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Evaluation of Lipid Profile, High-Sensitivity C-reactive Protein (hs-CRP), and Homocysteine in Premature Acute
Monika N Chavan1, Anup N Nillawar2, Anup S Hendre1
1Department of Biochemistry, Krishna Institute of Medical Sciences, Krishna Vishwa Vidyapeeth (Deemed to be University), Karad, IND.
Abstract:
Background The incidence of acute myocardial infarction (AMI) in young adults is progressively increasing, presenting a significant public health challenge. While traditional risk factors are documented, specific roles of atherogenic dyslipidemia and novel inflammatory biomarkers in premature AMI remain under-evaluated in semi-urban populations. Recent evidence suggests that biomarkers such as homocysteine (Hcy) and high-sensitivity C-reactive protein (hs-CRP) indicate endothelial dysfunction and vascular inflammation. Hyperhomocysteinemia (HHcy) is associated with oxidative stress and endothelial damage, while elevated hs-CRP levels are linked to plaque instability and a higher risk of cardiovascular events. Aims To evaluate the serum lipid profile, hs-CRP, and Hcy levels in patients with premature AMI in a semi-urban population, and to assess their correlations with glycemic markers. Methods A case-control analytical study was conducted at a tertiary care center in Maharashtra, India. The study enrolled 105 participants divided into three groups: Healthy controls (n=53), old age AMI (≥40 years, n=32), and premature AMI (<40 years, n=20). Fasting venous blood was analyzed for lipid profile, hs-CRP, Hcy, and glycemic markers. Results Patients with premature AMI were predominantly male (85%) with high rates of physical inactivity (90%). This cohort demonstrated profound atherogenic dyslipidemia, characterized by significantly elevated triglycerides (TGs) (238.00 ± 118.75 mg/dL). In premature AMI, TGs showed a significant positive correlation with fasting blood sugar (FBS) (r=0.681, p≤ 0.001), and glycated hemoglobin (HbA1c) (r=0.367, p=0.039). Inflammatory markers were also markedly elevated, with hs-CRP strongly correlating with FBS (r=0.658, p≤0.001). Older patients with AMI showed no such significant correlation between TGs and glycemic markers. Conclusions Premature AMI in this semi-urban population is metabolically distinct, driven by isolated hypertriglyceridemia and chronic inflammation linked to subclinical insulin resistance. A combined assessment of the lipid profile, hs-CRP, and Hcy levels may improve early risk stratification by capturing both atherogenic and inflammatory pathways. Early targeted screening for these biomarkers is crucial for prevention.
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