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Carotid intima-media thickness: assessment of sub-clinical atherosclerosis in HIV-infected patients
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AIDS: Volume 19(16) 4 November 2005
Letter to the Editor
Coll, Blai; Alonso-Villaverde, Carlos
Servei de Medicina Interna, Hospital Universitari Sant Joan, Reus, Spain.
With reference to the article by Currier et al. [1], we would like to highlight certain anomalies in their findings. These authors reported that neither the use of protease inhibitors nor the HIV infection itself have any impact on the carotid intima-media thickness (IMT); a validated method to assess subclinical atherosclerosis [2]. These results are in contradiction with previous studies published in AIDS. Maggi et al. [3] observed a higher prevalence of pathological carotid IMT, or atheromatous plaque, when comparing protease inhibitor-treated patients with those under a protease inhibitor-sparing scheme. Furthermore, Depairon et al. [4] observed a significantly higher presence of carotid, or femoral, atheromatous plaques in a group of HIV-infected patients compared with control subjects. Focusing on IMT in the common carotid artery could underestimate carotid IMT values. In the internal carotid artery, which has also been correlated with the risk of suffering a myocardial infarction or stroke, it is more likely to find focal IMT thickenings for flow-mediated reasons [5]. This could be one source of the contradictory results among the cited studies.
The normal rate of carotid IMT progression in the general population has been set at 0.01 mm/year [6]. In the report of Currier et al. [1] the follow-up period lasted for 96 weeks, but the data were analysed as a single measurement. It is likely that in this design the effects of time on the course of carotid IMT have been underestimated.
Atherosclerosis is an inflammatory disease [7] and HIV-infected patients are in a chronic inflammation status as a result of chronic infection. It is of particular interest to address non-classic cardiovascular risk factors, such as inflammatory-related factors, in the study of atherosclerosis in these patients. Alonso-Villaverde et al. [8] identified, in HIV-infected patients, a polymorphism in the promoter region of the monocyte chemoattractant protein 1 gene associated with a fivefold increased risk of developing subclinical atherosclerosis, and, no doubt, further studies will identify more candidate inflammation-related molecules implicated in the development of atherosclerosis [9].
The rate of myocardial infarction in HIV-infected patients is related to the years of exposure to protease inhibitors, and the cardiovascular risk in these patients is higher than that in control subjects [10]. A standardized, easy-to-use and reproducible method to assess asymptomatic atherosclerosis is highly desirable, and the measurement of carotid IMT would appear to be appropriate and effective for this purpose. We ought to implement a standardized IMT protocol, which, in turn, would lead us to a better understanding of subclinical atherosclerosis in these patients.
References
1. Currier JS, Kendall MA, Zackin R, Henry WK, Alston-Smith B, Torriani FJ, et al. Carotid artery intima-media thickness and HIV infection: traditional risk factors overshadow impact of protease inhibitor exposure. AIDS 2005; 19:927-933.
2. O'Leary DH, Polak JF. Intima-media thickness: a tool for atherosclerosis imaging and event prediction. Am J Cardiol 2002; 90:18L-21L.
3. Maggi P, Serio G, Epifani G, Fiorentino G, Saracino A, Fico C, et al. Premature lesions of the carotid vessels in HIV-1-infected patients treated with protease inhibitors. AIDS 2000; 14:123-128.
4. Depairon M, Chessex S, Sudre P, Rodondi N, Doser N, Chave JP, et al. Premature atherosclerosis in HIV-infected individuals focus on protease inhibitor therapy. AIDS 2001; 15:329-334.
5. O'Leary DH, Polak JF, Kronmal RA, Savage PJ, Borhani NO, Kittner SJ, et al. Thickening of the carotid wall. A marker for atherosclerosis in the elderly? Cardiovascular Health Collaborative Research Group. Stroke 1996; 27:224-231.
6. Hsue PY, Lo JC, Franklin A, Bolger AF, Martin JN, Deeks SG, Waters DD. Progression of atherosclerosis as assessed by carotid intima-media thickness in patients with HIV infection. Circulation 2004; 109:1603-1608.
7. Ross R. Atherosclerosis - an inflammatory disease. N Engl J Med 1999; 340:115-126.
8. Alonso-Villaverde C, Coll B, Parra S, Montero M, Calvo N, Tous M, et al. Atherosclerosis in patients infected with HIV is influenced by a mutant monocyte chemoattractant protein-1 allele. Circulation 2004; 110:2204-2209.
9. Coll B, Alonso-Villaverde C, Parra S, Montero M, Tous M, Joven J, Masana L. The stromal derived factor-1 mutated allele [SDF1-3'A] is associated with a lower presence of atherosclerosis in HIV-infected patients. AIDS 2005; 19: in press.
10. Friis-Moller N, Sabin CA, Weber R, d'Arminio Monforte A, El-Sadr WM, Reiss P, et al. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 2003; 349:1993-2003.
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