Disturbance of macro- and microcirculation: relations with pulse pressure and cardiac organ damage

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 293; no. 1; pp. H1 - H7
• Main Authors: Safar, Michel E, Lacolley, P
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2007
• Subjects: Animals; Blood Pressure; Cardiovascular system; Heart - physiopathology; Heart attacks; Heart Diseases - physiopathology; Humans; Kinases; Microcirculation - physiopathology; Models, Cardiovascular; Older people; Pressure; Pulsatile Flow; Signal transduction
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00063.2007

1 Paris-Descartes University, Faculty of Medicine; Hôtel-Dieu Hospital, Diagnosis Center Assistance Publique-Hôpitaux de Paris, Paris, France; and 2 Faculté de Médecine de Nancy, Nancy University, Nancy, France Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the heart. The transition from pulsatile to steady pressure is influenced by several factors as wave travel, damping, and reflections, which are mainly determined by the impedance mismatch between large vessels and arteriolar bifurcations. The mechanism(s) behind the dampening of pressure wave in the periphery and the links between central and peripheral pulsatile pressure (PP) may determine cardiac damage. Active pathways participate to pulse widening and changes in pulse amplitude in microvessels. Steady and cyclic stresses operate through different transduction mechanisms, the former being focal adhesion kinase and the latter being free radicals and oxidative stress. Independently of mechanics, calcifications and attachment molecules contribute to enhance vessel wall stiffness through changes in collagen cross-links, proteoglycans, integrins, and fibronectin. Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted. Such circumstances, observed in old subjects with systolic hypertension and/or Type 2 diabetes mellitus, particularly under high-sodium diet, cause cardiac damage and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly. microvessels; end-organ damage Address for reprint requests and other correspondence: Michel Safar, Centre de Diagnostic, Hôtel-Dieu, 1, place du Parvis Notre-Dame, 75181 Paris Cedex 04 (e-mail: michel.safar{at}htd.aphp.fr )