Markers of inflammation and endothelial activation in black South Africans with HIV and acute coronary syndromes

HIV infection is associated with a pro-inflammatory and thrombophilic state but little is known about the link between inflammation and thrombosis in treatment-naive patients with acute coronary syndromes (ACS). Prospective single centre study was conducted in Soweto, South Africa, comparing markers of inflammation and endothelial cell activation in highly active anti-retroviral therapy-naive HIV positive and negative patients presenting with ACS. Between March 2004 and February 2008, 30 consecutive black South African HIV patients with ACS were compared to 30 black HIV negative patients with ACS. The HIV patients were younger (43 ± 7 vs. 54 ± 13, p = 0.004) and besides smoking (73% vs. 33%, p = 0.002) and lower HDL levels (0.8 ± 0.3 vs. 1.1 ± 0.4, p = 0.001) had fewer risk factors than the control group. At baseline, HIV patients had higher levels of tumour necrosis factor-α [5.8 (1.7 - 15.0) vs. 0.19 (0.19 - 19.8) ng/ml, p = 0.0004] and vascular cell adhesion molecule-1 [263.3 (0.38 - 778.5) vs. 151.3 (80.6 - 416.3) ng/ml, p = 0.007] compared to HIV negative patients as well as higher levels of macrophage chemoattractant protein-1 at six months [70 (30 -130) vs. 50 (30 - 90) ng/L, p = 0.004]. Treatment-naive black South African patients with HIV and ACS have evidence of a pro-inflammatory state and greater degree of endothelial cell activation compared to HIV negative patients, both of which may play a direct role in the pathogenesis of ACS in this otherwise low risk population. MCP-1 may play an important role in HIV-associated coronary artery disease.   Key words: Human immunodeficiency virus (HIV), acute coronary syndrome (ACS), inflammation, endothelial dysfunction, thrombosis.

[1]  K. Sliwa,et al.  The Thrombotic Profile of Treatment-Naive HIV-Positive Black South Africans With Acute Coronary Syndromes , 2011, Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis.

[2]  K. Sliwa,et al.  Acute coronary syndromes in treatment-naïve black South africans with human immunodeficiency virus infection. , 2010, Journal of interventional cardiology.

[3]  P. Kolattukudy,et al.  Role of MCP-1 in cardiovascular disease: molecular mechanisms and clinical implications. , 2009, Clinical science.

[4]  M. Altfeld,et al.  Upregulation of PD-L1 on monocytes and dendritic cells by HIV-1 derived TLR ligands , 2008, AIDS.

[5]  E. Elm,et al.  The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies , 2007, The Lancet.

[6]  S. Pocock,et al.  Strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies , 2007, BMJ : British Medical Journal.

[7]  W. Koenig,et al.  Biomarkers of Atherosclerotic Plaque Instability and Rupture , 2007, Arteriosclerosis, thrombosis, and vascular biology.

[8]  B. Coll,et al.  The influence of HIV infection on the correlation between plasma concentrations of monocyte chemoattractant protein-1 and carotid atherosclerosis. , 2006, Clinica chimica acta; international journal of clinical chemistry.

[9]  D. Waters,et al.  What a Cardiologist Needs to Know About Patients With Human Immunodeficiency Virus Infection , 2005, Circulation.

[10]  S. Grinspoon,et al.  Cardiovascular risk and body-fat abnormalities in HIV-infected adults. , 2005, The New England journal of medicine.

[11]  B. Coll,et al.  Atherosclerosis in Patients Infected With HIV Is Influenced by a Mutant Monocyte Chemoattractant Protein-1 Allele , 2004, Circulation.

[12]  S. Yusuf,et al.  Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study , 2004, The Lancet.

[13]  Jeffrey N. Martin,et al.  Progression of Atherosclerosis as Assessed by Carotid Intima-Media Thickness in Patients With HIV Infection , 2004, Circulation.

[14]  L. Iacoviello,et al.  HIV infection, HAART, and endothelial adhesion molecules: current perspectives. , 2004, The Lancet. Infectious diseases.

[15]  D. Waters,et al.  Clinical Features of Acute Coronary Syndromes in Patients With Human Immunodeficiency Virus Infection , 2004, Circulation.

[16]  S. Blankenberg,et al.  Adhesion molecules and atherosclerosis. , 2003, Atherosclerosis.

[17]  E. Antman,et al.  Association Between Plasma Levels of Monocyte Chemoattractant Protein-1 and Long-Term Clinical Outcomes in Patients With Acute Coronary Syndromes , 2003, Circulation.

[18]  G. Specchia,et al.  Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation , 2002 .

[19]  Ryung S. Kim,et al.  Limited immune restoration after 3 years’ suppression of HIV-1 replication in patients with moderately advanced disease , 2002, AIDS.

[20]  Q. Yao,et al.  HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells , 2002, Laboratory Investigation.

[21]  U. Andersson,et al.  Cytokine expression in advanced human atherosclerotic plaques: dominance of pro-inflammatory (Th1) and macrophage-stimulating cytokines. , 1999, Atherosclerosis.

[22]  K. Williams,et al.  Atherosclerosis--an inflammatory disease. , 1999, The New England journal of medicine.

[23]  Warren Laskey.  Management of Acute Coronary Syndromes , 1999, Annals of Internal Medicine.

[24]  E. Boerwinkle,et al.  Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Communities (ARIC) study. , 1997, Circulation.

[25]  A. Blann,et al.  Soluble Adhesion Molecules and Endothelial Cell Damage in HIV Infected Patients , 1997, Thrombosis and Haemostasis.

[26]  G. Mariani,et al.  Productive HIV‐1 infection of human vascular endothelial cells requires cell proliferation and is stimulated by combined treatment with interleukin‐1β plus tumor necrosis factor‐α , 1995, Journal of medical virology.

[27]  John W. Ward,et al.  1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. , 1993, MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports.

[28]  A. D. Di Bisceglie,et al.  Myocardial infarction in an intensive care unit for blacks. A review over 6 years. , 1982, South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde.

[29]  E. Falk,et al.  Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. , 2003, European heart journal.

[30]  F Miedema,et al.  T-cell division in human immunodeficiency virus (HIV)-1 infection is mainly due to immune activation: a longitudinal analysis in patients before and during highly active antiretroviral therapy (HAART). , 2000, Blood.

[31]  A. Maiolo,et al.  Cytokines and hemostasis. , 2000, Haematologica.