Abstract
Objectives: General population studies have shown associations between copy number variation (CNV) of the LPA gene Kringle-IV type-2 (KIV-2) coding region, single-nucleotide polymorphism (SNP) rs6415084 in LPA and coronary heart disease (CHD). Because risk factors for HIV-infected patients may differ from the general population, we aimed to assess whether these potential associations also occur in HIV-infected patients. Methods: A unicenter, retrospective, case–control (1:3) study. Eighteen HIV-patients with confirmed diagnosis of acute myocardial infarction (AMI) were adjusted for age, gender, and time since HIV diagnosis to 54 HIV-patients without CHD. After gDNA extraction from frozen blood, both CNV and SNP genotyping were performed using real-time quantitative PCR. All genetic and non-genetic variables for AMI were assessed in a logistic regression analysis. Results: Our results did not confirm any association in terms of lipoprotein(a) LPA structural genetic variants when comparing KIV-2 CNV (p = 0.67) and SNP genotypes (p = 0.44) between AMI cases and controls. However, traditional risk factors such as diabetes mellitus, hypertension, and CD4+ T cell count showed association (p < 0.05) with CHD. Conclusion: Although significant associations of AMI with diabetes, hypertension and CD4+ T cell count in HIV-patients were found, this study could not confirm the feasibility neither of KIV-2 CNV nor rs6415084 in LPA as genetic markers of CHD in HIV-infected patients.Highlights:● Individuals with HIV infection are at higher risk of coronary heart disease (CHD) than the non-infected population.● Our results showed no evidence of LPA structural genetic variants associated with CHD in HIV-1-infected patients.● Associations were found between diabetes mellitus, arterial hypertension, CD4+ T cell count, and CHD.● The clinical usefulness of these biomarkers to predict CHD in HIV-1-infected population remains unproven.● Further studies are needed to assess the contribution of common genetic variations to CHD in HIV-infected individuals.
Highlights
Our results did not confirm any association in terms of lipoprotein(a) LPA structural genetic variants when comparing Kringle-IV type-2 (KIV-2) copy number variation (CNV) (p = 0.67) and single-nucleotide polymorphism (SNP) genotypes (p = 0.44) between acute myocardial infarction (AMI) cases and controls
Since the first case reports of acute myocardial infarction (AMI) in HIV-1-infected patients on highly active antiretroviral therapy (HAART) were described, it has become increasingly evident that individuals with HIV infection are at higher risk of cardiovascular events than the general population (Triant et al, 2007)
The contribution of classic risk factors, other factors such as viral replication, HIV-associated inflammation and/or immunodeficiency, and antiretroviral therapy have been associated with premature cardiovascular disease (CVD; Friis-Møller et al, 2003; Hansson, 2005)
Summary
Since the first case reports of acute myocardial infarction (AMI) in HIV-1-infected patients on highly active antiretroviral therapy (HAART) were described, it has become increasingly evident that individuals with HIV infection are at higher risk of cardiovascular events than the general population (Triant et al, 2007). The contribution of classic risk factors, other factors such as viral replication, HIV-associated inflammation and/or immunodeficiency, and antiretroviral therapy have been associated with premature cardiovascular disease (CVD; Friis-Møller et al, 2003; Hansson, 2005). Increased plasma concentrations of atherogenic lipoproteins play an important role in the development of atherosclerosis leading to premature AMI and ischemic stroke. Elevated plasma concentrations of Lp(a) have been associated with the risk of coronary heart disease (CHD) in the general population
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