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Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction.
Eur Heart J. 1999 Jul; 20(14):1039-43.EH

Abstract

AIMS

Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis. Cell adhesion molecules, expressed on endothelial cells and leukocytes, mediate transendothelial migration of leukocytes into the vessel wall, but also circulate in soluble forms. In the present study we related soluble cell adhesion molecules to the risk of suffering a cardiovascular death or a non-fatal myocardial infarction (cardiovascular death/myocardial infarction) in a substudy to the Angina Prognosis Study in Stockholm (APSIS).

METHODS AND RESULTS

Soluble intercellular adhesion molecule-1, vascular adhesion molecule-1 and E-selectin were measured in serum collected on inclusion in the APSIS study. During follow-up, seven patients suffered non-fatal myocardial infarction or cardiovascular death, whereas 86 patients were event-free. Cardiovascular death/myocardial infarction was associated with elevated intercellular adhesion molecule-1 (354+/-142 vs 282+/-62ng x ml-1;P<0.01) and vascular adhesion molecule-1 (538+/-138 vs 433+/-135ng x ml-1;P =0.05), and E-selectin levels tended to be higher (72+/-54 vs 49+/-20ng x ml-1). Clinical risk factors (history of hypertension, previous myocardial infarction, diabetes and smoking) were more abundant in the event group. Subgroup analyses showed that hypertension, smoking or male sex were associated with elevated intercellular adhesion molecule-1, whereas previous myocardial infarction or male sex were associated with elevated vascular adhesion molecule-1.

CONCLUSION

Patients with stable angina pectoris who developed cardiovascular death/myocardial infarction had elevated serum levels of soluble cell adhesion molecules, indicating increased inflammatory activity. The value of soluble cell adhesion molecules as prognostic markers in patients with stable ischaemic heart disease merits further study.

Authors+Show Affiliations

Department of Clinical Pharmacology, Karolinska Hospital, Stockholm, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10381855

Citation

Wallén, N H., et al. "Elevated Serum Intercellular Adhesion Molecule-1 and Vascular Adhesion Molecule-1 Among Patients With Stable Angina Pectoris Who Suffer Cardiovascular Death or Non-fatal Myocardial Infarction." European Heart Journal, vol. 20, no. 14, 1999, pp. 1039-43.
Wallén NH, Held C, Rehnqvist N, et al. Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction. Eur Heart J. 1999;20(14):1039-43.
Wallén, N. H., Held, C., Rehnqvist, N., & Hjemdahl, P. (1999). Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction. European Heart Journal, 20(14), 1039-43.
Wallén NH, et al. Elevated Serum Intercellular Adhesion Molecule-1 and Vascular Adhesion Molecule-1 Among Patients With Stable Angina Pectoris Who Suffer Cardiovascular Death or Non-fatal Myocardial Infarction. Eur Heart J. 1999;20(14):1039-43. PubMed PMID: 10381855.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction. AU - Wallén,N H, AU - Held,C, AU - Rehnqvist,N, AU - Hjemdahl,P, PY - 1999/6/26/pubmed PY - 1999/6/26/medline PY - 1999/6/26/entrez SP - 1039 EP - 43 JF - European heart journal JO - Eur Heart J VL - 20 IS - 14 N2 - AIMS: Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis. Cell adhesion molecules, expressed on endothelial cells and leukocytes, mediate transendothelial migration of leukocytes into the vessel wall, but also circulate in soluble forms. In the present study we related soluble cell adhesion molecules to the risk of suffering a cardiovascular death or a non-fatal myocardial infarction (cardiovascular death/myocardial infarction) in a substudy to the Angina Prognosis Study in Stockholm (APSIS). METHODS AND RESULTS: Soluble intercellular adhesion molecule-1, vascular adhesion molecule-1 and E-selectin were measured in serum collected on inclusion in the APSIS study. During follow-up, seven patients suffered non-fatal myocardial infarction or cardiovascular death, whereas 86 patients were event-free. Cardiovascular death/myocardial infarction was associated with elevated intercellular adhesion molecule-1 (354+/-142 vs 282+/-62ng x ml-1;P<0.01) and vascular adhesion molecule-1 (538+/-138 vs 433+/-135ng x ml-1;P =0.05), and E-selectin levels tended to be higher (72+/-54 vs 49+/-20ng x ml-1). Clinical risk factors (history of hypertension, previous myocardial infarction, diabetes and smoking) were more abundant in the event group. Subgroup analyses showed that hypertension, smoking or male sex were associated with elevated intercellular adhesion molecule-1, whereas previous myocardial infarction or male sex were associated with elevated vascular adhesion molecule-1. CONCLUSION: Patients with stable angina pectoris who developed cardiovascular death/myocardial infarction had elevated serum levels of soluble cell adhesion molecules, indicating increased inflammatory activity. The value of soluble cell adhesion molecules as prognostic markers in patients with stable ischaemic heart disease merits further study. SN - 0195-668X UR - https://www.unboundmedicine.com/medline/citation/10381855/Elevated_serum_intercellular_adhesion_molecule_1_and_vascular_adhesion_molecule_1_among_patients_with_stable_angina_pectoris_who_suffer_cardiovascular_death_or_non_fatal_myocardial_infarction_ L2 - https://academic.oup.com/eurheartj/article-lookup/doi/10.1053/euhj.1999.1451 DB - PRIME DP - Unbound Medicine ER -