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Results for “Atrial Function, Right”

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PubMed2002

Bi-atrial mapping of atrial arrhythmias.

Cardiac mapping of atrial activation was originally performed in animals during open chest preparations, using epicardial electrodes. The development of endocardial egg-shaped multiple electrodes provided detailed assessment of the minimum number of wavelengths required to sustain atrial fibrillation (AF), as well as the role of interatrial connections during AF. Subsequently, several studies on bi-atrial epicardial high-density mapping in animals and humans also reported on the importance of interatrial connections, as well as the specific characteristics of the left atrium as compared with the right atrium during chronic AF. Endocardial bi-atrial mapping studies using electrode catheters were reported using basket-shaped catheters carrying 64 electrodes. Animal studies suggested that septal activation was asynchronous and discordant, while a human study outlined the multiple origins of atrial ectopic beats following DC cardioversion in patients with chronic atrial fibrillation. The advent of non-fluoroscopic mapping systems significantly changed our approach to percutaneous endocardial mapping. Simultaneous bi-atrial studies using electroanatomic mapping were performed in sinus rhythm as well as in atrial flutter. These studies demonstrated the predominance of interatrial conduction over Bachmann's Bundle and the coronary sinus-left atrial connection during respectively, sinus rhythm and atrial flutter. Simultaneous bi-atrial non-contact mapping was initially performed during porcine studies and later in humans, demonstrating asynchronous and discordant septal activation both during sinus rhythm or left lateral atrial pacing. Preliminary studies from simultaneous bi-atrial non-contact mapping in humans in whom AF occurred spontaneously or was induced suggests three main types of atrial activation, consisting of left atrial drivers causing the right atrium to fibrillate following conduction over interatrial connections, the right atrium independently sustaining AF, even after pulmonary vein disconnection, and both atria fibrillating independently without activation over interatrial connections. Bi-atrial mapping has been essential for our understanding of normal and abnormal atrial activation, and ultimately may provide new approaches for ablation of atrial fibrillation.

Animals↗

PubMed2004

Catheter-based impedance measurements in the right atrium for continuously monitoring hematocrit and estimating blood viscosity changes; an in vivo feasibility study in swine.

Hematocrit is the most important determinant of whole blood viscosity and it affects thrombosis. As hematocrit can be measured accurately in vitro by using an electrical impedance technique, aim of the present study is to investigate the diagnostic potential of using this technique in vivo to continuously monitor hematocrit. Characteristics of a special catheter for in vivo measurement of electrical resistivity in blood in the right atrium are described. In five anesthetized swine hematocrit is monitored continuously with this catheter while different levels of hemoconcentration are induced. In addition, blood viscosity is increased by inducing 'acute phase' reaction the day before surgery, resulting in variable degree of elevated fibrinogen levels in the five swine. Good reproducibility of the resistivity measurements (S.D < 0.01) and excellent correlation between resistivity data in vivo and hematocrit levels in each swine are found (r2 = 0.95-0.99). Furthermore, stepwise regression analysis of data from all swine shows a highly significant contribution also of other important parameters of blood viscosity, such as fibrinogen, total protein and temperature (cumulative r2 = 0.97). Determining hematocrit continuously in vivo by electrical resistivity measurements with a catheter in the right atrium is feasible and these measurements correlate significantly also with other important parameters of blood viscosity.

Animals↗

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↗

PubMed1995

Tetralogy of Fallot in adults--107 cases.

Clinical and haemodynamic profile of 107 adult patients above the age of 15 years with TOF was analysed. Cardiac catherization and selective cine-angiography were performed in all cases. Infundibular pulmonary stenosis, mal-alignment type of ventricular septal defect, mitral-aortic fibrous continuity and equal systolic pressures in both the ventricles and aorta were considered mandatory for the diagnosis of Tetralogy of Fallot. Aortic regurgitation was seen in 26 cases (24%), tricuspid regurgitation in 22 cases (21%), absent pulmonary valve in 3 cases (3%), branch pulmonary artery stenosis in 9 case (8.4%), major aortopulmonary collaterals in 15 cases (14%), right atrial pressure was more than 10 mmHg in 10 cases (11%) and right ventricular end diastolic pressure more than 9 mmHg in 73 cases (68%). The left ventricular end diastolic pressure was above 13 mmHg in 58 cases (54%).

Adolescent↗

PubMed1997

Right ventricular function in human sepsis: a thermodilution study.

STUDY OBJECTIVE: To assess the relations among right ventricular (RV) pressures and volumes in sepsis. DESIGN: Prospective study. SETTING: ICU. PATIENTS: Eighteen patients with sepsis who were in hemodynamically stable condition. INTERVENTION: Stepwise increases and decreases in RV end-diastolic volume (EDV) as induced by military antishock trousers (MAST) inflation of 0, 15, 30, 50 and then 0 mm Hg over 15-min intervals. MEASUREMENTS AND RESULTS: RV volumes and pressures were measured using a rapid response thermistor pulmonary arterial catheter based on RV ejection fraction (RVEF) calculations. RV EDV was estimated as stroke volume (SV)/RVEF, while RV end-systolic volume (ESV) was estimated as EDV-SV. Right atrial pressure (Pra) was taken as end-diastolic pressure, and pulmonary artery pressures (Ppa), both mean and end-systolic, were used as RV ejection pressures. MAST inflation to 15 mm Hg had no measurable effects on the measured variables. However, inflation to 30 and 50 mm Hg increased Pra, both mean and end-systolic Ppa, EDV, and ESV, whereas SV and RVEF remained unchanged. The relation between either Pra and EDV (r=0.33) or the change in Pra and EDV, mean or end-systolic Ppa and ESV (r=0.5 and 0.28, respectively), or the change in mean or end-systolic Ppa and ESV for both the group and individual subjects was poor. Furthermore, SV correlated poorly with EDV (r=0.32), while RVEF correlated better with both EDV and ESV (r=-0.41 and -0.69, respectively), although it showed no definable relation to mean or end-systolic Ppa. However, both absolute and relative changes in EDV corresponded closely with respective ESV values (r=0.93). CONCLUSIONS: During sepsis, RV EDV and ESV vary independently of changes in Pra and ejection pressure. These data can be explained by assuming that the RV is a highly compliant chamber during filling, such that changes in RV EDV do not alter RV wall stress (preload) or ejection efficiency (RVEF). Thus, changes in RV EDV should proportionally alter RV ESV. Furthermore, the slope of the ESV/EDV relation should be inversely proportional to ejection efficiency.

Adult↗

PubMed1993

Pulsed Doppler echocardiographic assessment of portal venous flow patterns in patients after the Fontan operation.

OBJECTIVE: To assess the effect of the condition of the right heart after the Fontan operation on portal venous flow, and to determine whether the characteristics of portal venous flow were different when there was an atriopulmonary connection with atrial septal closure rather than an atriopulmonary or total cavopulmonary connection with intra-atrial routing. PATIENTS AND METHODS: After the Fontan operation six patients with an atriopulmonary connection (group 1), three patients with an atriosubpulmonary connection (group 2), four patients with intra-atrial routing and an atriopulmonary connection (group 3), and five patients with a total cavopulmonary connection (group 4) were studied by pulsed Doppler echocardiography. The flow signals were recorded for the pulmonary artery, hepatic vein, and intrahepatic portal vein in each patient. Postoperative cardiac catheterisation was performed in 16 of the 18 patients. The Doppler findings were compared with those of 14 controls. RESULTS: The portal flow was pulsatile in 13 patients and constant in five patients. Reversed flow was shown at or just after the QRS wave after hepatic venous regurgitation in two group 1 patients. The flow signal was interrupted in two group 1 patients and two group 2 patients. Decrease in velocity of flow was recorded in two group 1 patients, one group 2 patients, three group 3 patients, and one group 4 patient. Portal flow was constant in one group 3 patient and four group 4 patients. The pulsatility ratio ranged from -0.46 to 0.49 (mean (SD), 0.03 (0.32)) in the patients from group 1 and 2, from 0.41 to 0.76 (0.54 (0.15)) in group 3, and from 0.70 to 0.80 (0.75 (0.04)) in group 4. The ratio in the controls ranged from 0.29 to 0.83 (0.61 (0.13)). The ratio was significantly lower in groups 1 and 2 than in group 3 (p < 0.01), group 4 (p < 0.01), or the controls (p < 0.005). There was no significant difference in the ratio between group 3 and group 4 and no correlation between the pulsatility ratio and the cardiac index (r = 0.26), mean right atrial pressure (r = 0.25), or pulmonary vascular resistance (r = 0.17). CONCLUSION: The larger hepatic venous regurgitation caused by atrial contraction in patients with an atriopulmonary connection correlated with the higher portal pulsatility and a total cavopulmonary connection reduced portal pulsatility.

Atrial Function, Right↗

PubMed1998

[Large right atrial aneurysm: rare cause of recurrent pulmonary embolism].

Case report on a 72 year old female patient presenting with collapse and progressive dyspnea. X-ray of the chest showed a marked enlargement of the heart extending to the right. Echocardiography revealed an impressive displacement of the heart chambers to the left caused by a large aneurysm (11 x 5 x 5 cm) located anteriorly and medially from the right heart communicating with the right atrium. Pronounced compression of the basal part of the right ventricle was present. Within the aneurysmatic cavity several highly mobile thrombi and extensive spontaneous echo contrast were demonstrated. On magnetic resonance imaging and right heart angiocardiography the aneurysm was visualized as well. Coronary angiography revealed a marked curved displacement of the right coronary artery to the left side. Perfusion lung scanning suggested bilateral segmental pulmonary embolism proven by digital substraction angiography. With long-term oral anticoagulation the patient remained symptom-free during follow-up of now more than four years.

Aged↗

PubMed1995

Further evidence from functional studies for somatostatin receptor heterogeneity in guinea-pig isolated ileum, vas deferens and right atrium.

1. Somatostatin (SRIF) causes a concentration-dependent inhibition of neurotransmission in guinea-pig ileum and vas deferens as well as negative inotropy in guinea-pig isolated right atrium. The SRIF receptors mediating these effects have now been further characterized by use of the peptides BIM-23027, BIM-23056 and L-362855, reported as selective for the recombinant SRIF receptor types, sst2, sst3 and sst5, respectively. 2. BIM-23027 was a highly potent agonist at causing an inhibition of neurotransmission in the guinea-pig ileum (EC50 value 1.9 nM), being about 3 times more potent than SRIF (EC50 value 6.8 nM). In contrast, in both guinea-pig vas deferens and right atrial preparations, BIM-23027 was a relatively weak agonist being at least 30-100 times weaker than SRIF. In guinea-pig atria, BIM-23027 (3 microM) antagonized the negative inotropic action of SRIF28 (apparent pKB = 5.9 +/- 0.1) but had no effect on the negative inotropic action of cyclohexyladenosine. 3. The inhibitory effect of BIM-23027 in the guinea-pig ileum was readily desensitized. Prior exposure to BIM-23027 (0.3 microM) markedly attenuated the inhibitory effect of SRIF but had no effect on the inhibitory action of clonidine suggesting that BIM-23027 and SRIF act via a common receptor mechanism. 4. L-362855 caused a concentration-dependent inhibition of neurotransmission in both the guinea-pig ileum and vas deferens as well as causing negative inotropy in the guinea-pig atrium but was at least 30-100 times weaker than SRIF. In guinea-pig isolated atria, L-362855 (3 microM) did not antagonize the negative inotropic action of SRIF28. 5. BIM-23056 in concentrations up to 1 microM was inactive as an agonist in guinea-pig isolated ileum, vas deferens and atrium and did not antagonize the inhibitory actions of SRIF in any of these preparations.6. The results from this study support our previous contention that the sst2 receptor type mediates inhibition of neurotransmission by SRIF in the guinea-pig ileum. The SRIF receptor type mediating inhibition of neurotransmission in the guinea-pig vas deferens appears different, but similar, to that mediating negative inotropy in the atrium. However the characteristics of these latter receptors appear different from that of the recombinant sst2, sst3 and sst5 receptors for SRIF described for rat and man.

Animals↗

PubMedDate not supplied

Electrophysiological characteristics of the human atria after cardioversion of persistent atrial fibrillation.

BACKGROUND: In animal models, induced atrial fibrillation shortens the atrial effective refractory period (ERP) and reverses its physiological adaptation to rate. It is not clear whether this process, known as "electrical remodeling," occurs in humans. METHODS AND RESULTS: We determined the ERPs, at 5 pacing cycle lengths (300 to 700 ms) and in 5 right atrial sites, after internal cardioversion of chronic atrial fibrillation in 25 patients (14 in pharmacological washout and 11 on amiodarone). The ERPs were 195.5+/-18.8 ms in the washout and 206.3+/-17.9 ms in the amiodarone patients (P<0.0001). ERPs were closely correlated with the stimulation rates (r=0.95 in the washout and r=0.94 in the amiodarone group), and slope values indicating a normal (>/=0.07) or nearly normal (0.05 to 0.06) adaptation of ERP to rate were found in 77% of the 84 paced sites. The mean ERP was shorter in the lateral wall (198.1+/-17.9 ms) than in the atrial roof (203.3+/-21.5 ms) and in the septum (210.5+/-20.0 ms) (P<0.03). After 4 weeks of sinus rhythm, the mean ERP, determined again in 8 patients (4 in wash-out and 4 on amiodarone), was significantly increased compared with the basal study (221. 4+/-21.4 versus 197.8+/-18.3 ms, P<0.0001). CONCLUSIONS: After cardioversion of chronic atrial fibrillation, (1) atrial ERP adaptation to rate was normal or nearly normal in the majority of the cases, (2) a significant dispersion of refractoriness between different right atrial sites was present, and (3) ERPs were significantly increased after 4 weeks of sinus rhythm in both washout and amiodarone patients.

Adaptation, Physiological↗

PubMed2002

The impact of right atrial ischemia on inferior myocardial infarction with extension to right ventricle: transesophageal echocardiographic examination.

BACKGROUND: The role of the right atrium in adaptation to the hemodynamic changes produced by extension of myocardial infarction (MI) of the left ventricular inferior wall to the right ventricle is fundamental. HYPOTHESIS: The aim of this study was analyze a group of patients with MI with extension of right chambers, and particularly right atrial alterations, by transesophageal echocardiography and to correlate it with clinical and angiographic variables. METHODS: Thirty patients with right ventricular (RV) MI involving obstruction of the right coronary artery without stenosis of the left coronary artery were included; 18 underwent early reperfusion. Transesophageal echocardiography was performed on all within 5 days of coronary angiography. Follow-up was continued from hospitalization to the present. RESULTS: When patients with right atrial ischemia were compared with those with normal right atrium, the RV wall movement score was significantly greater in the group with right atrial ischemia, severe RV dilatation was more frequent, and association with proximal occlusion of the artery responsible for the MI, as well as absence of right atrial branches and poor collateral circulation, were significant. Hospitalization was more prolonged in this group, and there was a higher incidence of arrhythmias, complete atrioventricular block, and mortality. CONCLUSIONS: Right atrial ischemia associated with RV infarction leads to a higher incidence of complications and higher mortality. Transesophageal echocardiography is a safe, reproducible technique that provides detailed anatomic information about right chambers and aids in the determination of prognosis and therapeutic decisions.

Adult↗

PubMed1993

Simultaneous epicardial and endocardial activation sequence mapping in the isolated canine right atrium.

BACKGROUND: Since the atria are thin-walled structures, most studies that have examined the spread of activation in the atria have assumed that they behave electrophysiologically as a two-dimensional surface. It was the objective of this study to determine whether or not this assumption is true by simultaneously mapping the epicardial and endocardial activation sequences in the right atrium. METHODS AND RESULTS: Identical precisely superpositioned epicardial and endocardial electrode templates with 250 unipolar electrodes each were used to map the isolated canine right atrium (n = 8) during continuous perfusion and superfusion with Krebs-Henseleit buffer. Data were recorded during control conditions (normal sinus rhythm), continuous pacing (S1S1 = 300 msec), and premature stimulation (S1S2 = effective refractory period + 5 msec). Pacing was performed at two sites, one located on the inferior crista terminalis and one lateral to the crista terminalis on a pectinate muscle. Tachyarrhythmias were induced by a single extrastimulus during the continuous perfusion of acetylcholine (10(-3.5) mol/L). Individual electrode sites were correlated with the gross anatomy and histology. Activation time differences were calculated between each two corresponding epicardial and endocardial sites. There were differences in the activation times between the epicardium and endocardium during all experimental conditions. However, the average difference for each condition was < 1 msec, suggesting that overall activation did not spread faster on either the epicardium or the endocardium, even though in certain regions one surface could lead the other. The dispersion of time differences was smallest during normal sinus rhythm and continuous pacing (SD = 5.6-5.8 msec) and largest after premature stimulation (SD = 6.3 msec for crista pacing, p < 0.05; SD = 8.1 msec for pacing lateral to the crista, p < 0.001). Differences in the activation sequence correlated with the underlying anatomic architecture. The largest differences in activation times between the epicardium and endocardium were associated with those regions of the atrium where pectinate muscles ran below the epicardial surface. The pectinate muscles in those areas were often discontinuous with the epicardial surface and facilitated the discordant epicardial-endocardial activation. The discordant activation was also found in regions where the atrial wall thickness was < 0.5 mm and correlated with transmural differences in fiber orientation. A tachyarrhythmia induced in the presence of acetylcholine, which demonstrated a focal activation pattern, was shown to have a reentrant loop that used free-running muscle bundles connecting the epicardial and endocardial surfaces, resulting in a three-dimensional pathway. CONCLUSIONS: The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

Animals↗

PubMed1994

Effects of pimobendan on isolated human right atria strips and on isolated left atria of the rat.

The present study describes the effects of pimobendan on isolated human right atrial strips and on isolated left atria of the rat. Pimobendan induces a positive inotropic effect both in human and rat preparations. The maximal increase (28 +/- 2.0%) obtained with pimobendan in the strips from human right atria was similar to that obtained in left atria of the rat (31 +/- 1.8%). These observations may have some clinical relevance as pimobendan might prove to be an alternative to catecholamines for inotropic support in patients who undergo general anaesthesia.

Animals↗

PubMed2002

Bucindolol exerts agonistic activity on the propranolol-insensitive state of beta1-adrenoceptors in human myocardium.

In congestive heart failure patients, treatment with beta-adrenoceptor antagonists improves symptoms and decreases mortality. However, intrinsic sympathomimetic activity of beta-adrenoceptor antagonists might be disadvantageous in chronic heart failure. The nonselective beta1- and beta2-adrenoceptor antagonist bucindolol has failed to decrease mortality in clinical trials. A putative beta4-adrenoceptor, which mediates positive inotropic effects by activation of the adenylate cyclase has been described. Recently, this putative beta4-adrenoceptor has been identified to be a propranolol-insensitive state of the beta1-adrenoceptor. The present study aimed to characterize whether bucindolol exhibits agonistic activity on this atypical beta1-adrenoceptor state as one possible reason for clinical inefficiency. For comparison (S)-4-(3'-t-butylamino-1'-hydroxypropoxy)-benzimidozole-2 (CGP 12177), metoprolol, and nebivolol were investigated. Bucindolol did not reveal intrinsic sympathomimetic activity in electrically driven (1 Hz, 37 degrees C), forskolin-stimulated, left ventricular papillary muscle strips (donor hearts, nonfailing; n = 5) and in right auricular trabeculae (bypass operation; n = 4). Functional studies on the propranolol-insensitive state of beta1-adrenoceptors were performed in isolated muscle preparations after beta1- and beta2-adrenoceptor antagonism (propranolol, 1 microM), inhibition of beta3-mediated inotropic effects (N-nitro-L-arginine, 100 microM) and forskolin treatment (0.3 microM). Positive inotropic response to stimulation of atypical state beta1-adrenoceptors could be demonstrated in right auricular as well as left ventricular human myocardium (CGP 12177 treatment, 10 microM). Under these conditions, also bucindolol, but not metoprolol and nebivolol, significantly increased contractility (all 10 microM). In conclusion, bucindolol but not metoprolol or nebivolol mediate positive inotropic effects in human myocardium due to activation of atypical state beta1-adrenoceptors. Thus, the agonistic activity of bucindolol may influence outcome in heart failure patients.

Adrenergic beta-Agonists↗

PubMed2005

Improvement in sympatho-vagal imbalance and heart rate variability in patients with mitral stenosis after percutaneous balloon commissurotomy.

Elevated sympathetic nerve activity in patients with mitral stenosis (MS) may be an index of the severity of the disease. Percutaneous mitral balloon commissurotomy (PMBC) is now a standard treatment for many patients with symptomatic MS. We aimed to show the effects of PMBC on autonomic nervous system activity in the patients with MS by heart rate variability (HRV) analysis. Fifty-four consecutive patients with mitral stenosis and sinus rhythm who underwent percutaneous mitral commissurotomy were enrolled. Apart from significant haemodynamic improvements, mean heart rate (HR), LF day, LF night, LF/HF day and night significantly decreased and SDNN, RMSSD, PNN50, HF day and night significantly increased in the early period after PMBC and these changes were preserved for up to one month. SDNN was positively correlated with left ventricle ejection fraction (LVEF) but negatively correlated with mean valve area (MVA), left atrial (LA) diameter and pressure, right atrial (RA) pressure; LF/HF day ratio was positively correlated with LA diameter and pressure, mean transmitral gradient and negatively correlated with LVEF; LF/HF night ratio was positively correlated with LA pressure and mean transmitral gradient. The increase in SDNN was correlated with the change in LA and RA pressure. The decrease in LF/HF ratio after PMBC was significantly correlated with the changes in the mean transmitral gradient, LA pressure and RA pressure. As a result, the heart rate variability and autonomic nervous system function in patients with mitral stenosis are correlated with the atrial pressures and left ventricular function. These parameters significantly change in the early period after PMBC and are preserved at one month. The improvement in the heart rate variability and sympatho-vagal balance are significantly affected by the early changes in atrial pressures after PMBC.

Adult↗

PubMed1998

"Cristal tachycardias": origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography.

OBJECTIVES: We sought to use intracardiac echocardiography (ICE) to identify the anatomic origin of focal right atrial tachycardias and to define their relation with the crista terminalis (CT). BACKGROUND: Previous studies using ICE during mapping of atrial flutter and inappropriate sinus tachycardia have demonstrated an important relation between endocardial anatomy and electrophysiologic events. Recent studies have suggested that right atrial tachycardias may also have a characteristic anatomic distribution. METHODS: Twenty-three consecutive patients with 27 right atrial tachycardias were included in the study. ICE was used to facilitate activation mapping in relation to endocardial structures. A 20-pole catheter was positioned along the CT under ICE guidance. ICE was also used to assist in guiding detailed mapping with the ablation catheter in the right atrium. RESULTS: Of 27 focal right atrial tachycardias, 18 (67%, 95% confidence interval [CI] 46% to 83%) were on the CT (2 high medial, 8 high lateral, 6 mid and 2 low). ICE identified the location of the tip of the ablation catheter in immediate relation to the CT in all 18 cases. The 20-pole mapping catheter together with echocardiographic visualization of the CT provided a guide to the site of tachycardia origin along this structure. Radiofrequency ablation was successful in 26 (96%) of 27 (95% CI 81% to 100%) right atrial tachycardias. CONCLUSIONS: This study demonstrates that approximately two thirds of focal right atrial tachycardias occurring in the absence of structural heart disease will arise along the CT. Recognition of this common distribution may potentially facilitate mapping and ablation of these tachycardias.

Adolescent↗

PubMed1993

Effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances.

The effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances were examined in two groups of seven barbiturate-anesthetized open-chest pigs. Atrial diameters and pressures were recorded during atrioventricular (AV) pace and thereafter during atrial fibrillation. Both rhythms were studied with constant ventricular rate after complete AV block. Left atrial maximal diameter, which appeared at the end of the atrial filling phase, decreased from 32.4 (28.9-36.7; median and 95% confidence interval) to 31.3 (28.4-35.7) mm after induction of atrial fibrillation. The right atrial maximal diameter also decreased, although not significantly. Atrial pressure at the peak of the v wave rose from 7.0 (5.5-8.5) to 9.6 (8.3-11.2) mmHg in the left atrium and from 5.0 (4.3-5.6) to 7.3 (6.2-8.7) mmHg in the right atrium. Left and right atrial chamber stiffness constants increased from 0.25 (0.19-0.48) to 0.41 (0.28-0.66) mm-1 and from 0.21 (0.11-0.31) to 0.33 (0.30-0.39) mm-1, respectively. Instantaneous diastolic atrial compliance decreased in both atria after induction of atrial fibrillation. Thus, during atrial fibrillation with regular ventricular rate, changes in atrial diameter, pressure, and compliance take place.

Animals↗

PubMed1999

Evaluation of right atrial appendage blood flow by transesophageal echocardiography in subjects with a normal heart.

Right atrial appendage (RAA) blood flow pattern was analyzed in 42 normal subjects-without cardiovascular disease (aged 30 to 48 years, mean 40 +/- 6) who underwent transesophageal echocardiography. RAA flow pattern was demonstrated to be bi-, tri- or quadriphasic and heart rate dependent (p < 0.01) in this study. In 15 subjects (36%), a biphasic pattern was observed. A triphasic pattern was observed in 12 subjects (28%). Fifteen subjects (36%) had a quadriphasic pattern. In these subjects, we observed a pattern consisting of two diastolic forward flow waves, each followed by a backward flow wave. Mean heart rates among subjects with bi-, tri- and quadriphasic patterns were 110 +/- 6, 91 +/- 4 and 72 +/- 13 beats/min, respectively. In the triphasic pattern, the onset of superior vena cava diastolic forward flow began 18 +/- 4 ms after the onset of tricuspid E wave, whereas the first diastolic forward flow wave in the RAA began 40 +/- 7 ms after onset of the tricuspid E wave. A similar relation was also noted in the quadriphasic pattern. This sequence was constant and independent of heart rate (p < 0.05), suggesting a temporal relation between right ventricular relaxation and the first diastolic forward flow wave in the RAA. In normal subjects, the RAA flow pattern is heart rate dependent and three distinct flow patterns can be differentiated. Right ventricular relaxation appears to induce both the superior vena cava diastolic forward flow wave and the first diastolic forward flow wave of the RAA. These results can be used for comparison with patterns found in disease states.

Adult↗

PubMed1982

[Study on tricuspid regurgitation in Ebstein's anomaly using pulsed Doppler technique combined with two-dimensional echocardiography].

To investigate the localization of tricuspid regurgitant flow in Ebstein's anomaly, pulsed Doppler echocardiography (PDE) was performed on nine patients with or without associated cardiac lesions. The equipment used was characterized by the real time frequency analysis of Doppler signals obtained from the sampling sites confirmed on the cross-sectional images. We employed the apical four-chamber view or right ventricular inflow view in order to facilitate the sampling of Doppler signals from the three-sided heart chambers of this lesion. Doppler signals were recorded from several points in the functional right ventricle, atrialized right ventricle and right atrium. The PDE recording was made in conjunction with M-mode echocardiography at a paper speed of 50 mm per second. In eight of the nine patients, a systolic disturbed flow of wide band pattern was maximally located in the atrialized right ventricle in the vicinity of the tricuspid valve leaflets and had a delayed onset, which were seemed to be the findings characteristic of tricuspid regurgitation in Ebstein's anomaly. In the remaining one, a turbulent flow due to this lesion was obscured by a systolic jet of the associated ventricular septal defect in the vicinity of the tricuspid valve leaflet. In the right atrium, no disturbed flow of wide band pattern existed or only a faint abnormal blood flow was observed during systole. In the functional right ventricle, a smooth blood flow of the right ventricular inflow was recognized in diastole. In contrast, 15 patients with secondary tricuspid regurgitation revealed a holosystolic disturbed flow of wide band pattern maximally in the right atrium in the vicinity of the tricuspid valve leaflets. In eight healthy subjects, there was no systolic disturbed flow in the right atrium. Pulsed Doppler technique combined with two-dimensional echocardiography is thought useful to detect the localization of the disturbed flow in Ebstein's anomaly, thus contributing to the differentiation of various causes of tricuspid regurgitation.

Adult↗