Effect of left ventricular diastolic dysfunction on left atrial appendage function and thrombotic potential in nonvalvular atrial fibrillation

2014 ◽  
Vol 14 (3) ◽  
pp. 256-260 ◽  
Author(s):  
Muhammed Bora Demircelik ◽  
Mustafa Cetin ◽  
Hulya Cicekcioglu ◽  
Ozgul Ucar ◽  
Mustafa Duran
2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Or Yosefy ◽  
Barucha Sharon ◽  
Chana Yagil ◽  
Mark Shlapoberski ◽  
Alejandro Livoff ◽  
...  

Abstract Background Diabetic patients have an increased predisposition to thromboembolic events, in most cases originating from thrombi in the left atrial appendage (LAA). Remodeling of the LAA, which predisposes to thrombi formation, has been previously described in diabetic patients with atrial fibrillation, but whether remodeling of the LAA occurs in diabetics also in the absence of atrial fibrillation is unknown. To investigate the contribution of diabetes, as opposed to atrial fibrillation, to remodeling of the LAA, we went from humans to the animal model. Methods We studied by echocardiography the structure and function of the heart over multiple time points during the evolution of diabetes in the Cohen diabetic sensitive rat (CDs/y) provided diabetogenic diet over a period of 4 months; CDs/y provided regular diet and the Cohen diabetic resistant (CDr/y), which do not develop diabetes, served as controls. All animals were in sinus rhythm throughout the study period. Results Compared to controls, CDs/y developed during the evolution of diabetes a greater heart mass, larger left atrial diameter, wider LAA orifice, increased LAA depth, greater end-diastolic and end-systolic diameter, and lower E/A ratio—all indicative of remodeling of the LAA and left atrium (LA), as well as the development of left ventricular diastolic dysfunction. To investigate the pathophysiology involved, we studied the histology of the hearts at the end of the study. We found in diabetic CDs/y, but not in any of the other groups, abundance of glycogen granules in the atrial appendages , atria  and ventricles, which may be of significance as glycogen granules have previously been associated with cell and organ dysfunction in the diabetic heart. Conclusions We conclude that our rodent model of diabetes, which was in sinus rhythm, reproduced structural and functional alterations previously observed in hearts of human diabetics with atrial fibrillation. Remodeling of the LAA and of the LA in our model was unrelated to atrial fibrillation and associated with accumulation of glycogen granules. We suggest that myocardial accumulation of glycogen granules is related to the development of diabetes and may play a pathophysiological role in remodeling of the LAA and LA, which predisposes to atrial fibrillation, thromboembolic events and left ventricular diastolic dysfunction in the diabetic heart.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sotirios Nedios ◽  
Ole-A. Breithardt ◽  
Emmanuel Koutalas ◽  
Jedrzej Kosiuk ◽  
Philipp Sommer ◽  
...  

Introduction: Atrial fibrillation (AF) progression has been associated with asymmetric left atrial (LA) dilatation and left ventricular diastolic dysfunction (LVDD). LVDD has been also correlated with symptom severity. Hypothesis: Aim of this study was to test the hypothesis that the pattern of LA asymmetry is associated to LVDD and symptom severity. Methods: In 104 patients (58±10 years old, 69% male) referred for AF ablation, CT data were used to determine the LA volume (LAV) after exclusion of the appendage and the pulmonary veins (PVs). A cutting plane, between the PV ostia and the appendage and parallel to the posterior wall, divided LAV into anterior- (LA-A) and posterior-LA (LA-P) parts. The ratio LA-A/LAV was defined as asymmetry index (ASI). LVDD was evaluated according to current guidelines and symptom severity was quantified using the European Heart Rhythm Association score. Results: Univariate linear regression revealed that ASI is associated with LVDD, LAV and mitral regurgitation. ASI was higher in patients with LVDD (n=35, 62±5% vs. 59±6%, p=0.013) and in patients with mitral regurgitation (n=67, 61±6% vs. 58±5%, p=0.025) than those without. LAV increase was associated with an ASI increase (r=0.26, p=0.008). Multiple linear regression analysis revealed that LAV (β=0.211, 95% CI: 0.003-0.071, p=0.033) and LVDD (β=0.207, 95% CI: 0.167-5.011, p=0.036) were the only independent predictors of ASI increase (adjusted r2=0.92, F=6.2, p=0.003). Patients with moderate-severe AF symptoms (n=61) had higher ASI (61±6% vs. 58±5%, p=0.012) and higher prevalence of LVDD (43% vs. 21%, p=0.034) than those with mild symptoms. Conclusions: LA symmetry changes are associated with dilatation and left ventricular diastolic dysfunction and correlate with symptom severity in AF.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Gizatulina ◽  
N Y Khorkova ◽  
A V Belokurova ◽  
V E Kharats ◽  
L U Martyanova

Abstract Background Nonvalvular atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia and the most frequent cause of cardio-embolic stroke. It is well known that left atrial appendage thrombi (LAAT) are the source of most embolic strokes in patients with AF, and can be easily identified by transesophageal echocardiography (TEE). Purpose To determine additional LAAT predictors not included in the CHA2DS2-VASc score in patients with nonvalvular AF. Methods Retrospective study enrolled 636 patients with nonvalvular AF (400 males) aged 24–84 years (mean age 57.8±9.1), admitted to our Research Center in 2014–2017 for catheter ablation or electrical cardioversion. All patients had scheduled transthoracic echocardiography (TTE), as well as TEE performed to exclude LAAT. Four forms of cardiac geometry were revealed with the help of TTE according to Recommendations of ASE and EACI: normal geometry, concentric remodeling, eccentric hypertrophy and concentric hypertrophy. Results According to TEE results, LAAT (6.6%) was detected in 42 patients from 636. Patients with LAAT more often had persistent and permanent AF (assigned as “AF stability”), had bigger sizes and volumes of left and right cardiac chambers, lower left ventricular ejection fraction, more expressed LV hypertrophy and lower blood flow velocity in the LA appendage compared to patients without LAAT. Remodeling types also varied: less LAAT patients had normal cardiac geometry and more LAAT patients had LV eccentric hypertrophy. To analyze factors associated with AF, we used a multivariable logistic regression model, involving the potential independent, clinically relevant variables and echocardiographic parameters. Logistic regression analysis identified the latter three as independent predictors for LAAT (Table 1). According to ROC-analysis the quality of the received model was assessed as good: AUC=0.763 (p<0.01), sensitivity – 75.8%, specificity – 72.2%. Table 1 Predictors B Wald statistics χ2 P OR 95% CI AF stability 0.913 4.143 0.042 2.491 1.034–6.000 LA diameter, mm 0.149 8.684 0.003 1.160 1.051–1.281 Eccentric hypertrophy 1.440 7.411 0.006 4.222 1.497–11.908 Constant −10.613 24.088 0.000 Conclusion From risk factors, not included in the CHA2DS2-VASc score, in addition to such predictable values as AF stability and left atrial diameter, such predictor as eccentric left ventricular hypertrophy was revealed, which in our study was associated with more than a 4-fold increase in the risk of LAAT.


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