Review articleCoronary pressure-flow relations as basis for the understanding of coronary physiology
Highlights
► Hyperemic coronary pressure–flow relations are curvilinear, expressing pressure and cardiac contraction effects. ► Hyperemic coronary perfusion is heterogeneous, with subendocardium especially at risk for underperfusion. ► Physiological indices are preferable over angiographically derived stenosis parameters for clinical decision making. ► Combined pressure and flow velocity data comprehensively assess both epicardial and microvascular compartments. ► Coronary resistance adapts to lowered perfusion pressure distal to a stenosis by microvascular remodeling.
Introduction
The oxygen extraction from the coronary circulation is high and even at baseline conditions approximates 75%, while the overall oxygen extraction in the systemic circulation amounts to 25–30% [1]. In extreme exercise in dogs, coronary venous saturation may be reduced further from 25% to approximately 10% [2], but this increased extraction is much too small to account for the 4 to 5 times increase in oxygen demand that may occur and consequently necessitates an increase in coronary blood flow [1]. Normally, coronary blood flow is well controlled and matched to the oxygen needs of the heart by adapting the caliber of the coronary resistance arteries, including arterioles, via inter-related processes involving mechanisms intrinsic to the vascular wall, as well as metabolic and neurohumoral factors [3], [4].
One of the first observations on coronary physiology several centuries ago was that coronary arterial flow is pulsatile, high in diastole and low in systole [5]. This is opposite to the flow pattern in arteries feeding other organs where flow is high in systole. The particular coronary bi-phasic flow pattern is the result of compressive forces that are exerted by the contracting heart muscle on the embedded microvessels. Hence, the heart impedes its own perfusion by the contraction that is needed to fulfill its principal function.
Many of the physiological phenomena underlying coronary flow regulation have been studied in conscious and unconscious animal preparations where there is great freedom in instrumentation and interventions. More recently, investigation of human coronary physiology has become possible in clinical studies owing to the miniaturization of pressure and flow sensors at the tip of coronary guide wires used during cardiac catheterization and by myocardial perfusion imaging via magnetic resonance imaging, positron emission tomography and contrast echocardiography [6], [7].
The purpose of this paper is to provide a brief overview of some principles of coronary physiology, and how these principles translate to diagnostic applications in clinical practice.
Section snippets
Characteristics and limits of coronary blood flow control
In functional terms, the two major determinants of coronary flow are coronary arterial pressure and myocardial oxygen consumption. It was found very early on that, at constant oxygen consumption, coronary flow is relatively independent of arterial pressure which is referred to as coronary autoregulation [8]. Similarly, at a given coronary arterial pressure, coronary flow increases with oxygen consumption, which is defined as metabolic adaptation. These two mechanisms are interrelated and may
Stenosis pressure gradient–flow velocity relationship
In order to properly assess the physiological significance of an epicardial stenosis on coronary blood flow, it is important to understand the hemodynamic effect of a focal diameter reduction formed by a stenosis.
Total pressure drop across a stenosis is the sum of viscous losses due to friction (Law of Poiseuille) and losses incurred at the exit after acceleration along the throat of the lesion (Law of Bernoulli). The relationship between pressure drop (ΔP) and velocity (v) can be described by
Microvascular resistance and the distribution of myocardial perfusion
Up to this point we have discussed the myocardium as an entity and its perfusion at the level of epicardial arteries. However, perfusion of the myocardium is far from homogeneous and the hemodynamic characteristics measured at the epicardial level reflect a space average state. This implies that overall, the myocardium is perfused well but that certain local areas are predisposed for ischemia. Heterogeneity occurs at different spatial scales, and it is well established that especially the
Conclusions
Coronary pressure–flow relations are at the heart of the mechanistic interpretation of coronary hemodynamics. The autoregulation curves with their parallel shift depending on oxygen consumption are essential for understanding the interplay between coronary pressure and oxygen consumption with the control of blood flow. The hyperemic pressure–flow relation describes the maximal flow that is possible at a given coronary pressure and plays an important role in the definition of coronary flow
Disclosures
None.
Acknowledgments
We acknowledge support by the following grants: The Netherlands Heart Foundation (NHF 2006B186 and NHF 2006B226), the Netherlands Organization for Health Research and Development (ZonMw 911.05.008), and the European Community's Seventh Framework Programme (FP7/2007–2013) under grant agreement no. 224495 (euHeart project). M. C. Rolandi is supported by a PhD Scholarship of the Academic Medical Center. J. P. H. M. van den Wijngaard is funded by a personal grant in the Innovational Research
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