Inhibition of coronary blood flow by a vascular waterfall mechanism.

Downey, James M.; Kirk, Edward S.

doi:10.1161/01.res.36.6.753

Cited by 319 publications

(171 citation statements)

References 23 publications

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“…Moreover, this value agrees well with the intercept pressure measured in experimental studies on the effects of wall stress and intravascular pressure (7). Therefore, the data in the present study were divided into one group, where P w was lower than 25 mmHg, and one with higher values, assuming that relevant collateral function would only be present in the high P w group.…”

Section: Discussionsupporting

confidence: 88%

“…These mechanical determinants of coronary resistance yield a pressure-flow relation that is straight in the physiological range of arterial pressures, but is curvilinear for pressures below 40 mmHg. This has been clearly demonstrated by observations on pressure-flow relations obtained under experimental conditions where collateral effects were absent because of lack of a pressure gradient between the epicardial arteries (7,13,19). Moreover, the coronary pressure-flow relation is also shifted rightward in ventricles with elevated wall stress, e.g., because of hypertrophy, again without any contribution of collateral flow (12).…”

Section: Discussionmentioning

confidence: 80%

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Minimal effect of collateral flow on coronary microvascular resistance in the presence of intermediate and noncritical coronary stenoses

Verhoeff

Hoef

Spaan

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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-Depending on stenosis severity, collateral flow can be a confounding factor in the determination of coronary hyperemic microvascular resistance (HMR). Under certain assumptions, the calculation of HMR can be corrected for collateral flow by incorporating the wedge pressure (P w) in the calculation. However, although P w Ͼ 25 mmHg is indicative of collateral flow, Pw does in part also reflect myocardial wall stress neglected in the assumptions. Therefore, the aim of this study was to establish whether adjusting HMR by P w is pertinent for a diagnostically relevant range of stenosis severities as expressed by fractional flow reserve (FFR). Accordingly, intracoronary pressure and Doppler flow velocity were measured a total of 95 times in 29 patients distal to a coronary stenosis before and after stepwise percutaneous coronary intervention. HMR was calculated without (HMR) and with Pw-based adjustment for collateral flow (HMRC). FFR ranged from 0.3 to 1. HMR varied between 1 and 5 and HMRC between 0.5 and 4.2 mmHg·cm Ϫ1 ·s. HMR was about 37% higher than HMRC for stenoses with FFR Ͻ 0.6, but for FFR Ͼ 0.8, the relative difference was reduced to 4.4 Ϯ 3.4%. In the diagnostically relevant range of FFR between 0.6 and 0.8, this difference was 16.5 Ϯ 10.4%. In conclusion, P w-based adjustment likely overestimates the effect of potential collateral flow and is not needed for the assessment of coronary HMR in the presence of a flow-limiting stenosis characterized by FFR between 0.6 and 0.8 or for nonsignificant lesions. wedge pressure; fractional flow reserve; coronary circulation CORONARY MICROVASCULAR DYSFUNCTION is increasingly being recognized as a major contributor to myocardial ischemia (3) and is likely associated with an altered coronary hyperemic microvascular resistance (HMR). Hence, a reliable assessment of microvascular resistance is needed that accurately reflects the status of the microcirculation and supports further development of diagnostic tools for microvascular disease.Resistance of a vascular compartment is defined as the ratio between the pressure drop over it and flow through it. Application of the resistance concept to the coronary circulation is challenging in the clinical setting, since volume flow cannot practically be measured directly and coronary back pressure is governed by multiple factors including microvascular conductance and extravascular compressive forces (16,17,32,37). At present, two guidewire-based systems are capable of the combined measurement of pressure and a surrogate of flow through a coronary stenosis. In the first system, flow velocity is measured by a Doppler crystal next to a pressure sensor (31, 35). The second system exploits the temperature sensitivity of the pressure sensor to determine the mean transit time of a temperature change induced by a bolus of saline (10). The corresponding indexes of HMR are respectively defined as the mean distal pressure (P d ) divided by mean distal flow velocity (35) The entrance of the microcirculation is not uniquely defined. Colla...

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 80%

Minimal effect of collateral flow on coronary microvascular resistance in the presence of intermediate and noncritical coronary stenoses

Verhoeff

Hoef

Spaan

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…Since then, the "vascular waterfall" 3 and "intramyocardial pump" 4 models have considered the importance of increasing myocardial pressure in impeding coronary blood flow. The "time-varying elastance" 5 model described the importance of left ventricular stiffness and contraction of fibers surrounding intramyocardial blood vessels on coronary blood flow.…”

Section: Editorial P 1721 Clinical Perspective P 1778mentioning

confidence: 99%

Evidence of a Dominant Backward-Propagating “Suction” Wave Responsible for Diastolic Coronary Filling in Humans, Attenuated in Left Ventricular Hypertrophy

et al. 2006

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Background-Coronary blood flow peaks in diastole when aortic blood pressure has fallen. Current models fail to completely explain this phenomenon. We present a new approach-using wave intensity analysis-to explain this phenomenon in normal subjects and to evaluate the effects of left ventricular hypertrophy (LVH). Method and Results-We measured simultaneous pressure and Doppler velocity with intracoronary wires in the left main stem, left anterior descending, and circumflex arteries of 20 subjects after a normal coronary arteriogram. Wave intensity analysis was used to identify and quantify individual pressure and velocity waves within the coronary artery circulation.A consistent pattern of 6 predominating waves was identified. Ninety-four percent of wave energy, accelerating blood forward along the coronary artery, came from 2 waves: first a pushing wave caused by left ventricular ejection-the dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compression-the dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2Ϯ13.7ϫ10 3 W m Ϫ2 s

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“…Subendocardial vulnerability to ischemia has been previously attributed to several mechanisms, namely, the greater subendocardial systolic compression was proposed to induce one or more of the following: 1) increased subendocardial vessel resistance (5,36), 2) systolic backflow from endocardial to epicardial vessels (14) induced by systolic-diastolic interactions (23,39), or 3) transient vessel collapse (12), which would result in effectively higher subendocardial backpressures (2). The first two mechanisms account for a preferentially epicardial blood flow (i.e., Endo/Epi decrease) under increased systolic compression.…”

mentioning

confidence: 99%

Why is the subendocardium more vulnerable to ischemia? A new paradigm

Algranati

Kassab

Lanir

2011

American Journal of Physiology-Heart and Circulatory Physiology

113

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Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in deeper vessels, 2) consequent higher compliance of the subendocardial vasculature, and 3) substantial flow redistribution, i.e., a 20% drop in the subendocardial-to-subepicardial flow ratio under the prescribed reduction in perfusion pressure. This flow redistribution was found to occur primarily because the vessel compliance is nonlinear (pressure dependent). The observed thinner subendocardial vessel walls were predicted to induce a higher compliance of the subendocardial vasculature and greater flow redistribution. Subendocardial perfusion was predicted to improve with a reduction of either heart rate or left ventricular pressure under low perfusion pressure. In conclusion, subendocardial vulnerability to a acute reduction in perfusion pressure stems primarily from differences in vascular compliance induced by transmural differences in both extravascular loading and vessel wall thickness. Subendocardial ischemia can be improved by a reduction of heart rate and left ventricular pressure. coronary flow; stress and flow analysis; coronary network anatomy; myocardial contraction effects; myocardial ischemia MYOCARDIAL ISCHEMIA, a major cause of morbidity and mortality, is transmurally heterogeneous where the subendocardium is at higher risk than the midwall or epicardium (22). Despite the significant clinical relevance, the physical determinants of subendocardial vulnerability remain controversial. Although subendocardial metabolic demands are somewhat higher than subepicardial ones (22), data have suggested that it is the lower blood supply to the subendocardium, rather than the higher demand, that induces subendocardial vulnerability (23). For example, under partial occlusions (2) or otherwise decreased (9) perfusion pressure in the nonautoregulated coronary circulation, subendocardial blood supply has been observed to be compromised to a higher extent than subepicardial flow, whereas increased perfusion pressure was found to improve primarily the subendocardial supply (3). Hence, changes in perfusion pressure induce transmural flow redistribution, i.e., changes in the subendocardial-to-subepicardial perfusion ratio (Endo/Epi).Subendocardial vulnerability to ischemia has been previously attributed to several mechanisms, namely, ...

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Inhibition of coronary blood flow by a vascular waterfall mechanism.

Cited by 319 publications

References 23 publications

Minimal effect of collateral flow on coronary microvascular resistance in the presence of intermediate and noncritical coronary stenoses

Minimal effect of collateral flow on coronary microvascular resistance in the presence of intermediate and noncritical coronary stenoses

Evidence of a Dominant Backward-Propagating “Suction” Wave Responsible for Diastolic Coronary Filling in Humans, Attenuated in Left Ventricular Hypertrophy

Why is the subendocardium more vulnerable to ischemia? A new paradigm

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