Intramyocardial Pressure and Coronary Extravascular Resistance

1985 ◽  
Vol 107 (1) ◽  
pp. 46-50 ◽  
Author(s):  
P. D. Stein ◽  
H. N. Sabbah ◽  
M. Marzilli
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Ventricular Pressure ◽  
Intramyocardial Pressure ◽  
Extravascular Resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastole, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blood flow.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Effects of aminophylline on behaviorally induced coronary blood flow increases

1987 ◽  
Vol 253 (3) ◽  
pp. H548-H555
Author(s):  
G. E. Billman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Left Ventricular Pressure ◽  
Aversive Conditioning ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adenosine Antagonist ◽  
Blood Flow Increase ◽  
Myocardial Oxygen Supply

It has been proposed that adenosine is a metabolic vasodilator that matches myocardial oxygen supply to demand by regulating coronary blood flow. In the present study, the adenosine antagonist aminophylline (Am) was used to evaluate the role adenosine plays in the coronary blood flow increase elicited by a controlled aversive stress, namely, classical aversive conditioning (a 30-s tone reinforced with a 1-s shock). Fifteen mongrel dogs were chronically instrumented to measure left circumflex coronary blood flow (CBF), left ventricular pressure (LVP), and heart rate. Am significantly (P greater than 0.01) attenuated the CBF response to the aversive stress without affecting the prestress levels (pre-Am control 40.9 +/- 2.4, peak 64.6 +/- 3.3 ml/min; post-Am control 41.7 +/- 2.2, peak 55.0 +/- 2.5 ml/min). The maximal CBF increase was reduced by 38.9 +/- 6.7% when compared with the control (no drug) condition. In a similar manner, neither heart rate nor LVP was affected by Am. However, Am significantly increased prestress level of first derivative of left ventricular pressure with reference to time [LV dP/dt] (pre-Am control 3,793.5 +/- 289.8 and Am 4,599.6 +/- 331.2 mmHg/s, respectively). These data suggest that adenosine contributes significantly to the regulation of CBF during a controlled emotional stress.

Estimation of intramyocardial pressure and coronary blood flow distribution

1988 ◽  
Vol 255 (3) ◽  
pp. H664-H672 ◽  
Author(s):  
Y. Sun ◽  
H. Gewirtz
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Circulation ◽  
Regression Line ◽  
Flow Distribution ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Flow Distribution ◽  
Intramyocardial Pressure ◽  
D Model

To characterize the intramyocardial pressure (IMP) and coronary blood flow distribution in a stenosed coronary circulation, we compared four analog circuits for modeling coronary impedance. The resistor (R)-diode (D) model simulates vascular collapse, and the capacitor (C) simulates compliance effect. Identification of the best model and magnitudes of the endocardial and epicardial IMPs (IMPendo and IMPepi) was done retrospectively using data from studies in 28 anesthetized swine. Performance evaluation was based on comparison of model predicted vs. observed coronary distal pressure (DP) waveforms and endocardial-to-epicardial (endo-epi) flow ratios as determined by radiolabeled microspheres. The R-D-C model gave the best performance at IMPendo = 1.1 times left ventricular pressure (LVP), and IMPepi = 0.1.LVP + 15 mmHg; with good fit to DP (r = 0.98, slope of regression line = 1.0) and estimates of endo-epi flow ratio (r = 0.78, slope = 1.01, P less than 0.02, SEE = 0.21, n = 139). The R-D model gave comparable results even though capacitance was omitted. Although R-C and R models predicted distal coronary pressure well, they failed to predict endo-epi flow ratios (r less than 0.50). The R-D-C and R-D models were applied in seven prospective studies. Both models generated reasonable estimates of endo-epi flow distribution (r = 0.78, n = 50). Thus the R-D-C or R-D models of the stenosed coronary circulation can be used to provide reliable estimates of transmural blood flow distribution.

Fluid-Structure Interaction Simulation of Blood Flow Inside a Diseased Left Ventricle With Obstructive Hypertrophic Cardiomyopathy in Early Systole

2009 ◽  
Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricle ◽  
Fluid Structure Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Systolic Phase

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.

Role of site of microsphere injection and catheter position on systemic and regional hemodynamics in rat

1984 ◽  
Vol 247 (1) ◽  
pp. H35-H39 ◽  
Author(s):  
I. Kobrin ◽  
M. B. Kardon ◽  
W. Oigman ◽  
B. L. Pegram ◽  
E. D. Frohlich
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Ventricular Catheter ◽  
Catheter Position ◽  
Flow Measurements ◽  
Conscious Rats ◽  
Anesthetized Rats ◽  
Regional Hemodynamics

The influences of the site of microsphere injection (intra-atrial vs. intraventricular) and positioning of the left ventricular catheter (aortoventricular vs. atrioventricular) on systemic, renal, and coronary hemodynamics were evaluated in anesthetized rats. The effect of anesthesia on aortoventricular catheter positioning was also evaluated. In anesthetized and open-chest preparations, the systemic and renal hemodynamics were not affected by catheter position or site of microsphere injection; however, myocardial blood flow was dependent on these variables. Variations in coronary blood flow were significantly greater when the catheter was in the aortoventricular position (34 +/- 3%) than with an atrioventricular catheter (11 +/- 2%, P less than 0.01), irrespective of whether the microspheres were injected into the atrium or ventricle. Comparison of anesthetized and conscious rats with aortoventricular catheter indicated lesser variability in coronary blood flow in the conscious rats (P less than 0.01). Therefore, the greater variability of coronary flow measurements in anesthetized rats was caused by the position of the cardiac catheter in the aortoventricular route. However, the variability caused by the aortoventricular catheter was much less in conscious rats. Therefore, coronary flow hemodynamic measurements (microsphere technique) are less variable when they are made in conscious rats.

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

2001 ◽  
Vol 280 (2) ◽  
pp. H576-H581 ◽  
Author(s):  
Wei Wang ◽  
Harold D. Schultz ◽  
Rong Ma
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Volume Expansion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Volume Expansion ◽  
Cardiac Sympathetic Afferent Reflex

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 μg) and capsaicin (10 and 100 μg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 μg) of epicardial bradykinin (17. 3 ± 1.9 vs. 10.6 ± 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 ± 4.1 vs. 5.0 ± 1.3% for 5 μg, P < 0.05, and 28.9 ± 3.7 vs. 10.6 ± 4.8% for 50 μg, P < 0.05) and capsaicin (29.8 ± 6.0 vs. 9.3 ± 3.1% for 10 μg, P < 0.05, and 34.2 ± 2.7 vs. 15.1 ± 2.7% for 100 μg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.

Anesthetic Preconditioning

2003 ◽  
Vol 99 (2) ◽  
pp. 385-391 ◽  
Author(s):  
Leo G. Kevin ◽  
Peter Katz ◽  
Amadou K. S. Camara ◽  
Enis Novalija ◽  
Matthias L. Riess ◽  
...  
Keyword(s):  
Coronary Flow ◽  
Vascular Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Ischemic Time ◽  
Langendorff Preparation ◽  
Anesthetic Preconditioning ◽  
Structural Variables ◽  
Serious Injury

Background Anesthetic preconditioning (APC) is protective for several aspects of cardiac function and structure, including left ventricular pressure, coronary flow, and infarction. APC may be protective, however, only if the duration of ischemia is within a certain, as yet undefined range. Brief ischemia causes minimal injury, and APC would be expected to provide little benefit. Conversely, very prolonged ischemia would ultimately cause serious injury with or without APC. Previous investigations used a constant ischemic time as the independent variable to assess ischemia-induced changes in dependent functional and structural variables. The purpose of the study was to define the critical limits of efficacy of APC by varying ischemic time. Methods Guinea pig hearts (Langendorff preparation; n = 96) underwent pretreatment with sevoflurane (APC) or no treatment (control), before global ischemia and 120 min reperfusion. Ischemia durations were 20, 25, 30, 35, 40, and 45 min. Results At 120 min reperfusion, developed (systolic-diastolic) left ventricular pressure was increased by APC compared with control for ischemia durations of 25-40 min. Infarction was decreased by APC for ischemia durations of 25-40 min, but not 20 or 45 min. APC improved coronary flow and vasodilator responses for all ischemia durations longer than 25 min, and decreased ventricular fibrillation on reperfusion for ischemia durations longer than 30 min. Conclusions Although APC protects against vascular dysfunction and dysrhythmias after prolonged ischemia, protection against contractile dysfunction and infarction in this model is restricted to a range of ischemia durations of 25-40 min. These results suggest that APC may be effective in a subset of patients who have cardiac ischemia of intermediate duration.

Image-Based Modeling of Blood Flow in Human Coronary Arteries With and Without Bypass Grafts During Rest and Simulated Exercise

2008 ◽  
Author(s):  
Jessica Shih ◽  
Hyun Jin Kim ◽  
Charles A. Taylor
Keyword(s):  
Coronary Artery ◽  
Coronary Bypass ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Bypass Grafts ◽  
Heart Model ◽  
Intramyocardial Pressure ◽  
Image Based Modeling ◽  
Lumped Parameter

The number of patients with coronary artery disease continues to rise, with approximately 469,000 coronary bypass procedures in 2005 alone [1]. A priori knowledge of the flow features within the coronary vascular system could prove useful in predicting flow changes due to coronary bypass surgery. Image-based modeling and 3-D computational simulations could be used to compute flow and pressure in a patient-specific manner. However, modeling coronary flow requires knowledge of the intramyocardial pressure that compresses coronary vessels, resulting in decreased flow in systole and increased flow in diastole. Left ventricular pressure can provide an estimate to intramyocardial pressure, but the aortic pressure and left ventricular pressure must be coupled in systole when the aortic valve is open. Previously, we have developed a method to couple a lumped-parameter heart model to the inlet of a 3-D model to compute aortic and ventricular pressure [2]. In this study, we use the lumped-parameter heart model and computational fluid dynamics to calculate flow dynamics in a patient model with coronary artery bypass grafts.

Epicardial Coronary Blood Flow Including the Presence of Stenoses and Aorto-Coronary Bypasses—I: Model and Numerical Method

1985 ◽  
Vol 107 (4) ◽  
pp. 361-367 ◽  
Author(s):  
E. Rooz ◽  
T. F. Wiesner ◽  
R. M. Nerem
Keyword(s):  
Blood Flow ◽  
Numerical Method ◽  
Coronary Blood Flow ◽  
Wave Speed ◽  
Peripheral Resistance ◽  
Left Ventricular Pressure ◽  
Systematic Investigation ◽  
Left Ventricular ◽  
Resistive Component ◽  
The One

A computer model and numerical method for calculating left epicardial coronary blood flow has been developed. This model employs a finite-branching geometry of the coronary vasculature and the one-dimensional, unsteady equations for flow with friction. The epicardial coronary geometry includes the left main and its bifurcation, the left anterior descending and left circumflex coronary arteries, and a selected number of small branches. Each of the latter terminate in an impedance, whose resistive component is related to intramyocardial compression through a linear dependence on left ventricular pressure. The elastic properties of the epicardial arteries are taken to be non-linear and are prescribed by specifying the local small-disturbance wave speed. The model allows for the incorporation of multiple stenoses as well as aorto-coronary bypasses. Calculations using this model predict pressure and flow waveform development and allow for the systematic investigation of the dependence of coronary flow on various parameters, e.g., peripheral resistance, wall properties, and branching pattern, as well as the presence of stenoses and bypass grafts. Reasonable comparison between calculations and earlier experiments in horses has been obtained.

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