70 +/- 18 watts/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Evaluation of transesophageal atrial pacing stethoscope in adult surgical patients under general anesthesia.

Sinus bradycardia (SB) and atrioventricular junctional rhythm (AVJR) commonly cause circulatory insufficiency in anesthetized surgical patients. Treatment is usually with drugs, which can be ineffective or have adverse effects. Cardiac pacing might be preferred, but the transvenous or epicardial routes are too invasive for routine use, and transcutaneous pacing fails to preserve atrial transport function. Transesophageal atrial pacing (TAP) lacks these disadvantages, yet unavailability of inexpensive products has prevented more widespread use. Therefore, a pacing esophageal stethoscope (PES) fabricated by addition of bipolar electrodes to disposable esophageal stethoscopes routinely used for intraoperative monitoring, was evaluated in 100 anesthetized adults. TAP thresholds (10-msec pulses) and hemodynamic effects of TAP as treatment for incidental SB (< or = 60 beats/min) or AVJR were determined. Minimum TAP thresholds (mean +/- standard error) in 48 males were 7.3 +/- 0.3 mA and in 51 females were 8.5 +/- 0.4 mA. Corresponding inferior alveolar ridge-to-electrode distances were 32.5 +/- 0.2 and 30.4 +/- 0.2 cm. For 48 patients with SB < or = 60 beats/min (54 +/- 1 beats/min), TAP (81 +/- 1 ppm) produced average 15, 11, and 14 mmHg increases in systolic, diastolic, and mean arterial pressure, respectively (P < 0.001). For 11 patients with AVJR (71 +/- 5 beats/min), TAP (92 +/- 3 ppm) produced average 23 and 15 mmHg increases in systolic and mean arterial pressure, respectively (P < 0.05). There were no apparent complications of TAP. TAP with a PES appears practical, safe, and effective for prophylaxis and treatment of SB or AVJR in anesthetized surgical patients.

Adult↗

Effects of procainamide and dl-sotalol on the changes of atrial electrophysiology induced by high current stimulation.

The relation between high current atrial stimulation and antiarrhythmic drugs was not clear. We evaluated the effects of procainamide and dl-sotalol on the electrophysiological changes induced by high current stimulation. Effects of high current atrial stimulation on effective refractory period, dispersion of refractoriness, conduction velocity, and wavelength of the earliest atrial premature beat were evaluated at baseline and after infusion of procainamide (10 patients) and dl-sotalol (10 patients). High current atrial stimulation shortened effective refractory period locally (-12% +/- 4.0%, -7.0% +/- 3.0%, -5.1 +/- 3.3%, and -3.0 +/- 2.0%, at 0, 7, 14, and 21 mm from the S1 stimulation site, respectively; P < 0.001); increased the dispersion of refractoriness (from 17.8 +/- 8.5 to 27.4 +/- 12.5 ms, P < 0.001); decreased conduction velocity of the earliest premature beat (from 0.58 +/- 0.10 to 0.52 +/- 0.09 ms, P = 0.01); and decreased wavelength of the earliest atrial premature beat (from 10.9 +/- 2.4 to 8.8 +/- 2.1 cm, P < 0.001). These effects of high current stimulation persisted after procainamide infusion. However, after dl-sotalol infusion, high current atrial stimuli did not change the dispersion of refractoriness (23.1 +/- 10 ms vs 26.4 +/- 10.4 ms; P > 0.05, twice diastolic threshold vs 10 mA); conduction velocity of the earliest premature beat (0.54 +/- 0.06 ms vs 0.50 +/- 0.06 ms, P > 0.05); or wavelength of the earliest premature atrial beat (11.5 +/- 1.6 m/s vs 10.1 +/- 1.7 cm; P > 0.05). Although high current atrial stimulation shortened effective refractory period locally, increased dispersion of refractoriness, and decreased the wavelength of the earliest premature atrial impulse, these effects were abolished by dl-sotalol but not procainamide.

Adult↗

Results from the use of a preshaped lead for single-pass VDD/DDD stimulation.

Main criticisms about single-pass VDD stimulation in patients with AV block and normal sinus node function concern atrial undersensing in a lead with floating atrial electrodes, and loss of AV synchrony if sinus node dysfunction develops after implantation. We evaluated the concept of a preshaped single-pass lead designed to place the atrial ring electrodes in a constant position close to, or in contact with, the atrial wall. A preshaped lead (Model 2775, Medtronic Inc.) was implanted in 14 patients and followed for up to 2 years. Mean P wave amplitudes (PWAs) were 3.1 mV at implantation, 1.2 mV at predischarge, and 1.3 mV after 12 months. In all patients, minimal PWAs were well above maximal atrial sensitivity of the pacemaker in all body positions during the complete follow-up; atrial undersensing was not observed. Effective atrial stimulation was possible in all patients at implantation (mean stimulation threshold 2.5 V at 0.50 ms), in 11 patients on the first day after implant (mean stimulation threshold 0.22 ms at 5.0 V), in 10 patients after 1 month (mean stimulation threshold 0.57 ms at 5.0 V), and in 10 patients after 1 year (mean stimulation threshold 0.65 ms at 5.0 V). Intermittent phrenic nerve stimulation could be provoked in six patients. In conclusion, the concept of a preshaped single-pass lead facilitated implantation, improved atrial sensing performance, and allowed atrial stimulation in some patients. Still, further improvements are necessary to decrease the atrial stimulation thresholds to acceptable values in all patients.

Aged↗

The role of atrial electrical remodeling in the progression of focal atrial ectopy to persistent atrial fibrillation.

Although atrial fibrillation- (AF) induced changes in atrial refractoriness (atrial electrical remodeling) have been demonstrated in a number of different animal models, the clinical significance of this process is unknown. We describe a patient in whom there has been documented progression of atrial ectopy to persistent AF accompanied by evidence of atrial electrical remodeling, with reversal of remodeling following successful ablation of the focal source of AF. A second patient with focal AF, but with a "nonfocal" appearance on the ECG, is also described. These cases illustrate: (1) the possibility that a significant proportion of younger patients with idiopathic persistent AF may well have a focal source as the underlying abnormality; and (2) atrial electrical remodeling reverses following ablation of the underlying source.

Action Potentials↗

Atrial natriuretic peptide has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization in anesthetized dogs.

INTRODUCTION: Atrial natriuretic peptide (ANP) may alter electrophysiological properties of the heart and possibly have a role in arrhythmogenesis. However, previous studies have yielded conflicting results and have not fully considered whether ANP's cardiac electrophysiological effects are mediated via direct actions and/or indirectly via the autonomic nervous system. This study's aim was to establish whether ANP infused at pathophysiological and pharmacological doses has significant in vivo cardiac electrophysiological effects and to determine whether these effects are directly or autonomically mediated. METHODS AND RESULTS: Electrophysiologic and hemodynamic effects of ANP infusion (human ANP at 15-600 ng/kg per minute) were examined in chloralose-anesthetized dogs under conditions of varying autonomic blockade. In autonomically intact dogs (n = 12), low-dose ANP (15 ng/kg per minute) shortened atrial effective refractory period (ERP) (P < 0.001) and monophasic action potential duration (MAPD90) (P < 0.05) at 600, 500, and 400 msec atrial paced cycle lengths and reduced right atrial pressure (P < 0.05) but did not alter mean arterial pressure. After either combined vagal and beta-adrenergic blockade (vagotomy plus atropine plus propranolol, n = 7) or selective vagal blockade (n = 9), low-dose ANP no longer altered atrial ERP or MAPD90. Higher ANP doses (150 and 600 ng/kg per minute) decreased mean arterial and right atrial pressures (P < 0.001) but did not alter atrial ERP, MAPD90, or other electrophysiological parameters including atrial fibrillation threshold, ventricular ERP, and MAPD90. CONCLUSION: ANP has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization.

Action Potentials↗

Plasma ANP during hypertonic NaCl infusion in man.

To determine the relationship between hyperosmolality and immunoreactive atrial natriuretic peptide of heart atrial plasma six healthy men were given 0.06 ml kg-1 min-1 855 mmol l-1 NaCl, i.v., for 2 h. The right atrial pressure and atrial plasma atrial natriuretic peptide were measured. During the infusion, right atrial pressure was kept constant by lowering the legs of the subject in a supine position downwards if any increase in the pressure was seen. There was a significant and linear increase in atrial serum osmolality, from 288 +/- 3.3 to 307 +/- 3.2 mOsm kg-1 (P less than 0.001). No statistically significant changes in right atrial pressure were seen. Regression analysis revealed that there was a statistically significant correlation between serum osmolality and plasma ANP in three subjects (responders) (r2: 0.5241, 0.8965, 0.6695). In three other subjects (nonresponders), there was no correlation between osmolality and ANP. The mean basal osmolality of responders was 280 mOsm kg-1 and the mean basal osmolality of nonresponders was 295 mOsm kg-1. In contrast, all subjects responded with an increase in plasma ANP (P less than 0.05) after RAP had been increased by tilting the legs of the subject upwards for 30 min. We conclude that the right atrial pressure regulates the release of atrial natriuretic peptide. Serum hyperosmolality may also contribute to the regulation of atrial natriuretic peptide independently of the right atrial pressure in man.

Adolescent↗

Influence of right atrial stretch and atrial natriuretic factor on rat intestinal fluid content.

1. Studies were made on the effects of right atrial stretch and atrial natriuretic factor (ANF) infusion on fluid movement into the intestinal tract. 2. Stimulation of the atrial volume receptors by inflation of an intracardiac balloon in the conscious, unrestrained rat did not change intestinal fluid content under normovolaemic conditions. 3. When the rat was rendered hypovolaemic by peritoneal dialysis (34% deficit in extracellular fluid volume), right atrial stretch significantly increased intestinal fluid content. Under these conditions, inflation of the balloon restored large intestinal fluid content to the pre-dialysis state, i.e. right atrial stretch completely abolished that component of fluid absorption attributable to the extracellular fluid volume deficit. 4. These data suggest that stimulation of the right atrial receptors inhibits intestinal fluid reabsorption but probably does not initiate fluid secretion. 5. There was no evidence that this might be mediated by ANF since rat ANF (twenty-eight residue peptide, Ser-99-Tyr-126), infused for 1 h at doses of 0, 0.05, 0.1 and 0.5 microgram/min, did not cause any detectable changes in the fluid content of the large or small intestine of similarly prepared hypovolaemic rats.

Animals↗

Atrial natriuretic factor release during pregnancy in rats.

1. We investigated the control of atrial natriuretic factor (ANF) secretion during pregnancy. 2. Plasma ANF levels were measured in conscious virgin female rats under basal conditions, and after atrial distension with an indwelling balloon catheter. The rats were then mated, and the measurements repeated at 7, 14 and 21 days of pregnancy, and at 1 week postpartum. Plasma ANF levels were also measured in ovariectomized rats injected with progesterone, oestradiol, or oestradiol plus progesterone. 3. Basal plasma ANF levels were elevated at 7 and 14 days of pregnancy, but returned to prepregnant levels by 21 days. At 1 week postpartum, they were again elevated. 4. In response to atrial stretch, plasma ANF increased significantly in virgin rats (from 100 +/- 10 to 148 +/- 13 pg ml-1, P < 0.001, n = 20). In contrast, there was no such secretory response observed in the pregnant and postpartum animals i.e. stretch-induced secretion of ANF was markedly attenuated. 5. Treatment with exogenous oestradiol caused a significant increase in plasma ANF levels in acyclic rats. However, neither progesterone nor a combination of oestradiol plus progesterone had any effect. 6. It is concluded that basal and stretch-induced ANF secretion are differentially influenced by pregnancy; oestradiol is identified as a potential stimulatory factor.

Animals↗

Nitric oxide signalling by selective beta(2)-adrenoceptor stimulation prevents ACh-induced inhibition of beta(2)-stimulated Ca(2+) current in cat atrial myocytes.

The present study determined the effects of acetylcholine (ACh) on the L-type Ca(2+) current (I(Ca,L)) stimulated by beta(1)- or beta(2)-adrenergic receptor (AR) agonists in cat atrial myocytes. When isoproterenol (ISO; 0.1 microM) plus the beta(2)-AR antagonist ICI 118,551 (ISO-beta(1)-AR stimulation) or 0.1 microM fenoterol, a beta(2)-AR agonist (FEN-beta(2)-AR stimulation) increased I(Ca,L), ACh (1 microM) inhibited I(Ca,L) by -60 +/- 4 and -63 +/- 6 %, respectively. When ISO plus the beta(1)-AR antagonist atenolol (ISO-beta(2)-AR stimulation) or 1 microM zinterol (ZIN-beta(2)-AR stimulation) increased I(Ca,L), ACh-induced inhibition of I(Ca,L) was significantly smaller, at -21 +/- 3 and -24 +/- 3 %, respectively. L-N(5)-(1-iminoethyl)ornithine (L-NIO, 10 microM), an inhibitor of nitric oxide (NO) synthase, enhanced ACh-induced inhibition of I(Ca,L) when stimulated by ZIN-beta(2)-ARs, but not when stimulated by ISO-beta(1)-ARs or FEN-beta(2)-ARs. Haemoglobin (50 microM), a NO scavenger, also enhanced ACh-induced inhibition when I(Ca,L) was stimulated by ZIN-beta(2)-ARs, but not when stimulated by FEN-beta(2)-ARs. ACh-induced inhibition of I(Ca,L) stimulated by ZIN-beta(2)-ARs was not affected by 10 microM 1H-[1,2,4] oxadiazolo[4,3-a] quinoxaline-1-one (ODQ) a guanylate cyclase inhibitor, but was significantly enhanced by 500 microM reduced glutathione or 100 microM dithiothreitol, agents that act as sinks for S-nitrosylation. ACh-induced inhibition was smaller when I(Ca,L) was stimulated by spermine/NO, a NO donor, than by milrinone, a phosphodiesterase type III inhibitor. ISO (ISO-beta(1)/beta(2)-AR stimulation) increased I(Ca,L) and even though ISO releases NO, ACh prominently inhibited I(Ca,L). This inhibitory effect of ACh was enhanced by L-NIO. Stimulation of ZIN-beta(2)-ARs increased intracellular NO, whereas ISO-beta(1)-ARs or FEN-beta(2)-ARs failed to increase intracellular NO. These results indicate that in atrial myocytes, NO released by selective beta(2)-AR stimulation prevents ACh-induced inhibition of I(Ca,L) stimulated by beta(2)-ARs. NO acts via a cGMP-independent, S-nitrosylation mechanism. Although FEN acts via beta(2)-ARs, it fails to stimulate G(i)-/NO signalling and preferentially stimulates G(s)-/adenylate cyclase signalling, similar to beta(1)-ARs. These findings indicate that NO signalling modulates muscarinic receptor inhibition of atrial function stimulated by beta(2)-ARs.

Acetylcholine↗

Alignment of rat cardionatrin sequences with the preprocardionatrin sequence from complementary DNA.

Mammalian atria contain peptides that promote the excretion of salt and water from the kidney. When rat atrial tissue is extracted under conditions known to inhibit proteolysis, four natriuretic peptides, cardionatrins I to IV, are consistently isolated. These peptides derive from a common precursor, preprocardionatrin, of 152 amino acids, whose sequence was determined by DNA sequencing of a complementary DNA clone. Amino acid sequencing located the start points of cardionatrins I, III, and IV in the overall sequence. Cardionatrin IV most closely resembles procardionatrin because it begins immediately after the signal sequence at residue 25. Cardionatrin III begins at residue 73, and cardionatrin I, sequenced previously, begins at residue 123. Compositional analysis indicated that each of these cardionatrins extends up to tyrosine at position 150 but lacks the terminal two arginine residues.

Amino Acid Sequence↗

Ser-Leu-Arg-Arg-atriopeptin III: the major circulating form of atrial peptide.

Vasopressin induces a concentration-dependent increase in atriopeptin immunoreactivity in plasma. Rat plasma, rat atrial extract, and synthetic atriopeptin III (APIII) produced parallel displacement curves of iodine-125-labeled APIII binding to specific antiserum. Fractionation of plasma atriopeptin immunoreactivity by reverse-phase high-performance liquid chromatography showed that the major portion consists of two species of low molecular weight peptides in a ratio of 10 to 1. Both peaks exhibited potent vasorelaxant activity, suggesting the presence of the carboxyl terminal Phe-Arg sequence of atriopeptin in each species. Sequence determination of the purified peptides indicated that the major peptide is Ser-Leu-Arg-Arg-APIII and the minor peptide APIII. It appears that the former is the major species of atrial peptide in the rat circulation and that it is the product of selective cleavage of the high molecular weight precursor.

Animals↗