Accounting for the Gregg effect in tetanised coronary arterial pressure-flow relationships

Livingston, J. Z.; Halperin, Henry R.; Yin, F. C. P.

doi:10.1093/cvr/28.2.228

Cited by 12 publications

(6 citation statements)

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“…They found the slope equal to 0.007 g·mm −2 /mmHg or 0.069 kPa/mmHg. As explained above, after dividing by 3, the shear modulus value is calculated as 0.023 kPa/mmHg [27]. This value for the slope is the same order of magnitude as the value we found in this experiment.…”

Section: Discussionsupporting

confidence: 79%

Ultrasound Shear Wave Elasticity Imaging Quantifies Coronary Perfusion Pressure Effect on Cardiac Compliance

Vejdani‐Jahromi

Nagle

Trahey

et al. 2015

IEEE Trans. Med. Imaging

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Diastolic heart failure (DHF) is a major source of cardiac related morbidity and mortality in the world today. A major contributor to, or indicator of DHF is a change in cardiac compliance. Currently, there is no accepted clinical method to evaluate the compliance of cardiac tissue in diastolic dysfunction. Shear wave elasticity imaging (SWEI) is a novel ultrasound-based elastography technique that provides a measure of tissue stiffness. Coronary perfusion pressure affects cardiac stiffness during diastole; we sought to characterize the relationship between these two parameters using the SWEI technique. In this work, we demonstrate how changes in coronary perfusion pressure are reflected in a local SWEI measurement of stiffness during diastole. Eight Langendorff perfused isolated rabbit hearts were used in this study. Coronary perfusion pressure was changed in a randomized order (0–90 mmHg range) and SWEI measurements were recorded during diastole with each change. Coronary perfusion pressure and the SWEI measurement of stiffness had a positive linear correlation with the 95% confidence interval (CI) for the slope of 0.009–0.011 m/s/mmHg (R2 = 0.88). Furthermore, shear modulus was linearly correlated to the coronary perfusion pressure with the 95% CI of this slope of 0.035–0.042 kPa/mmHg (R2 = 0.83). In conclusion, diastolic SWEI measurements of stiffness can be used to characterize factors affecting cardiac compliance specifically the mechanical interaction (cross-talk) between perfusion pressure in the coronary vasculature and cardiac muscle. This relationship was found to be linear over the range of pressures tested.

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Section: Discussionsupporting

confidence: 79%

Ultrasound Shear Wave Elasticity Imaging Quantifies Coronary Perfusion Pressure Effect on Cardiac Compliance

Vejdani‐Jahromi

Nagle

Trahey

et al. 2015

IEEE Trans. Med. Imaging

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“…Reviews of this effect can be found in Downey et al and Westerhof et al 21,22 . Livingston et al showed that there is a linear relationship between the myocardial stiffness and the perfusion pressure corresponding to this effect 4 . The Gregg effect can be small when auto-regulation is intact as the coronary circulation adjusts to maintain flow; however, it has been shown to be pronounced in the isolated heart preparation and during auto-regulation blockade 23 .…”

Section: Discussionmentioning

confidence: 99%

“…Recently, echocardiography-based tissue Doppler, tissue strain and strain rate imaging have been used clinically to assess contractility; however, these techniques do not provide a contractility measurement of the myocardium independent of factors such as intra-ventricular volume or cardiac motion 1–3 . It has been shown that transverse stiffness, measured using small high frequency indentations, is an index of contractility in beating canine inter-ventricular septum 4 . However, none of the available clinical techniques measure systolic stiffness this directly.…”

Section: Introductionmentioning

confidence: 99%

Quantifying Myocardial Contractility Changes Using Ultrasound-Based Shear Wave Elastography

Vejdani‐Jahromi

Freedman

Nagle

et al. 2017

Journal of the American Society of Echocardiography

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BACKGROUND Myocardial contractility, a significant determinant of cardiac function, is valuable for diagnosis and evaluation of treatment in cardiovascular disorders including heart failure. Shear Wave Elasticity Imaging (SWEI) is a newly developed ultrasound-based elastography technique that can directly assess the stiffness of cardiac tissue. The aim of the study was to verify the ability of technique to quantify contractility changes in the myocardium. METHODS In 12 isolated rabbit hearts we made SWEI measurements of systolic stiffness at 5 different coronary perfusion pressures from 0 to 92 mmHg. The changes in coronary perfusion were used to induce acute stepwise reversible changes in cardiac contractility via the Gregg effect. The Gregg effect is the dependency of contractility on coronary perfusion. In 4 of the hearts, we repeated the measurements after delivery of Gadolinium, which is known to block the Gregg effect. RESULTS Systolic stiffness measured by SWEI changed linearly with coronary perfusion pressure with a slope of 0.27 kPa/mmHg (mean of 95% CI, R2=0.73). As expected the change in contractility due to the Gregg effect was blocked by Gadolinium with a significant reduction of the slope to 0.08 kPa/mmHg. CONCLUSION SWEI measurements of systolic stiffness provide an index of contractility in the unloaded isolated rabbit heart. While this study was done under ideal imaging conditions and with non-physiological loading conditions, it reinforces the concept that this ultrasound technique has the potential to provide a direct and noninvasive index of cardiac contractility.

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“…A) SYSTOLIC STIFFNESS. Another suggested explanation of the Gregg effect is based on the concept of systolic ventricular stiffness, defined as the slope of the wall forcesegment length relationship in systole (43,109,183,272) [for details, see Fig. 1 of the publication by Bian and Downey (43)].…”

Section: The Gregg Effectmentioning

confidence: 99%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

231

209

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall model and the intramyocardial pump model are based on an intramyocardial pressure, assumed to be proportional to ventricular pressure. They explain the global effects of contraction on coronary flow and the effects of contraction in the layers of the heart wall. The varying elastance model, the muscle shortening and thickening model, and the vascular deformation model are based on direct contact between muscles and vessels. They predict global effects as well as differences on flow in layers and flow heterogeneity due to contraction. The relative contributions of these two mechanisms depend on the wall layer (epi- or endocardial) and type of contraction (isovolumic or shortening). Intramyocardial pressure results from (local) muscle contraction and to what extent the interstitial cavity contracts isovolumically. This explains why small arterioles and venules do not collapse in systole. Coronary vasculature affects the cardiac muscle. In diastole, at physiological ventricular volumes, an increase in coronary perfusion pressure increases ventricular stiffness, but the effect is small. In systole, there are two mechanisms by which coronary perfusion affects cardiac contractility. Increased perfusion pressure increases microvascular volume, thereby opening stretch-activated ion channels, resulting in an increased intracellular Ca2+ transient, which is followed by an increase in Ca2+ sensitivity and higher muscle contractility (Gregg effect). Thickening of the shortening cardiac muscle takes place at the expense of the vascular volume, which causes build-up of intracellular pressure. The intracellular pressure counteracts the tension generated by the contractile apparatus, leading to lower net force. Therefore, cardiac muscle contraction is augmented when vascular emptying is facilitated. During autoregulation, the microvasculature is protected against volume changes, and the Gregg effect is negligible. However, the effect is present in the right ventricle, as well as in pathological conditions with ineffective autoregulation. The beneficial effect of vascular emptying may be reduced in the presence of a stenosis. Thus cardiac contraction affects vascular diameters thereby reducing coronary inflow and enhancing venous outflow. Emptying of the vasculature, however, enhances muscle contraction. The extracellular matrix exerts its effect mainly on cardiac properties rather than on the cross-talk between cardiac muscle and coronary c...

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Accounting for the Gregg effect in tetanised coronary arterial pressure-flow relationships

Abstract: A small but clearly discernible portion of the shift in tetanised pressure-flow relationships is attributable to the Gregg effect. Similar conclusions pertained when quadratic regressions were fitted to the pressure-flow data.

Cited by 12 publications

References 0 publications

Ultrasound Shear Wave Elasticity Imaging Quantifies Coronary Perfusion Pressure Effect on Cardiac Compliance

Ultrasound Shear Wave Elasticity Imaging Quantifies Coronary Perfusion Pressure Effect on Cardiac Compliance

Quantifying Myocardial Contractility Changes Using Ultrasound-Based Shear Wave Elastography

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

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