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

B. Khan, W. A. Bauman, A. K. Sinha, N. N. Kahn

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

Abstract

Study design: Review. Objectives: 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.ConclusionsSubjects 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.

Original languageEnglish
Pages (from-to)858-866
Number of pages9
JournalSpinal Cord
Volume49
Issue number8
DOIs
StatePublished - Aug 2011

Keywords

  • antibody
  • coronary heart disease
  • insulin
  • platelets
  • prostacyclin

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