Inflammatory changes during the 'common cold' are associated with platelet activation and increased reactivity of platelets to agonists

Rolf Kreutz, Udaya S. Tantry, Kevin P. Bliden, Paul A. Gurbel

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Epidemiologic studies have shown increased rates of myocardial infarction after upper respiratory tract infections. We hypothesized that changes in platelet activation and reactivity and inflammation occur during the 'common cold'. Previously healthy individuals with viral upper respiratory tract infections were studied (n = 18). Venous blood samples were obtained during the time of infection and again after 6 weeks. Platelet reactivity was higher during the 'common cold' as measured by low-dose ADP-induced aggregation (46 ± 28 versus 27 ± 21% 6 weeks after presentation, P = 0.003) and was higher than control individuals (22 ± 8%, P = 0.003). Platelet P-selectin expression increased during illness (2.3 ± 0.2% CD62-positive platelets versus 1.8 ± 0.1% at 6 weeks after presentation, P = 0.017; and 1.7 ± 0.2% in the control group, P = 0.03). C-reactive protein (3.7 ± 1.3 versus 2.2 ± 1.5 mg/l, P = 0.004) and tumor necrosis factor-α (27.6 ± 28 versus 12.7 ± 9 pg/ml, P = 0.03) were increased during the 'common cold'. There were no significant differences in levels of soluble P-selectin (P = 0.18), soluble vascular adhesion molecule-1 (P = 0.59) and soluble intercellular adhesion molecule-1 (P = 0.23). Increased platelet reactivity and activation during the 'common cold' are associated with inflammation as measured by increased levels of C-reactive protein and tumor necrosis factor-α, but not increased levels of endothelial markers. These findings support a pro-aggregatory state that, in part, explains the thrombotic events shown by epidemiological studies.

Original languageEnglish (US)
Pages (from-to)713-718
Number of pages6
JournalBlood Coagulation and Fibrinolysis
Volume18
Issue number8
DOIs
StatePublished - Dec 2007
Externally publishedYes

Fingerprint

Common Cold
Platelet Activation
Blood Platelets
P-Selectin
Respiratory Tract Infections
C-Reactive Protein
Epidemiologic Studies
Tumor Necrosis Factor-alpha
Inflammation
Intercellular Adhesion Molecule-1
Adenosine Diphosphate
Blood Vessels
Myocardial Infarction
Control Groups
Infection

Keywords

  • C-reactive protein
  • Infection
  • P-selectin
  • Platelets
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Hematology

Cite this

Inflammatory changes during the 'common cold' are associated with platelet activation and increased reactivity of platelets to agonists. / Kreutz, Rolf; Tantry, Udaya S.; Bliden, Kevin P.; Gurbel, Paul A.

In: Blood Coagulation and Fibrinolysis, Vol. 18, No. 8, 12.2007, p. 713-718.

Research output: Contribution to journalArticle

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abstract = "Epidemiologic studies have shown increased rates of myocardial infarction after upper respiratory tract infections. We hypothesized that changes in platelet activation and reactivity and inflammation occur during the 'common cold'. Previously healthy individuals with viral upper respiratory tract infections were studied (n = 18). Venous blood samples were obtained during the time of infection and again after 6 weeks. Platelet reactivity was higher during the 'common cold' as measured by low-dose ADP-induced aggregation (46 ± 28 versus 27 ± 21{\%} 6 weeks after presentation, P = 0.003) and was higher than control individuals (22 ± 8{\%}, P = 0.003). Platelet P-selectin expression increased during illness (2.3 ± 0.2{\%} CD62-positive platelets versus 1.8 ± 0.1{\%} at 6 weeks after presentation, P = 0.017; and 1.7 ± 0.2{\%} in the control group, P = 0.03). C-reactive protein (3.7 ± 1.3 versus 2.2 ± 1.5 mg/l, P = 0.004) and tumor necrosis factor-α (27.6 ± 28 versus 12.7 ± 9 pg/ml, P = 0.03) were increased during the 'common cold'. There were no significant differences in levels of soluble P-selectin (P = 0.18), soluble vascular adhesion molecule-1 (P = 0.59) and soluble intercellular adhesion molecule-1 (P = 0.23). Increased platelet reactivity and activation during the 'common cold' are associated with inflammation as measured by increased levels of C-reactive protein and tumor necrosis factor-α, but not increased levels of endothelial markers. These findings support a pro-aggregatory state that, in part, explains the thrombotic events shown by epidemiological studies.",
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