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Updated: Dec 30, 2025
Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
Left ventricular mass index and subendocardial myocardial function in children with chronic kidney disease, a
Amira Esmat El Tantawy1, Fatina Fadel2, Safaa M Abdelrahman2
1Pediatric Cardiology.
Insights
Insulin resistance significantly contributes to left ventricular hypertrophy (LVH) in chronic kidney disease (CKD) patients, negatively impacting subendocardial function. Further research into insulin sensitizers is recommended for potential therapeutic benefits.
Area of Science:
- Cardiology
- Nephrology
- Metabolic Syndrome
Background:
- Left ventricular hypertrophy (LVH) is a common and detrimental cardiac complication in chronic kidney disease (CKD).
- LVH in CKD impairs myocardial blood flow and leads to progressive cardiac dysfunction, particularly affecting subendocardial layers.
- Understanding the determinants of LVH and its impact on myocardial function is crucial for managing CKD patients.
Purpose of the Study:
- To investigate the key determinants of left ventricular hypertrophy (LVH) in patients with chronic kidney disease (CKD).
- To assess the impact of LVH on subendocardial systolic function in CKD patients.
- To explore the role of insulin resistance as a determinant of LVH and its effect on myocardial function.
Main Methods:
- The study included 40 CKD patients and 40 age-matched controls.
- Transmural echocardiography was used to measure subepicardial and subendocardial global longitudinal strain (GLS) and left ventricle mass index (LVMI).
- Ambulatory blood pressure monitoring, lipid profile, and homeostasis model assessment of insulin resistance (HOMA-IR) were performed in CKD patients.
Main Results:
- Insulin resistance (HOMA-IR) was identified as a more significant determinant of LVH than systolic and diastolic blood pressure (P=0.01).
- Subendocardial GLS showed a significant negative correlation with LVMI (r=0.69, P<0.01), indicating impaired function with increased LVH.
- LVH appears to negatively affect subendocardial function, likely through impaired myocardial perfusion.
Conclusions:
- Insulin resistance plays a critical role in the progression of myocardial remodeling in CKD patients.
- Further research is warranted to explore the potential of insulin sensitizers in reversing cardiac remodeling and improving subendocardial function in CKD.
- Targeting insulin resistance may be a key strategy in managing cardiac complications associated with CKD.
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.
