Progressive Left Atrial Enlargement Research Articles

An unknown wide persistent ductus arteriosus debuting with atrial fibrillation in older adult: a case report

BackgroundThe persistently patent ductus arteriosus represents a well-known common congenital heart defect; it is uncommon in adult patients, and in any case, it debuts with atrial fibrillation.Case presentationA 75-year-old woman suffering from persistent ductus arteriosus (PDA) was admitted to the cardiology department because of atrial fibrillation, dyspnea and exercise intolerance. A PDA was detected on echocardiography and globally assessed through ECG-gated CT angiography.ConclusionsPatent ductus arteriosus is an uncommon clinical finding in adulthood, and atrial fibrillation, as a consequence of chronic, progressive left atrial enlargement, may be the initial symptom. We describe the ECG-gated CT angiography imaging features of unknown patent ductus arteriosus in an elderly patient who debuted with atrial fibrillation.

Identification of factors associated with progression of left atrial enlargement in patients with atrial fibrillation.

Left atrial (LA) enlargement frequently occurs in atrial fibrillation (AF) patients, and this enlargement is associated with the development of heart failure, thromboembolism, or atrial functional mitral regurgitation (AFMR). AF patients can develop LA enlargement over time, but its progression depends on the individual. So far, the factors that cause progressive LA enlargement in AF patients have thus not been elucidated, so that the aim of this study was to identify the factors associated with the progression of LA enlargement in AF patients. We studied 100 patients with persistent or permanent AF (aged: 67±2 years, 40 females). Echocardiography was performed at baseline and 12 (5-30) months after follow-up. LA size was evaluated as the LA volume index which was calculated with the biplane modified Simpson's method from apical four-and two-chamber views, and then normalized to the body surface area (LAVI). The deterioration of AFMR after follow-up was defined as a deterioration in severity of mitral regurgitation (MR) by a grade of 1 or more. Multivariate regression analysis demonstrated that hypertension (p=.03) was an independently associated parameter of progressive LA enlargement, as was baseline LAVI. In addition, the Kaplan-Meier curve indicated that patients with hypertension tended to show greater deterioration of AFMR after follow-up than those without hypertension (log-rank p=.08). Hypertension proved to be strongly associated with progression of LA enlargement over time in patients with AF. Our findings provide new insights for better management of patients with AF to prevent the development of AFMR.

Long-term Clinical Impacts of Functional Mitral Stenosis After Mitral Valve Repair

The relationship between functional mitral stenosis (MS) after mitral valve (MV) repair and long-term clinical outcomes is not fully understood. Therefore, we reviewed an institutional series to identify the determinants of functional MS and its effect on long-term clinical outcomes after MV repair for degenerative mitral regurgitation. Between January 1990 and December 2015, 792 patients who underwent MV repair for degenerative mitral regurgitation were retrospectively enrolled and divided into 2 groups: functional MS (n= 192) (≥5 mm Hg mean diastolic pressure gradient across the MV) and nonfunctional MS (n= 600) (<5 mm Hg mean diastolic pressure gradient). Mean follow-up was 11.6 ± 5.8 years. After propensity-score matching, patients' characteristics were comparable between groups (n=192/group). At 20 years, the functional MS group had significantly lower rates of freedom from new-onset atrial fibrillation (73.0% ± 5.6% versus 93.2% ± 2.3%; P= .003), overall survival (72.1% ± 4.6% versus 85.6%±4.3%; P= .010), and freedom from MV reoperation(82.8% ± 4.1% versus 92.5% ± 4.2%; P= .019) than the nonfunctional group. The functional MS group also had a significantly greater postoperative left atrialvolume index and tricuspid regurgitation grade. A small left ventricular end-diastolic dimension (hazard ratio= 0.975; 95% confidence interval, 0.955-0.996; P=.022) and annuloplasty ring (hazard ratio= 0.757; 95% confidence interval, 0.685-0.837; P < .001) were independentrisk factors for functional MS. A small left ventricle and annuloplasty ring increased the risk for functional MS after MV repair and was associated with progressive left atrial enlargement and tricuspid regurgitation exacerbation. As a result, functional MS increased the risk for new-onset atrial fibrillation, MV reoperation, and decreased long-term survival.

THE 5-YEAR DYNAMICS OF CARDIAC STRUCTURE AND FUNCTION IN PATIENTS WITH CORONARY ARTERY DISEASE AFTER MYOCARDIAL REVASCULARIZATION

The aim: To estimate the dynamics of echocardiographic parameters in patients with CAD within 5 years after revascularization. Material and methods: 50 persons (males/females 39/11; mean age 59.9±9.3 years; STEMI 76%, non-STEMI 24%) were divided into two groups: n=38 after PCI with stenting (PCIwS); n=12 after CABG. Observation included regular echocardiography with LV myocardial mass (LVMM) and geometry estimation. Results: Groups were comparable by age, co-morbidity, BP, heart rate and BMI. Significantly severe baseline LV hypertrophy (LVH) and left atrial enlargement (LAE) in group 2 explained by spread coronary atherosclerosis. Later progressive LAE (4.37±0.22 cm, P0-60<0.05) in group 1, and aortic/LV dilatation (+0.4/+1.0 cm, respectively, both P0-60<0.05) in group 2 developed. In two years LVMM index increased by 13.4/17.5% in groups 1/2, respectively. Normal geometry and concentric remodeling completely disappeared in 3/1.5 years after PCIwS/CABG, respectively. Conclusions: Within the 1st year after revascularization, patients with CABG had more severe LVH. In 5 years after PCIwS the ratio between concentric/eccentric LVH was 2:1, whereas after CABG - 1:2.

Contribution of the left atrial remodeling to the elevated pulmonary capillary wedge pressure in patients with WHO Group II pulmonary hypertension.

The contribution of progressive left atrial (LA) enlargement to elevated pulmonary capillary wedge pressure (PCWP) in patients with WHO Group II pulmonary hypertension (PH) has not been well studied. We hypothesized that progressive LA enlargement is associated with increased PCWP. A cross-sectional retrospective cohort consisted of 166 patients with HF and WHO Group II PH, confirmed by right heart catheterization (RHC). LA anteroposterior dimension and volume were measured on TTE. PCWP and other hemodynamic parameters were measured by RHC. Univariate and multivariate logistic regression models were used for analysis. LA enlargement was associated with advanced age, increased BMI, and LV ejection fraction < 40%. PCWP was progressively increased in patients with dilated LA: 16.9 ± 7.4mmHg in normal LA, 17.6 ± 7.2mmHg in mildly dilated LA, 22.6 ± 6.3mmHg in moderately and 22 ± 7.6 in severely dilated LA (p < 0.001). In multiple logistic regression, after adjustment for echocardiographic and clinical variables, severe LA enlargement was independently predictive of elevated PCWP (OR 3.468; 95% CI 1.046-11.504; p = 0.042). After excluding significant mitral regurgitation, progressive LA dilatation was associated with higher PCWP V-wave amplitude: from 21.3 ± 10.4mmHg in patients with normal LA size, to 30.9 ± 11.7mmHg in moderately dilated and 31.0 ± 11.6mmHg in severely dilated LA (p < 0.001). In patients with HF and WHO Group II PH, progressive LA enlargement was independently associated with elevated PCWP. After excluding significant mitral regurgitation, LA enlargement was also associated with increased V-wave amplitude, indicative of decreased atrial compliance.

Sickle cell anemia mice develop a unique cardiomyopathy with restrictive physiology

Cardiopulmonary complications are the leading cause of mortality in sickle cell anemia (SCA). Elevated tricuspid regurgitant jet velocity, pulmonary hypertension, diastolic, and autonomic dysfunction have all been described, but a unifying pathophysiology and mechanism explaining the poor prognosis and propensity to sudden death has been elusive. Herein, SCA mice underwent a longitudinal comprehensive cardiac analysis, combining state-of-the-art cardiac imaging with electrocardiography, histopathology, and molecular analysis to determine the basis of cardiac dysfunction. We show that in SCA mice, anemia-induced hyperdynamic physiology was gradually superimposed with restrictive physiology, characterized by progressive left atrial enlargement and diastolic dysfunction with preserved systolic function. This phenomenon was absent in WT mice with experimentally induced chronic anemia of similar degree and duration. Restrictive physiology was associated with microscopic cardiomyocyte loss and secondary fibrosis detectable as increased extracellular volume by cardiac-MRI. Ultrastructural mitochondrial changes were consistent with severe chronic hypoxia/ischemia and sarcomere diastolic-length was shortened. Transcriptome analysis revealed up-regulation of genes involving angiogenesis, extracellular-matrix, circadian-rhythm, oxidative stress, and hypoxia, whereas ion-channel transport and cardiac conduction were down-regulated. Indeed, progressive corrected QT prolongation, arrhythmias, and ischemic changes were noted in SCA mice before sudden death. Sudden cardiac death is common in humans with restrictive cardiomyopathies and long QT syndromes. Our findings may thus provide a unifying cardiac pathophysiology that explains the reported cardiac abnormalities and sudden death seen in humans with SCA.

21 Left atrial remodelling following treatment of symptomatic severe aortic stenosis

<h3>Background</h3> Left atrial (LA) size is an adverse prognostic marker. Aortic stenosis results in increased filling pressures with progressive left atrial enlargement and dysfunction. Intervention for aortic stenosis results in LV reverse remodelling, however the effect of TAVI or SAVR upon LA function remains poorly understood and the two treatments have not been directly compared. <h3>Aim</h3> We assessed LA size and function in patients with severe symptomatic aortic stenosis before and 6 months TAVI and SAVR. <h3>Methods</h3> All patients underwent an identical 1.5T CMR protocol and were in sinus rhythm at time of imaging. LA volumes were derived using the biplane area–length method (Figure 1). The total LA emptying fraction was derived as: (LAVmax–LAVmin)*100/LAVmax. <h3>Results</h3> 23 SAVR patients (age 72.7 ± 7.5 years, 83% male, EuroSCORE II 1.40 ± 1.11%) and 23 TAVI patients (age 80.7 ± 6.9 years, 57% male, EuroSCORE II 4.99 ± 2.97%). The left atria of the TAVI group were significantly more dilated at baseline than those of the SAVR group (p = 0.039) however both groups were comparable at 6 months (p = 0.227). Similarly, the LA emptying fraction of the TAVI group was significantly lower than the SAVR group at baseline (p = 0.003) with comparable function seen at 6 months (p = 0.08) (Table 1). <h3>Conclusions</h3> TAVI, but not SAVR, was associated with a significant reduction in LA volume and concomitant improvement in emptying fraction at 6 months. These preliminary findings may reflect worse LA function at baseline in the TAVI group or improved valvular haemodynamics with TAVI compared to SAVR.

Left atrial remodelling following transcatheter aortic valve implantation (TAVI) and surgical aortic valve replacement (SAVR)

Background Left atrial (LA) size is a marker of poor prognosis in a variety of cardiovascular conditions. Severe aortic stenosis results in elevated LV afterload with compensatory hypertrophy and increased filling pressures. This is associated with progressive left atrial enlargement and dysfunction. Intervention for aortic stenosis results in LV reverse remodelling, however the effect of TAVI or SAVR upon LA function remains poorly understood and the two treatments have not been directly compared. We sought to accurately determine LA size and function using CMR in patients with severe symptomatic aortic stenosis and identify changes following TAVI compared to SAVR.

Left Atrial Enlargement and Phasic Function in Patients Following Non–ST Elevation Myocardial Infarction

Changes in left atrial (LA) volumes after ST elevation myocardial infarction are reported but have not been well described following non-ST elevation myocardial infarction (NSTEMI). Seventy-five patients with NSTEMIs were studied within 48 hours of presentation and in follow-up at 6 and 12 months; they were compared with age-matched normal controls (n = 100). Biplane indexed LA volumes were measured, and phasic LA volumes (conduit, passive, and active emptying) were calculated. LA remodeling was defined as an increase in LA maximum volume over 12 months. LA maximum volume was significantly larger at baseline in patients with NSTEMIs. At 12 months, maximum LA volume increased (27.6 ± 7.4 vs 30.2 ± 8.9 mL/m² P = .002), with LA remodeling present in 64% of the patients with NSTEMIs. LA passive emptying volume increased, with concurrent reductions in conduit and active emptying volumes. Although diabetes, major coronary artery disease, and a larger myocardial score were predictive of LA remodeling, E' velocity was the only independent predictor. Patients with NSTEMIs had progressive LA enlargement with reductions in conduit and active emptying volumes, reflecting persistent left ventricular diastolic dysfunction consequent to coronary artery disease and associated diabetes. The measurement of LA volumes after NSTEMI may be useful to monitor chronic diastolic dysfunction resulting from ischemic burden.