Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atrial function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,423 records · Page 79Linked to original sources
PubMed1984

Alterations in subsidiary pacemaker function after prolonged subsidiary pacemaker dominance in the canine right atrium.

In vivo and in vitro techniques were used to study the functional characteristics of subsidiary atrial pacemaker activity 4 to 11 months after surgical excision of the sinoatrial node region of the dog heart. Characteristics of this long-term subsidiary atrial pacemaker activity were compared with those of sinoatrial node and short-term subsidiary atrial pacemaker activities. Extracellular bipolar electrodes were used to estimate the site of earliest activation and monitor spontaneous rate. Under both in vivo and in vitro conditions, long-term pacemaker activity was located in the same region of the inferior right atrium as was short-term pacemaker activity. Under in vitro conditions, long-term activity was characterized by a reduced sensitivity to acetylcholine and overdrive pacing and by a lack of dependence on beta-adrenergic stimulation compared with short-term activity. Furthermore, long-term pacemaker activity was more sensitive to acetylcholine and less sensitive to norepinephrine (greater than 10(-7) M) compared with sinoatrial node activity. It is concluded that the subsidiary atrial pacemakers that emerge soon after removal of the sinoatrial node are the same as those pacemakers that ultimately assume long-term control of the heart. In addition, after subsidiary atrial pacemakers assume dominant pacemaker function, their dependence on norepinephrine and their response to acetylcholine and overdrive pacing are reduced. These changes facilitate a more stable regulation of atrial pacemaker rhythm and, thereby, make subsidiary atrial pacemaker function more like that of the sinoatrial node.

Acetylcholine↗
PubMed1988

Electrophysiologic effects of intravenous and oral sotalol for sustained ventricular tachycardia secondary to coronary artery disease.

The electrophysiologic effects of intravenous sotalol (1.5 mg/kg load followed by 0.008 mg/kg maintenance, mean dose 150 +/- 23 mg) and oral sotalol (mean dose 583 +/- 204 mg daily) were prospectively evaluated in 16 patients undergoing electrophysiologic evaluation for sustained ventricular tachycardia (VT) secondary to coronary artery disease. Electrocardiographic intervals, indexes of sinus and atrioventricular node function and indexes of atrial and ventricular function were assessed. Inducibility or noninducibility of sustained VT and characteristics of the induced arrhythmia were also evaluated. Intravenous and oral sotalol exerted similar beta-blocking effects, which included significant prolongation of sinus cycle length (baseline 820 +/- 165 ms, intravenous sotalol 1,077 +/- 206 ms, oral sotalol 1,141 +/- 306 ms), AH interval (baseline 126 +/- 43, intravenous sotalol 169 +/- 42, oral sotalol 197 +/- 55 ms) and Wenckebach cycle length (baseline 375 +/- 70, intravenous sotalol 460 +/- 84, oral sotalol 449 +/- 68 ms). Both intravenous and oral sotalol also prolonged repolarization and refractoriness including significant increases in QT interval (baseline 338 +/- 47, intravenous sotalol 417 +/- 35, oral sotalol 450 +/- 70 ms), atrial effective refractory period (baseline 240 +/- 38, intravenous sotalol 330 +/- 71, oral sotalol 299 +/- 26 ms) and right ventricular effective refractory period (baseline 241 +/- 16, intravenous sotalol 289 +/- 35, oral sotalol 291 +/- 22 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Bilateral atrial appendectomy abolishes increased plasma atrial natriuretic peptide release and blunts sodium and water excretion during volume loading in conscious dogs.

The atrial appendages contain most of the atrial natriuretic factor (ANF) in the mammalian heart, and atrial appendage mechanical function predicts ANF secretion during volume loading. To demonstrate the crucial role of the atrial appendages in ANF release, we first measured hemodynamics and changes in plasma ANF after injection of 1,000 ml i.v. normal saline in conscious dogs and again after bilateral atrial appendectomy; we next measured changes in renal function using infusions of atriopeptin 24 to achieve plasma levels corresponding to levels achieved during volume loading; and we lastly measured renal function during acute volume expansion and also after atrial appendectomy. Plasma ANF increased from 65 +/- 11 to 246 +/- 54 pg/ml after volume loading but did not increase after atrial appendectomy. Atrial appendectomy did not alter the tachycardia or hemodynamic effects of volume loading. Infusion of 10 ng/kg/min atriopeptin 24 increased plasma ANF from 50 +/- 9 to 234 +/- 54 pg/ml, increased urine output 34 +/- 10%, and increased sodium excretion 62 +/- 10% in dogs with intact atrial appendages. Renal function was compared in dogs before atrial appendectomy: 20, 40, and 60 minutes after volume loading, urine flow rate increased by 5.9 +/- 0.5, 6.9 +/- 0.4, and 4.4 +/- 0.8 ml/min, while sodium excretion increased by 717 +/- 60, 839 +/- 84, and 582 +/- 57 mueq/min. After atrial appendectomy urine flow rate increased 2.1 +/- 0.7, 2.7 +/- 0.7, and 2.0 +/- 0.6 ml/min, and sodium excretion increased only by 327 +/- 110, 324 +/- 77, and 340 +/- 92 mueq/min (p less than 0.01) during volume loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Disturbed atrioventricular electromechanical function long after Mustard operation for transposition of great arteries: a potential contributing factor to atrial flutter.

OBJECTIVE: The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. METHODS: Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. RESULTS: There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. CONCLUSION: Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.

Adult↗
PubMed1992

Modulation of kidney function in conscious Pekin ducks by atrial natriuretic factor.

The influence of avian atrial natriuretic factor (ANF) on renal function was examined in conscious saltwater-acclimated Pekin ducks undergoing a steady state diuresis maintained by iv infused isotonic avian Krebs-Ringer solution at a rate of 1.0 ml/min. Synthetic chicken ANF (chANF) was applied iv at doses of 10, 50, and 90 ng/min.kg BW for 10 min and caused dose-dependent transient increases in urine flow, osmolal excretion, glomerular filtration rate, effective renal plasma flow, and fractional water clearance at decreased urinary osmolality. Using receptor autoradiography, binding sites for [125I]Bolton-Hunter-labeled chANF [( 125I]BH-chANF) were localized in both the reptilian-type glomeruli and the collecting duct system throughout the duck kidney. A RRA for [125I]BH-chANF, established using an enriched kidney membrane fraction, indicated that unlabeled chANF and human ANF competitively displaced [125I]BH-chANF with comparable potencies. ANF-induced modulation of renal salt and water elimination via glomerular and tubular receptor interactions is consistent with the concept that this hormone has a physiological role in avian volume homeostasis.

Animals↗
PubMed1999

Predictors and significance of atrial rhythm before and six months after percutaneous balloon mitral commissurotomy.

Clinical, echocardiographic, and cardiac catheterization data were evaluated in 263 patients with mitral stenosis who were undergoing balloon commissurotomy to determine the predictors of atrial rhythm and its effect on functional status. Conversion from atrial fibrillation to sinus rhythm at 6 months after the procedure occurred in 16 of 86 patients (19%) and was predicted by the duration of atrial fibrillation, baseline functional class, and antiarrhythmic therapy; patients who remained in atrial fibrillation had a poorer functional status compared with those in sinus rhythm despite similar procedural results.

Adult↗
PubMed1987

Atrial granules in the dog heart after cardiac denervation.

Because the increase in sodium excretion during left atrial distension in conscious dogs is abolished after chronic cardiac denervation, we have investigated whether this is a result of the disappearance of specific atrial granules. Electron microscopy and light-microscopical and ultrastructural immunohistochemistry of canine atria show that atrial granules displaying immunoreactivity for cardiac hormones of the cardiodilatin/atrial natriuretic polypeptide (CDD/ANP) family are still present in denervated left and right atria, although reduced in quantity. It is concluded that the "atrial-induced natriuresis" is not only related to the existence of specific atrial granules. The functional link between atrial-induced natriuresis provoked by atrial distension and the release of atrial polypeptide hormones remains uncertain because the denervated heart can secrete CDD although the diuretic-natriuretic effect is altered.

Animals↗
PubMed1989

Perioperative cardiac pacing using an atrioventricular pacing pulmonary artery catheter.

An atrioventricular pacing thermodilution pulmonary artery catheter was evaluated in 40 patients undergoing cardiac surgery. The catheter was inserted in all study patients in a timely fashion without difficulty and functioned well during the perioperative period. Before the start of cardiopulmonary bypass, atrial capture was achieved in 98% of the patients (threshold mean 4.9 mA), ventricular capture in 100% (threshold mean 3.0 mA) and atrioventricular sequential (AVS) pacing in 98%. After cardiopulmonary bypass, atrial capture was achieved in 95% of the patients (threshold mean 5.2 mA), ventricular pacing in 100% (threshold mean 3.1 mA), and sequential pacing in 95%. In 27 patients in whom cardiac outputs were recorded, cardiac index increased an average of 45% (range 8% to 95%) with atrial or AVS pacing over ventricular pacing alone. In 11 patients, extended atrial pacing was used postoperatively, the longest for 93 hours. No major complications could be attributed to the study catheter. Minor complications included diaphragmatic stimulation in one patient and supraventricular tachycardia, possibly related to atrial pacing postoperatively, in one patient. These data suggest that this catheter/pacing system is effective and reliable for hemodynamic monitoring and temporary atrial or AVS pacing. In addition, the atrial pacing probe can be used perioperatively to record atrial electrograms to facilitate the diagnosis of supraventricular tachyarrhythmias.

Aged↗
PubMed2003

Inter-relationships between atrial flutter and atrial fibrillation.

It has been appreciated for a long time that atrial flutter and atrial fibrillation have a clinical relationship. Now, with the technological advances that permit more sophisticated electrophysiological studies, especially mapping studies, we have significantly advanced our understanding of this interrelationship. Regarding the relationship at atrial fibrillation to atrial flutter: Atrial fibrillation of variable duration (very brief to prolonged episodes) precedes the onset of atrial flutter in most instances. It seems that during the period of atrial fibrillation, the functional components of the atrial flutter reentrant circuit are formed. This is principally a line of block between the venae cavae. If this line of block does not form, classical atrial flutter does not form. And if this line of block shortens or disappears, classical atrial flutter disappear as well. In fact, it might be said that the major difference in whether classical atrial flutter or atrial fibrillation develops is whether a line of block forms between the venae cavae. Regarding the relationship of atrial flutter to atrial fibrillation: Studies have demonstrated that a driver (a single focus or reentrant circuit of very short cycle length) can be responsible for causing atrial fibrillation by producing fibrillatory conduction to the rest of the atria. In experimental models and now beginning to be demonstrated in patients, this driver may be a stable reentrant circuit of very short cycle length, i.e., a fast form of atrial flutter, if you will. In fact, there is probably a spectrum of these short cycle lengths that depend, in part, on where the reentrant circuit (i.e., "atrial flutter") exists. When the stable reentrant circuit is of sufficiently short cycle length, it will only activate small portions of the atria in a 1 : 1 manner. The rest of the atria will be activated irregularly, resulting in atrial fibrillation. Unstable reentrant circuits can also do the same thing. In short, it appears that there are several mechanisms of atrial fibrillation, one of which is due to a form of very rapid atrial flutter.

Animals↗
PubMed1988

Natriuresis during atrial distension and a concurrent decline in plasma atriopeptin.

In the conscious dog, left atrial distension elicits a composite response that modulates both cardiovascular and renal function. The response to atrial distension may be mediated by the combined effects of neural reflexes and the release of atriopeptin. To assess the relative contributions of atrial reflex mechanisms and circulating atriopeptin to the renal response elicited by atrial distension, alpha-human atrial natriuretic peptide (alpha-hANP) was infused into conscious dogs at 50 ng.kg-1.min-1 for 60 min. Then the infusion was stopped abruptly, and left atrial pressure was increased 8 mmHg by inflating a balloon positioned above the mitral valve. Plasma atriopeptin decreased during the 40-min period of atrial distension, but urine flow and sodium excretion increased during this time. In another series of experiments, volume expansion was substituted for atrial distension. Saline (24 ml/kg) was infused intravenously for 5 min immediately after the 60-min period of alpha-hANP infusion. Urine flow and sodium excretion increased after administration of saline even though plasma atriopeptin decreased substantially during the same time period. These results provide evidence that circulating levels of atriopeptin do not play a dominant role in influencing sodium excretion either during atrial distension or in response to saline infusion.

Aldosterone↗
PubMed2006

Functional mitral regurgitation in heart failure.

Mitral regurgitation commonly occurs in patients with heart failure. Systolic dysfunction is the hallmark of dilated cardiomyopathy. Mitral functional regurgitation is mitral incompetence in the absence of intrinsic lesions of the mitral valve apparatus. Echocardiography can make a major contribution to the diagnosis of cardiomyopathies. A more careful anatomic and hemodynamic evaluation of mitral regurgitation mechanisms is possible with spectral Doppler, color Doppler, three-dimensional echocardiography and transesophageal echocardiography. Functional mitral regurgitation is due to the incomplete closure of mitral leaflets and is based on alterations of mitral annulus, left ventricular dimensions, function and geometry, left atrial dimensions and function. Knowledge of the mechanisms of mitral regurgitation helps us to gain an insight into therapeutic interventions that modify the mechanistic factors. Medical therapy reduces the tethering forces and also augments transmitral pressure; surgical approaches can modify geometric relationships in the left ventricular chamber and resynchronization therapy can improve co-ordinated timing of mechanical activation of papillary muscles.

Cardiomyopathy, Dilated↗
PubMedDate not supplied

[Atrial natriuretic factor].

The atrial natriuretic factor represents a group of atrial peptides structurally and functionally related. These peptides produce the following effects: natriuresis, diuresis, vasodilation and inhibition of aldosterone release. Its discovery in 1981 opened a new horizon in the studies on body sodium and water homeostasis, as well as on blood pressure regulation. In a few years there have been spectacular advances in the knowledge of this new hormone. However, there are still many doubts and controversies concerning its exact physiological role. Its effects on renal function, vascular contractility and its relationship with other physiological systems are not completely understood. The versatility of functions in which atrial natriuretic factor participates has pointed new trends in the research of important clinical entities such as arterial hypertension and cardiac failure, and could be a starting point for the development of novel therapeutic agents. In this work, the experimental findings dealing with the participation of atrial natriuretic factor in several biological events are reviewed.

Animals↗
PubMed1995

[Cardioversion in atrial fibrillation. Results and complications in 1,152 prospective patients. Study Group of the Working Society of Leading Cardiologic Hospital Physicians].

BACKGROUND: Pharmacological and direct-current cardioversion of atrial fibrillation are often performed interventions. Little is known about results and complications of cardioversion in daily practise. PATIENTS AND METHODS: Demographic, procedural and outcome data from patients with cardioversion of atrial fibrillation were collected in a prospective, multicenter registry of 61 hospitals. RESULTS: Between July 1994 and December 1994 1152 patients with a mean age of 64 +/- 11 years were registered on an intention-to-treat basis. 62% were male. The most prevalent underlying disorders were coronary artery disease (34.7%), valvular heart disease (18.1%), and cardiomyopathy (6.9%). 16.4% of patients had lone atrial fibrillation. New onset atrial fibrillation was reported in 21%, paroxysmal in 32% and chronic in 47% of patients. The mean duration of atrial fibrillation was 7 +/- 26 weeks (range 1 day to 7 years, median 5 days). In 3.8% of patients no cardioversion attempt was made and follow-up was not possible in another 5.5%. 19.2% of patients cardioverted spontaneously. Direct current cardioversion was attempted in 39.7% and pharmacological cardioversion in 31.8% of patients. Cardioversion was successful (sinus rhythm at discharge) in 96.4% of spontaneous cardioversion, in 73.1% of direct current cardioversion and in 84.4% of pharmacological cardioversion. Success of cardioversion was significantly related to duration of atrial fibrillation, NYHA functional class and left atrial diameter (p < 0.001). In 55 (4.8%) cases complications were reported of which 14 were fatal. Five cases of sudden death occurred, all of which were related to quinidine therapy for pharmacological cardioversion. Five cases of embolism were reported. Two were not associated with cardioversion attempts and 3 occurred within 24 hours after successful direct current cardioversion. Two of these patients were effectively anticoagulated at the time of cardioversion. A total of only 62% of patients with atrial fibrillation of more than 48 hours duration were anticoagulated for cardioversion with coumadine or i.v. heparin. CONCLUSIONS: The main risks of cardioversion are fatal proarrhythmic events in pharmacological attempts to restore sinus rhythm. The risk of embolism is despite low rates of effective anticoagulation low.

Aged↗
PubMed1991

[The effects of atrial natriuretic peptide on left ventricular function in subjects with heart failure].

The effects of atrial natriuretic peptide (ANP) infusion was evaluated in 11 patients with congestive heart failure undergoing cardiac catheterization. Data were obtained at rest and during steady-state phase of alpha-human (1-28) ANP infusion (1 microgram/kg bolus dose, 0.1 microgram/kg/min iv for 30 min). Mean blood pressure decreased from 104 +/- 20 to 89 +/- 21 mmHg (p less than 0.05) 15 min after ANP infusion, as well as left ventricular end-diastolic pressure (from 27 +/- 6 to 14 +/- 11 mmHg, p less than 0.05) and wedge pressure (from 22 +/- 5 to 13 +/- 7 mmHg, p less than 0.05). Left ventricular ejection fraction increased significantly after ANP infusion from 39 +/- 7 to 47 +/- 2%, p less than 0.01. The ANP infusion significantly increased cardiac output from 4.9 +/- 0.8 to 5.8 +/- 1.41/min, p less than 0.05, and decreased the relaxation constant from 69 +/- 17 to 48 +/- 18, p less than 0.05. These results demonstrate that in patients with congestive heart failure ANP infusion decreased wedge pulmonary pressure, left ventricular end-diastolic pressure and increased cardiac output and left ventricular ejection fraction.

Adult↗
PubMedDate not supplied

Time-course of left atrial performance during coronary artery occlusion followed by reperfusion in anesthetized dogs by densitometric analysis of digital atrioventriculographic images.

The left atrial (LA) function during coronary artery occlusion followed by reperfusion using densitometric analysis of digital atrioventriculographic images was evaluated. Eight anesthetized dogs underwent atrioventriculography at baseline, 10 and 60 min after left circumflex coronary artery (LCX) occlusion and 5, 30, 60, and 120 min of reperfusion. Time-density curves were obtained for LA and left ventricle (LV). The ratios of passive atrial video-densitometric change (VC) to total VC (Passive Ratio), and active VC to total VC (Active Ratio) were calculated. Left ventricular ejection fraction (LVEF), peak ejection rate (PER), and peak filling rate (PFR) were derived. Active Ratio, an index of atrial contraction, increased to 144%, and Passive Ratio decreased to 75% of baseline at 60 min of LCX occlusion. Two hours after reperfusion, both Active and Passive Ratios returned to control level. While LVEF reduced to 70%, PER to 67%, LV peak positive dP/dt to 88% of baseline at 60 min after occlusion, and remained depressed at 2 h after reperfusion. However, PFR, LV peak negative dP/dt and LV isovolumic pressure decay rate showed recovery at 2 h after reperfusion. There were significant correlations between PFR and Passive Ratio (r = 0.41), and between Active and Passive Ratios (r = 0.55). Thus, time-course of recovery of LV post-ischemic systolic and diastolic function was different. Return of LA function to control level during 2 h after reperfusion may be depend on recovery of LV diastolic function.

Animals↗