Dilatory capacity of the coronary circulation and its correlation to the arterial vasculature in the canine left ventricle

Wüsten, B.; Buss, Daryl D.; Deist, Hellmuth; Schäper, Wolfgang

doi:10.1007/bf01907044

Cited by 83 publications

(39 citation statements)

References 74 publications

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“…The distensibility of the arteries depends on the active vasomotor tone and relaxes to the passive pressure-volume relationships when there is complete vasodilation (106). Kassab and Malloi (51) show that coronary compliances are small in large coronaries and proportionately higher in smaller vessels, consistent with the data of Cornelissen et al (28).…”

Section: Vasomotor Influencesmentioning

confidence: 52%

The mechanical and metabolic basis of myocardial blood flow heterogeneity

Bassingthwaighte

Beard

2001

Basic Research in Cardiology

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Precise measurements of regional myocardial blood flow heterogeneity had to be developed before one could seek causation for the heterogeneity. Deposition techniques (particles or molecular microspheres) are the most precise, but imaging techniques have begun to provide high enough resolution to allow in vivo studies. Assigning causation has been difficult. There is no apparent association with the regional concentrations of energy-related enzymes or substrates, but these are measures of status, not of metabolism. There is statistical correlation between flow and regional substrate uptake and utilization. Attribution of regional flow variation to vascular anatomy or to vasomotor control appears not to be causative on a long-term basis. The closest relationships appear to be with mechanical function, but one cannot say for sure whether this is related to ATP hydrolysis at the crossbridge or associated metabolic reactions such as calcium uptake by the sarcoplasmic reticulum.

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Section: Vasomotor Influencesmentioning

confidence: 52%

The mechanical and metabolic basis of myocardial blood flow heterogeneity

Bassingthwaighte

Beard

2001

Basic Research in Cardiology

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“…2 of Wüsten et al (77). The interface between 1D and 0D in our model was at the level of these penetrating arteries.…”

Section: D Model Of Conduit Coronary Arteries Most Sheepmentioning

confidence: 84%

Scalability and in vivo validation of a multiscale numerical model of the left coronary circulation

Mynard

Penny

Smolich

2014

American Journal of Physiology-Heart and Circulatory Physiology

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Mynard JP, Penny DJ, Smolich JJ. Scalability and in vivo validation of a multiscale numerical model of the left coronary circulation. Am J Physiol Heart Circ Physiol 306: H517-H528, 2014. First published December 20, 2013 doi:10.1152/ajpheart.00603.2013.-Multiscale modeling is a promising tool for the study of coronary hemodynamics. A key strength of this approach is that it accounts for microvascular properties and extravascular forces that differ regionally and transmurally, as well as wave propagation effects in the conduit arteries. However, little validation of such models has been reported and no models of the newborn coronary circulation have been described. We therefore validated a multiscale model of the left coronary circulation using high-fidelity data from nine adult sheep and nine newborn lambs and investigated whether wave propagation effects are more prominent in adults, whose body size (and hence wave transit distance) is greater. The model consisted of a one-dimensional (1D) network of the major conduit arteries and a lumped parameter model of microvascular beds. Intramyocardial pressure was considered to arise via contraction-related myocyte thickening and transmission of ventricular cavity pressure into the heart wall. 1D network geometry from published human anatomical data was scaled using myocardial weights, while subject-specific aortic pressure/flow and ventricular pressure formed model inputs. Total vascular resistance was determined iteratively from measured mean circumflex coronary flow (CxQ), but no fitting of phasic aspects of the waveform was performed. Excellent agreement was obtained between simulated and measured CxQ waveforms in most cases. Detailed flow waveform analysis did not clearly reveal a greater prominence of wave propagation effects in adults compared with newborns. This multiscale model is likely to be useful for investigating wave phenomena and phasic aspects of coronary flow in adults and during development. coronary arteries; wave propagation; allometric scaling; computer model; hemodynamics; newborn MATHEMATICAL MODELING, in concert with experimental studies, has played an important role in building our current understanding of coronary hemodynamics, providing insights into the role of intramyocardial pressure, large microvascular compliance, and transmural differences of vascular impedance and flow patterns (4, 9 -12, 18, 64, 67, 70). Many models of the coronary circulation have been of the lumped parameter [or zero-dimensional (0D)] type, where the resistive and capacitive properties of all coronary vessels are combined into a small number of elements. For example, the main conduit coronary arteries lying on the epicardium (or traversing the ventricular septum) have generally been represented by a single compliance (10, 12, 64) or windkessel compartment (4, 9, 18).One limitation of an exclusively 0D modeling approach is that wave propagation effects are neglected. That these effects play a role in shaping the coronary arterial flow waveform was first suggested ...

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“…The coronary circulation was filled with contrast medium by modification of the methodology for micro-CT study in the rats. 10 Preparation of contrast medium was according to Wusten et al, 11 consisting of barium sulfate (60 g, No.…”

Section: Coronary Microvascular Imaging With Micro-ctmentioning

confidence: 99%

“…A sham heart with balloon implantation but no RI showed 4 visible collaterals (top left). A heart in the control group after RI showed higher visible vascularity and more connections 11 between the LAD vascular tree and adjacent arteries (bottom left) compared with the sham. However, there was no evidence of collateral growth (4 collateral connections; PϾ0.05 versus sham) in anti-VEGF group after RI (bottom right).…”

Section: Coronary Vascular Architecturementioning

confidence: 99%

Vascular Endothelial Growth Factor Is Required for Coronary Collateral Growth in the Rat

et al. 2005

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Background— The goal of this study was to determine whether the expression of vascular endothelial growth factor (VEGF) is critical for coronary collateral growth. Previous studies have provided an association between coronary collateral growth and VEGF, but none have allowed determination of a causal role. Methods and Results— We measured coronary collateral growth in rats subjected to repetitive episodes of myocardial ischemia (RI; one 40-second occlusion every 20 minutes for 2 hours 40 minutes, followed by 5 hours 20 minutes of rest, with this 8-hour cycle repeated 3 times per day for 10 days). Collateral growth was measured from blood flow (radioactive microspheres), visualization of arterial-arterial anastomoses (x-ray micro-CT), and maintenance of function during complete coronary occlusion in 3 groups of animals: sham (received instrumentation but no RI), experimental (subjected to RI), and anti–vascular endothelial growth factor (RI+anti-VEGF 0.6 mg/100 g per day) to block the endogenous actions of VEGF. In the 3 groups, native collateral flow (measurement for RI or sham protocol) averaged 0.2 to 0.3 mL · min −1 · g −1 of tissue. In the sham group, collateral flow did not increase during the protocol. Collateral flow in the control RI group increased by ≈6-fold to 1.63 mL · min −1 · g −1 tissue, but in the anti-VEGF group, collateral flow did not increase after the RI protocol (0.22 mL · min −1 · g −1 ). In acute experiments, collateral flow was unchanged during vasodilation with dipyridamole, indicating the increases in collateral flow are due to collateral growth and not vasodilation. X-ray micro-CT analysis revealed a 3-fold increase (versus sham group) in the number of arterial-arterial anastomoses per heart after RI, which was prevented by treatment with anti-VEGF. The growth of the collateral circulation was functional in the RI group because complete coronary occlusion did not induce any untoward effects on hemodynamics or arrhythmias. In the sham or anti-VEGF groups, coronary occlusion at the end of the protocol induced many arrhythmias and deterioration of function. Conclusions— From these results, we conclude that the expression of VEGF is critical to the growth of coronary collaterals.

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Dilatory capacity of the coronary circulation and its correlation to the arterial vasculature in the canine left ventricle

Cited by 83 publications

References 74 publications

The mechanical and metabolic basis of myocardial blood flow heterogeneity

The mechanical and metabolic basis of myocardial blood flow heterogeneity

Scalability and in vivo validation of a multiscale numerical model of the left coronary circulation

Vascular Endothelial Growth Factor Is Required for Coronary Collateral Growth in the Rat

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