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PubMed1981

[Electrophysiologic effects of lorcainide (R 15889) in man].

The electrophysiological effects of lorcainide (R 15 899) were studied in 15 patients. Atrioventricular conduction was analysed by His bundle recording and cardiac refractory periods were determined by the extra stimulus method. The assessment of sino atrial function was performed by measuring sinus node recovery times and sino atrial conduction times. The electrophysiological data was recorded before and 10 minutes after a slow intravenous injection of 1,5 mg/Kg of lorcainide followed by a continuous infusion at 0,02 mg/Kg/min. The following results were obtained; 1) The HV interval increased in all cases (average : II ms) 2) The QRS and QT intervals were significantly prolonged 3) Lorcainide produced a slowing of conduction and an increase in the refractory periods at atrial level 4) AV nodal conduction was unaffected 5) The sinus rate slightly increased. There were no significant changes in sinus node recovery time or sino atrial conduction. It must be concluded that, in man, lorcainide produces electrophysiological effects of antiarrhythmic agents of the quinidine type.

Adolescent↗
PubMedDate not supplied

[The role of adenosine on the anti-arrhythmic action of digitalis glycosides].

UNLABELLED: The action of adenosine on atrial functional refractory period, as well as on its ability to interrupt atrial flutter is similar to that of digitalis. The latter suggests the possible existence of an adenilic component to digitalis action. To test this possibility, we measured the plasma concentrations of adenosine after ouabain infusion in dogs, and we investigated the effect of digitalis on atrial refractory period and on flutter in conditions of cholinergic inhibition and purinergic blockade. Ouabain was administered until ventricular fibrillation was induced. Blood was obtained from both the coronary sinus and the femoral vein, and adenosine was measured by liquid chromatography. The refractory period was measured by applying an extra stimulus at variable intervals following a train of 10 basic beats. Flutter was induced by stimulation of the posterior internodal pathway. RESULTS: The concentration of adenosine in plasma collected from the coronary sinus increased by more than 100%; the effect of digitalis on atrial refractory period was independent of cholinergic blockade, but it was inhibited by aminophylline; the ability of digitalis to interrupt flutter was modified by aminophylline. CONCLUSION: The antiarrhythmic action of digitalis seems to include an adenilic component, that results from the liberation of adenosine in the heart.

Adenosine↗
PubMed2000

Left atrial and appendage mechanical function after pharmacological or electrical cardioversion in patients with chronic atrial fibrillation: a multicenter, randomized study.

BACKGROUND: Transient atrial and appendage dysfunction occurs after cardioversion of atrial fibrillation. It has been suggested that one component of early dysfunction is related to the method of restoration of sinus rhythm and it is less severe in patients undergoing pharmacological than electrical cardioversion. The aim of this study was to compare left atrial chamber and left atrial appendage mechanical function before and after 48 hours from electrical or pharmacological cardioversion in patients with chronic atrial fibrillation. METHODS: We studied the effects of the mode of cardioversion on Doppler left atrial and appendage function in 19 patients with persistent atrial fibrillation (> or = 4 weeks), who were randomized to pharmacological (quinidine) or electrical cardioversion (protocol: 200, 300, 360 J) after pre-treatment with verapamil. Transthoracic and transesophageal echocardiography were performed before and 48 hours after the restoration of sinus rhythm. To determine left atrial and appendage mechanical dysfunction, the peak A wave velocities were obtained from transmitral flow velocity profiles recorded in the apical 4-chamber view, and peak emptying and filling appendage velocities were measured by the transesophageal approach with the sample volume placed at the orifice of the left atrial appendage. All the patients were pre-treated with verapamil before cardioversion in order to achieve a satisfactory control of heart rate. RESULTS: Mean peak A wave velocities were 0.52 +/- 0.12 m/s in the patients treated electrically and 0.54 +/- 0.08 m/s in those treated pharmacologically (p = NS). Before and after electrical cardioversion, the peak filling velocities of the left atrial appendage were 0.42 +/- 0.17 and 0.43 +/- 0.17 m/s respectively, and the peak emptying velocities 0.30 +/- 0.14 and 0.36 +/- 0.17 m/s respectively; before and after pharmacological treatment, the peak filling velocities were 0.38 +/- 0.1 and 0.43 +/- 0.1 m/s respectively, and the peak emptying velocities were 0.30 +/- 0.13 and 0.43 +/- 0.24 m/s respectively (p = 0.08). CONCLUSIONS: Even a long period of atrial fibrillation does not lead to a marked depression of global left atrial and left atrial appendage function 48 hours after the restoration of sinus rhythm by means of electrical or pharmacological cardioversion. There is no evidence that electrical cardioversion causes greater post-cardioversion atrial and/or appendage dysfunction than pharmacological treatment after 48 hours. Pre-treatment with verapamil may have reduced the dysfunction (probably because of a reduction in mechanical remodeling during atrial fibrillation).

Aged↗
PubMed1995

[Pulsed Doppler findings of the pulmonary vein flow in mitral stenosis].

Left atrial function was assessed by transesophageal echocardiography in 8 patients with mitral stenosis and sinus rhythm (MS group), and 16 age-matched normal controls (C group). Pulsed Doppler findings of left upper pulmonary vein flow were classified into first and second forward waves during systole (S1, S2), forward wave during diastole (D), and backward flow during left atrial contraction (PVA). Peak velocity (P) and time-velocity integral (TVI) of each wave and acceleration and deceleration slope of S2 wave (S2-Ac, S2-Dc) were obtained. TVI-S2 and P-D in the MS group were significantly lower than those in the C group (TVI-S2: 4 +/- 2 vs 12 +/- 3 cm, P-D: 27 +/- 13 vs 41 +/- 12 cm/sec). S2-Ac and S2-Dc in the MS group were significantly higher than those in the C group (S2-Ac: 456 +/- 116 vs 323 +/- 118 cm/sec2, S2-Dc: 380 +/- 102 vs 165 +/- 48- cm/sec2). There were no differences in S1 and PVA. Lower TVI-S2 in the MS group suggests decreased reservoir function of the left atrium. Lower TVI-S2 in the MS group was caused by increased S2-Ac and S2-Dc which suggests increased left atrial preload and deterioration of left atrial compliance. Decreased P-D in the MS group reflects dysfunction of mitral valve opening.

Adult↗
PubMed1985

Atrial vulnerability in the immature canine heart.

The induction of repetitive atrial responses during atrial extrastimulation (atrial vulnerability) was studied in 3 groups of dogs. Group I consisted of 19 neonatal puppies (age 3 to 15 days), group II of 10 older puppies (age 5 to 11 weeks) and group III of 10 adult dogs. In all dogs, atrial extrastimulation was performed coupled to a constant paced rhythm that was 85 +/- 7% of the sinus cycle length at rest in group I, 86 +/- 6% in group II and 83 +/- 10% in group III. In all groups, atrial repetitive responses were observed as the atrial functional refractory periods were approached during extrastimulation; however, the number of repetitive atrial responses was greater and the duration of repetitive firing longer in the neonates. In the neonatal group as many as 28 repetitive atrial responses were induced (9.4 +/- 8.2 beats) and the duration of repetitive atrial firing averaged 838 ms (range 120 to 2,425). In contrast, in only 1 of 20 older puppies and adult dogs were more than 2 repetitive atrial beats observed (number of repetitive atrial beats in group II, 1.7 +/- 1; in group III, 1.2 +/- 0.5). Thus, the normal neonatal atrium is more susceptible to intraatrial reentry in response to premature extrastimulation than the more mature canine atrium. This enhanced atrial vulnerability may be related to the shorter atrial refractory periods of the neonate and may be of importance in understanding the genesis of certain dysrhythmias in the human neonate.

Aging↗
PubMed1977

Effects of cycle length on atrial vulnerability.

The effect of cycle length on atrial vulnerability was studied in 14 patients manifesting reproducible repetitive atrial firing during atrial extra-stimulus (A2) testing. Repetitive atrial firing was defined as the occurrence of two or more premature atrial responses with return cycle (A2-A3) of 250 msec or less and subsequent mean cycle length of 300 msec or less, following A2. The zone of repetitive atrial firing could be defined in terms of its longest and shortest A1-A2 coupling intervals. Each patient was tested at a long cycle length (CL1) (mean 884 msec) and a short cycle length (CL2) (mean 557 msec). CL1 was sinus rhythm and CL2, an atrial paced rhythm. Repetitive atrial firing occurred in two patients at CL1 and in all patients at CL2. Of the former two patients (group 2), the zone of repetitive atrial firing was markedly widened in one at CL2 due to a shortening of atrial functional refractory period (FRP) at CL2. In the other, zone of repetitive atrial firing could not be totally defined due to induction of sustained atrial flutter preventing definition of atrial FRP. The occurrence of repetitive atrial firing at only CL2 in 12 patients (group 1) reflected: 1) a shortening of atrial FRP from 294 +/- 11 msec at CL1 to 242 +/- 10 msec at CL2 (mean +/- SEM; P less than 0.01), allowing delivery of A2 at shorter coupling intervals (9); 2) the new occurrence of repetitive atrial firing at A1-A2 coupling intervals achievable at both cycle lengths (1); or 3) both effects (2). In conclusion, decrease of cycle length potentiated atrial vulnerability. This demonstration implies that atrial pacing could potentiate occurrence of paroxysmal atrial fibrillation or flutter.

Adult↗
PubMed1995

Chronic rapid atrial pacing. Structural, functional, and electrophysiological characteristics of a new model of sustained atrial fibrillation.

BACKGROUND: Despite the clinical importance of atrial fibrillation (AF), the development of chronic nonvalvular AF models has been difficult. Animal models of sustained AF have been developed primarily in the short-term setting. Recently, models of chronic ventricular myopathy and fibrillation have been developed after several weeks of continuous rapid ventricular pacing. We hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, yielding a reproducible model of sustained AF. METHODS AND RESULTS: Twenty-two halothane-anesthetized mongrel dogs underwent insertion of a transvenous lead at the right atrial appendage that was continuously paced at 400 beats per minute for 6 weeks. Two-dimensional echocardiography was performed in 11 dogs to assess the effects of rapid atrial pacing on atrial size. Atrial vulnerability was defined as the ability to induce sustained repetitive atrial responses during programmed electrical stimulation and was assessed by extrastimulus and burst-pacing techniques. Effective refractory period (ERP) was measured at two endocardial sites in the right atrium. Sustained AF was defined as AF > or = 15 minutes. In animals with sustained AF, 10 quadripolar epicardial electrodes were surgically attached to the right and left atria. The local atrial fibrillatory cycle length (AFCL) was measured in a 20-second window, and the mean AFCL was measured at each site. Marked biatrial enlargement was documented; after 6 weeks of continuous rapid atrial pacing, the left atrium was 7.8 +/- 1 cm2 at baseline versus 11.3 +/- 1 cm2 after pacing, and the right atrium was 4.3 +/- 0.7 cm2 at baseline versus 7.2 +/- 1.3 cm2 after pacing. An increase in atrial area of at least 40% was necessary to induce sustained AF and was strongly correlated with the inducibility of AF (r = .87). Electron microscopy of atrial tissue demonstrated structural changes that were characterized by an increase in mitochondrial size and number and by disruption of the sarcoplasmic reticulum. After 6 weeks of continuous rapid atrial pacing, sustained AF was induced in 18 dogs (82%) and nonsustained AF was induced in 2 dogs (9%). AF occurred spontaneously in 4 dogs (18%). Right atrial ERP, measured at cycle lengths of 400 and 300 milliseconds at baseline, was significantly shortened after pacing, from 150 +/- 8 to 127 +/- 10 milliseconds and from 147 +/- 11 to 123 +/- 12 milliseconds, respectively (P < .001). This finding was highly predictive of inducibility of AF (90%). Increased atrial area (40%) and ERP shortening were highly predictive for the induction of sustained AF (88%). Local epicardial ERP correlated well with local AFCL (R2 = .93). Mean AFCL was significantly shorter in the left atrium (81 +/- 8 milliseconds) compared with the right atrium 94 +/- 9 milliseconds (P < .05). An area in the posterior left atrium was consistently found to have a shorter AFCL (74 +/- 5 milliseconds). Cryoablation of this area was attempted in 11 dogs. In 9 dogs (82%; mean, 9.0 +/- 4.0; range, 5 to 14), AF was terminated and no longer induced after serial cryoablation. CONCLUSIONS: Sustained AF was readily inducible in most dogs (82%) after rapid atrial pacing. This model was consistently associated with biatrial myopathy and marked changes in atrial vulnerability. An area in the posterior left atrium was uniformly shown to have the shortest AFCL. The results of restoration of sinus rhythm and prevention of inducibility of AF after cryoablation of this area of the left atrium suggest that this area may be critical in the maintenance of AF in this model.

Animals↗
PubMed2000

Electrophysiological effect of adenosine triphosphate and adenosine on atrial and ventricular action potential duration in humans.

Bolus injection of adenosine triphosphate (ATP) or adenosine is widely used clinically for terminating supraventricular tachycardia. However, bolus injection of these drugs has been reported to provoke atrial fibrillation (Afib). The effects of ATP and adenosine on the monophasic action potential duration (MAPD) of atrial and ventricular muscle was investigated, as well as the changes in the spatial distribution of atrial functional refractoriness caused by adenosine. Bolus injection of ATP and adenosine shortened atrial MAPD; no change was observed in the ventricle. Because local f-f intervals during atrial fibrillation correlate with the atrial refractory period, changes in mean f-f intervals in the right atrial appendage, His bundle region, coronary sinus ostium and distal coronary sinus were compared before and after injection of adenosine during induced Afib. Maximal shortening of f-f intervals was observed in the right atrial appendage. Inhomogeneous shortening of atrial refractoriness may account for the Afib following bolus injection of ATP or adenosine.

Action Potentials↗
PubMed1997

Doppler echocardiographic parameters predictive of recurrence of atrial fibrillation of different etiologic origins.

Atrial fibrillation is a common arrhythmia associated with an increased risk for the occurrence of embolism. Recurrences of atrial fibrillation are very frequent and increase the risk for an embolic event. The aim of the present study was to identify the clinical and echocardiographic parameters that are predictive of the recurrence of atrial fibrillation. One hundred and twenty consecutive patients with non-rheumatic atrial fibrillation were followed for 1 year after cardioversion. The following parameters were evaluated: cause and duration of atrial fibrillation, modality of cardioversion, atrial function after cardioversion (peak A wave velocity and A wave integral), left atrial dimension, peak E wave velocity of the transmitral inflow pattern, acceleration and deceleration times, and the integral of E wave. At 1 year, 72 patients maintained sinus rhythm whereas 48 patients had a recurrence of atrial fibrillation. The univariate analysis revealed that the parameter with the strongest influence on the recurrence of atrial fibrillation was the peak A velocity after cardioversion (P < 0.001). The other parameters associated with recurrences were cause of atrial fibrillation (P < 0.001), duration of arrhythmia (P = 0.002), and left atrial dimension (P = 0.05). The modality of cardioversion and the E wave variables did not influence the recurrence of atrial fibrillation. The peak A velocity was smaller in the group of patients who had a recurrence. We suggest that clinical and echocardiographic parameters, such as A wave variables, be used to identify patients at risk for recurrence. These patients should be monitored more frequently and should eventually be treated with antiarrhythmic drugs.

Aged↗
PubMed1989

[Relation of parameters of frequent transesophageal electric stimulation of the atria during the treatment of atrial flutter and electrophysiologic characteristics of the myocardium].

After arresting paroxysms with frequent transesophageal cardiostimulation (TECS), 20 patients with coronary heart disease accompanied by episodes of Type 1 atrial flutter (AF) were studied by using a technique of intracardiac electrophysiological examination. The length of the atrial cycle in AF was found to correlate with that of successful TECS (r = 0.83). The correlation increases when a difference of atrial functional and effective refractory periods is subtracted from the length of the atrial cycle in tachycardia (r = 0.92). The equations of simple and multiple linear regression were derived, which defined the optimal frequency parameters of stimulation with a sufficient accuracy to stop Type I AF episodes. The efficacy of frequent TECS in arresting 324 spontaneous AF episodes was 92.9%.

Adult↗
PubMed2002

Assessment of the left atrial appendage mechanical function by three-dimensional echocardiography.

AIMS: We evaluated the feasibility of three-dimensional echocardiography, in the assessment of left atrial appendage (LAA) function. METHODS AND RESULTS: Forty-five patients underwent multiplane transoesophageal echocardiography. In addition to Doppler and two-dimensional echocardiography, data for three-dimensional echocardiography reconstruction were obtained during transoesophageal echocardiography. Left atrial appendage ejection fraction based on three-dimensional echocardiography volume measurements (EFv) and two-dimensional echocardiography area measurements (EFa), coupled with other echocardiographic data, were related to left atrial appendage late peak emptying velocity, a frequently used indicator of left atrial appendage function. Multiple regression analysis has revealed a significant association of peak emptying velocity with EFv (P<0.0001), spontaneous echocardiographic contrast (P=0.001), tricuspid regurgitation (P=0.03) and left ventricular hypertrophy (P=0.05). No significant relation was observed between peak emptying velocity and EFa, presence or absence of atrial fibrillation, left ventricular dysfunction, mitral stenosis and insufficiency, left atrial dilatation, pulmonary venous peak systolic, diastolic and peak reverse flow velocity at atrial contraction as well as left atrial appendage volumes derived from two-dimensional echocardiography and three-dimensional echocardiography. In a simple linear correlation, the degree of association between peak emptying velocity and EFv was higher as between peak emptying velocity and EFa (r=0.7 vs 0.4, both P<0.001). Observer variabilities for calculating EFv were considerably lower than for two-dimensional echocardiography derived EFa. Ejection fractions determined by two-dimensional echocardiography area measurements at 45 degrees, 90 degrees and 135 degrees cutplane angulations were related to EFv only at 135 degrees. CONCLUSIONS: Left atrial appendage ejection fraction calculation by three-dimensional echocardiography is feasible, more accurate than by two-dimensional echocardiography and has lower observer variability. Furthermore, an optimal cutplane angulation of the left atrial appendage view at 135 degrees has been demonstrated.

Adult↗
PubMed1988

Characteristics of patients operated on because of suspected arterial embolism: a multivariate analysis.

In order to improve the understanding and classification of patients with suspected arterial embolism, we performed a loglinear analysis to study the interactions among eight characteristics in 202 patients operated on as a result of this diagnosis. Female patients were generally older, were in a poorer cardiac state (NYHA class), and had shorter duration of symptoms before operation than male patients. Atrial dysrhythmias were more common in women than in men less than 75 years of age. After the age of 75, however, the incidence was similar in both sexes. Thus, apparently, poor cardiac function is more commonly associated with acute arterial occlusion in women than in men. In men arterial thrombosis secondary to arteriosclerotic occlusive disease may be more frequent. Ischemic heart disease, age of more than 75 years, and the fact that the patient was a woman were independent predictors of poor cardiac function. Atrial dysrhythmias increased the odds for proximal arterial occlusion compared with distal occlusion, but only in NYHA class 1-2, which suggests that low cardiac output might be of importance in distal thrombotic occlusion in patients with both atrial dysrhythmia and poor cardiac function. Patients with arteriosclerosis had symptoms of longer duration than patients without arteriosclerosis and men had symptoms of longer duration than women, which indicate that the diagnosis was more uncertain, or the disease less severe, in these patients. In patients without evidence of ischemic heart disease, poor cardiac function was a predictor of short duration of symptoms, which suggests that patients with nonatherosclerotic heart disease were correctly treated for arterial emboli without undue delay.

Age Factors↗
PubMed1997

Nitric oxide does not mediate lipopolysaccharide-induced myocardial depression in guinea pigs.

OBJECTIVE: To determine the role of nitric oxide as a mediator of lipopolysaccharide-induced myocardial depression. DESIGN: Prospective, controlled study. SETTING: University research laboratory. SUBJECTS: Male and female Hartley guinea pigs. INTERVENTIONS: Animals (n = 97) received intraperitoneal injections of either saline or Escherichia coli lipopolysaccharide (2 mg/kg). Some (n = 5) animals received two injections of dexamethasone before lipopolysaccharide. Left atria were harvested 6 hrs (n = 20) or 16 hrs (n = 77) later and placed in a tissue bath with Krebs-Henseleit buffer. Contractile tension was measured in the presence or absence of two inhibitors of nitric oxide synthase (NG-nitroarginine [NNA] or aminoguanidine). Atrial and serum nitrite/ nitrate and atrial cyclic guanosine monophosphate (cGMP) concentrations were assayed. MEASUREMENTS AND MAIN RESULTS: Lipopolysaccharide caused significant atrial contractile depression at 16 hrs but not 6 hrs compared with control animals. Neither NNA nor aminoguanidine reversed the depression in atrial function. In contrast, exposure of control atria to NNA worsened contractile function. There were no significant differences between control and lipopolysaccharide-treated animals in atrial and serum nitrite/nitrate and atrial cGMP concentrations. CONCLUSIONS: Nitric oxide does not mediate lipopolysaccharide-induced myocardial depression in this animal model. Basal concentrations of nitric oxide may be important since NNA worsened contractile function in control atria.

Animals↗
PubMed1991

Atrial compliance determines the nature of passive atrial stretch and plasma atrial natriuretic factor in the conscious dog.

STUDY OBJECTIVE: The aim was to measure changes in atrial wall function over a wide range of atrial filling pressures in order to determine the relationship governing the atrial stretch in vivo. DESIGN: Acute graded haemorrhage, 30 ml.kg-1, was used to reduce atrial stretch, and volume loading with 1000 ml saline was used to increase atrial stretch. EXPERIMENTAL MATERIAL: Awake mongrel dogs (n = 6) were instrumented for the measurement of left atrial appendage pressure and diameter; awake mongrel dogs (n = 4) were instrumented for measurement of left and right atrial appendage pressures and diameters. MEASUREMENTS AND MAIN RESULTS: During haemorrhage, left atrial pressure and diameter decreased progressively, and plasma atrial natriuretic factor fell from 44 (SEM 10) to 25(5) pg.ml-1 (p less than 0.05). Calculated left atrial wall stress and minute wall stress fell by 80(5.8)% and 72(15)% (p less than 0.05 from control). During volume expansion, however, atrial wall stress and minute wall stress markedly increased and plasma atrial natriuretic factor increased by more than 500%. The relationship between left atrial pressure and diameter was a typical exponential compliance curve during volume loading and haemorrhage for atrial systole, the A wave, and for atrial diastole, the V wave. During volume expansion right atrial pressure and diameter were also related exponentially. Left atrial passive stretch, as measured by V wave wall stress, increased more than right atrial stretch during volume loading. Changes in atrial filling in conscious dogs therefore result in typical exponential changes in atrial pressure and diameter in both atria. Plasma atrial natriuretic factor only increased at high filling pressures. The relationship between passive V wave minute wall stress and plasma atrial natriuretic factor also fitted an exponential curve. Thus when atrial filling was reduced, plasma atrial natriuretic factor fell by only 50% from control, while when atrial filling increased over the physiological range (up to 15 mm Hg left atrial pressure), it rose only to 100 pg.ml-1. CONCLUSIONS: Very high atrial appendage wall stresses are required to increase plasma atrial natriuretic factor markedly. Atrial stretch and the release of atrial natriuretic factor are non-linearly related. The stimulus for atrial natriuretic factor release is related to the exponential changes in atrial function due to the underlying atrial compliance relationship.

Animals↗
PubMed1992

The hemodynamic importance of atrial systole: a function of the kinetic energy of blood flow?

The relative importance of atrial systole on left ventricular filling was investigated at rest and during exercise in 25 patients with dual chamber pacemakers. The mean blood flow velocity over the mitral valve, the velocities of the rapid filling phase (E), the active filling phase (A), and the E/A ratio were determined by pulsed Doppler-echocardiography. The patients were first examined at rest during AV sequential pacing (DVI) at 70 and 104 beats/min. The investigation was subsequently repeated during atrial synchronous pacing (VDD) at rest and during supine submaximal exercise at workloads adjusted to achieve heart rates corresponding to those during DVI pacing. The mean blood flow velocity at rest did not differ between DVI and VDD pacing at 70 beats/min (0.46 vs 0.49 m/sec). When the resting heart rate was increased to 104 beats/min (DVI) the mean blood flow velocity increased to 0.56 msec (P < 0.001). At a corresponding heart rate during exercise (VDD) the velocity increased to 0.70 msec (P < 0.001). At a resting heart rate of 70 beats/min the E/A ratio (n = 14) did not differ significantly between DVI and VDD pacing. With an increased resting heart rate (DVI) the E/A ratio decreased from 0.94 +/- 0.45 to 0.78 +/- 0.18; NS. When the heart rate increased during exercise (VDD) the E/A ratio increased from 0.75 +/- 0.14 to 0.97 +/- 0.16; P < 0.001. There was a positive correlation between the increase of the mean blood flow velocity and the increase of the E/A ratio during exercise (r = 0.69, P < 0.01). No such correlation was found when the heart rate was changed at rest. Thus, the importance of atrial systole on ventricular filling diminishes during exercise in accordance with increasing blood flow velocity, which by physical principles is related to the kinetic energy. The relative importance of atrial systole is hence inversely correlated to the kinetic energy of the blood flow.

Aged↗
PubMed1999

When the body and appendage of the left atrium disagree: "Focal" atrial fibrillation-implications for atrial thrombus formation and risk of thromboembolism.

A case is presented of a man who had 5 hours of atrial fibrillation followed by spontaneous conversion and maintained sinus rhythm that persisted as shown by surface electrocardiography. Transesophageal echocardiography performed 24 hours after electrocardiographic conversion documented an atrial fibrillation pattern within the left atrial appendage, with a normal sinus Doppler pattern in the body of the left atrium. This apparent regional discrepancy in atrial function may partially explain the increased risk for "late" thromboembolism among patients with atrial fibrillation who appear to be successfully converted with sustained sinus rhythm.

Aged↗
PubMed2006

Identification, regulation and anti-proliferative role of the NPR-C receptor in gastric epithelial cells.

Evidence suggests that functional atrial natriuretic peptide (ANP) receptors occur in surface gastric mucosal epithelial cells. To evaluate functional aspects of ANP in a model of these cells we examined the expression of natriuretic peptide receptors (NPR) subtypes A and C in the non-transformed rat gastric mucosal epithelial cell line RGM1. Transcripts for NPR-A and NPR-C were detected in RGM1 cells by RT-PCR. However, only NPR-C protein was detected by Western blot and immunohistochemical analyses. Specific saturable binding of (125)I-ANP to RGM1 cells revealed a single class of high affinity binding sites (K (d) = 208 +/- 71pM, B (max) = 110,000 +/- 14,000 sites/cell, Hill coefficient = 0.97 +/- 0.05). ANP (IC(50) 130 +/- 47pM), BNP (IC(50) 716 +/- 26 pM), CNP (IC(50) 356 +/- 85pM) and C-ANP (IC(50) 134 +/- 13pM), a specific ligand for NPR-C, effectively displaced (125)I-ANP binding. Cross-linking of (125)I-ANP to cells labeled predominantly a protein of 66,000 Da. These data suggest that (125)I-ANP binding was primarily to NPR-C. ANP and C-ANP inhibited forskolin- and prostaglandin E(2) (PGE(2))-stimulated cAMP in a PTx-sensitive fashion. PGE(2), transforming growth factor-+/-1 (TGF-+/-1), forskolin, 8-bromo-cyclic AMP, and phorbol-12-myristate-13-acetate (PMA) caused a dose-dependent decrease in specific (125)I-ANP binding, whereas epidermal growth factor (EGF), 8-bromo-cyclic GMP and 4+/--phorbol didecanoate had no effect. PGE(2), forskolin, TGF-+/-1 and PMA significantly decreased (125)I-ANP B (max) values, NPR-C protein and steady-state NPR-C transcript levels. H89, a protein kinase A inhibitor, blocked the reduction of NPR-C mRNA produced by both forskolin and PGE(2.) GF109203X, a protein kinase C inhibitor, abolished the PMA-induced decrease in NPR-C transcripts but only partially blocked that produced by TGF-+/-1. RGM1 cells exhibited a dose-dependent decrease in both DNA synthesis and cell proliferation when cultured in the presence of ANP or C-ANP. These findings indicate that RGM1 cells express functional NPR-C receptors that can influence RGM1 cell proliferation and are down-regulated by PGE(2) and TGF-+/-1.

Adenylyl Cyclases↗