A Study of the Correlation between Echocardiography and Lipid-Based Genetic Markers among Children with Severe Acute Malnutrition

Background and Aims

Children with Severe Acute Malnutrition (SAM), especially those with edema, are believed to be at high risk for cardiovascular morbidity and sodium overload, both of which could lead to early death during treatment. This study evaluated the correlation between echocardiography and lipid molecular markers in children with SAM.

Materials and Methods

Lipid profiling & Echo test; M mode and 2D echocardiography were performed using Philips HD7XE Echo Machine. A molecular marker of cardiac risk i.e., LPLSer447Ter, LIPC-250G/A, ApoA1G-75A, ApoBC7673T and ApoCIII3238C>G genetic variation identification was done by using PCR-RFLP method. MUAC- WHO guidelines were used to identify SAM cases. LDL, HDL, VLDL, Triglycerides, and Total Cholesterol profiles were analyzed by using an automated biochemistry analyzer, while PCR-RFLP was used to identify variation in the ApoAI, ApoB, and ApoCIII genes.

Results

The mean values of IVSs, IVSd, LVPWs, LVPWd, LVM, LVMI, LVIDs, EF, FS, and SV between cases and controls were significantly different (p <0.001). We found no significant differences in genotypic and allelic frequencies among SAM cases and controls for the LPLSer447Ter, LIPC-250G/A, ApoA1G-75A, ApoBC7673T, and ApoCIII3238C>G polymorphisms. We found no correlation between IVSs, IVSd, LVPWs, LVPWd, LVM, LVMl, LVID, LVIDd, EF, FS, SV echo parameters and TC, TG, HDL, LDL, VLDL, Non-HDL lipid parameters in SAM cases. SAM children had significantly reduced structural (thickness of IVS, LVPW, and LVM) and functional echo parameters (EF, FS, and SV) in comparison to normal children.

Conclusion

Early evaluation of cardiac function in a malnourished child will significantly affect the management of severe acute mal-nutrition to prevent deaths from cardiac abnormalities. Genotype and allele frequencies of LPLSer447Ter, LIPC-250G/A, ApoA1G-75A, ApoBC7673T, and ApoCIII3238C>G polymorphisms were similar between SAM cases and controls. There was no significant difference in the lipid profile between the mutant SAM case and the non-mutant SAM case.