ABSTRACT
Acute aortic syndromes are fatal medical conditions including classic acute aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. Given the nonspecific symptoms and signs, a high clinical index of suspicion followed by an imaging study, namely transesophageal echocardiography, computed tomography, and magnetic resonance imaging (sensitivity 98-100% and specificity 95-100%), is a conditio sine qua non for prompt diagnosis of acute aortic syndromes. This article provides an overview of established and emerging approaches for the assessment of acute aortic syndromes, with focus on imaging and biomarkers. In this regard, D-dimer levels (cut-off: 500 ng/ml) may be useful to rule out aortic dissection, if used within the first 24 h after symptom onset.
Subject(s)
Aortic Aneurysm/diagnosis , Aortic Dissection/diagnosis , Atherosclerosis/diagnosis , Diagnostic Imaging/methods , Fibrin Fibrinogen Degradation Products/analysis , Thrombosis/diagnosis , Aortic Dissection/classification , Aortic Aneurysm/classification , Atherosclerosis/blood , Atherosclerosis/classification , Biomarkers/blood , Diagnosis, Differential , Humans , Syndrome , Thrombosis/blood , Thrombosis/classificationABSTRACT
- Vascular cell adhesion molecule-1 (VCAM-1/Vcam1) is a cytokine-inducible member of the immunoglobulin gene superfamily that is expressed by arterial endothelial cells in regions predisposed to atherosclerosis and at borders of atherosclerotic plaques. To determine whether VCAM-1 expression regulates atherosclerotic lesion formation, we crossed Vcam1 domain 4-deficient (D4D) mice, which partially circumvent the embryonic lethality of Vcam1 null mice, with apolipoprotein E null (Apoe(-/-)) mice, which spontaneously develop hypercholesterolemia and atherosclerosis. In the Apoe(-/-) background, mice homozygous for the Vcam1 D4D allele had markedly reduced arterial VCAM-1 expression, monocyte adherence in the aortic root, and fatty streak formation. Heterozygous Vcam1 D4D mice revealed a Vcam1 gene-dosage effect and had intermediate, yet significant, reductions in these parameters. Our data demonstrate that VCAM-1 plays a pivotal role in the initiation of atherosclerosis in Apoe(-/-) mice.
Subject(s)
Arteriosclerosis/etiology , Cell Adhesion , Endothelium, Vascular/physiology , Monocytes/physiology , Vascular Cell Adhesion Molecule-1/genetics , Vascular Cell Adhesion Molecule-1/physiology , Animals , Aorta/metabolism , Apolipoproteins E/genetics , Arteriosclerosis/metabolism , Arteriosclerosis/pathology , Female , Gene Dosage , Gene Targeting , Hypercholesterolemia/etiology , Leukocyte Count , Male , Mice , Mice, KnockoutABSTRACT
Ischemic cardiovascular disease is a common cause of morbidity and mortality in the United States population over the age of 65. Prior clinical studies have demonstrated that the severity of cardiovascular pathophysiology is increased in older individuals. Both in vitro and in vivo experimental studies have shown that age-associated clinical events parallel changes in vascular function. Aging is associated with systemic as well as cardiac alterations in three basic vascular regulatory functions: vascular tone, hemostasis, and vascular repair/angiogenesis. This article reviews the molecular and cellular events that may contribute to senescent cardiac pathology. Indeed, a better understanding of the biology of aging-associated vascular dysfunction is fundamental for the development of therapeutics targeted for the treatment of cardiovascular disease in older individuals.
