Degree Of Left Atrial Enlargement Research Articles

Clinical application of the novel 4S-AF scheme for the characterisation of patients with atrial fibrillation: a report from the ESC-EHRA EORP Atrial Fibrillation General Long-Term (AFGen LT) registry

Abstract Background Current classification systems recommended by major international guidelines are based on a single domain of atrial fibrillation (AF): temporal pattern, symptom severity or underlying comorbidity. Lack of integration between these various elements limits our approach to patients with AF and acts as a barrier against the delivery of better holistic care. The 4S-AF classification scheme was recently introduced as a means for the characterisation of patients with AF. It comprises of 4 domains: stroke risk (St), symptoms (Sy), severity of AF burden (Sb) and substrate (Su). We sought to examine the implementation of the 4S-AF scheme in the EORP-AF General Long-Term Registry and effects of individual domains on outcomes in AF. Methods Patients with AF from 250 centres across 27 participating European countries were included. All patients were over 18 years old and had electrocardiographic confirmation of AF within 12 months prior to enrolment. Data on demographics and comorbidities were collected at baseline. Individual domains of the 4S-AF scheme were assessed using the CHA2DS2-VASc score (St), European Heart Rhythm Association classification (Sy), temporal classification of AF (Sb), and cardiovascular risk factors and the degree of left atrial enlargement (Su). Each of these domains were used during multivariable cox regression analysis. Results A total of 6321 patients were included in the present analysis, corresponding to 57.0% of the original cohort of 11096 patients. The median age of patients was 70 (interquartile range [IQR] 62–77) years with 2615 (41.4%) females. Among these patients, 528 (8.4%) had low stroke risk (St=0), 3002 (47.5%) no or mild symptoms (Sy=0), 2558 (40.5%) newly diagnosed or paroxysmal AF (Sb=0), and 322 (5.1%) no cardiovascular risk factors or left atrial enlargement (Su=0). Median follow-up was 24 months. Using multivariable cox regression analysis, independent predictors of all-cause mortality were (St) (adjusted hazard ratio [aHR] 8.21 [95% CI, 2.60–25.9]), (Sb) (aHR 1.21 [95% CI, 1.08–1.35]) and (Su) (aHR 1.27 [95% CI, 1.14–1.41]). For cardiovascular mortality and any thromboembolic event, only (Su) (aHR 1.73 [95% CI, 1.45–2.06]) and (Sy) (aHR 1.29 [95% CI, 1.00–1.66]) were statistically important, respectively. None of the domains were independently linked to ischaemic stroke or major bleeding. Conclusion Overall, we demonstrated that the 4S-AF scheme may be used to provide clinical characterisation of patients with AF using routinely collected data, and each of the domains within the 4S-AF scheme were independently associated with adverse long-term outcomes of all-cause mortality, cardiovascular mortality and/or any thromboembolic event. Funding Acknowledgement Type of funding sources: None.

Atrial fibrillation, not atrial cardiopathy, is associated with stroke: A single center retrospective study

BackgroundAtrial fibrillation (AF) increases the risk of thromboembolism. Atrial cardiopathy, defined as structural left atrial enlargement (LAE), has been proposed to be a unifying risk factor for stroke, with or without atrial fibrillation (AF). We sought to understand the relative importance of LAE and AF as risk factors for stroke. MethodsWe performed a retrospective analysis of all patients who underwent echocardiography within the Henry Ford Health System between March and September 2016. Patients were categorized based on the degree of LAE (none, mild, moderate and severe). The diagnosis of prior stroke or AF was ascertained by the presence of these conditions in the electronic medical record (www.EPIC.com). ResultsTotal of 8679 cases, 54% were female, 41% were African-American, and mean age was 65 ± 17 years. Fifteen percent had mild, 12% had moderate and 18% had severe LAE; the frequency of AF was 22%; and prior stroke was 18%. In multivariate analysis, the odds of AF increased progressively with severity of LAE (adjusted OR for mild 1.81, moderate 2.13 and severe 4.38, all P < .001) and AF was confirmed as a risk factor for prior stroke (aOR 1.34, CI 1.15–1.56, p < .001). By contrast, there was no association between LAE and stroke (aOR 0.98 CI 0.86–1.12, p = .74), regardless of the severity of LAE, and regardless of whether AF was present or not. ConclusionStructural LAE, found in almost half of this population, has a significant association with AF. While AF was confirmed to have a significant association with prior stroke, we found no association between stroke and LAE. AF, not LAE, appears to be the true atrial factor associated with stroke.

PM313 From the Couch to the Cuff: The Relationship between Physical Activity levels and Blood Pressure in Older Australians

We sought to compare left atrial (LA) volume to LA area and diameter for the prediction of adverse cardiovascular outcomes.The incremental value of LA volume compared with LA area or diameter as a cardiovascular risk marker has not been evaluated prospectively for patients with sinus rhythm or atrial fibrillation (AF).Left atrial size was assessed with biplane LA volume, four-chamber LA area, and M-mode dimension for 423 patients (mean age 71 ± 8 years, 56% men) who were prospectively followed for development of first AF, congestive heart failure, stroke, transient ischemic attack, myocardial infarction, coronary revascularization, and cardiovascular death.Of the 317 subjects in sinus rhythm at baseline, 62 had 90 new events during a mean follow-up of 3.5 ± 2.3 years. All three LA size parameters were independently predictive of combined outcomes (all p < 0.0001). The overall performance for the prediction of cardiovascular events was greatest for LA volume (area under the receiver operator characteristic curve: indexed LA volume 0.71; LA area 0.64; LA diameter 0.59). A graded association between the degree of LA enlargement and risk of cardiovascular events was only evident for indexed LA volume. For subjects with AF, there was no association between LA size and cardiovascular events.Left atrial volume is a more robust marker of cardiovascular events than LA area or diameter in subjects with sinus rhythm. The predictive utility of LA size for cardiovascular events in AF was poor, irrespective of the method of LA size quantitation.

Young Investigator Award session - Clinical * Clinical applications

Young Investigator Award session - Clinical * Clinical applications

Left Atrial Deformation Analysis by Speckle Tracking Echocardiography for Prediction of Cardiovascular Outcomes

The incremental value of left atrial (LA) deformation analysis by speckle tracking echocardiography compared with LA volume or LA ejection fraction as a cardiovascular risk marker has not been evaluated prospectively. We sought to compare LA function by speckle tracking echocardiography to other conventional LA parameters for prediction of adverse cardiovascular outcomes. This prospective study included 312 adults (mean age 71 ± 6 years, 56% men) in sinus rhythm who were followed for development of first atrial fibrillation, congestive heart failure, stroke, transient ischemic attack, myocardial infarction, coronary revascularization, and cardiovascular death. Global peak atrial longitudinal strain (PALS) by speckle tracking echocardiography was measured in all subjects by averaging all atrial segments. Left atrium was assessed with biplane LA volume, LA ejection fraction, 4-chamber LA area, and M-mode dimension. Of 312 subjects at baseline, 43 had 61 new events during a mean follow-up of 3.1 ± 1.4 years. All LA parameters, traditional parameters, and parameters derived by speckle tracking echocardiography were independently predictive of combined outcomes (p <0.0001 for all comparisons). Overall performance for prediction of cardiovascular events was greatest for global PALS (area under receiver operator characteristic curve: global PALS 0.83, indexed LA volume 0.71, LA ejection fraction 0.69, LA area 0.64, LA diameter 0.59). A graded association between degree of LA enlargement and risk of cardiovascular events was evident only for global PALS and indexed LA volume. In conclusion, global PALS is a strong and independent predictor of cardiovascular events and appears to be superior to conventional parameters of LA analysis.

WITHDRAWN: Left atrial function and arterial hypertension.

Left atrial enlargement is frequently observed in many cardiac diseases. One of the main determinants of left atrial size is ventricular diastolic function. It has recently been suggested that left atrial volume might be the morphophysiologic expression of long-term modifications induced by diastolic function. Furthermore, left ventricular remodelling, such as it happens in hypertensive patients, is another important determinant of atrial volume. All the volumetric modifications of the left atrium, during cardiac cycle, are involved in hypertensive damage. Therefore, left atrial function impairment represents the result of morphological and haemodynamic alterations observed in hypertension. Actually, many techniques, invasive and non-invasive, are available with the purpose to investigate the real atrial dimensions and provide a suitable assessment of atrial function. Recently, it has been demonstrated that the degree of left atrial enlargement is associated with adverse prognosis in different clinical setting. The predictive value of left atrial volume seems to be independent of left ventricular systolic and diastolic function, but the use of left atrial volume for risk stratification is yet an evolving science: more data are required with respect to the natural history of left atrial remodelling in disease, the degree of left atrial modifiability with therapy and whether regression of left atrial size translates into improved cardiovascular outcome.Journal of Human Hypertension advance online publication, 14 August 2008; doi:10.1038/jhh.2008.96.

Prediction of Cardiovascular Outcomes With Left Atrial Size: Is Volume Superior to Area or Diameter?

We sought to compare left atrial (LA) volume to LA area and diameter for the prediction of adverse cardiovascular outcomes. The incremental value of LA volume compared with LA area or diameter as a cardiovascular risk marker has not been evaluated prospectively for patients with sinus rhythm or atrial fibrillation (AF). Left atrial size was assessed with biplane LA volume, four-chamber LA area, and M-mode dimension for 423 patients (mean age 71 +/- 8 years, 56% men) who were prospectively followed for development of first AF, congestive heart failure, stroke, transient ischemic attack, myocardial infarction, coronary revascularization, and cardiovascular death. Of the 317 subjects in sinus rhythm at baseline, 62 had 90 new events during a mean follow-up of 3.5 +/- 2.3 years. All three LA size parameters were independently predictive of combined outcomes (all p < 0.0001). The overall performance for the prediction of cardiovascular events was greatest for LA volume (area under the receiver operator characteristic curve: indexed LA volume 0.71; LA area 0.64; LA diameter 0.59). A graded association between the degree of LA enlargement and risk of cardiovascular events was only evident for indexed LA volume. For subjects with AF, there was no association between LA size and cardiovascular events. Left atrial volume is a more robust marker of cardiovascular events than LA area or diameter in subjects with sinus rhythm. The predictive utility of LA size for cardiovascular events in AF was poor, irrespective of the method of LA size quantitation.

Relationship between left ventricular geometry and left atrial size and function in patients with systemic hypertension.

Arterial hypertension determines distinct adaptive left ventricular geometric responses, which may differently affect left ventricular function and left atrial performance. In this study, the effect of left ventricular geometry on left atrial size and function, and the relationship between left atrial size and left ventricular mass were assessed in 336 patients with systemic arterial hypertension who had undergone Doppler echocardiography. Patients were classified into concentric (110 patients with concentric left ventricular geometry defined as relative wall thickness > or = 0.44) and eccentric groups (226 patients with relative wall thickness < 0.44). Comparison to the latter, the former had greater left atrial size, left atrial ejection force, left ventricular mass and lower left ventricular midwall fractional shortening. Left ventricular concentric, rather than eccentric, geometry emerged by multivariate analysis as a factor independently associated with the highest degree of left atrial ejection force. Left atrial size was positively related to left ventricular mass in the whole population (r = 0.65, SEE = 6 ml, P < 0.00001). This relationship was maintained in the subgroups with concentric (r = 0.65, SEE = 6 ml, P < 0.00001) or eccentric geometry (r = 0.59, SEE = 6 ml, P < 0.00001). Our results indicate that the relationship of left ventricular geometry to both left atrial size and ejection force in hypertensive patients is relevant. Concentric left ventricular geometry is associated with greater left atrial size and ejection force than eccentric geometry, suggesting that increased left ventricular stiffness has a greater effect in stimulating left atrial performance than left ventricular end-systolic stress. The degree of left atrial enlargement similarly depends on left ventricular mass in patients with concentric and eccentric geometry.

798-4 Predictors of the Efficacy of Sotalol, a Class III Antiarrhythmic Agent, in the Treatment of Atrial Arrhythmias

Sotalol, a class III antiarrhythmic drug (AAD) approved for use in ventricular arrhythmias, is being used with increasing frequency for supraventricular arrhythmias (SVA). To determine the efficacy of sotalol in the treatment of SVA and the predictors of sotalol failure or intolerance, 114 pts in whom Sotalol was begun for SVA were reviewed. All pts had atrial fibrillation (109) and/or atrial flutter (32) (AF: paroxysmal in 76, chronic in 35), except for 3 who had SVT. Mean duration after diagnosis of SVA was 5.2 ± 8.2 yrs. The mean number of priorfailed AADs was 1.96 ± 1.27 (range 0–6). Electrical cardioversion was achieved in 38/41 pts; 18 pts pharmacologically converted. Sotalol was stopped prior to discharge in 16 pts (inefficacy in 8, side effects in 4, prolonged QT in 2, and no longer indicated in 2). Prior to discharge, proarrhythmia occurred in 1 pt and bradycardia in 15 pts. 26 pts had prior pacemakers, and 11 pts required pacemakers for sotalol. Mean discharge dose was 229 ± 78 mg/day and mean discharge QTc was 462 ± 59 ms. Predictors for discontinuation of sotalol prior to discharge included degree of left atrial enlargement (LAE, p = 0.03) and QTc on sotalol (p = 0.063). Of 88 pts discharged on sotalol in sinus rhythm, 52 developed recurrent SVA (mean f/u 7.8 mos). After dose changes, 3 more pts became recurrence free. Of 36 recurrence-free pts, 12 had sotalol discontinued (side effects in 7, no longer indicated in 5). 2 pts discharged on sotalol developed proarrhythmia, and 2 pts died (1 noncardiac and 1 CVA). Overall, 27/114 pts (23.6%) begun on sotalol remained recurrence free and on the drug. Of 10 pts who began sotalol as first line antiarrhythmic therapy, 2 stopped sotalol in the hospital, 2 after hospital discharge, and 2 recurred after discharge (overall 40% recurrence free on sotalol). Univariate predictors of recurrent SVA on sotalol for pts discharged in NSR included younger age (60 ± 13 vs 68 ± 9 yrs, p = 0.001), longer duration since diagnosis of SVA (7.7 ± 11 vs 2.8 ± 4.0 yrs, p = 0.009), prior CABG (p = 0.01), number of failed AADs (2.4 ± 1.3 vs 1.4 ± 1.1, p = 0.0003), and shorter baseline QTc (441 ± 46 vs 465 ± 59 ms, p = 0.049) and discharge QRS (109 ± 32 vs 128 ± 41 ms, p = 0.025). Changes in HR or QTc were not significant predictors of sotalol success. Significant multivariate predictors of SVA recurrence adjusted for the follow-up period included number of failed AADs (p = 0.0024), discharge QRS (p = 0.0038) and age (p = 0.03). In summary, sotalol showed moderate (24%) efficacy in pts previously refractory to AADs and comparable efficacy as a first-line agent to that reported with other AADs. Changes in QT interval or HR could not be used to predict long term efficacy.

CORRELATION OF RADIOGRAPHIC, ECHOCARDIOGRAPHIC, AND ELECTROCARDIOGRAPHIC SIGNS OF LEFT HEART ENLARGEMENT IN DOGS WITH MITRAL REGURGITATION

Thoracic radiographs of 40 dogs with mitral regurgitation were evaluated for signs of left heart enlargement and classified into three groups based on the degree of left atrial enlargement (mild = group A, moderate = group B, and severe = group C). Echocardiographic enlargement ratios were calculated for the left atrium (LAEecho), the left ventricle (LVEecho), and the aorta (AOEecho) by dividing the measured dimension with the expected dimension normalized for body weight. The incidence of LVH patterns and p‐mitrale was recorded on electrocardiograms. With advanced stages of the disease, there was good agreement of the radiographs and echocardiograms with significant differences of the left atrial enlargement ratio between groups. Nine of the 16 dogs from groups A and B, however, had LAEecho ratios within the normal range. Sixteen dogs with radiographic signs of left ventricular enlargement had normal LVEecho ratios. These disagreements were interpreted as either cardiac enlargement not manifest in the dimensional change measured by the echocardiogram or as overreading of radiographs. The left ventricular wall thickness did not vary significantly between groups. The incidence of p‐mitrale was 30%, but this ECG abnormality, when present, reliably identified enlarged left atrial dimensions. Left ventricular hypertrophy patterns of the ECG did not correlate with either the radiographic diagnosis of left ventricular enlargement or the echocardiographic enlargement ratios.

Mechanisms for atrial arrhythmias associated with cardiomyopathy: a study of feline hearts with primary myocardial disease.

The cellular electrophysiologic and structural characteristics of arrhythmic and non-arrhythmic atria isolated from feline hearts with spontaneously occurring cardiomyopathy were studied. The animals were divided into three groups according to the degree of left atrial enlargement: mild (group I), moderate (group II), and severe (group III). The right atria were of relatively normal size. Microelectrode recordings showed that inexcitable cells were present in both left and right atria of all groups but were most numerous in the left atria of group III animals. Most inexcitable cells had low resting membrane potentials. There was also a significant reduction in resting membrane potentials, maximum rate of phase 0 depolarization, and action potential amplitude of excitable cells in left atria of animals in groups II and III, whereas action potentials of excitable cells in the right atria were normal. Acetylcholine or norepinephrine often restored excitability to cells that originally did not generate action potentials. Norepinephrine also caused slow-response action potentials as well as abnormal automaticity and triggered activity due to delayed afterpotentials. The diseased atria showed marked structural abnormalities, which were most pronounced in group III cats, including large amounts of interstitial fibrosis, cellular hypertrophy and degeneration, and thickened basement membranes. Therefore electrophysiologic abnormalities and concurrent changes in cell structure may be involved in the genesis of atrial tachyarrhythmias caused by cardiomyopathy.

Atrial fibrillation in congestive cardiomyopathy: echocardiographic and hemodynamic correlates.

AbstractPrevious studies have suggested an unexpectedly low incidence of atrial fibrillation in patients with congestive cardiomyopathy. To further investigate the incidence of chronic atrial fibrillation in these patients and its relationship to left atrial dimension and pressure, we retrospectively examined M‐mode echocardiographic and cardiac catheterization data from 54 patients with idiopathic (n = 29) and ischemic (n = 25) congestive cardiomyopathy. The incidence of atrial fibrillation (17%) was surprisingly low given the degree of left atrial enlargement (51 ± 5 mm; mean ± SD) and left atrial hypertension (19 ± 8 mm Hg). In addition, there were no significant differences in left atrial pressure or left atrial dimension between those congestive cardiomyopathy patients in sinus rhythm and those in atrial fibrillation, nor was there a higher incidence of secondary mitral regurgitation in patients in atrial fibrillation.Comparisons were also made between congestive cardiomyopathy patients and 21 patients with primary mitral valve disease and atrial fibrillation. Left atrial pressure was not significantly different between these groups. However, the mean left atrial dimension of the patients with mitral valve disease (56 ± 8 mm) was greater (P &lt; 0.01) than that of patients with idiopathic (51 ± 6 mm) or ischemic (50 ± 4 mm) cardiomyopathy in sinus rhythm and also greater (P = 0.07) than left atrial dimension (51 ± 6 mm) of congestive cardiomyopathy patients in atrial fibrillation. Furthermore, massive enlargement of the left atrium (greater than 60 mm) was a common feature of mitral valve disease (33% incidence) but occurred only rarely in congestive car‐diomyopathy (5% incidence).We conclude that while left atrial volume and pressure loads may be important contributors to the pathogenesis of atrial fibrillation, these factors are not sufficient to produce the arrhythmia in most patients with congestive cardiomyopathy. Other variables such as disease duration or the degree of atrial fibrosis or inflammation may also be important in determining which patients with left atrial enlargement will develop atrial fibrillation. Furthermore, massive left atrial enlargement (left atrial dimension &gt; 60 mm) is rarely associated with ischemic or idiopathic congestive car‐diomyopathy and suggests underlying primary mitral valve disease.

Left ventricular function in rheumatic mitral stenosis. Clinical echocardiographic study.

Echocardiography was used to examine the extent and significance of impairment in left ventricular function in 20 patients with rheumatic mitral stenosis. Indices of left ventricular performance--normalised mean rate of circumferential fibre shortening (Vcf), ejection fraction, normalised posterior wall velocity, and stroke volume were reduced. The impairment in left ventricular function was related to the degree of functional disability (NYHA), right ventricular dilatation, and left atrial enlargement. Vcf was inversely related to both the internal right ventricular diameter (r=-0.767, P less than 0.001) and the degree of left atrial enlargement (r=-0.554; P less than 0.05). The normalised velocity of the interventricular septum and the maximum systolic and diastolic endocardial velocities were also reduced. These results suggest that abnormalities in contractility of left ventricular myocardium are responsible for the impaired myocardial function in patients with mitral stenosis and that such impairment is clinically significant.

HIS bundle electrogram in rheumatic mitral valve disease with special reference to Bachmann's bundle block in P mitrale.

HBEs were recorded from either the right or left ventricle or simultaneously from both in 26 patients with chronic rheumatic mitral stenosis alone or in association with other mild valvular lesions during the diagnostic cardiac catheterization. Eleven of the patients had auricular fibrillation. Of the remaining 15 patients with sinus mechanism and P mitrale in the surface electrocardiogram, 12 were noted to have H potential preceded the termination of P wave and gave P2H interval of negative value- so-called "Bachmann's bundle block". Among these, double atrial activities (A and A' waves) could be identified on the HBE recorded from the left ventricular endocardial surface with catheter electrodes positioned at the subarotic region in 7 patients studied. Interatrial conduction time (P1A' interval) measured in these patients was prolonged in all and ranged from 47 to 82 with an average of 66 msec. Prolongation of intraatrial (or internodal) conduction time was noted in only one patient who also had first degree A-V block and prolonged A-H interval. There was no correlation of either P1P2 or P2H interval to the degree of left atrial enlargement. The P1P2 or P2H interval also had no correlation with hemodynamic parameters. In patients with auricular fibrillation, all impulses unable to conduct to the ventricle were blocked proximal to the His bundle and concealed conduction was not observed distal to it.