PMID- 20172413
OWN - NLM
STAT- MEDLINE
DCOM- 20100511
LR  - 20131121
IS  - 0213-005X (Print)
IS  - 0213-005X (Linking)
VI  - 27 Suppl 1
DP  - 2009 Sep
TI  - [Physiopathology of cardiovascular disease in HIV-infected patients].
PG  - 33-9
LID - 10.1016/S0213-005X(09)73443-3 [doi]
AB  - Patients with HIV have an increased risk of cardiovascular events related to 
      arteriosclerosis. The virus is able to replicate in the arterial wall, implying 
      severe inflammatory dysfunction. When this inflammatory dysfunction is 
      accompanied by the metabolic disorders associated with HIV infection and its 
      treatment, progression of the atheroma plaque is accelerated. HIV shows high 
      replication in CD4+ T lymphocytes, which accumulate in the subendothelial space. 
      CD4+ T lymphocytes produce viral proteins such as Tat, which leads to synthesis 
      of chemokines such as monocyte chemoattractant protein-1 (MCP-1) or vascular cell 
      adhesion molecule-1. This combination will attract monocytes into the 
      subendothelial space, which penetrate rapidly if infected. These monocytes will 
      also infect the smooth muscle cells, producing the initiation of endothelial 
      dysfunction. Dyslipidemia and insulin resistance will then provoke modification 
      of lipoproteins, which will be phagocytized through CD36 receptors by macrophages 
      of the subendothelial space. Reverse cholesterol transport will be damaged, since 
      the Nef viral protein is able to block the ABCA1 receptor. These events will 
      produce rapid cholesterol accumulation in the atheroma plaque nucleus. 
      Subsequently, the plaque will become complicated, either by rupture or erosion. 
      Then, a juxtalesional thrombus is formed, where the platelet is activated.
CI  - Copyright 2009 Elsevier Espana S.L. All rights reserved.
FAU - Alonso-Villaverde Lozano, Carlos
AU  - Alonso-Villaverde Lozano C
AD  - Unidad VIH, Servicio de Medicina Interna, Centre de Recerca Biomedica, Hospital 
      Universitario San Juan de Reus, Reus, Tarragona, Espana. 
      cavillaverde@grupsagessa.com
LA  - spa
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Fisiopatologia de la enfermedad cardiovascular en pacientes con VIH.
PL  - Spain
TA  - Enferm Infecc Microbiol Clin
JT  - Enfermedades infecciosas y microbiologia clinica
JID - 9104081
RN  - 0 (Chemokines)
RN  - 0 (Human Immunodeficiency Virus Proteins)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Arteriosclerosis/etiology/physiopathology
MH  - CD4-Positive T-Lymphocytes/pathology/virology
MH  - Cardiovascular Diseases/etiology/*physiopathology/virology
MH  - Chemokines/metabolism
MH  - Chemotaxis, Leukocyte
MH  - Cholesterol/metabolism
MH  - Disease Progression
MH  - Dyslipidemias/complications
MH  - Endothelium, Vascular/physiopathology/*virology
MH  - HIV/physiology
MH  - HIV Infections/*complications/drug therapy/metabolism
MH  - Human Immunodeficiency Virus Proteins/physiology
MH  - Humans
MH  - Inflammation
MH  - Insulin Resistance
MH  - Macrophages/physiology
MH  - Models, Biological
MH  - Phagocytosis
MH  - Risk
MH  - Thrombosis/etiology
MH  - Virus Replication
RF  - 61
EDAT- 2010/02/23 06:00
MHDA- 2010/05/12 06:00
CRDT- 2010/02/23 06:00
PHST- 2010/02/23 06:00 [entrez]
PHST- 2010/02/23 06:00 [pubmed]
PHST- 2010/05/12 06:00 [medline]
AID - S0213-005X(09)73443-3 [pii]
AID - 10.1016/S0213-005X(09)73443-3 [doi]
PST - ppublish
SO  - Enferm Infecc Microbiol Clin. 2009 Sep;27 Suppl 1:33-9. doi: 
      10.1016/S0213-005X(09)73443-3.