scholarly journals Left Ventricular Pressure Gating in Ovine Cardiac Studies: A Software-Based Method

2013 ◽  
Vol 135 (3) ◽  
Author(s):  
Gabriel Acevedo-Bolton ◽  
Takamaro Suzuki ◽  
Deepak Malhotra ◽  
Zhihong Zhang ◽  
Arthur W. Wallace ◽  
...  
Keyword(s):  
Cardiac Imaging ◽  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Digital Circuit ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Diastolic Phase ◽  
Tissue Tagging ◽  
Phase Images ◽  
Systolic Phase

Cardiac imaging using magnetic resonance requires a gating signal in order to compensate for motion. Human patients are routinely scanned using an electrocardiogram (ECG) as a gating signal during imaging. However, we found that in sheep the ECG is not a reliable method for gating. We developed a software based method that allowed us to use the left ventricular pressure (LVP) as a reliable gating signal. By taking the time derivative of the LVP (dP/dt), we were able to start imaging at both end-diastole for systolic phase images, and end-systole for diastolic phase images. We also used MR tissue tagging to calculate 3D strain information during diastole. Using the LVP in combination with our digital circuit provided a reliable and time efficient method for ovine cardiac imaging. Unlike the ECG signal the left ventricular pressure was a clean signal and allowed for accurate, nondelay based triggering during systole and diastole.

Impairment of contraction increases sensitivity of epicardial lymph pressure for left ventricular pressure

1998 ◽  
Vol 274 (1) ◽  
pp. H187-H192 ◽  
Author(s):  
Jurgen W. G. E. Vanteeffelen ◽  
Daphne Merkus ◽  
Luc J. Bos ◽  
Isabelle Vergroesen ◽  
Jos A. E. Spaan
Keyword(s):  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Relative Increase ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Local Contraction ◽  
Lymphatic Vasculature ◽  
Anesthetized Dogs ◽  
Lidocaine Administration

In the present study, cardiac contraction was regionally impaired to investigate the relationship between contractility [maximum first time derivative of left ventricular pressure (dPLV/d tmax)] and PLVon epicardial lymph pressure (Plymph) generation. Measurements were performed in open-chest anesthetized dogs under control conditions and while local contraction was abolished by intracoronary administration of lidocaine. Lidocaine significantly lowered dPLV/d tmaxand PLVpulse to 77 ± 9 (SD; n = 5) and 82 ± 5% of control, respectively, whereas Plymphpulse increased to 186 ± 101%. The relative increase of maximum Plymphto PLVrelated inversely to the change in dPLV/d tmaxafter lidocaine administration. Additional data were obtained when PLVwas transiently increased by constriction of the descending aorta. The ratio of pulse Plymphto PLVduring aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of PLVto the cardiac lymphatic vasculature is enhanced when regional contraction is impaired. These findings imply that during normal, unimpaired contraction lymph vessels are shielded from high systolic PLVby the myocardium itself.

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.

Abstract 5728: Abrupt Early Intraventricular Septal Motion In Not Passive But Active In Left Bundle Brunch Block

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Azusa Furugen ◽  
Naoki Matsuda ◽  
Tsuyoshi Shiga ◽  
Daigo Yagishita ◽  
Asako Mochida ◽  
...  
Keyword(s):  
Speckle Tracking ◽  
Interventricular Septum ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Speckle Tracking Imaging ◽  
Systolic Phase ◽  
Qrs Duration ◽  
The Right ◽  
Septal Motion

Abnormal early septal motion observed in patients with left bundle brunch block (LBBB) has been explained as a difference in right-to-left ventricular pressure. The interventricular septum was thought to be displaced passively into the LV because the right ventricle contracts prior to the LV and the right ventricular pressure exceeds the LV pressure during early systolic phase. Assuming that this theory is right, the interventricular septal wall would be stretched and shown positive strain value in circumferential and longitudinal directions during early systolic phase. We investigated the mechanism of the early septal motion with LBBB using speckle tracking imaging (STI). Methods: Systolic septal motion on the middle LV portion level was analyzed in 44 patients with complete LBBB (mean QRS duration 166 ± 35 ms) using M-mode echocardiography and speckle tracking imaging (STI). Time from onset of QRS configuration to peak circumferential strain and longitudinal strain were measured in parasternal short axis and apical views by STI. Furthermore, 20 healthy individuals (mean QRS duration 84 ± 6 ms) were also analyzed. Changes in LV pressure and septal strain were simultaneously measured to evaluate the relationship between them in 6 patients with LBBB. Results: Septal displacement into the LV was early and abrupt on M-mode echocardiograms from all patients with LBBB. During this displacement, the STI of the interventricular septum of all patients showed negative strain in both the circumferential and longitudinal directions. Furthermore, early septal displacement almost coincided with peak negative strain. Time to peak septal strain in LBBB patients was significantly shorter than in normal controls in the circumferential (296 ± 80 vs. 356 ± 30 ms; p < 0.05) and longitudinal (317 ± 104 vs. 369 ± 17 ms; p < 0.05) directions. The peak of septal negative strain was followed by an increase in LV pressure in all patients. Conclusion: Early motion of the interventricular septum is provoked by its active contraction in LBBB. The septal contraction starts very early and almost isotonically toward a very low load. However, further shortening is suppressed by a subsequently increased load of pressure elevation due to the contraction of other LV segments.

Effects of vasoactive intestinal peptide on myocardial performance

1994 ◽  
Vol 266 (2) ◽  
pp. H399-H405 ◽  
Author(s):  
N. P. Xenopoulos ◽  
R. J. Applegate
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Contractile Function ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adrenergic Blockade ◽  
Volume Relation ◽  
First Time

It is now recognized that stimulation of the vagus releases both acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Whereas ACh depresses cardiac function, recent data indicate that VIP may have a cardiostimulatory effect. Exogenously administered VIP appears to enhance left ventricular (LV) contractile function; however, whether endogenously released VIP alters LV performance is not known. Accordingly, we evaluated the effects of exogenous VIP and endogenously released VIP during vagal stimulation after muscarinic and beta-adrenergic blockade (VS-B) on LV performance using pressure-volume analysis. Eight anesthetized open-chest dogs instrumented to measure LV pressure and volume (conductance catheter) were pretreated with atropine (0.1 mg/kg) and propranolol (1 mg/kg). The cervical vagi were transected. Hemodynamic data were obtained at steady state and during transient vena caval occlusion. Exogenous intravenous VIP (0.05 microgram/kg-1 x min-1) increased HR minimally [2.1 +/- 0.9% increase; P = not significant (NS)] but significantly increased maximum first time derivative of left ventricular pressure (dP/dtmax; 29.4 +/- 19.9% increase; P < 0.05) and the slope of the end-systolic pressure-volume relation (Ees; 3.1 +/- 1.3 to 8.9 +/- 4.2 mmHg/ml; P < 0.05). Minimum first time derivative of left ventricular pressure (dP/dtmin) decreased 22 +/- 16.2% (P < 0.05), and the time constant of isovolumic relaxation (tau) decreased 38 +/- 18% (P < 0.05). During VS-B (20 Hz, 15 v, 5 min), HR increased significantly (98 +/- 11 to 130 +/- 26 beats/min; P < 0.05). Ees also increased significantly (3.3 +/- 1.6 vs. 5.2 +/- 2.8 mmHg/ml; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Sign in / Sign up

Export Citation Format

Share Document