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Non-conventional hemostatic risk factors for coronary heart disease in individuals with spinal cord injury

KHAN B; BAUMAN WA; SINHA AK; KAHN N
SPINAL CORD , 2011, vol. 49, n° 8, p. 858-866
Doc n°: 153063
Localisation : Centre de Réadaptation de Lay St Christophe

D.O.I. : http://dx.doi.org/DOI:10.1038/sc.2011.33
Descripteurs : AE21 - ORIGINE TRAUMATIQUE, FA331 - MALADIE CORONARIENNE

In subjects with spinal cord injury (SCI),
there is strong evidence for platelet hyperactivity, which may stimulate
atherosclerosis and coronary heart disease (CHD). The literature was reviewed.
BACKGROUND: Individuals with SCI develop premature CHD. In addition to the
conventional risk factors associated with CHD, there are pathologic hematological
factors involved in atherogenesis that are similar to those that have been
demonstrated in individuals with diabetes, and these hematological factors might
affect individuals with SCI. One such hematological factor, platelet aggregation,
is essential for the development of CHD, which results from thrombus formation in
the coronary vasculature. Prostacyclin (PGI(2)) is a potent inhibitor of platelet
aggregation and is thought to have a beneficial role in inhibiting atherogenesis;
therefore, it is possible that individuals with SCI have impaired PGI(2) receptor
function. METHODS: We reviewed the literature by conducting a search using PubMed
(1970-2007). RESULTS: Acute thrombosis is emerging as an important factor in the
etiology of CHD and therefore could mediate the risk of CHD in persons with SCI,
in addition to previously known risk factors such as hyperlipidemia,
hypertension, hyperlipidemia, diabetes mellitus and hyperinsulinemia. Because
PGI(2) may retard atherogenesis through its inhibitory effects on platelet
function, we discuss the effects of PGI(2) on platelets in persons with SCI in
this review. CONCLUSIONS: Subjects with chronic SCI develop abnormal platelet
function, resulting in the production of atherogenic and thrombogenic factors for
the following reasons: (1) the PGI(2) and insulin receptors on their platelets
are impaired; (2) thrombin generation and platelet-derived growth factor release
are elevated; (3) insulin-induced nitric oxide production by platelets is
markedly impaired; and (4) a circulating antibody (immunoglobulin G (IgG)) blocks
the antithrombotic effect of both insulin and PGI(2) receptors. Thus, this IgG
molecule is thought to be one of the pathological mediators of the increased
incidence of CHD in individuals with SCI.

Langue : ANGLAIS

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