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Coronary Hemodynamics and Atherosclerotic Wall Stiffness: a Vicious Cycle Q Medical Hypotheses (2007) 69, 349–355 http://intl.elsevierhealth.com/journals/mehy Coronary hemodynamics and atherosclerotic wall stiffness: A vicious cycle q Yiannis S. Chatzizisis *, George D. Giannoglou Cardiovascular Engineering and Atherosclerosis Laboratory, 1st Cardiology Department, AHEPA University Hospital, Aristotle University Medical School, Thessaloniki, Greece Received 23 November 2006; accepted 26 November 2006 Summary Local hemodynamic environment, including low shear stress and increased tensile stress, determines the localization, growth and progression of coronary atherosclerosis. As atherosclerotic lesions evolve, the diseased coronary arteries undergo local quantitative and qualitative changes in their wall, and progressively become stiff. Arterial stiffening amplifies the atherogenic local hemodynamic environment, initiating a self-perpetuating vicious cycle, which drives the progression of atherosclerosis and the formation of atherosclerotic plaque. In vivo evidence indicates that endothelial dysfunction is associated with arterial stiffness, an association that creates a challenging perspective of utilizing stiffness as an early marker of endothelial dysfunction and future atherosclerosis. Coronary stiffening is also associated with vascular remodeling, which is a major determinant of the natural history of atherosclerotic plaques. Thus, arterial stiffness may constitute a useful marker for the identification of the remodeling pattern, in particular expansive remodeling, which is closely associated with high-risk plaques. The early identification of endothelial dysfunction, or a high-risk plaque may enable the early adoption of preventive measures to improve endothelial function, or justify pre-emptive local interventions in high-risk regions to prevent future acute coronary syndromes. Further experimental and perspective clinical studies are needed for the investigation of these perspectives, whereas the development of new modalities for non-invasive and reliable assessment of coronary stiffness is anticipated to serve these studies. c 2007 Elsevier Ltd. All rights reserved. Introduction Although several studies have focused on the patho- physiology of stiffening of large elastic-type arter- Arterial stiffness has been proposed to be an impor- ies (e.g. aorta, carotid arteries, brachial arteries) tant determinant of cardiovascular risk [1]. [2–4], the pathophysiology of coronary arterial stiffening remains unclear. In this work we provide q This work was funded by the Greek State Scholarships Foundation, the Aristotle University Research Committee, and the theoretical foundation of normal coronary arte- the Hellenic Harvard Foundation. rial structure and function, and discuss the patho- * Corresponding author. Present address: Cardiovascular Divi- physiologic basis of the continuous and dynamic sion, Brigham and Women’s Hospital, Harvard Medical School, interplay between the local coronary hemodynamic 1620 Tremont Street, 3rd Floor, Boston, MA 02120, United environment and wall stiffness, an interplay that States. Tel.: +1 617 525 7745; fax: +1 617 734 1874. E-mail address: [email protected] (Y.S. Chatzizisis). eventually drives the development and progression 0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2006.11.053 350 Chatzizisis and Giannoglou of atherosclerosis, as well as arterial remodeling. slow systolic anterograde flow accompanied by an Better understanding of the pathogenetic mecha- increase in their diameter [7–10]. Although it nisms of atherosclerotic wall stiffening is antici- would be anticipated that during systole the back- pated to advance our knowledge about the ward flow derived by the collapsed subendocardial pathobiology of coronary atherosclerosis. vessels would induce a retrograde flow in the sub- epicardial and epicardial arteries, in fact, this ret- rograde flow is concealed by the high capacitance Structural, functional and flow of the extramural epicardial arteries, which are di- characteristics of normal coronary lated due to their elastic properties. Also, forward arteries compression waves derived by the increased aortic pressure contribute to the systolic forward epicar- The coronary arteries originate from the aorta, con- dial flow [7,8]. However, a small component of tinue along the surface of the heart surrounded by backward flow may occur, especially at the onset the pericardium (i.e. epicardial segments), and pen- of ventricular contraction, accounting for the com- etrate into the myocardium (i.e. intramyocardial plexity of the systolic flow [8]. In diastole, as the segments), where they deliver blood [5]. There are ventricular myocardium relaxes, the compressive several structural and functional differences be- impediment to intramyocardial arteries resolves, tween the epicardial and intramyocardial coronary and the dilated extramural segments discharge segments [5]. The former are elastic-type conduit the stored blood through the microcirculation, arteries, and their wall extracellular matrix (ECM) resulting in a forward and accelerated flow in the contains a complex mixture of collagen and elastin entire coronary arterial bed in order to maintain fibers within a ground substance of proteoglycans myocardial perfusion [7,8]. and glycosaminoglycans. Collagen fibres primarily provide integrity and tensile strength to the arterial wall, whereas elastin fibres regulate the elastic Local hemodynamic environment properties of the wall. Both these ECM proteins, as promotes atherosclerosis well as their cellular sources (i.e. vascular smooth muscle cells, VSMCs) are the major structural deter- The local hemodynamic environment within the minants of the ability of an artery to distend, the so- coronary arteries constitutes a major determinant called compliance [6]. The content of collagen and of focal atherogenesis and atherosclerotic plaque elastin within the arterial wall remains relatively development [11] (Fig. 2). The main components stable through a dynamic process of synthesis and of this environment include shear stress (SS) and breakdown, thereby maintaining normal wall com- tensile stress (TS) [6]. SS is the tangential force de- pliance. Functionally, the epicardial arteries are rived by the friction of the flowing blood on the responsible for the conduction of blood to intramu- endothelial cells (ECs). SS is defined as the product ral segments, as well as for the buffering effect, of the blood viscosity (l) and the flow velocity gra- storing blood during systole and discharging it in dient at the wall (SS = l\dv/ds). TS is the blood diastole. Contrary to extramural arteries, intramu- pressure-derived force imposed circumferentially ral arteries are primarily muscle-type arteries on the arterial wall. TS is primarily sensed by responsible for the coronary peripheral resistances. VSMCs, and can be approximated by an equation In normal, non-atherosclerotic coronary arter- related to the law of Laplace, T = P\r/t, where P ies, blood flow varies over the cardiac cycle [5] is the blood pressure, r is the lumen radius, and t (Fig. 1). The major determinants of coronary flow is the wall thickness. According to this equation, are the compressive resistance of the ventricular higher blood pressures, larger lumen diameters, myocardium and the driving pressure (i.e. the dif- and thinner arterial walls lead to increased TS. ference between aortic and intraventricular pres- Although the entire coronary tree is exposed to sure); these forces create forward and backward the atherogenic effect of the systemic risk factors, compression waves (‘‘pushing’’ effect) and expan- atherosclerotic lesions form at specific regions of sion waves (‘‘pulling’’ effect), which interplay with the arterial tree, such as in the vicinity of branch each other and determine eventually the direction points, the outer wall of bifurcations, and the inner of flow at each time-point of the cardiac cycle wall of curvatures [11]. In these regions disturbed [7,8]. In systole, the intramural arteries, especially laminar flow occurs, yielding a low and oscillatory in the left coronary system, experience a retro- SS, which is characterized by low time-averaged grade flow due to the myocardial compression. Un- values (<10–12 dyn/cm2), as well as significant like subendocardial arteries, the subepicardial and variations in direction and magnitude over short epicardial segments are mainly characterized by a distances [11–13] (Fig. 2). Low and oscillatory SS Coronary hemodynamics and atherosclerotic wall stiffness: A vicious cycle 351 Figure 1 Conceptual model presenting the implication of reduced coronary wall compliance in the modulation of a local atherogenic hemodynamic environment. Physiologically, the systolic buffering effect in non-diseased elastic epicardial segments (upper left) results in a normal biphasic flow pattern during the cardiac cycle with a difference Dn between peak systolic and peak diastolic flow (upper right) [5,6,10]. On the contrary, in atherosclerotic coronaries, reduced compliance attenuates the systolic buffering effect (lower left), thereby augmenting the biphasic flow pattern (Dr > Dn), and leading to lower and more oscillatory shear stress, especially in regions susceptible to atherosclerosis (lower right). Dashed lines represent the change of the coronary lumen during systole. Figure 2 Local hemodynamic environment, atherosclerosis, and arterial stiffness are involved in a self-perpetuating vicious cycle, ultimately regulating coronary wall function, plaque
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