Left Atrial Volume Overload Research Articles

The hemodynamic and atrial electrophysiologic consequences of chronic left atrial volume overload in a controllable canine model

ObjectiveThe purpose of this study was to determine the effects of chronic left atrial volume overload on atrial anatomy, hemodynamics, and electrophysiology using a titratable left ventriculoatrial shunt in a canine model. MethodsCanines (n = 16) underwent implantation of a shunt between the left ventricle and the left atrium. Sham animals (n = 8) underwent a median sternotomy without a shunt. Atrial activation times and effective refractory periods were determined using 250-bipolar epicardial electrodes. Biatrial pressures, systemic pressures, left atrial and left ventricle diameters and volumes, atrial fibrillation inducibility, and durations were recorded at the initial and at 6-month terminal study. ResultsBaseline shunt fraction was 46% ± 8%. The left atrial pressure increased from 9.7 ± 3.5 mm Hg to 13.8 ± 4 mm Hg (P < .001). At the terminal study, the left atrial diameter increased from a baseline of 2.9 ± 0.05 cm to 4.1 ± 0.6 cm (P < .001) and left ventricular ejection fraction decreased from 64% ± 1.5% to 54% ± 2.7% (P < .001). Induced atrial fibrillation duration (median, range) was 95 seconds (0-7200) compared with 0 seconds (0-40) in the sham group (P = .02). The total activation time was longer in the shunt group compared with the sham group (72 ± 11 ms vs 62 ± 3 ms, P = .003). The right atrial and not left atrial effective refractory periods were shorter in the shunt compared with the sham group (right atrial effective refractory period: 156 ± 11 ms vs 141 ± 11 ms, P = .005; left atrial effective refractory period: 142 ± 23 ms vs 133 ± 11 ms, P = .35). ConclusionsThis canine model of mitral regurgitation reproduced the mechanical and electrical remodeling seen in clinical mitral regurgitation. Left atrial size increased, with a corresponding decrease in left ventricle systolic function, and an increased atrial activation times, lower effective refractory periods, and increased atrial fibrillation inducibility. This model provides a means to understand the remodeling by which mitral regurgitation causes atrial fibrillation.

The Electrophysiologic Effects of Acute Mitral Regurgitation in a Canine Model

Atrial fibrillation (AF) occurs in 30% of patients with mitral regurgitation referred for surgical intervention. However, the underlying mechanisms in this population are poorly understood. This study examined the effects of acute left atrial volume overload on atrial electrophysiology and the inducibility of AF. Ten canines underwent insertion of an atrioventricular shunt between the left ventricle and left atrium. Shunt and aortic flows were calculated, and the shunt was titrated to a shunt fraction to 40% to 50% of cardiac output. An epicardial plaque with 250 bipolar electrodes was used to determine activation and refractory periods. Biatrial pressures and volumes, conduction times, and atrial fibrillation inducibility were recorded. Data were collected at baseline and 20 minutes after shunt opening and closure. Mean shunt flow was 1.3 ± 0.5 L/min with a shunt fraction of 43% ± 6% simulating moderate to severe mitral regurgitation. Compared with baseline, left atrial volumes and maximum pressures increased by 27% and 29%, respectively, after shunt opening. Biatrial effective refractory periods did not change significantly after shunt opening or closure. Conduction times increased by 9% with shunt opening and returned to baseline after closure. AF duration or inducibility did not change with shunt opening. This canine model of mitral regurgitation demonstrated that acute left atrial volume overload did not increase the inducibility of atrial arrhythmias in contrast with experimental and clinical findings of chronic left atrial volume overload. This suggests that the substrates for AF in patients with mitral regurgitation are a result of chronic remodeling.

Ultrasonographic Identification of the Pulmonary Veins in Adult Horses

Reasons for performing studyIn man, pulmonary veins (PV) are of major importance in atrial fibrillation pathophysiology as ectopy often originates in atrial myocardial sleeves extending in the PV wall. In addition, PV size on ultrasound is used to assess left atrial volume overload. In horses, PV anatomy and ultrasound have hardly been studied.ObjectivesTo study PV anatomy and establish a standard approach for echocardiographic identification of the PV from a right and left parasternal view.Study designAnatomical and echocardiographic description.MethodsFirstly, post mortem left atrial and PV silicone corrosion casts were made in 10 horses to investigate normal PV anatomy. Secondly, left and right parasternal ultrasound images and silicone casts were made in 3 horses, to compare images and casts.ResultsFour major PV ostia were identified on the casts, draining specific lung areas. From a right parasternal longitudinal view, ostium III was identified between the right atrial wall and right pulmonary artery, and ostium II left‐dorsal to it. From a left parasternal oblique short‐axis view, ostium III, its antrum and side‐branches were used as anatomical landmarks (adjacent to the right atrial wall). Slightly more caudal, ostium II was visualised with, in one horse, its antrum and 2 branches. Ostium I was only seen in one horse, slightly ventral to ostium II. Ostium IV was always identified in cross‐section on a left short‐axis view, left to the pulmonary artery bifurcation.ConclusionsA standard echocardiographic approach allows identification of pulmonary veins in adult horses. Left oblique and short axis views were superior although right long‐axis views also showed ostiums II and III. These data allow reference values to be established for pulmonary venous size and flow, and to investigate new treatment strategies for atrial fibrillation.Ethical animal research: Post mortem study with owner's informed consent; ultrasound with owner's informed consent. Study performed following the local ethical guidelines. Source of funding: Ghent University (institutional). Competing interests: None declared.

Left atrial function in volume versus pressure overloaded left atrium

Left atrial (LA) pressure and volume overload both result in cavity enlargement and complications. LA volume has been shown to predict such complications, but it does not reflect myocardial function, which can be accurately assessed using myocardial deformation measurements. We hypothesized that volume overloaded LA have maintained myocardial function compared to pressure overloaded ones. We tested this hypothesis in 44 patient (mean age 62 ± 12 years) with LA volume overload (LAVOL) due to severe mitral regurgitation (MR) with no indirect signs of elevated left ventricular (LV) filling pressures based on Doppler measured isovolumic relaxation time >60 ms. We compared them with 24 (mean age 64 ± 12 years) patient with LA pressure overload (LAPOL) who proved to have PCWP >15 mmHg on right heart catheterization. Twenty-seven healthy controls (mean age 57 ± 10 years) constituted a control group. Patients with LAVOL had larger LA volumes, higher LV ejection fraction, global LV strain (LVGLS) and transmitral and pulmonary veins flow velocities (p < 0.05) and better LA atrial strain rate (LASR) function compared to LAPOL (p < 0.001). In LAVOL, the LASR during atrial contraction (LASRa) was lower than in controls (p < 0.05) indicating LA mechanical disturbances. LVGLS correlated with peak atrial longitudinal systolic strain in the whole group (r = -0.65, p < 0.001) and less so with LASRa (r = -0.43, p < 0.001) CONCLUSION: Irrespective of a smaller LA volume, LAVOL had less negative effect on LA myocardial function than LAPOL. Thus, monitoring atrial myocardial contraction might be useful in following patients with significant MR.

Rupture of atrial septum in a Pomeranian dog secondary to advanced degenerative mitral valve disease

A 12-year-old spayed female Pomeranian (weighing 2.4 ㎏) was referred with primary complaints of acute dyspnea, cough, and lethargy. Diagnostic imaging studies found degenerative mitral valve cusps, chordae tendinae rupture, severe mitral regurgitation (5.45 ㎧ of peak velocity), and marked left atrial and ventricular dilation. The dog was diagnosed as having degenerative mitral valve disease (DMVD) with ISACHC stage IIIa heart failure. Her clinical condition was stabilized after administration of cardiac medication (e.g. diuretics and pimobendan). Ten months later, the dog was referred back to the clinic due to a sudden worsening of clinical signs. Echocardiographic study found pulmonary hypertension in addition to DMVD. After medication was adjusted, clinical signs were stabilized in 2 weeks. The patient was returned after 4 months for cardiac recheck and there was no obvious worsening of clinical signs. Incidental finding of a left-to-right atrial septal defect from rupture of the atrial septum secondary to marked left atrial dilation by DMVD was noted by echocardiography. To diminish left atrial volume overload, the frequencies of both furosemide and pimobendan were increased (i.e. from q 12 hr to q 8 hr) in addition to adding spironolactone (1 ㎎/㎏ q 12 hr). Based on diagnostic findings, this case was re-diagnosed as acquired atrial septal defect secondary to rupture of the atrial septum with advanced stage DMVD. The dog was then stabilized and is currently being regularly monitored.

Chronic left atrial volume overload abbreviates the action potential duration of the canine pulmonary vein myocardium via activation of IK channel

Electrophysiological properties of the pulmonary vein myocardium were assessed in a canine chronic atrioventricular block model resulting in left atrial volume overload. Five chronic atrioventricular block dogs and five sham-operated dogs were used. The heart was removed two months after a surgical procedure causing atrioventricular block, when atrial structural remodeling was established. Standard microelectrode penetrations were made with glass microelectrodes to obtain action potential signals of left atrium and pulmonary vein myocardia. The resting membrane potential in the pulmonary vein was more positive than that in the left atrium (− 69 mV vs − 74 mV) in both animal groups. The action potential duration at 50% repolarization of the pulmonary vein was shorter in the chronic atrioventricular block dogs than in the sham-operated dogs (38 ms vs 63 ms), whereas no significant difference was detected in the action potential duration of the left atrium between the two animal groups (67 ms vs 61 ms). The action potential duration of the pulmonary vein in the chronic atrioventricular block dogs was prolonged by charybdotoxin but not by iberiotoxin. Such prolongation was not observed in the normal pulmonary vein. These results suggest that long-term left atrial dilatation shortened the action potential duration of pulmonary vein myocardium, which may be associated with activation of the intermediate conductance Ca 2+-activated K + channel (IK channel).

Assessment of Left Ventricular Function Using Pulsed Tissue Doppler Imaging in Healthy Dogs and Dogs with Spontaneous Mitral Regurgitation

Pulsed tissue Doppler imaging (pulsed TDI) has been demonstrated to be useful for the estimation of left ventricular (LV) systolic and diastolic functions in various human cardiac diseases. The objectives of this study were to investigate the relationship between pulsed TDI and LV function by using cardiac catheterization in healthy dogs and to evaluate the clinical usefulness of pulsed TDI in dogs with spontaneous mitral regurgitation (MR). The peak early diastolic velocity (E'), peak atrial systolic velocity (A'), and peak systolic velocity (S') were detectable in the velocity profiles of the mitral annulus in all the dogs. In the healthy dogs, S' and E' were correlated with LV peak +dP/dt and -dP/dt, respectively. E' was lower in dogs with MR than in dogs without cardiac diseases. E/E' in the MR dogs with decompensated heart failure was significantly increased in comparison with those with compensated heart failure. The sensitivity and specificity of the E/E' cutoff value of 13.0 for identifying decompensated heart failure were 80% and 83%, respectively. In addition, E/E' was significantly correlated with the ratio of left atrial to aortic diameter. These findings suggest that canine pulsed TDI can be applied clinically for estimation of cardiac function and detection of cardiac decompensation and left atrial volume overload in dogs with MR.

Evaluation of ventricular septal defects in horses using two-dimensional and Doppler echocardiography.

Ventricular septal defects (VSDs) were diagnosed in 27 horses; in 26 affected horses systolic murmurs were detected over both sides of the chest. Holodiastolic decrescendo murmurs were also detected in 5 horses. Standardbreds and Arabian horses were over-represented, while Thoroughbred horses were under-represented, when compared to the hospital population (P < 0.0001). Five horses had previously raced successfully, one 2-year-old was training successfully and close to racing, and 4 horses had competed successfully in other types of competition. Eleven horses had a history of exercise intolerance or poor performance, 5 horses were stunted and 3 horses were in congestive heart failure at the time of presentation. The VSD murmur was detected as an incidental finding in 14 horses. Membranous VSD were most commonly detected (in 23/27 affected horses) and were typically found underneath the septal leaflet of the tricuspid valve and the right and/or noncoronary leaflet of the aortic valve. Muscular VSDs were much less common and were located in any portion of the muscular septum. The VSDs ranged in size from 1-4.6 cm (maximal diameter) in affected horses. A left to right shunt through the VSD was detected in 26/27 affected horses with Doppler echocardiography. The peak velocity of shunt flow detected through the VSD was 0-5.8 m/s. The interventricular pressure gradients estimated from the peak shunt velocity obtained with Doppler echocardiography were 0-135 mmHg. Right ventricular pressures estimated with Doppler echocardiography were 15-84 mmHg, similar to invasively obtained measurements of right ventricular pressure in 80% of horses in which right sided cardiac catheterisation was performed (n = 5). Left ventricular and left atrial volume overload was detected in the majority (23/27) of horses. Right atrial and right ventricular volume overload was severe in 3 horses with muscular VSDs, mild in 1 horse with a perimembranous VSD, and mild in 2 horses with membranous VSDs. Concurrent left ventricular dysfunction was detected in 2 horses. Aortic valve prolapse was seen in 7 horses associated with the membranous location of the VSD; 6 of these horses had very mild (1+) or mild (2+) aortic regurgitation. Severe (4+) aortic regurgitation was present in one horse, severe mitral regurgitation in 2 horses, severe tricuspid regurgitation in 3 horses, and severe pulmonary regurgitation was detected in 2 horses. Mitral valve prolapse, tricuspid valve dysplasia, a flail aortic valve leaflet, and a bicuspid pulmonary valve were additional findings detected in one horse each. Post mortem examinations were performed in 8 horses which confirmed the echocardiographic findings. Sixteen out of 27 horses had a history of racing or competing successfully either before or after the diagnosis of the VSD. Two horses were useful pleasure horses, 3 horses presented in congestive heart failure, 1 horse developed signs of congestive heart failure, 2 horses were lost to follow-up and 2 are still alive but are small and stunted. The successful racehorses usually had a membranous VSD that measured < or = 2.5 cm in its largest diameter and a peak velocity of shunt flow through the VSD of > or = 4 m/s. Two-dimensional (2-D) and Doppler echocardiography is useful in assessing the haemodynamic significance of VSDs in horses and can be used to help formulate a prognosis for life and performance.

Two-dimensional echocardiographic assessment of left atrial size in children

The ability of 2-dimensional echocardiography (2-D echo) to estimate end-systolic left atrial (LA) size and volume was assessed in 140 infants and children. These subjects were divided into 2 groups. Group A included 91 patients with normal LA volume and Group B included 49 patients with LA volume overload. Five echocardiographic views (left parasternal long-axis, left parasternal short-axis, apical 4-chamber, apical 2-chamber and subcostal 4-chamber) were used. From these views, the LA long-axis and minor-axis lengths were measured and the area was planimetered. These echocardiographically derived measurements were compared with angiographically calculated LA volume. Although all echocardiographic measurements correlated well with angiographic LA volume measurements, the echocardiographic area tracked better than length measurements. Echo LA volume was calculated using 5 single-plane and 3 biplane area-length methods. LA volume calculated from either single- or biplane methods correlated well with angiographically determined LA volume. The degree of correlation depended on the method used. Echocardiographic area and estimated LA volume measured from the parasternal long-axis and apical 2-chamber views best separated patients with LA volume overload from normal. Two-dimensional echo using these views accurately segregated all patients with a LA volume >180% of normal and 15 of 21 patients (71%) with an LA volume between 138% and 179% of normal. Thus, 2-D echo is useful in the evaluation of LA size and volume in Infants and children.

Left atrial volume overload in mitral regurgitation: A two dimensional echocardiographic study

Left atrial volume in patients with mitral valve disease was studied with two dimensional echocardiography. The left atrial dimension was derived by planimetry of the left atrial area and, assuming spherical geometry, left atrial volume was calculated. Patients with severe mitral regurgitation had marked systolic expansion of the left atrium with large phasic changes in left atrial cubic dimension. Conversely, patients with severe mitral stenosis had small changes in the cubic dimension in comparison with the large left atrial size. Left atrial volumetric changes were similar among patients with atrial fibrillation and normal sinus rhythm. Therefore, left atrial volume overload is an additional two dimensional echocardiographic diagnostic feature of severe mitral regurgitation.

The electrocardiographic recognition of left atrial enlargement in childhood

The P wave of the scalar electrocardiogram has been evaluated in a group of normal infants and children, and in a group of children with left atrial volume overload due either to ventricular septal defect or mitral regurgitation. In the normal group the P wave in Lead V 1 was frequently diphasic, with the terminal negative deflection smaller than the initial positive component, however. With left atrial overload, the negative P-V 1 deflection becomes more prominent, and the P wave in Lead V 2 may also become diphasic. Amplitude and duration of the terminal negative P-V 1 have been measured, and their product, the “terminal P-V 1 index”, obtained. In the absence of left atrial overload, the terminal P-V 1 index is ordinarily not greater than 0.015 mm. sec., the 90th percentile, or one half of a small square on ECG paper. Patients with left atrial overload have a significantly greater terminal P-V 1 index and can thus be identified. Abnormal negativity of the P-V 1 deflection, as expressed in the terminal P-V 1 index, does not occur with mild left atrial overload, but is consistently present with more significant degrees of overload. In a group of patients with prominent left atrial overload, the terminal P-V 1 index was abnormal in 92 per cent. The terminal P-V 1 index is compared with other electrocardiographic measures of left atrial abnormality. Prolonged P duration is more sensitive an indicator than terminal P-V 1 index, but is frequently not present in patients with prominent overload. Abnormal P morphology is confined to patients with more severe left atrial overload, but identifies less than half the number of these who are identified by an abnormal terminal P-V 1 index. An increased P P -R segment ratio is often a nonspecific finding. Unusual negativity of the P wave in Lead V 1, as indicated by an abnormal terminal P-V 1 index, correlates quite well with roentgenographic evidence of increased left atrial size. To date, abnormal negativity of the P wave in Lead V 1 is the sole electrocardiographic measure of left atrial enlargement which has this advantage.