Faculty Opinions recommendation of The relative contribution of prosthetic gradients, systemic arterial pressure, and pulse pressure to the left ventricular pressure in patients with aortic prosthetic valves.

2011 ◽  
Author(s):  
Olav F Münter Sellevold
Keyword(s):  
Arterial Pressure ◽  
Pulse Pressure ◽  
Left Ventricular Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Relative Contribution ◽  
Prosthetic Valves

Reflex sympathetic augmentation of left-ventricular inotropic state in the conscious dog

1981 ◽  
Vol 241 (6) ◽  
pp. H857-H863
Author(s):  
C. Yoran ◽  
L. Higginson ◽  
M. A. Romero ◽  
J. W. Covell ◽  
J. Ross
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Conscious Dog ◽  
Inotropic State ◽  
Simultaneous Decrease

Cardiac reflex responses to a series of partial inferior vena caval occlusions were studied in conscious previously instrumented dogs. Heart rate responses during the fall of systemic arterial pressure were mediated both by increased sympathetic tone and withdrawal of parasympathetic tone. Responses of the left-ventricular inotropic state, estimated from changes in left ventricular pressure rise (LV dP/dt), were studied early after release of a series of partial vena caval occlusions, and a positive linear relation between the prior fall in the systemic arterial pressure and the increase in LV dP/dt was demonstrated. Serial studies showed this effect of persist for at least 12 s beyond the reflex slowing of heart rate early after release of vena caval occlusion. The positive inotropic response was markedly attenuated by beta-adrenergic blockade and also occurred at a constant heart rate. It was present after adrenalectomy. These studies suggest that the integrated baroreceptor responses that are activated by a simultaneous decrease in the venous return and systemic arterial pressure play an important role in the regulation of left-ventricular inotropic state in the conscious dog.

Enkephalin lowers vascular resistance in dog hindlimb via a peripheral nonlimb site

1991 ◽  
Vol 260 (2) ◽  
pp. H386-H392 ◽  
Author(s):  
J. L. Caffrey ◽  
H. Gu ◽  
B. A. Barron ◽  
J. F. Gaugl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Opiate Receptors ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Sharp Decline ◽  
Descending Aorta ◽  
A Site

The intravenous administration of methionine enkephalin in anesthetized dogs produces an abrupt decline in mean arterial pressure, left ventricular pressure, and the maximal rate of left ventricular pressure development. All of these changes are prevented by receptor blockade with the opiate antagonist, naloxone. To evaluate peripheral vascular contributions to these responses, experiments were conducted in a constant pressure-isolated perfused hindlimb. In this model, the sharp decline in mean arterial pressure associated with enkephalin injection (5 micrograms/kg iv) coincided with an equally sharp decline in vascular resistance (rise in blood flow) in the hindlimb. Both were blocked by naloxone pretreatment (1 mg/kg). When equal doses of enkephalin were administered directly into the femoral inflow (external iliac artery), both arterial pressure and hindlimb flow responses were all but eliminated. This observation ruled out significant direct vascular interactions in the response and indicated a site of action outside the hindlimb. Additional catheters were placed in the bracheocephalic artery and descending aorta to permit the comparison of arterial injections conducted, respectively, into the cerebral or abdominal circulations. Injections introduced into the descending aorta consistently produced the greatest response, followed by injections (in descending order of effectiveness) into the jugular, the brachiocephalic, and external iliac. The response in the hindlimb vasculature was initiated at a site somewhere between the diaphragm and terminal aorta. The vascular response to enkephalin was subsequently eliminated by blocking ganglionic transmission with the nicotinic antagonist mecamylamine. These observations suggest that the opioids probably interrupt local vasomotor traffic via opiate receptors in regional sympathetic ganglia or in the spinal cord.

Abstract 16747: The Artificial Pulse of the HeartMate3 LVAD Alters Mean Arterial Pressure Calculation, and the Relationship Between Arterial Pulse Pressure and Pulsatility Index

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lorenzo Braghieri ◽  
Alberto Pinsino ◽  
Giulio Mondellini ◽  
Antonia Gaudig ◽  
Azka Javaid ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pulsatility Index ◽  
Left Ventricular ◽  
Absolute Difference ◽  
Arterial Line ◽  
Arterial Pulse ◽  
Relative Contribution ◽  
Arterial Pulse Pressure

Introduction: The HeartMate (HM3) left ventricular assist device (LVAD) uniquely features an artificial pulse (AP) (designed to reduce blood stasis and simulate physiologic pulsatility) that alters arterial blood pressure (BP) tracings ( Fig. 1A ). Pulsatility Index (PI) corresponds to the magnitude of flow pulse through the LVAD and is used as a surrogate measure of arterial pulse pressure (PP). The effect of the AP on: i) relative contribution of systolic BP (SBP) and diastolic BP (DBP) to mean arterial pressure (MAP) calculation; and ii) association between PP and PI is presently unknown. Thus, we aimed to compare: i) MAP calculations; and ii) relation of PI with PP in HM3 vs HM II (LVAD with no AP) pts with arterial line (A-line) monitoring. Methods: A-line BP and LVAD PI data were prospectively collected in 48 HM3 and 29 HMII pts. MAP was calculated with the formula conventionally used in non LVAD pts (MAP = 2/3 DBP + 1/3 SBP) and compared to A-line MAP. Among HM3 pts, a multiple linear regression model was fit with A-line SBP and DBP as predictor variables, and A-line MAP as the dependent variable to derive the HM3 MAP Formula . The relation between arterial PP and PI in HM3 and HMII pts was assessed using Pearson’s correlation. Results: MAP calculated using the conventional formula accurately estimated A-line MAP in HMII pts, but overestimated A-line MAP in HM3 pts. The HM3 MAP Formula more closely approximated A-line MAP. Mean observed difference (MOD) and mean absolute difference (MAD) between calculated MAPs and A-line MAPs are reported in Fig. 1B . While median PP was similar in HM3 and HMII pts (16 vs 20 mmHg, p=0.11), median PI was significantly higher in HMII pts (3.45 vs 5.6, p<0.001). PI correlated with PP in HMII pts ( r 0.47, p=0.01). However, no significant correlation was found between PI and PP in HM3 pts ( r 0.24, p=0.1; Fig. 1C ). Conclusions: In HM3 pts, the AP significantly alters the relative contribution of SBP and DBP to MAP. Unlike in HM2 pts, PI does not relate to arterial PP in HM3 pts.

Perfusion-induced changes in cardiac O2 consumption and contractility are based on different mechanisms

1996 ◽  
Vol 271 (3) ◽  
pp. H984-H989 ◽  
Author(s):  
M. A. Dijkman ◽  
J. W. Heslinga ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Shear Stress ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Isolated Heart ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Cardiac Perfusion ◽  
Induced Changes ◽  
Pressure Measure

Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms.

Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 2010-2017 ◽  
Author(s):  
J.J. Schreuder ◽  
F.H. van der Veen ◽  
E.T. van der Velde ◽  
F. Delahaye ◽  
O. Alfieri ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter ◽  
Volume Relation

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.

scholarly journals The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jingtao Na ◽  
Haifeng Jin ◽  
Xin Wang ◽  
Kan Huang ◽  
Shuang Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Expression Patterns ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Luciferase Reporter ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction

Abstract Background Heart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating  targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3. Methods Firstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry. Results HDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined. Conclusion Collectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

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