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The impact of functional mitral valve regurgitation in 1600 patients with chronic heart Failure
UntitledBook1.book Page 170 Monday, March 20, 2017 2:28 PM
170
Archives of Cardiovascular Diseases Supplements (2017) 9, 170-171
Topic 10 -Heart failure and cardiomyopathies + rehabilitation, exercise and prevention April 06th, Thursday 2017
004 A Novel myocardial fibrosis risk score in Heart Failure with preserved ejection fraction A. Secq*, JN. Dacher, V. Richard, V. Brunel, C. Vallet, H. Eltchaninoff, F. Bauer CHU Rouen, Rouen, France *Corresponding author: [email protected]
ventricle (LV) tissue of male and female Tgb3 and wild type rats (WT) (n=68). The expression level of some potential targeted genes were confirmed with quantitative RT-PCR analysis (n=8-10). Results At 45 weeks, Tgb3 female cardiac function appeared to be normal while males showed an increase in LV end diastolic pressure (5.6 ± 3.2mmHg vs 11.7 ± 3.2mmHg in Tgb3) associated with an increased E/A wave ratio (1.14 ± 0.05 vs 1.32 ± 0.13 in Tgb3) confirming a diastolic dysfunction. Transcriptome analysis highlighted 241 altered genes in males (15 up– and 226 down-regulated) and 182 in females (122 up– and 60 down-regulated). Among them, we identified genes implicated in different signalling pathways such as autophagy and cardiac metabolism. Lipocalin 2 (Lcn2), involved in inflammation, and Calmodulin 3 (Calm3), involved in calcium homeostasis, were significantly up (+59%) and down (–11%) regulated, respectively. Conclusion In our model, we demonstrated that Lcn2 and Calm3 are altered in HFpEF development. These genes are known to be altered in HF with reduced ejection fraction, but this is the first time that their alteration is described in HFpEF. An in depth analysis of these genes involved in inflammation and calcium handling will be performed. The author hereby declares no conflict of interest
Background Half of patients with heart failure have a preserved ejection fraction (HFpEF). Myocardial fibrosis is highly involved in the pathophysiology of HFpEF, but is only detectable by MRI. The purpose of this study is to create a simple risk score identifying HFPEF patients at risk of developing fibrosis, irrespective of MRI.
243
Methods We prospectively followed 123 patients hospitalized for acute HFpEF (EF> 50%, BNP >400pg/ml) between 2010 and 2012 at Rouen University Hospital. The primary endpoint was the presence of intramyocardial fibrosis identified by late gadolinium enhancement on MRI 2 months after the acute decompensation. Independant risk factors of fibrosis were determined using stepwise regression from echocardiographic date and biological marker, to build a risk score.
I. El Haddad* (1), K. Kharbouche (2), L. Azzouzi (1), R. Habbal (1) (1) cardiologie, CHU Casablanca-Maroc – (2) cardiologie, chu ibn ochd, Casablanca, Maroc *Corresponding author: [email protected]
Results 77 patients benefited from an MRI. Among them, 43 presented fibrosis. Independent predictors of fibrosis were high sensitivity Troponine (p=0.015), presence of arterial hypertension (HTN, p=0.013) and left atrium area (LA, p=0.09). Accordingly, the score could be calculated as follows: score= [0.007 x troponine (ng/L)] – [0.017 x LA area (cm²)] – [0.49 x (1 if HTN, 0 if absent)] + 1.25. Area under the ROC curve was 0.77. A value ≥0.6 was associated with fibrosis with a sensitivity and a specificity of 0.56 and 0.97, respectively. Conclusion Using a simple score with 3 traditional parameters, we are able to detect myocardial fibrosis in patients with HFpEF without the need of MRI. Our new score may be useful to identify patients with HFpEF who might benefit from early diagnosis and treatment. Keywords heart failure, preserved ejection fraction, risk score, LGE MRI, fibrosis. The author hereby declares no conflict of interest
148 Identification of signalling pathways potentially involved in the development of heart failure with preserved ejection fraction J. Dhot* (1), M. Steenman (1), V. Prat (1), M. Ferron (1), A. Persello (1), A. Erraud (1), B. Rozec (2), B. Lauzier (1), C. Gauthier (1) (1) Institut du thorax, INSERM UMR 1087-CNRS UMR 6291, UNIV Nantes – (2) Institut du thorax, INSERM UMR 1087-CNRS UMR 6291, UNIV Nantes, CHU Nantes, Nantes, France *Corresponding author: [email protected] Background Heart failure (HF) with preserved ejection fraction (pEF) is a common cardiac disease associated with a high morbi-mortality. The incidence of HFpEF increases with ageing of the population and affects mainly women. Thus far, no treatment is able to reduce the HFpEF burden. Our team developed a new HFpEF model, a transgenic rat (Tgb3) overexpressing the human b3-adrenoreceptor gene in endothelium leading to diastolic dysfunction with ageing. Purpose The aim of our study was to identify the different signalling pathways potentially implicated in HFpEF development. Methods At 45 weeks, cardiac function was evaluated by echocardiography and invasive haemodynamics. Transcriptome analysis was performed on left
© Elsevier Masson SAS. All rights reserved.
The impact of functional mitral valve regurgitation in 1600 patients with chronic heart Failure
Purpose To examine the prognostic impact of functional mitral valve regurgitation (FMR) among patients with chronic heart failure (HF). Methods We examined a historical cohort of 1600 patients with HF. All patients fulfilled the ESC criteria for HF. Patients with HF secondary to MI, organic mitral valve disease and severe aortic valve stenosis and patients with valve prosthesis were excluded. Cox-proportional-hazard analysis was used to compute the Hazard ratio (HR) and confidence intervals (CI) of all-cause mortality controlling for potential confounding factors. Results The median age was 75.1 years. A total of 788 (49.3%) had died after a median follow-up time of 2.9 years. Mild FMR was present in 36.9%, moderate FMR in 13.8% and severe FMR in 4.5% of the patients. We found a significant association between the presence and grade of FMR and risk of death. the HR for death (patients with no FMR as reference) in patients with mild FMR was 1.06 (95% CI 0.78-1.44), in patients with moderate FMR 1.42 (95% CI 0.97p. 0.05); 2.08) and 2.60 (95% CI 1.49p. 0.05); 4.54) in patients with severe FMR. HR for death did not change in subgroup analysis of patients who were classified in the New York Heart Associations groups I-II and III-IV. Conclusion FMR is present in almost half of the patients with chronic HF and is an independent prognostic determinant of all-cause mortality. The author hereby declares no conflict of interest
036 Inhibition of PIKfyve improves cardiometabolic phenotype in chronic diet-induced obesity through activation of SIRT3 M. Cinato (1), H. Tronchere (1), A. Timotin (1), L. Guitou (1), D. Baetz (2), H. Thibault (2), B. Payrastre (1), P. Valet (1), A. Parini (1), O. Kunduzova (1), F. Boal* (1) (1) I2MC INSERM U1048 and Université Paul Sabatier, Toulouse – (2) Univ-Lyon, CarMeN Laboratory, Inserm U1060, Université Claude Bernard Lyon 1, Bron, France *Corresponding author: [email protected] PIKfyve is an evolutionarily conserved lipid kinase that regulates pleiotropic cellular functions. Here we identify PIKfyve as a key regulator of cardiometabolic status and mitochondria integrity in chronic diet-induced obesity.
170
Archives of Cardiovascular Diseases Supplements (2017) 9, 170-171
Topic 10 -Heart failure and cardiomyopathies + rehabilitation, exercise and prevention April 06th, Thursday 2017
004 A Novel myocardial fibrosis risk score in Heart Failure with preserved ejection fraction A. Secq*, JN. Dacher, V. Richard, V. Brunel, C. Vallet, H. Eltchaninoff, F. Bauer CHU Rouen, Rouen, France *Corresponding author: [email protected]
ventricle (LV) tissue of male and female Tgb3 and wild type rats (WT) (n=68). The expression level of some potential targeted genes were confirmed with quantitative RT-PCR analysis (n=8-10). Results At 45 weeks, Tgb3 female cardiac function appeared to be normal while males showed an increase in LV end diastolic pressure (5.6 ± 3.2mmHg vs 11.7 ± 3.2mmHg in Tgb3) associated with an increased E/A wave ratio (1.14 ± 0.05 vs 1.32 ± 0.13 in Tgb3) confirming a diastolic dysfunction. Transcriptome analysis highlighted 241 altered genes in males (15 up– and 226 down-regulated) and 182 in females (122 up– and 60 down-regulated). Among them, we identified genes implicated in different signalling pathways such as autophagy and cardiac metabolism. Lipocalin 2 (Lcn2), involved in inflammation, and Calmodulin 3 (Calm3), involved in calcium homeostasis, were significantly up (+59%) and down (–11%) regulated, respectively. Conclusion In our model, we demonstrated that Lcn2 and Calm3 are altered in HFpEF development. These genes are known to be altered in HF with reduced ejection fraction, but this is the first time that their alteration is described in HFpEF. An in depth analysis of these genes involved in inflammation and calcium handling will be performed. The author hereby declares no conflict of interest
Background Half of patients with heart failure have a preserved ejection fraction (HFpEF). Myocardial fibrosis is highly involved in the pathophysiology of HFpEF, but is only detectable by MRI. The purpose of this study is to create a simple risk score identifying HFPEF patients at risk of developing fibrosis, irrespective of MRI.
243
Methods We prospectively followed 123 patients hospitalized for acute HFpEF (EF> 50%, BNP >400pg/ml) between 2010 and 2012 at Rouen University Hospital. The primary endpoint was the presence of intramyocardial fibrosis identified by late gadolinium enhancement on MRI 2 months after the acute decompensation. Independant risk factors of fibrosis were determined using stepwise regression from echocardiographic date and biological marker, to build a risk score.
I. El Haddad* (1), K. Kharbouche (2), L. Azzouzi (1), R. Habbal (1) (1) cardiologie, CHU Casablanca-Maroc – (2) cardiologie, chu ibn ochd, Casablanca, Maroc *Corresponding author: [email protected]
Results 77 patients benefited from an MRI. Among them, 43 presented fibrosis. Independent predictors of fibrosis were high sensitivity Troponine (p=0.015), presence of arterial hypertension (HTN, p=0.013) and left atrium area (LA, p=0.09). Accordingly, the score could be calculated as follows: score= [0.007 x troponine (ng/L)] – [0.017 x LA area (cm²)] – [0.49 x (1 if HTN, 0 if absent)] + 1.25. Area under the ROC curve was 0.77. A value ≥0.6 was associated with fibrosis with a sensitivity and a specificity of 0.56 and 0.97, respectively. Conclusion Using a simple score with 3 traditional parameters, we are able to detect myocardial fibrosis in patients with HFpEF without the need of MRI. Our new score may be useful to identify patients with HFpEF who might benefit from early diagnosis and treatment. Keywords heart failure, preserved ejection fraction, risk score, LGE MRI, fibrosis. The author hereby declares no conflict of interest
148 Identification of signalling pathways potentially involved in the development of heart failure with preserved ejection fraction J. Dhot* (1), M. Steenman (1), V. Prat (1), M. Ferron (1), A. Persello (1), A. Erraud (1), B. Rozec (2), B. Lauzier (1), C. Gauthier (1) (1) Institut du thorax, INSERM UMR 1087-CNRS UMR 6291, UNIV Nantes – (2) Institut du thorax, INSERM UMR 1087-CNRS UMR 6291, UNIV Nantes, CHU Nantes, Nantes, France *Corresponding author: [email protected] Background Heart failure (HF) with preserved ejection fraction (pEF) is a common cardiac disease associated with a high morbi-mortality. The incidence of HFpEF increases with ageing of the population and affects mainly women. Thus far, no treatment is able to reduce the HFpEF burden. Our team developed a new HFpEF model, a transgenic rat (Tgb3) overexpressing the human b3-adrenoreceptor gene in endothelium leading to diastolic dysfunction with ageing. Purpose The aim of our study was to identify the different signalling pathways potentially implicated in HFpEF development. Methods At 45 weeks, cardiac function was evaluated by echocardiography and invasive haemodynamics. Transcriptome analysis was performed on left
© Elsevier Masson SAS. All rights reserved.
The impact of functional mitral valve regurgitation in 1600 patients with chronic heart Failure
Purpose To examine the prognostic impact of functional mitral valve regurgitation (FMR) among patients with chronic heart failure (HF). Methods We examined a historical cohort of 1600 patients with HF. All patients fulfilled the ESC criteria for HF. Patients with HF secondary to MI, organic mitral valve disease and severe aortic valve stenosis and patients with valve prosthesis were excluded. Cox-proportional-hazard analysis was used to compute the Hazard ratio (HR) and confidence intervals (CI) of all-cause mortality controlling for potential confounding factors. Results The median age was 75.1 years. A total of 788 (49.3%) had died after a median follow-up time of 2.9 years. Mild FMR was present in 36.9%, moderate FMR in 13.8% and severe FMR in 4.5% of the patients. We found a significant association between the presence and grade of FMR and risk of death. the HR for death (patients with no FMR as reference) in patients with mild FMR was 1.06 (95% CI 0.78-1.44), in patients with moderate FMR 1.42 (95% CI 0.97p. 0.05); 2.08) and 2.60 (95% CI 1.49p. 0.05); 4.54) in patients with severe FMR. HR for death did not change in subgroup analysis of patients who were classified in the New York Heart Associations groups I-II and III-IV. Conclusion FMR is present in almost half of the patients with chronic HF and is an independent prognostic determinant of all-cause mortality. The author hereby declares no conflict of interest
036 Inhibition of PIKfyve improves cardiometabolic phenotype in chronic diet-induced obesity through activation of SIRT3 M. Cinato (1), H. Tronchere (1), A. Timotin (1), L. Guitou (1), D. Baetz (2), H. Thibault (2), B. Payrastre (1), P. Valet (1), A. Parini (1), O. Kunduzova (1), F. Boal* (1) (1) I2MC INSERM U1048 and Université Paul Sabatier, Toulouse – (2) Univ-Lyon, CarMeN Laboratory, Inserm U1060, Université Claude Bernard Lyon 1, Bron, France *Corresponding author: [email protected] PIKfyve is an evolutionarily conserved lipid kinase that regulates pleiotropic cellular functions. Here we identify PIKfyve as a key regulator of cardiometabolic status and mitochondria integrity in chronic diet-induced obesity.