Coronary Sinus Assessment of Left Ventricular Pressure in Man

We hypothesized that endothelin (ET) release during exercise may be triggered by α-adrenergic-receptor activation and thereby influence coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min−1 · g−1) and in a fall ( P < 0.01) in coronary sinus O2saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas myocardial O2 consumption (MV˙o 2) increased (109 ± 13% from 145 ± 16 μl O2 · min−1 · g−1). Tezosentan, a dual ETA/ETB-receptor blocker, slightly reduced mean arterial pressure (MAP) and increased heart rate throughout exercise. The relationship between coronary sinus O2 saturation and MV˙o 2 was shifted upward ( P < 0.05) after tezosentan administration; i.e., as MV˙o 2 increased during exercise, coronary sinus O2 saturation was disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases ( P < 0.05) in left ventricular pressure, the first derivative of left ventricular pressure over time, and MAP during exercise. As MV˙o 2 increased during exercise, coronary sinus O2 saturation levels after tezosentan became superimposable over those observed before ET-receptor blockade. Thus dual blockade of ETA/ETBreceptors alters coronary hemodynamics and O2 metabolism during exercise, but ET activity failed to increase beyond baseline levels.

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Transcardiac gradients of circulating apelin: extraction by normal hearts vs. release by hearts failing due to pressure overload

Journal of Applied Physiology ◽

10.1152/japplphysiol.00474.2010 ◽

2010 ◽

Vol 109 (6) ◽

pp. 1744-1748 ◽

Cited By ~ 5

Author(s):

Satu Helske ◽

Petri T. Kovanen ◽

Jyri Lommi ◽

Heikki Turto ◽

Markku Kupari

Keyword(s):

Coronary Sinus ◽

Aortic Root ◽

Pressure Overload ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Control Group ◽

Electrophysiological Studies ◽

Plasma Apelin

Apelin is a newly discovered inotropic peptide tentatively linked up with the pathophysiology of heart failure (HF). To further assess the role of apelin in HF, we measured its transcardiac arteriovenous gradients in patients with left ventricular pressure overload with or without HF and in patients with structurally normal hearts. Blood samples from the aortic root and coronary sinus were drawn from 49 adult patients undergoing preoperative cardiac catheterization for severe aortic valve stenosis (AS). Similar samples were taken from 12 control patients with structurally normal hearts undergoing electrophysiological studies. Plasma apelin was determined by enzyme immunoassay. In the control group, apelin decreased from a median of 0.39 (0.16–1.94) ng/ml in the aortic root to 0.18 (0.13–1.04) ng/ml in the coronary sinus ( P = 0.004). In AS patients free of HF ( n = 33), apelin concentration remained unaltered across the heart, but in those with HF ( n = 15) apelin rose from a median of 0.26 (0.20–0.82) ng/ml in the aorta to 0.45 (0.24–1.17) ng/ml in the coronary sinus ( P = 0.002). The transcardiac apelin gradients differed statistically highly significantly across the three groups ( P = 0.00005), and each of the two-group differences was also statistically significant ( P < 0.05). In conclusion, left ventricular pressure overload changes the transcardiac arteriovenous differences of circulating apelin. Although normal hearts extract apelin from the coronary blood, hearts failing due to left ventricular pressure overload release apelin into the circulation. Loss of cardiac apelin may be involved in the mechanisms of HF development in AS.

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Endothelin Receptor Blockade Improves Left Ventricular Pressure-Volume Relationships Without Altering the Hypertrophic Response During Congestive Heart Failure in Rats

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(97)84967-4 ◽

1998 ◽

Vol 31 (2) ◽

pp. 289A

Author(s):

E Øie

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Receptor Blockade ◽

Endothelin Receptor ◽

Hypertrophic Response

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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.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.9881957.10592055 ◽

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

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

Circulation ◽

10.1161/01.cir.91.7.2010 ◽

1995 ◽

Vol 91 (7) ◽

pp. 2010-2017 ◽

Cited By ~ 57

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

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Contribution of extravascular compression to reduction of maximal coronary blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h68 ◽

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.

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

Cell & Bioscience ◽

10.1186/s13578-020-00523-y ◽

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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