Der intramyokardiale Druck des Hundes in verschiedenen Tiefen, bei Druckbelastung und bei Ischämie des Herzmuskels

Gerke, E; Juchelka, W.; Mittmann, U.; Schmier, J

doi:10.1007/bf01906385

Cited by 7 publications

(5 citation statements)

References 24 publications

(2 reference statements)

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“…It has been shown that intramyocardial pressure increases from the epicardial to the endocardial surface of the ventricular wall. This was demonstrable from direct measurements of intramyocardial pressure by various methods (15,16,17,18,19,20) and was established indirectly by perfusion studies at increased ventricular load and lowered perfusion pressure (11,13,14,19,21). From these investigations it became evident that the intramyocardial tissue pressure as the determinant of extravascular coronary resistance increases with wall depth which became obvious under resting conditions at normal ventricular load and perfusion pressure and became more marked in experiments when systolic and diastolic load was increased when coronary perfusion was limited to systole and when coronary pressure was lowered by a decrease of the systemic pressure or by stenotic or occluded coronary arteries.…”

Section: Discussionmentioning

confidence: 98%

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

et al. 1977

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The functional capacity of flow limiting myocardial conductance vessels was evaluated in canine hearts. In an isolated heart preparation transmural coronary flow distribution during maximal vasodilation was measured in the unloaded diastolic arrested left ventricle with tracer microspheres. The ratio of subendocardial versus subepicardial (ENDO/EPI) flow in the left ventricular free wall was 1.6. Measurements in 8 different wall layers showed a successive increase in maximal coronary flow from the subepicardium towards the deeper layers. A decreased subendocardial vascular resistance due to a better vascularization is forwarded as a mechanism to compensate for the extravascular compression during cardiac contraction. This statement contradicts the commonly accepted hypothesis that a diminished vascular tone with a reduction of the dilatory reserve in the subendocardium accounts for a homogeneous flow distribution in the normal beating heart. An augmentation of subendocardial supplying vessel capacity could be established from the angiographic determination of the coronary arterial volume of intramural small arteries and arterioles. From a strict parallelity in maximal coronary flow and coronary arterial volume within the wall, it becomes probable that these vascular structures are the flow-limiting factors which determine regional coronary flow reserve in the absence of extravascular compressive forces.

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Section: Discussionmentioning

confidence: 98%

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

et al. 1977

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“…The system is assumed to behave as a Starling resistor so that flow will cease when intramyocardial (external) pressure equals perfusion pressure (11, 13-15, 26, 28, 34, 37, 51, 52, 54). Most investigators report a smaller intramyocardial pressure than left ventricular pressure, but some report conditions where the inverse is true (26,37). Baird et al (15) found intramyocardial pressures in isobaric beats, at a perfusion pressure of 100 mm Hg, to be 123 _+ 43 mm Hg in the endocardial third and 22 + 11 mm Hg in the epicardial third of the wall.…”

Section: Perfusion Methodsmentioning

confidence: 96%

“…With all methods systolic intramyocardial pressures can be obtained that are higher than systolic aortic or ventricular pressure. Often epicardial intramyocardial pressures are found well above zero, i.e., more than 30 % of left ventricular pressure (5,6,13,14,26,34,66). In fibrillation intramyocardial pressures are found that are higher than left ventricular pressure (22).…”

Section: Summary Of Measurementsmentioning

confidence: 98%

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Westerhof

1990

Basic Res Cardiol

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Intramyocardial pressure is supposed to play a major role in systolic coronary flow impediment. Via its assumed relation with radial wall stress it is supposed to be similar to ventricular pressure at the endocardium and decreases linearly to negligible values epicardially. Many attempts to measure intramyocardial pressure have been reported in the literature with rather different results. For instance, with most of the various methods, intramyocardial pressures both higher and lower than left ventricular pressure have been obtained and intramyocardial pressures of more than 125 mm Hg have been found in low-loaded isobaric beats (negligible pressure development in systole). In this "physiological hypotheses paper" I suggest left ventricular pressure and intramyocardial pressure both to result from the varying stiffness of cardiac muscle over the heart cycle. For any intramuscular cavity a time varying pressure-volume (P-V) relation results from the changes in muscle stiffness, the so-called time varying elastance defined as E(t) = P(t)/V(t), and with maximal or systolic elastance called Emax. For a constant contractile state the time varying elastance (E(t)) is suggested to be almost independent of preload and afterload. This concept has been well established for the ventricular cavities, but is here proposed to hold for the interstitial space as well. If a cavity is subject to isovolumic conditions the pressure will be high, but when volume in systole decreases (ventricular ejection or squeezing out of interstitial fluid) pressures will be lower. Thus for constant load on the interstitial cavities, but different loads on the ventricle, left ventricular pressure will vary while intramyocardial pressure remains the same. For low-loaded isobaric beats where left ventricular pressure is minimal intramyocardial pressure will remain the same as during normal ventricular loads and isovolumic beats. Augmented contractility will increase Emax and this will increase left ventricular and intramyocardial pressure only by the same amount if loading conditions of both cavities remain the same. Both ventricular pressure and intramyocardial pressure arise from varying stiffness of cardiac muscle and intramyocardial pressure does not result from left ventricular pressure. A proportionality of left ventricular and intramyocardial pressure is therefore not to be expected. The results on intramyocardial pressure obtained by the different methods used in the literature should be re-interpreted taking this concept into account.

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“…The solutions for p Cap are mapped onto the segmented 3D models to provide the CFD simulations with a well‐defined set of BCs. The capillary pressure is scaled depending on the depth within the myocardium of the outlet under consideration . For each model outlet, a downstream arterial resistance R i is calculated according to the self‐similarity of the coronary tree …”

Section: Methodsmentioning

confidence: 99%

“…The capillary pressure is scaled depending on the depth within the myocardium of the outlet under consideration. 42 For each model outlet, a downstream arterial resistance R i is calculated according to the self-similarity of the coronary tree. 40,[43][44][45] Finally, for each time step t of the Navier-Stokes simulation, the pressure is computed and assigned at outlet i, where F i denotes outlet flow.…”

Section: Blood Flowmentioning

confidence: 99%

Influence of contrast agent dispersion on bolus‐based MRI myocardial perfusion measurements: A computational fluid dynamics study

Martens

Panzer

Wijngaard

et al. 2019

Magnetic Resonance in Med

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Purpose Bolus‐based dynamic contrast agent (CA) perfusion measurements of the heart are subject to systematic errors due to CA bolus dispersion in the coronary arteries. To better understand these effects on quantification of myocardial blood flow and myocardial perfusion reserve (MPR), an in‐silico model of the coronary arteries down to the pre‐arteriolar vessels has been developed. Methods In this work, a computational fluid dynamics analysis is performed to investigate these errors on the basis of realistic 3D models of the left and right porcine coronary artery trees, including vessels at the pre‐arteriolar level. Using advanced boundary conditions, simulations of blood flow and CA transport are conducted at rest and under stress. These are evaluated with regard to dispersion (assessed by the width of CA concentration time curves and associated vascular transport functions) and errors of myocardial blood flow and myocardial perfusion reserve quantification. Results Contrast agent dispersion increases with traveled distance as well as vessel diameter, and decreases with higher flow velocities. Overall, the average myocardial blood flow errors are −28% ± 16% and −8.5% ± 3.3% at rest and stress, respectively, and the average myocardial perfusion reserve error is 26% ± 22%. The calculated values are different in the left and right coronary tree. Conclusion Contrast agent dispersion is dependent on a complex interplay of several different factors characterizing the cardiovascular bed, including vessel size and integrated vascular length. Quantification errors evoked by the observed CA dispersion show nonnegligible distortion in dynamic CA bolus‐based perfusion measurements. We expect future improvements of quantitative perfusion measurements to make the systematic errors described here more apparent.

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Der intramyokardiale Druck des Hundes in verschiedenen Tiefen, bei Druckbelastung und bei Ischämie des Herzmuskels

Cited by 7 publications

References 24 publications

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

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

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Influence of contrast agent dispersion on bolus‐based MRI myocardial perfusion measurements: A computational fluid dynamics study

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