Analysis of the relationship between left ventricular pressure and motor current for evaluation of native cardiac function during left ventricular support with a centrifugal blood pump

2001 ◽  
Vol 4 (4) ◽  
pp. 269-272
Author(s):  
Daiki Kikugawa ◽  
Katsuhiro Ohuchi ◽  
Makoto Nakamura ◽  
Setsuo Takatani ◽  
Taiji Murakami ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Blood Pump ◽  
Centrifugal Blood Pump ◽  
Motor Current ◽  
Ventricular Support ◽  
The Relationship

scholarly journals Influence of dual ETA/ETB-receptor blockade on coronary responses to treadmill exercise in dogs

2000 ◽  
Vol 89 (5) ◽  
pp. 2041-2048 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Peter Cernacek ◽  
Michel Lavallée
Keyword(s):  
Coronary Sinus ◽  
Adrenergic Receptor ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Receptor Blockade ◽  
Etb Receptor ◽  
Dual Blockade ◽  
The Relationship

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.

scholarly journals Synergistic Model of Cardiac Function with a Heart Assist Device

2019 ◽  
Vol 7 (1) ◽  
pp. 1
Author(s):  
Eun-jin Kim ◽  
Massimo Capoccia
Keyword(s):  
Cardiac Function ◽  
Heart Diseases ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Self Organization ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Assist Device ◽  
Clinical Scenarios ◽  
Volume Relation

The breakdown of cardiac self-organization leads to heart diseases and failure, the number one cause of death worldwide. The left ventricular pressure–volume relation plays a key role in the diagnosis and treatment of heart diseases. Lumped-parameter models combined with pressure–volume loop analysis are very effective in simulating clinical scenarios with a view to treatment optimization and outcome prediction. Unfortunately, often invoked in this analysis is the traditional, time-varying elastance concept, in which the ratio of the ventricular pressure to its volume is prescribed by a periodic function of time, instead of being calculated consistently according to the change in feedback mechanisms (e.g., the lack or breakdown of self-organization) in heart diseases. Therefore, the application of the time-varying elastance for the analysis of left ventricular assist device (LVAD)–heart interactions has been questioned. We propose a paradigm shift from the time-varying elastance concept to a synergistic model of cardiac function by integrating the mechanical, electric, and chemical activity on microscale sarcomere and macroscale heart levels and investigating the effect of an axial rotary pump on a failing heart. We show that our synergistic model works better than the time-varying elastance model in reproducing LVAD–heart interactions with sufficient accuracy to describe the left ventricular pressure–volume relation.

Inhibition of vascular peroxidase alleviates cardiac dysfunction and apoptosis induced by ischemia–reperfusion

2012 ◽  
Vol 90 (7) ◽  
pp. 851-862 ◽  
Author(s):  
Ting-Ting Li ◽  
Yi-Shuai Zhang ◽  
Lan He ◽  
Bin Liu ◽  
Rui-Zheng Shi ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Clinical Value ◽  
Pharmacologic Inhibition

Myeloperoxidase (MPO) is involved in myocardial ischemia–reperfusion (IR) injury and vascular peroxidase (VPO) is a newly identified isoform of MPO. This study was conducted to explore whether VPO is involved in IR-induced cardiac dysfunction and apoptosis. In a rat Langendorff model of myocardial IR, the cardiac function parameters (left ventricular pressure and the maximum derivatives of left ventricular pressure and coronary flow), creatine kinase (CK) activity, apoptosis, VPO1 activity were measured. In a cell (rat-heart-derived H9c2 cells) model of hypoxia–reoxygenation (HR), apoptosis, VPO activity, and VPO1 mRNA expression were examined. In isolated heart, IR caused a marked decrease in cardiac function and a significant increase in apoptosis, CK, and VPO activity. These effects were attenuated by pharmacologic inhibition of VPO. In vitro, pharmacologic inhibition of VPO activity or silencing of VPO1 expression significantly suppressed HR-induced cellular apoptosis. Our results suggest that increased VPO activity contributes to IR-induced cardiac dysfunction and inhibition of VPO activity may have the potential clinical value in protecting the myocardium against IR injury.

Stopped-flow epicardial lymph pressure is affected by left ventricular pressure in anesthetized goats

1993 ◽  
Vol 264 (5) ◽  
pp. H1624-H1628 ◽  
Author(s):  
Y. Han ◽  
I. Vergroesen ◽  
J. A. Spaan
Keyword(s):  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beating Heart ◽  
Ventricular Pressure ◽  
Stopped Flow ◽  
Pressure Waveform ◽  
Descending Aorta ◽  
Aortic Clamping ◽  
The Relationship

We measured epicardial lymph pressure (Plymph) in the anesthetized goat (n = 5 goats). To study the transmission of systolic left ventricular pressure (PLV) to Plymph, the effect of an increase in PLV caused by clamping of the descending aorta on Plymph was evaluated. Peak systolic PLV was 131 +/- 4 (+/- SE) mmHg during control (43 beats) and 188 +/- 4 mmHg when elevated due to aortic clamping (157 beats). Peak systolic Plymph was 24.8 +/- 1.0 and 34.8 +/- 1.1 mmHg during control and elevated PLV, respectively. In the first beat of elevated PLV, peak Plymph did not change, although the pressure waveform did. In the subsequent beats, Plymph increased proportionally with increased PLV. When PLV was decreased back to control, Plymph also decreased but did not reach control level until after three beats. The relationship between normalized Plymph and normalized PLV is given by Plymph = 0.70 x PLV + 0.09. The results show that PLV does affect Plymph in a normal beating heart.

Cardiac function and exercise training in conscious dogs

1977 ◽  
Vol 42 (6) ◽  
pp. 824-832 ◽  
Author(s):  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Exercise Training ◽  
Cardiac Function ◽  
Heart Rate Response ◽  
Exercise Program ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Time Intervals ◽  
Similar Time

Exercise training (T) was accomplished in 21 mongrel dogs. The animals were instrumented to measure ascending aortic flow, left ventricular pressure, and left atrial pressure. They were allowed to recover for 4 wk following surgery before accomplishing a standardized submaximal test (SMT). The exercise program alternated daily between sprint and endurance training. During T, the animals were tested while lying quietly on a laboratory table as well as during the SMT. In six animals, ventricular function curves (VFC) were obtained by rapid volume loading at similar time intervals as the SMT. Heart rate increased during the SMT but was found to be reduced in the T animals by an average of 20 beats/min. The maximum derivative of left ventricular pressure (P) increased during the SMT in T animals by an average of 2,200 Torr/s above the untrained animals. The VFC was lower in T animals than untrained animals because of a reduction in heart rate response. Results indicate a reflex adaptation of the nervous system with training to improve cardiac function.

scholarly journals Protective Effects of Thyroid Hormone Deprivation on Progression of Maladaptive Cardiac Hypertrophy and Heart Failure

2021 ◽  
Vol 8 ◽  
Author(s):  
Helena Kerp ◽  
Georg Sebastian Hönes ◽  
Elen Tolstik ◽  
Judith Hönes-Wendland ◽  
Janina Gassen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Heart Function ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Cardiovascular Morbidity And Mortality ◽  
The Impact

Purpose: Thyroid hormones (TH) play a central role for cardiac function. TH influence heart rate and cardiac contractility, and altered thyroid function is associated with increased cardiovascular morbidity and mortality. The precise role of TH in onset and progression of heart failure still requires clarification.Methods: Chronic left ventricular pressure overload was induced in mouse hearts by transverse aortic constriction (TAC). One week after TAC, alteration of TH status was induced and the impact on cardiac disease progression was studied longitudinally over 4 weeks in mice with hypo- or hyperthyroidism and was compared to euthyroid TAC controls. Serial assessment was performed for heart function (2D M-mode echocardiography), heart morphology (weight, fibrosis, and cardiomyocyte cross-sectional area), and molecular changes in heart tissues (TH target gene expression, apoptosis, and mTOR activation) at 2 and 4 weeks.Results: In diseased heart, subsequent TH restriction stopped progression of maladaptive cardiac hypertrophy and improved cardiac function. In contrast and compared to euthyroid TAC controls, increased TH availability after TAC propelled maladaptive cardiac growth and development of heart failure. This was accompanied by a rise in cardiomyocyte apoptosis and mTOR pathway activation.Conclusion: This study shows, for the first time, a protective effect of TH deprivation against progression of pathological cardiac hypertrophy and development of congestive heart failure in mice with left ventricular pressure overload. Whether this also applies to the human situation needs to be determined in clinical studies and would infer a critical re-thinking of management of TH status in patients with hypertensive heart disease.

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