Introduction: Left ventricular hypertrophy (LVH) is the commonest myocardial response to chronic kidney disease (CKD); this response has been regarded detrimental as it impairs the blood flow to the deepest layers of the myocardium causing progressive myocardial dysfunction. The aim of these series is to assess the determinants of LVH in CKD patients and its impact on subendocardial function in such patients. Methods: This study has been conducted on 40 CKD patients (Group 1) and 40 age-matched controls, both groups were assessed by transmural echocardiography to determine the subepicardial and subendocardial global longitudinal strain (GLS) as an expression of the systolic function of each of those layers. LVH was assessed by calculation of left ventricle mass index (LVMI). Both groups underwent ambulatory blood pressure monitoring. Group 1 was assessed as regards lipid profile and insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR). Results: HOMA-IR proved to be a more important determinant of LV hypertrophy than SBP and DBP with a P of 0.01. Moreover subendocardial GLS was negatively correlated with LVMI with r = 0.69 and P < 0.01 denoting the negative effect. LVH plays on subendocardial function probably by impairing myocardial perfusion. Conclusion: This study points toward the importance of insulin resistance in aggravation of myocardial remodeling in CKD patients; more studies are warranted to examine the role of insulin Sensitizers in reversing such remodeling and restoring subendocardial function in such important systemic disorder.
Introduction: Left ventricular hypertrophy (LVH) is the commonest myocardial response to chronic kidney disease (CKD); this response has been regarded detrimental as it impairs the blood flow to the deepest layers of the myocardium causing progressive myocardial dysfunction. The aim of these series is to assess the determinants of LVH in CKDpatients and its impact on subendocardial function in such patients. Methods: This study has been conducted on 40 CKDpatients (Group 1) and 40 age-matched controls, both groups were assessed by transmural echocardiography to determine the subepicardial and subendocardial global longitudinal strain (GLS) as an expression of the systolic function of each of those layers. LVH was assessed by calculation of left ventricle mass index (LVMI). Both groups underwent ambulatory blood pressure monitoring. Group 1 was assessed as regards lipid profile and insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR). Results: HOMA-IR proved to be a more important determinant of LV hypertrophy than SBP and DBP with a P of 0.01. Moreover subendocardial GLS was negatively correlated with LVMI with r = 0.69 and P < 0.01 denoting the negative effect. LVH plays on subendocardial function probably by impairing myocardial perfusion. Conclusion: This study points toward the importance of insulin resistance in aggravation of myocardial remodeling in CKDpatients; more studies are warranted to examine the role of insulin Sensitizers in reversing such remodeling and restoring subendocardial function in such important systemic disorder.
Authors: Melvin D Cheitlin; William F Armstrong; Gerard P Aurigemma; George A Beller; Fredrick Z Bierman; Jack L Davis; Pamela S Douglas; David P Faxon; Linda D Gillam; Thomas R Kimball; William G Kussmaul; Alan S Pearlman; John T Philbrick; Harry Rakowski; Daniel M Thys; Elliott M Antman; Sidney C Smith; Joseph S Alpert; Gabriel Gregoratos; Jeffrey L Anderson; Loren F Hiratzka; David P Faxon; Sharon Ann Hunt; Valentin Fuster; Alice K Jacobs; Raymond J Gibbons; Richard O Russell Journal: J Am Soc Echocardiogr Date: 2003-10 Impact factor: 5.251
Authors: Sonia A El Saiedi; Marwa F Mira; Sahar A Sharaf; Maysoun M Al Musaddar; Rania M H El Kaffas; Antoine F AbdelMassih; Ihab H Y Barsoum Journal: Cardiol Young Date: 2017-08-07 Impact factor: 1.093
Authors: Luca Di Lullo; Antonio Gorini; Domenico Russo; Alberto Santoboni; Claudio Ronco Journal: Cardiorenal Med Date: 2015-07-15 Impact factor: 2.041