0365 : Prognostic value of left atrial volume in patients with non-ischemic dilated cardiomyopathy

0365 : Prognostic value of left atrial volume in patients with non-ischemic dilated cardiomyopathy

241 Archives of Cardiovascular Diseases Supplements (2016) 8, 240-242 0365 Prognostic value of left atrial volume in patients with non-ischemic dila...

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241

Archives of Cardiovascular Diseases Supplements (2016) 8, 240-242

0365 Prognostic value of left atrial volume in patients with non-ischemic dilated cardiomyopathy Ichraq Nassiri *, Fatima Aghlad, Malika Nourddine, Leila Azzouzi, Rachida Habbal CHU Ibn Rochd, Casablanca, Maroc * Corresponding author: [email protected] (Ichraq Nassiri) Background Increased left atrial (LA) size is a prognostic marker of mortality in the general population. LA size varies considerably in patients with non ischemic dilated cardiomyopathy (DCM), but its clinical significance has not been widely studied. Our objective is to evaluate the long-term prognostic value of LA volume (LAV) in patients with non ischemic DCM. Methods We prospectively studied 102 patients followed with non ischemic (we exclude also valvular heart diseases) dilated cardiomyopathy and reduced ejection fraction, in sinus rhythm. Complete echocardiographic study at rest was performed in all patients. The composite endpoint of acute heart failure during follow-up was assessed. Results The average age of patients was 56 years±10. The sexe ratio was 2,5/1. 67% of patients were smokers. 2/3 of the population had hypertension. 52% of them had diabete mellitus which was insulino-dependant in the majority of cases. The average of ejection fraction of left ventricle (SIMPSON BP) was 35,7%±9. During 5 years of follow-up, 10 patients were lost, 5 died and 46 patients were hospitalized for acute hearte failure. Univariate Cox analysis showed various potential echocardiographic markers of prognosis in our population, including LA size in M-mode (44 VS 38mm, p=0.36), LA area (24 VS 20 cm2, p=0,58), LA volume (121,7 VS 79,3ml/mm2, p=0.007), E/A ratio (1,81 vs 1,1; p=0.019); E/A >2 (, p=0.0001) and mitral E/e’ ratio (16 vs 14,8, p=2.74). The only variable that remained in the multivariate model was LA volum (p=0.005). Conclusion LA volum was shown to be an echocardiographic determinant of acute heart failure in our population with non ischemic and non valvular DCM. The results of this study suggest that LA volum assessment, which can be performed using echocardiography, a non-invasive, readily available and inexpensive imaging modality, contributes to risk stratification and should be a routine part of echocardiographic study in patients with DCM. The author hereby declares no conflict of interest

0178 Global and regional echocardiographic strain to assess early phase of hypertrophic cardiomyopathy due to sarcomeric mutations Guillaume Baudry * (1), Nicolas Mansencal (2), Riadh Cheikh-Khelifa (1), Pascale Richard (1), Richard Isnard (1), Olivier Dubourg (2), Michel Komadja (1), Philippe Charron (1) (1) APHP-GH Pitié-Salpêtrière, Paris, France – (2) APHP-Hôpital Ambroise Paré, Boulogne-Billancourt, France * Corresponding author: [email protected] (Guillaume Baudry) Introduction Hypertrophic cardiomyopathy (HCM) is a genetic disease with delayed cardiac expression. Our objective was to characterize global and regional LV myocardial strain by two-dimensional imaging in sarcomeric HCM families and hypothesized that early systolic dysfunction, before hypertrophic stage, may be diagnosed by this technique. Methods and results We analyzed 79 adults: HCM patients with LV hypertrophy (LVH+, n=38), mutation carriers without LV hypertrophy (LVH-/G+, n=20), and normal control subjects (n=21). We calculated global longitudinal strain (GLS) and regional peak longitudinal strain. Age, sex ratio and body surface area were not significantly different between groups. Maximal 2D wall thickness of left ventricle was 10.1±1.6 mm in LVH-/G+ and not different from controls (9.9 ±1.2 mm). We observed that LV GLS was not different in LVH-/G+ as compared to controls (–20.6% IQ:–24.2/– 8.3 vs –22.9% IQ:-26.8/-20.9) but was reduced in HCM patients (–14.1% IQ:–18.5/–11.8) although a normal ejection fraction. Interestingly, regional peak longitudinal strain was similar in LVH-/G+ and controls except in four segments: basal anteroseptal (BAS) wall (–16% vs –19%,



p=0.018), basal inferoseptal wall (–16.0% vs –19.0%, p=0.047), basal inferior wall (–21.0% vs –24.0%, p=0.006) and mid anteroseptal wall (–21.0% vs –22.5%, p=0.022). Regional BAS strain <-16.5% yielded a sensitivity of 57% and a specificity of 90% to differentiate LVH-/G+ patients from controls. We also evaluated accuracy of ratio between normal and abnormal segments. Septo-basal/Latero-basal strain ratio <0.76 yielded a sensitivity of 73% and a specificity of 92% to differentiate LVH-/G+ patients from controls. Conclusion Regional longitudinal strain but not global strain, was significantly reduced at early stage of HCM before development of LVH. This suggests the integration of myocardial deformation in the evaluation of HCM relatives to identify better mutation carriers and early LV abnormalities. The author hereby declares no conflict of interest

0483 HFE gene knock-out induce cardiac dysfunction in a mouse model of hereditary hemochromatosis Damien Vitiello *, Yvan Trzaskus, Rémi Thomasson, Haidar Djemai, Jean-François Toussaint, Philippe Noirez Université Paris Descartes, Paris, France * Corresponding author: [email protected] (Damien Vitiello) Introduction Mechanisms involved in cardiac dysfunction induced by iron overload are not fully elucidated. The goal of our study is to evaluate cardiac function in HFE gene knock-out mice and determine the potential mechanisms involved in cardiac dysfunction. Material and methods Male wild type (WT, n=9), HFE gene knock-out (KO, n=8) and HFE heterozygote (Hete, n=9) mice were used in this study. Body composition (nuclear magnetic resonance) and cardiac function (echocardiography) were assessed at 7 and 20 months. Mice were sacrificed and hearts were stored at –80°C. Repeated measures ANOVA and Wilcoxon's test were performed. Differences were considered statistically significant at p<0.05. Results The corporal mass of HFE KO mice was significantly higher than WT and Hete mice at 7 months (respectively in g: 32.3±3.1 vs. 28.3±2.3, p<0.01 vs. 26.4±1.5, p<0.001) and at 20 months (32.7±5.2 vs. 30.4±2.9, p<0.05 vs. 28.2±1.9, p<0.01). The muscle mass was also significantly higher in HFE KO mice at 7 months (+19% vs. WT and Hete mice, p<0.001) and at 20 months (+12% vs. WT and Hete mice, p<0.05). Left ventricle end-systolic volumes were significantly greater in HFE KO mice than WT and Hete mice at 7 months (in mL: 0.043±0.008 vs. 0.022±0.004, p<0.01 vs. 0.036±0.012, p<0.01) and at 20 months (0.083±0.041 vs. 0.050±0.017, p<0.01 vs. 0.074±0.025, p<0.01). The left ventricle end-systolic diameters where higher in HFE KO mice at both 7 and 20 months compared to WT and Hete mice. The shortening fraction was significantly reduced at 7 months compared to WT (–7%, p<0.01) but not Hete mice and was significantly reduced at 20 months compared to WT (–10%, p<0.01) and Hete (–2%, p<0.01) mice. Conclusion Our study showed that HFE KO mice exhibit cardiac dysfunctions and myocardial structural modifications at 7 and 20 months. Analyses of heart tissues are currently under progress to determine the potential mechanisms involved in these cardiac dysfunctions. The author hereby declares no conflict of interest

0004 Overweight in mice induced by perinatal programming exacerbates doxorubicin and trastuzumab cardiotoxicity Charles Guenancia * (1), Olivier Hachet (1), Mona Aboutabl (2), Na Li (2), Yves Cottin (1), Luc Rochette (2), Catherine Vergely (2) (1) CHU Dijon, Bocage, Dijon, France – (2) Université de Bourgogne, UMR INSERM 866, Dijon, France * Corresponding author: [email protected] (Charles Guenancia) Background Trastuzumab (TRZ) is believed to potentiate doxorubicin (DOX) cardiotoxicity, resulting in left ventricular dysfunction. There is some evidence that overweight could influence anticancer drug-induced cardio-

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