scholarly journals The Cardiovascular Implications of Thoracic Endovascular Aortic Repair: how aortic stenting impacts LV function and coronary artery flow

2021 ◽  
Author(s):  
David P Stonko ◽  
Hossam Abdou ◽  
Joseph Edwards ◽  
Noha N Elansary ◽  
Eric Lang ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiovascular System ◽  
Coronary Flow ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Aortic Compliance ◽  
Flow Measurements ◽  
Aortic Stenting

Abstract Aortic stents are known to have harmful effects on the cardiovascular system. They augment left ventricular function by decreasing aortic compliance. How these cardiovascular parameters change during and immediately after deployment of aortic stents has not been rigorously quantified, despite the development of heart failure in as many as 40% of post-TEVAR survivors within one-year. Without a comprehensive understanding of how the cardiovascular system changes in response to aortic stenting, surgical or medical strategies to augment prevent these changes cannot be developed. The goal of this study is to evaluate alterations in cardiovascular physiology that develop during and after total aortic endografting in a swine model. We will employ left ventricular (LV) pressure-volume (PV) loop analysis, which provides comprehensive pump mechanical information about LV function including stroke work and cardiac output, coupled with direct coronary flow measurements to understand how these parameters change when an aortic stent is placed. Our hypotheses are that aortic stenting: 1) is associated with decreased aortic compliance and increased LV afterload, 2) augments the LV end systolic pressure relationship (i.e., stroke work and end systolic pressure increase) and 3) increases coronary blood flow but decreases the coronary flow/cardiac output ratio.

Direct cardiac effects of vasopressin and their reversal by a vascular antagonist

1986 ◽  
Vol 251 (4) ◽  
pp. H734-H741 ◽  
Author(s):  
W. A. Boyle ◽  
L. D. Segel
Keyword(s):  
Coronary Flow ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Total Output ◽  
Stroke Work ◽  
Cardiac Effects ◽  
Myocardial O2 Consumption ◽  
Dose Dependent

We studied the direct cardiac effects of arginine vasopressin (AVP) by use of an isolated working rat heart model perfused with Krebs-Henseleit medium. At a concentration of 878 +/- 15 pg/ml, AVP produced significant (P less than 0.05) decreases in coronary flow (-31 +/- 2%); myocardial O2 consumption (-12 +/- 2%); left ventricular peak systolic pressure (-5 +/- 1%); dP/dtmax (-7 +/- 1%); -dP/dtmax (-6 +/- 3%); peak aortic flow rate (-5 +/- 1%); stroke work (-3 +/- 1%); peak power (-8 +/- 1%); and total output (-3 +/- 1%). Aortic output increased significantly (+7 +/- 1%) as did arteriovenous O2 difference (+108 +/- 14 mmHg); left ventricular end-diastolic pressure (+0.4 +/- 0.1 mmHg); efficiency (+1.5 +/- 0.4%); and rate of lactate release (+1.27 +/- 0.21 nmol/ml perfusate/min). Dose-response relationships were studied at 9 +/- 1, 25 +/- 1, 75 +/- 3, 303 +/- 15, and 817 +/- 42 pg AVP/ml. Significant dose-dependent depression of coronary flow occurred at the three highest AVP concentrations; cardiac function was significantly depressed at the highest dose. The AVP analogue d(CH2)5[Tyr(Me)]AVP (20 ng/ml) completely reversed the cardiac effects attributed to AVP. The data indicate that AVP is a potent direct coronary constrictor that produces myocardial ischemia and decreased contractile function at AVP concentrations that are observed in some pathophysiologic states.(ABSTRACT TRUNCATED AT 250 WORDS)

Crystalloid and perfluorochemical perfusates in an isolated working rabbit heart preparation

1985 ◽  
Vol 249 (2) ◽  
pp. H285-H292 ◽  
Author(s):  
J. M. Chemnitius ◽  
W. Burger ◽  
R. J. Bing
Keyword(s):  
Cardiac Output ◽  
Coronary Flow ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Heart Weight ◽  
Perfused Heart ◽  
Heart Preparation ◽  
Perfused Hearts

Krebs-Henseleit buffer (KH) and a perfluorochemical (FC-43) were compared as perfusates in an isolated working rabbit heart preparation. Both perfusates were oxygenated in an identical manner using an infant bubble oxygenator. After 60 min of perfusion, no difference could be detected in the ratio of wet to dry heart weight between KH- and FC-43-perfused hearts (KH, 6.25 +/- 0.3; FC-43, 5.99 +/- 0.20). Left ventricular systolic pressure, maximal rate of left ventricular pressure rise, mean aortic systolic pressure, cardiac output, aortic flow, left ventricular power, and myocardial O2 consumption (MVO2) were significantly higher in FC-43-perfused hearts throughout the time of perfusion. However, there were no differences in resistance to cardiac output and heart rate. In KH- and FC-43-perfused hearts, MVO2 and left ventricular power were closely correlated (KH, r = 0.793; FC-43, r = 0.831). Significantly higher coronary flow of KH-perfused hearts could be attributed to the lower viscosity of KH (1.05 Pa . s) compared with FC-43 (1.91 Pa . s). Increased O2 extraction during KH perfusion could not compensate for low O2-carrying capacity of KH buffer (345 compared with 705 nmol O2 X ml-1 in FC-43 emulsion). A postischemic increase of coronary flow was observed only in FC-43-perfused hearts (28%). These results demonstrate a different response of perfused heart preparations to FC-43 and KH buffer.

scholarly journals Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism

2010 ◽  
Vol 299 (2) ◽  
pp. H492-H501 ◽  
Author(s):  
Li Jianhui ◽  
Nathalie Rosenblatt-Velin ◽  
Noureddine Loukili ◽  
Pal Pacher ◽  
François Feihl ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Myocardial Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Laboratory Animals ◽  
Lv Function ◽  
Stroke Work ◽  
Loading Conditions ◽  
Arterial Elastance ◽  
End Diastolic Volume

Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin [lipopolysacharride (LPS)] to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indexes of cardiac function [including ejection fraction (EF) and maximal systolic pressure increment (dP/d tmax)], which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6, or 20 h, cardiac function was analyzed in anesthetized, mechanically ventilated mice. All doses of LPS induced a significant drop in LV stroke volume and a trend toward reduced cardiac output after 6 h. Concomitantly, there was a significant decrease of LV preload (LV end-diastolic volume), with no apparent change in LV afterload (evaluated by effective arterial elastance and systemic vascular resistance). Load-dependent indexes of LV function were markedly reduced at 6 h, including EF, stroke work, and dP/d tmax. In contrast, there was no reduction of load-independent indexes of LV contractility, including end-systolic elastance (ejection phase measure of contractility) and the ratio dP/d tmax/end-diastolic volume (isovolumic phase measure of contractility), the latter showing instead a significant increase after 6 h. All changes were transient, returning to baseline values after 20 h. Therefore, the alterations of cardiac function induced by LPS are entirely due to altered loading conditions, but not to reduced contractility, which may instead be slightly increased.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Ryanodine and left ventricular function in intact dogs: dissociation of force-based and velocity-based indexes

1997 ◽  
Vol 273 (3) ◽  
pp. H1561-H1568 ◽  
Author(s):  
S. D. Prabhu ◽  
M. M. Rozek ◽  
D. R. Murray ◽  
G. L. Freeman
Keyword(s):  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Systolic Pressure ◽  
Specific Inhibitor ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Mean Velocity ◽  
Release Channel

After anesthesia and autonomic blockade, nine dogs chronically instrumented with left ventricular (LV) micromanometers and piezoelectric dimension crystals were studied before and after the intravenous administration of 4 micrograms/kg ryanodine, a specific inhibitor of the sarcoplasmic reticulum Ca2+ release channel. Ryanodine prolonged LV contraction and relaxation (P < 0.001) without changing heart rate, end-diastolic volume (EDV), or end-systolic pressure. Velocity-dependent mechanical parameters were significantly depressed, including the maximal rate of LV pressure rise (dP/dtmax; P < 0.002), the mean velocity of circumferential fiber shortening (P < 0.002), the slope of the dP/dtmax-EDV relation (P < 0.05), and the time constant of LV relaxation (P < 0.01). In contrast, the slopes of the end-systolic pressure-volume (PES-VES) and stroke work (SW)-EDV relations, both force-based parameters, were increased (P < 0.05) or maintained, respectively. Ryanodine reduced overall LV contractile performance, evidenced by significant rightward shifts of the PES-VES, dP/dtmax-EDV, and SW-EDV relations and reduced SW at constant preload (P < 0.02). Thus, in the closed-chest dog, low-dose ryanodine resulted in 1) generalized slowing of LV mechanical events without changes in heart rate or load, 2) dissociation of velocity-based and force-based measures of LV function, with depression of the former but enhancement or maintenance of the latter, and 3) reduced overall LV inotropic performance. These effects are consistent with ryanodine-induced alterations of the Ca2+ transient and altered sarcoplasmic reticulum Ca2+ availability.

Age-related left ventricular function in the mouse: analysis based on in vivo pressure-volume relationships

1999 ◽  
Vol 277 (5) ◽  
pp. H1906-H1913 ◽  
Author(s):  
Bo Yang ◽  
Douglas F. Larson ◽  
Ronald Watson
Keyword(s):  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Lv Function ◽  
Mouse Heart ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Systolic Volume ◽  
End Systolic Volume

Our study compared left ventricular (LV) function between senescent and young adult mice through in situ pressure-volume loop analysis. Two groups of mice ( n = 9 each), 6-mo-old and 16-mo-old (senescent) mice, were anesthetized with urethan and α-chloralose, and their LV were instrumented with a Millar 1.4-Fr conductance micromanometer catheter for the acquisition of the pressure-volume loops. The senescent mice had a significantly decreased contractile function related to load-dependent parameters, including stroke volume index, ejection fraction, cardiac output index, stroke work index, and maximum derivative of change in systolic pressure over time. The load-independent parameters, preload recruitable stroke work and the slope (end-systolic volume elastance) of the end-systolic pressure-volume relationship, were significantly decreased in the senescent mice. Heart rate and arterial elastance were not different between the two groups; however, the ventricular-to-vascular coupling ratio (ratio of elastance of artery to end-systolic volume elastance) was increased by threefold in the senescent mice ( P < 0.001). Thus there were significant decreases in contractile function in the senescent mouse heart that appeared to be related to reduced mechanical efficiency but not related to arterial elastance.

scholarly journals Environmentally persistent free radicals compromise left ventricular function during ischemia/reperfusion injury

2015 ◽  
Vol 308 (9) ◽  
pp. H998-H1006 ◽  
Author(s):  
Brendan R. Burn ◽  
Kurt J. Varner
Keyword(s):  
Free Radicals ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Halogenated Hydrocarbons ◽  
Lv Function ◽  
Stroke Work

Increases in airborne particulate matter (PM) are linked to increased mortality from myocardial ischemia. PM contains environmentally persistent free radicals (EPFRs) that form as halogenated hydrocarbons chemisorb to transition metal oxide-coated particles, and are capable of sustained redox cycling. We hypothesized that exposure to the EPFR DCB230 would increase cardiac vulnerability to subsequent myocardial ischemia-reperfusion (MI/R) injury. Rats were exposed to DCB230 or vehicle via nose-only inhalation (230 μg max/day) over 30 min/day for 7 days. MI/R or sham MI/R (sham) was initiated 24 h after the final exposure. Following 1 or 7 days of reperfusion, left ventricular (LV) function was assessed and infarct size measured. In vehicle-exposed rats, MI/R injury did not significantly reduce cardiac output (CO), stroke volume (SV), stroke work (SW), end-diastolic volume (EDV), or end-systolic volume (ESV) after 1 day of reperfusion, despite significant reductions in end-systolic pressure (ESP). Preload-recruitable SW (PRSW; contractility) was elevated, presumably to maintain LV function. MI/R 1-day rats exposed to DCB230 also had similarly reduced ESP. Compared with vehicle controls, CO, SV, and SW were significantly reduced in DCB230-exposed MI/R 1-day rats; moreover, PRSW did not increase. DCB230’s effects on LV function dissipated within 8 days of exposure. These data show that inhalation of EPFRs can exacerbate the deficits in LV function produced by subsequent MI/R injury. Infarct size was not different between the MI/R groups. We conclude that inhalation of EPFRs can compromise cardiac function during MI/R injury and may help to explain the link between PM and MI/R-related mortality.

Length-dependent Regulation of Left Ventricular Function in Coronary Surgery Patients 

1999 ◽  
Vol 91 (2) ◽  
pp. 379-387 ◽  
Author(s):  
Stefan G. De Hert ◽  
Thierry C. Gillebert ◽  
Pieter W. Ten Broecke ◽  
Adriaan C. Moulijn
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Coronary Surgery ◽  
Volume Data ◽  
Load Dependence ◽  
End Diastolic Volume ◽  
Lv Volume ◽  
Underlying Mechanisms

Background Load-dependent impairment of left ventricular (LV) function was observed after leg elevation in a subgroup of coronary surgery patients. The present study investigated underlying mechanisms by comparing hemodynamic effects of an increase in LV systolic pressures with leg elevation to effects of a similar increase in systolic pressures with phenylephrine. Methods The study was performed in patients undergoing elective coronary surgery prior to cardiopulmonary bypass. High-fidelity LV pressure tracings (n = 25) and conductance LV volume data (n = 10) were obtained consecutively during leg elevation and after phenylephrine administration (5 microg/kg). Results Leg elevation resulted in a homogeneous increase in end-diastolic volume. The change in stroke volume (SV), stroke work (SW) and dP/dtmax was variable, with an increase in some patients but no change or a decrease in other patients. For a matched increase in systolic pressures, phenylephrine increased SW and dP/dtmax in all patients with no change in SV. Load dependence of relaxation (slope R of the tau-end-systolic pressure relation) was inversely related for changes in SV, SW, and dP/dtmax with leg elevation but not with phenylephrine. Conclusions The different effects of leg elevation and phenylephrine suggest that the observed decrease in SV, SW, and dP/dtmax with leg elevation in some patients could not be attributed to an impaired contractile response to increased systolic LV pressures. Instead, load-dependent impairment of LV function after leg elevation appeared related to a deficient length-dependent regulation of myocardial function.

Hemodynamic responses to acute carboxyhemoglobinemia in the rat

1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.

Left ventricular pressure-volume relationship in conscious mice

2007 ◽  
Vol 292 (1) ◽  
pp. H369-H377 ◽  
Author(s):  
Shuji Joho ◽  
Shinji Ishizaka ◽  
Richard Sievers ◽  
Elyse Foster ◽  
Paul C. Simpson ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Conscious State ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Polyethylene Tube ◽  
End Diastolic Volume ◽  
Volume Relationship ◽  
Pressure Volume Relationship

With the availability of transgenic models, the mouse has become an increasingly important subject for genetic-hemodynamic studies. Recently, we developed a technique to measure left ventricular (LV) pressure in conscious mice with an implanted LV polyethylene tube. We extended our new method by evaluating the LV pressure-volume relationship and examined the feasibility of this method in this study. We studied 17 male mice (age, 11–20 wk) with a conductance catheter inserted into the LV through the polyethylene tube. Load-independent parameters of contractility derived from pressure-volume relationship [slope of the end-systolic pressure-volume relationship ( Ees), slope of the maximum first derivative of LV pressure (dP/d tmax)-end-diastolic volume (EDV) relation, and preload-recruitable stroke work (PRSW)] were evaluated by inferior vena caval occlusion with an implanted snare. LV function assessed by this technique on two different days showed that the parameters were very similar, indicating reproducibility. Both linear and nonlinear regression analyses were performed for Ees. Contractility was enhanced by isoproterenol ( Ees, 13.1 ± 6.6 to 20.8 ± 8.7 mmHg/μl; dP/d tmax-EDV, 496 ± 139 to 825 ± 178 mmHg·s−1·μl−1; and PRSW, 110 ± 23 to 127 ± 21 mmHg), depressed by atenolol ( Ees, 14.5 ± 6.1 to 4.6 ± 2.0 mmHg/μl; dP/d tmax-EDV, 543 ± 188 to 185 ± 94 mmHg·s−1·μl−1; and PRSW, 117 ± 20 to 70 ± 15 mmHg) and isoflurane ( Ees, 12.3 ± 6.0 to 5.7 ± 2.1 mmHg/μl; dP/d tmax-EDV, 528 ± 172 to 164 ± 68 mmHg/s·μl; and PRSW, 124 ± 19 to 48 ± 10 mmHg), significantly. In conclusion, this is the first description of the LV pressure-volume relationship in conscious mice. These findings suggest that this method is feasible to detect changes of contractility in the conscious state, allowing serial assessment of pressure-volume-derived cardiac function indexes over time without anesthesia or repeated surgery.

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