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PubMed2002

Compensatory changes in atrial volumes with normal aging: is atrial enlargement inevitable?

OBJECTIVES: The aim of this study was to evaluate left atrial volume and its changes with the phases (active and passive) of atrial filling, and to examine the effect of normal aging on these parameters and pulmonary vein (PV) flow patterns. BACKGROUND: Atrial volume change with normal aging has not been adequately described. Pulmonary vein flow patterns have not been volumetrically evaluated in normal aging. Combining atrial volumes and PV flow patterns obtained using transthoracic echocardiography could estimate shifts in left atrial mechanical function with normal aging. METHODS: A total of 92 healthy subjects, divided into two groups: Group Y (young <50 years) and Group O (old > or =50 years), were prospectively studied. Maximal (Vol(max)) and minimal (Vol(min)) left atrial volumes were measured using the biplane method of discs and by three-dimensional echocardiographic reconstruction using the cubic spline interpolation algorithm. The passive filling, conduit, and active emptying volumes were also estimated. Traditional measures of atrial function, mitral peak A-wave velocity, velocity time integral (VTI), atrial emptying fraction, and atrial ejection force were measured. RESULTS: As age increased, Vol(max), Vol(min), and total atrial contribution to left ventricle (LV) stroke volume were not significantly altered. However, the passive emptying volume was significantly higher (14.2 +/- 6.4 ml vs. 11.6 +/- 5.7 ml; p = 0.03) whereas the active emptying volume was lower (8.6 +/- 3.7 ml vs. 10.2 +/- 3.8 ml; p = 0.04) in Group Y versus Group O. Pulmonary vein flow demonstrated an increase in peak diastolic velocity (Group Y vs. Group O) with no corresponding change in diastolic VTI or systolic fraction. CONCLUSIONS: Normal aging does not increase maximum (end-systolic) atrial size. The atrium compensates for changes in LV diastolic properties by augmenting active atrial contraction. Pulmonary vein flow patterns, although diastolic dominant using peak velocity, demonstrated no volumetric change with aging.

Adolescent↗
PubMed1988

Functional multiplicity of atrial natriuretic peptide receptors on cultured rat Leydig tumor cells.

Native rat atrial natriuretic peptide (NANP) was shown to bind with high affinity and to increase intracellular levels of cGMP in cultured rat Leydig tumor cells. A linear analog of NANP which lacks the disulfide-linked bridge structure also bound with high affinity but did not increase levels of intracellular cGMP or antagonize the increase of this cyclic nucleotide by NANP. These data are consistent with the existence of two functional subpopulations of ANP receptors on cultured rat Leydig tumor cells; one which is capable of activating guanylate cyclase and one which is not linked to this enzyme.

Amino Acid Sequence↗
PubMed2006

Atrial and ventricular volume and function evaluated by magnetic resonance imaging in patients with persistent atrial fibrillation before and after cardioversion.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and 25% of those >40 years old will experience AF. Left atrial size and left ventricular function are independently related to cardiovascular morbidity and mortality. Our aim was to evaluate cardiac volume and function using magnetic resonance imaging in patients with persistent AF and to describe the changes after cardioversion (CV). Sixty consecutive patients with persistent AF and 19 healthy volunteers had cardiac volumes evaluated by cinematographic breath-hold magnetic resonance imaging. Patients with AF were evaluated before CV and at 1, 30, and 180 days after CV, if still in sinus rhythm. All atrial and ventricular volumes and left ventricular mass decreased and ejection fractions increased significantly after CV (p <0.0001 for all variables). Atrial and ventricular diastolic volumes increased significantly the day after CV. The atrial diastolic volumes had decreased significantly at 30 days and ventricular volumes at 180 days. The atrial systolic volumes decreased significantly the day after CV, but the ventricular systolic volumes remained constant the day after CV and decreased thereafter. Only the right atrial volumes were normalized 180 days after CV. The same results were found in a subgroup of patients with lone AF. In conclusion, reversal of atrial dimensions and function happened earlier than ventricular reversal after CV in persistent AF. Atrial reversal began immediately and ventricular reversal was not seen before 30 days after CV. Our results suggest that the changes to the left atrium and both ventricles caused by AF could be permanent and that CV of AF may be preferable.

Adult↗
PubMed2005

[Effect of atrial fibrillation on left ventricle function in the elderly].

INTRODUCTION: Atrial fibrillation (FA) coexists with heart failure, and its occurrence frequency increases with age. This arrhythmia can precede heart failure as well as can be a consequence of cardiac function deterioration. AIM OF STUDY: The influence of atrial fibrillation on left ventricle (LV) function assessed by echocardiography in the elderly. Investigated group. Study group consists of 30 older patients 75,9 (+/- 4,6) years old with chronic atrial fibrillation, mean duration 319,5 (+/- 292,5) days and 30 younger patients 56,7 (+/- 3,7) years old with atrial fibrillation, mean duration 254,2 (+/- 191,2) days. In control group were 30 persons 74,7 (+/- 5,1) years old with sinus rhythm (SR). In all patients transthoracic (TTE) echocardiography was performed to assess following parameters: end-diastolic diameter of LV (LVEDd), end-systolic diameter of LV (LVESd), fractional shortening of LV (FS LK), stroke volume of LV (SV LK), cardiac output (CO), ejection fraction of LV (EF LK), preejection period of LV (PEP LK), ejection period of LV (LVET), maximal aortic flow velocity (V max LK), maximal velocity of mitral early diastolic flow (E ampl LK), deceleration time of mitral early diastolic flow (E dcct LK). Consequently transoesophageal (TEE) echocardiography was made to record flow in left superior pulmonary vein (LSPV) and following parameters were measured: maximal systolic flow velocity in LSPV (PVS), maximal diastolic flow velocity in LSPV (PVD), integral of systolic flow in LSPV (PVS intg), deceleration time of diastolic flow in LSPV (PVD dcct). During Holter electrocardiographic recording were calculated: maximal heart rate (HR max), minimal heart rate (HR min), mean heart rate (Hr sr). RESULTS: Older patients with atrial fibrillation characterised significantly lower EF LK and FS LK than younger patients and older patients with sinus rhythm. Most of Doppler echocardiographic parameters recorded from aortic flow as well as measured in left superior pulmonary vein have lower values in older patients with arrhythmia compared to younger ones. LVEDd was significantly greater in older patients with atrial fibrillation than in those with sinus rhythm. E ampl LK was markedly lower in older patients with atrial fibrillation and coexisted with shortening deceleration time of this flow in this group of patients. PVD did not differ in studied groups but deceleration time of this flow similarly to deceleration time of mitral flow was markedly shortened in older group of patients with arrhythmia. HR mean and Hr max in older patients with atrial fibrillation were significantly higher in older patients with atrial fibrillation compared to those without arrhythmia whereas HR min did not differ between mentioned groups. HR mean calculated from 24 hours correlated with poorer hemodynamic parameters of left ventricle. CONCLUSIONS: Atrial fibrillation in the elderly causes greater systolic and diastolic dysfunction of left ventricle compared to younger patients with this kind of arrhythmia. The left ventricle contractility deterioration in older patients with atrial fibrillation correlates with high maximal and mean diurnal heart rate.

Aged↗
PubMedDate not supplied

Relationship of left atrial pressure and pulmonary venous flow velocities: importance of baseline mitral and pulmonary venous flow velocity patterns studied in lightly sedated dogs.

Prior clinical and animal studies have shown a markedly different relationship between left atrial pressure and the systolic fraction of pulmonary venous flow but have not discussed possible reasons for this discrepancy. To examine the possibility that these disparate results are due to differences in baseline mitral and pulmonary venous flow velocities, we recorded both velocities with left atrial and left ventricular pressure under different loading conditions in eight lightly sedated normal dogs. With constant atrial pacing at 85 beats/min, mean left atrial pressure was increased from 5.3 +/- 1.1 mm Hg at baseline to 16.1 +/- 1.7 mm Hg with volume and methoxamine infusion (p < 0.05). As left atrial pressure increased, the operating compliance of the left atrium decreased, whereas left atrial volumes and ejection fraction increased. Baseline pulmonary venous diastolic flow velocity was larger than systolic velocity (66 +/- 9 versus 36 +/- 11 cm/sec), with the systolic fraction of pulmonary venous flow 31% +/- 8%. With increasing left atrial pressure, pulmonary venous diastolic velocity did not change, but peak systolic velocity (57 +/- 16 cm/sec) and the systolic fraction (48% +/- 9%) both increased (p < 0.05). Changes in pulmonary venous diastolic flow velocity closely followed changes in early diastolic mitral flow velocity (r = 0.85, p < 0.05). Mean left atrial pressure, or change in mean left atrial pressure, was related to the ratio of pulmonary venous systolic to diastolic velocity time integral (r = 0.59 to 0.62, p < 0.01) and the pulmonary venous systolic fraction (r = 0.58 to 0.60; p < 0.01). When expressed as change from baseline, these variables showed even stronger correlations with left atrial pressure (r = 0.72 to 0.76, p < 0.001). These results are consistent with previous animal and clinical results that indicate pulmonary venous diastolic flow is closely related to early mitral flow velocity, whereas systolic flow is determined primarily by left atrial systolic function. The markedly different relationships observed between left atrial pressure and pulmonary venous systolic flow in animal and clinical studies are most likely due to different baseline flow velocity patterns and differences in left atrial systolic reserve. Future studies investigating these relationships should include data on mitral and pulmonary venous flow velocities as well as left atrial size and systolic function.

Animals↗
PubMed1995

Temporal (circadian) and functional relationship between atrial natriuretic peptides and blood pressure.

Long-acting natriuretic peptide, vessel dilator, and atrial natriuretic factor consisting of amino acids (a.a.) 1 to 30, 31 to 67, and 99 to 126 of the 126-a.a. atrial natriuretic factor (ANF) prohormone, respectively, circulate in humans and have potent vasodilatory properties. To determine if these atrial natriuretic peptides are directly related to blood pressure in clinically healthy normotensive humans, we obtained 24-h profiles of vessel dilator, long-acting natriuretic peptide, ANF, and blood pressure in 10 men in 1988 and 11 men in 1993 (seven men were studied twice) to compare circulating concentrations of atrial natriuretic peptides with naturally occurring changes in blood pressure. Overall, vessel dilator, long-acting natriuretic peptide, and ANF each had significant (p<0.001) circadian rhythms, with peak concentrations late during sleep (at 04:00 h) being nearly twice their concentrations in the afternoon and evening. This high-amplitude circadian change allowed for the refinement of normal limits for ANF peptides by computing 3-hourly tolerance intervals (chronodesms) against which to compare time-specified single samples for normality. Systolic, diastolic, and mean arterial blood pressure also had significant circadian rhythms (p<0.001) with peaks and troughs that were exactly opposite those of the ANF peptides. In addition to this inverse temporal relationship, there was a significant inverse correlation between absolute values for blood pressure and each ANF peptide (p<0.001), implying a functional relationship. These data suggest that in addition to other well-established neurochemical factors, the ANF peptides (vessel dilator, long-acting natriuretic peptide, and ANF) are important for the maintenance of blood pressure and modulation of its circadian rhythm.

Adult↗
PubMed1997

Left atrial appendage "stunning" after electrical cardioversion of atrial flutter: an attenuated response compared with atrial fibrillation as the mechanism for lower susceptibility to thromboembolic events.

OBJECTIVES: This study sought to determine whether left atrial appendage stunning occurs in patients with atrial flutter and to compare left atrial appendage function in the pericardioversion period with that in patients with atrial fibrillation. BACKGROUND: Left atrial appendage stunning has recently been proposed as a key mechanistic phenomenon in the etiology of postcardioversion thromboembolic events in atrial fibrillation. Atrial flutter is thought to be associated with a negligible risk of thromboembolic events; therefore, anticoagulation is commonly withheld before and after cardioversion in these patients. METHODS: Sixty-three patients with atrial flutter (n = 19) or atrial fibrillation (n = 44) underwent transesophageal echocardiography immediately before and after electrical cardioversion. In addition to assessing the presence of thrombus and spontaneous echo contrast, we measured left atrial appendage emptying velocity and calculated shear rates by pulsed wave Doppler and two-dimensional echocardiography. RESULTS: Patients with atrial flutter exhibited greater left atrial appendage flow velocities before cardioversion than those with atrial fibrillation (42 +/- 19 vs. 28 +/- 15 cm/s [mean +/- SD], p < 0.001). Left atrial appendage shear rates were also higher in patients with atrial flutter (103 +/- 82 vs. 59 +/- 37 s-1, p < 0.001). After cardioversion, left atrial appendage flow velocities decreased compared with precardioversion values in patients with atrial fibrillation (28 +/- 15 before to 15 +/- 14 cm/s after cardioversion, p < 0.001) and atrial flutter (42 +/- 19 to 27 +/- 18 cm/s, respectively, p < 0.001). Shear rates decreased from 59 +/- 37 before cardioversion to 30 +/- 31 s-1 after cardioversion in atrial fibrillation (p < 0.001), and from 103 +/- 82 s to 65 +/- 52 s-1, respectively (p < 0.001), in atrial flutter. This decrease in flow velocity from before to after cardioversion occurred in 36 (82%) of 44 patients with atrial fibrillation and 14 (74%) of 19 with atrial flutter. The impaired left atrial appendage function after cardioversion was less pronounced in the group with atrial flutter (27 +/- 18 cm/s for atrial flutter vs. 15 +/- 14 cm/s for atrial fibrillation, p < 0.001). New or increased spontaneous echo contrast occurred in 22 (50%) of 44 patients with atrial fibrillation versus 4 (21%) of 19 with atrial flutter (p < 0.05). CONCLUSIONS: Left atrial appendage stunning also occurs in patients with atrial flutter, although to a lesser degree than in those with atrial fibrillation. These data suggest that patients with atrial flutter are at risk for thromboembolic events after cardioversion, although this risk is most likely lower than that in patients with atrial fibrillation because of better preserved left atrial appendage function.

Aged↗
PubMed1994

Altered left ventricular diastolic function post-atrial pacing in coronary artery disease and left ventricular hypertrophy: further insights by pulmonary venous flow analysis.

Left ventricular filling dynamics during acute pacing-induced myocardial ischaemia were assessed using transoesophageal atrial pacing and simultaneous Doppler measurements of pulmonary venous and mitral flow. All patients (10 with CAD and 12 with left ventricular hypertrophy due to hypertrophic cardiomyopathy; HCM) were in sinus rhythm and patients with mitral insufficiency were excluded. Data were compared with those of a control group (n = 10). Measurements were obtained at baseline (heart rate 84 +/- 14 beats.min-1) and immediately after atrial pacing via the same transoesophageal echocardiography (TEE) probe after stepwise increase of the pacing rate to 133 +/- 12 beats.min-1. Heart rate immediately after pacing was 83 +/- 13 beats.min-1. Time velocity integrals (TVI) were calculated at baseline and after pacing for the following flows: early (E) and late (A) mitral flows, as well as antegrade systolic (S), diastolic (D) and retrograde diastolic (R) pulmonary venous flows. In the control group none of the flow parameters changed significantly after pacing compared with baseline data. In contrast, in CAD patients, the TVI of the E wave, the TVI E/A ratio as well as the pulmonary venous flow changed significantly after pacing (7.3 to 5.5 cm, P < 0.05, 1.7 to 1.1, P < 0.01 and 1.0 to 2.1 cm, P < 0.001, respectively). HCM patients also showed significant changes: TVI E/A ratio post-pacing decreased from 1.9 to 1.4 (P < 0.05), and the pulmonary venous reverse flow integral increased from 1.3 to 2.8 cm (P < 0.0001). Analysis of variance showed the TVI E/A ratio to be significantly dependent on pacing (P = 0.012). The pulmonary venous retrograde flow was found to be influenced by the presence of disease (P = 0.033 before and P = 0.0001 after pacing) and in all cases by pacing (before vs after pacing; P = 0.0001). Pacing resulted in significantly different changes in the TVI E/A ratio and the TVI of the retrograde pulmonary venous flow for CAD and HCM patients compared with those of control subjects. In patients with CAD and HCM, rapid atrial pacing results in a decreased early to late ventricular filling ratio because of impaired relaxation, despite presumably increased filling pressure. Retrograde pulmonary venous flow increased because of increased filling pressure and operating left ventricular stiffness.

Adult↗
PubMed1999

Evaluation of left atrial wall elasticity using acoustic microscopy.

Left atrial wall elasticity is one of the important factors regulating left atrial stiffness and functions. The authors evaluated left atrial wall elasticity by measuring the sound speed through the left atrial wall, based on the hypothesis that high elasticity tissues will yield larger sound speed values through the tissue, and examined age-associated changes in left atrial wall elasticity. Left atrium specimens were obtained from 30 normal subjects (age, 15-95 years) at autopsy. An acoustic microscope, operating at 450 MHz, was used to measure the sound speed in the endocardium and the myocardium of the left atrium. The sound speeds in endocardium and myocardium demonstrated significant correlation with age (r = 0.74, p<0.0001 and r = 0.47, p<0.01, respectively). These findings indicate that left atrial wall elasticity increased with advancing age. These changes may lead to deterioration of left atrial compliance and eventual left atrial failure in older subjects.

Adolescent↗
PubMed1999

Functional studies in atrium overexpressing A1-adenosine receptors.

1. Adenosine and the A1-adenosine receptor agonist R-PIA, exerted a negative inotropic effect in isolated, electrically driven left atria of wild-type mice. 2. In left atria of mice overexpressing the A1-adenosine receptor, adenosine and R-PIA exerted a positive inotropic effect. 3. The positive inotropic effect of adenosine and R-PIA in transgenic atria could be blocked by the A1-adenosine receptor antagonist DPCPX. 4. In the presence of isoprenaline, adenosine exerted a negative inotropic effect in wild-type atria but a positive inotropic effect in atria from A1-adenosine receptor overexpressing mice. 5. The rate of beating in right atria was lower in mice overexpressing A1-adenosine receptors compared with wild-type. 6. Adenosine exerted comparable negative chronotropic effects in right atria from both A1-adenosine receptor overexpressing and wild-type mice. 7. A1-adenosine receptor overexpression in the mouse heart can reverse the inotropic but not the chronotropic effects of adenosine, implying different receptor-effector coupling mechanisms.

Adenosine↗
PubMed2001

Radiofrequency modified maze in patients with atrial fibrillation undergoing concomitant cardiac surgery.

OBJECTIVE: In the majority of patients with chronic atrial fibrillation the arrhythmia will persist after correction of the underlying structural abnormality. The maze procedure is an effective surgical method to eliminate atrial fibrillation and to restore atrial contractility. METHODS: In this study we used radiofrequency energy to create lines of conduction block in both atria during cardiac surgery as a modification of the maze III procedure. One hundred twenty-two patients with atrial fibrillation for at least 1 year and structural heart disease underwent open heart operation and a radiofrequency modified maze procedure. RESULTS: In 108 (89%) of 122 patients mitral valve surgery was performed, and in this group 86 patients (80%) underwent 121 concomitant procedures. Fourteen patients (11%) underwent cardiac surgery not involving the mitral valve. The additional crossclamp time required for the left atrial part of the radiofrequency modified maze procedure was 14 +/- 3 minutes. The in-hospital mortality rate was 4.1%. The overall 39-month survival was 90%, and freedom of atrial flutter or atrial fibrillation was 78.5% +/- 5.1%. Eighty-nine survivors with sinus, atrial rhythm, or atrioventricular sequential pacemaker had Doppler echocardiography, and right atrial transport function was documented in 83% and left atrial transport function in 77% of patients. CONCLUSION: We concluded that the radiofrequency modified maze procedure as an adjunctive procedure is safe, time-sparing, and effective in eliminating atrial fibrillation and restoring atrial transport function.

Aged↗
PubMed2002

Reversal of atrial mechanical stunning after cardioversion of atrial arrhythmias: implications for the mechanisms of tachycardia-mediated atrial cardiomyopathy.

BACKGROUND: Atrial mechanical stunning develops on termination of chronic atrial arrhythmias and is implicated in the genesis of thromboembolic complications after cardioversion. The mechanisms responsible for atrial mechanical stunning are unknown. The effects of atrial rate, isoproterenol, and calcium on atrial mechanical function in patients with atrial stunning have not been evaluated, and it is not known if atrial stunning can be reversed. METHODS AND RESULTS: Thirty-five patients with chronic atrial flutter (AFL) undergoing radiofrequency ablation were studied. Fifteen patients in sinus rhythm undergoing ablation for paroxysmal AFL were studied as control for effects of the procedure. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AFL, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol or calcium. With termination of AFL, LAAEV decreased from 59.0+/-3.7 cm/s to 18.8+/-1.4 cm/s (P<0.0001) and LASEC grade increased from 0.9+/-0.1 to 2.2+/-0.2 (P<0.0001). Pacing increased LAAEV to a maximum of 38.4+/-3.2 cm/s (P<0.0001) and reduced LASEC grade to 1.9+/-0.2 (P=0.005). Isoproterenol and calcium reversed atrial mechanical stunning with LAAEV increasing to 89.3+/-12.6 cm/s (P=0.0007) and 50.2+/-10.5 cm/s (P=0.005), respectively, and LASEC grade decreasing to 0.2+/-0.1 (P=0.001) and 1.4+/-0.2 (P=0.01), respectively. The postpacing pause increased LAAEV to 69.3+/-3.7 cm/s (P<0.0001). No change in LAAEV was observed in the paroxysmal AFL group. CONCLUSION: Atrial mechanical stunning can be reversed by pacing at increased rates and through the administration of isoproterenol or calcium. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium as a result of chronic atrial flutter.

Atrial Flutter↗
PubMed1979

Ultrastructure and possible function of an atrial paraganglion not directly related to atrial ganglion in the albino mouse.

The ultrastructure of a paraganglion found in right atrium of albino mouse close to the superior cava vein is described. A capillary, which occupied the central part of the paraganglion, was surrounded by three chromaffin cells. Two other chromaffin cells were also present, but neither nerve fibers nor nerve endings were seen. The possible physiological role of paraganglia is discussed.

Albinism↗
PubMed1991

Modulation of acetylcholine-activated K+ channel function in rat atrial cells by phosphorylation.

1. In voltage-clamped whole cells dialysed with GTP, extracellular application of ACh elicits an inwardly rectifying K+ current which subsequently decreases to a steady-state level well below the maximally induced current (desensitization). The mechanism of desensitization of the acetylcholine (ACh)-activated K+ channel current was studied in rat neonatal atrial cells at the single-channel level using the patch-clamp technique. 2. In cell-attached patches with ACh in the pipette, a similar pattern of K+ channel current desensitization was present. Single-channel analyses revealed that the initial rapid decrease in channel activity was associated with progressive shortening of the mean open time (tau o) and prolongation of the mean closed time (tau c) of the K+ channel. 3. In excised, inside-out patches with ACh in the pipette, GTP activated K+ channels with a tau o of approximately 1.0 ms. Addition of ATP to the cytosolic surface resulted in progressive increases in tau o (from 1 to 5 ms) and channel activity. These changes are similar but opposite in direction to those observed during the early phase of ACh-induced channel desensitization in cell-attached patches. 4. The effect of ATP on the channel kinetics was abolished in Mg(2+)-free solution AMP-PNP (adenylyl-imidodiphosphate, a non-hydrolysable analogue of ATP), ADP, CTP (cytidine triphosphate), ITP (inosine triphosphate) or UTP (uridine triphosphate) did not alter the channel kinetics, suggesting that the ATP effect on channel gating probably occurs via phosphorylation by a membrane-bound kinase. H-8 (an isoquinolinesulphonamide derivative which inhibits protein kinases A and C) failed to prevent the action of ATP on the channel. 5. The increases in tau o and channel activity produced by ATP could be completely reversed by an elevation of cytosolic [Ca2+] to 3 x 10(-5) M or above. 6. The effect of Ca2+ on the ATP-induced changes in channel kinetics was blocked by sodium vanadate, a general phosphatase inhibitor. Okadaic acid, an inhibitor of protein phosphatase 1 and 2A, did not block the Ca2+ effect. Calmodulin antagonists, N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7), trifluoroperazine, and calmidazolium, partially blocked the effect of Ca2+. 7. Alkaline phosphatase (20 units/ml) reversed the ATP-induced increases in tau o and channel activity. These results suggest that the ACh-activated K+ channel can be modulated by phosphorylation and dephosphorylation.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗