Review article
Coronary pressure-flow relations as basis for the understanding of coronary physiology

https://doi.org/10.1016/j.yjmcc.2011.07.025Get rights and content

Abstract

Recent technological advancements in the area of intracoronary physiology, as well as non-invasive contrast perfusion imaging, allow to make clinical decisions with respect to percutaneous coronary interventions and to identify microcirculatory coronary pathophysiology. The basic characteristics of coronary hemodynamics, as described by pressure–flow relations in the normal and diseased heart, need to be understood for a proper interpretation of these physiological measurements. Especially the hyperemic coronary pressure–flow relation, as well as the influence of cardiac function on it, bears great clinical significance. The interaction of a coronary stenosis with the coronary pressure–flow relation can be understood from the stenosis pressure drop–flow velocity relationship. Based on these relationships the clinically applied concepts of coronary flow velocity reserve, fractional flow reserve, stenosis resistance and microvascular resistance are discussed. Attention is further paid to the heterogeneous nature of myocardial perfusion, the vulnerability of the subendocardium and the role of collateral flow on hyperemic coronary pressure–flow relations. This article is part of a Special Issue entitled “Coronary Blood Flow”.

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

References (85)

  • J.D. Tune et al.

    Matching coronary blood flow to myocardial oxygen consumption

    J Appl Physiol

    (2004)
  • W.V. Restorff et al.

    Exercise induced augmentation of myocardial oxygen extraction in spite of normal coronary dilatory capacity in dogs

    Pflugers Arch Eur J Phys

    (1977)
  • E. Bassenge et al.

    Endothelial and neuro-humoral control of coronary blood flow in health and disease

    Rev Physiol Biochem Pharmacol

    (1990)
  • G.B. Scaramucci

    De motu cordis

  • P. Knaapen et al.

    Coronary microvascular resistance: methods for its quantification in humans

    Basic Res Cardiol

    (2009)
  • S. Plein et al.

    High spatial resolution myocardial perfusion cardiac magnetic resonance for the detection of coronary artery disease

    Eur Heart J

    (2008)
  • P. Mosher et al.

    Control of coronary blood flow by an autoregulatory mechanism

    Circ Res

    (1964)
  • I. Vergroesen et al.

    Quantification of O2 consumption and arterial pressure as independent determinants of coronary flow

    Am J Physiol

    (1987)
  • A.J. Drake-Holland et al.

    Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog

    J Physiol

    (1984)
  • J.D. Tune et al.

    Adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise

    Am J Physiol Heart Circ Physiol

    (2000)
  • D. Duncker et al.

    Alterations in vasomotor control of coronary resistance vessels in remodelled myocardium of swine with a recent myocardial infarction

    Med Biol Eng Comput

    (2008)
  • I. Vergroesen et al.

    Myocardial oxygen supply: demand ratio as reference for coronary vasodilatory drug effects in humans

    Heart

    (1997)
  • A.J.M. Cornelissen et al.

    Balance between myogenic, flow-dependent, and metabolic flow control in coronary arterial tree: a model study

    Am J Physiol Heart Circ Physiol

    (2002)
  • C.J. Jones et al.

    Regulation of coronary blood flow: coordination of heterogeneous control mechanisms in vascular microdomains

    Cardiovasc Res

    (1995)
  • C.J. Jones et al.

    In vivo and in vitro vasoactive reactions of coronary arteriolar microvessels to nitroglycerin

    Am J Physiol Heart Circ Physiol

    (1996)
  • M. Siebes

    Intracoronary doppler-based techniques for stenosis appraisal

  • M. Siebes et al.

    Single-wire pressure and flow velocity measurement to quantify coronary stenosis hemodynamics and effects of percutaneous interventions

    Circulation

    (2004)
  • W. Wijns et al.

    Guidelines on myocardial revascularization: The task force on myocardial revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)

    Eur Heart J

    (2010)
  • G. Heusch

    Adenosine and maximum coronary vasodilation in humans: myth and misconceptions in the assessment of coronary reserve

    Basic Res Cardiol

    (2010)
  • K.L. Gould

    Quantification of coronary artery stenosis in vivo

    Circ Res

    (1985)
  • J.I.E. Hoffman

    Maximal coronary flow and the concept of coronary vascular reserve

    Circulation

    (1984)
  • M.J. Kern et al.

    Physiological assessment of coronary artery disease in the cardiac catheterization laboratory: a scientific statement from the American Heart Association Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology

    Circulation

    (2006)
  • J.I.E. Hoffman

    Problems of coronary flow reserve

    Ann Biomed Eng

    (2000)
  • N.G. Uren et al.

    Effect of aging on myocardial perfusion reserve

    J Nucl Med

    (1995)
  • K. Rajappan et al.

    Mechanisms of coronary microcirculatory dysfunction in patients with aortic stenosis and angiographically normal coronary arteries

    Circulation

    (2002)
  • D. Baumgart et al.

    Improved assessment of coronary stenosis severity using the relative flow velocity reserve

    Circulation

    (1998)
  • C. Ince et al.

    Heterogeneity of the hypoxic state in rat heart is determined at capillary level

    Am J Physiol

    (1993)
  • R.E. Austin et al.

    Profound spatial heterogeneity of coronary reserve. Discordance between patterns of resting and maximal myocardial blood flow

    Circ Res

    (1990)
  • J.I. Hoffman

    Heterogeneity of myocardial blood flow

    Basic Res Cardiol

    (1995)
  • D.F. Young et al.

    Hemodynamics of arterial stenoses at elevated flow rates

    Circ Res

    (1977)
  • N.H.J. Pijls et al.

    Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty

    Circulation

    (1993)
  • F.L. Hanley et al.

    The effect of coronary inflow pressure on coronary vascular resistance in the isolated dog heart

    Circ Res

    (1984)
  • Cited by (90)

    • Unraveling the Gordian knot of coronary pressure-flow autoregulation

      2024, Journal of Molecular and Cellular Cardiology
    • The Impact of Blood Pressure Variability on Coronary Arterial Lumen Dimensions as Assessed by Optical Coherence Tomography in Patients with ST-Elevation Myocardial Infarction

      2019, Cardiovascular Revascularization Medicine
      Citation Excerpt :

      Both metabolic and myogenic theories have been proposed to explain the autoregulation of coronary flow. Based on the metabolic theory, a decrease in coronary artery pressure reduces flow, which results in coronary vasodilation by decreasing myocardial substrate availability or increasing production of metabolites [16–18]. While according to the myogenic theory, an intrinsic mechanism in vascular smooth muscle regulates resistance in response to changes in transmural pressure thus can change coronary vessel diameter in response to pressure.

    • Coronary Hemodynamics in Patients With Severe Aortic Stenosis and Coronary Artery Disease Undergoing Transcatheter Aortic Valve Replacement: Implications for Clinical Indices of Coronary Stenosis Severity

      2018, JACC: Cardiovascular Interventions
      Citation Excerpt :

      Restriction of aortic valve opening, a systolic phenomenon, therefore does not affect flow during the wave-free period of diastole, because regardless of the severity of AS, the aortic valve leaflets are closed and therefore the aortic valve is not actively contributing to coronary flow. Maximal blood flow in a coronary artery is affected by microvascular structure, function, LV end-diastolic pressure, and right atrial pressure (20–23). Any condition that affects 1 of these determinants will affect maximal flow.

    View all citing articles on Scopus
    View full text