Mechanics of left ventricular relaxation, early diastolic lengthening, and suction investigated in a mathematical model

2011 ◽  
Vol 300 (5) ◽  
pp. H1678-H1687 ◽  
Author(s):  
Espen W. Remme ◽  
Anders Opdahl ◽  
Otto A. Smiseth
Keyword(s):  
Mathematical Model ◽  
Relaxation Rate ◽  
Left Ventricular ◽  
Force Balance ◽  
Passive Stiffness ◽  
Ventricular Relaxation ◽  
Active Fiber ◽  
Restoring Forces ◽  
Definition Of ◽  
Early Filling

We investigated the determinants of ventricular early diastolic lengthening and mechanics of suction using a mathematical model of the left ventricle (LV). The model was based on a force balance between the force represented by LV pressure (LVP) and active and passive myocardial forces. The predicted lengthening velocity ( e′) from the model agreed well with measurements from 10 dogs during 5 different interventions ( R = 0.69, P < 0.001). The model showed that e′ was increased when relaxation rate and systolic shortening increased, when passive stiffness was decreased, and when the rate of fall of LVP during early filling was decreased relative to the rate of fall of active stress. We first defined suction as the work the myocardium performed to pull blood into the ventricle. This occurred when contractile active forces decayed below and became weaker than restoring forces, producing a negative LVP. An alternative definition of suction is filling during falling pressure, commonly believed to be caused by release of restoring forces. However, the model showed that this phenomenon also occurred when there had been no systolic compression below unstressed length and therefore in the absence of restoring forces. In conclusion, relaxation rate, LVP, systolic shortening, and passive stiffness were all independent determinants of e′. The model generated a suction effect seen as lengthening occurring during falling pressure. However, this was not equivalent with the myocardium performing pulling work on the blood, which was performed only when restoring forces were higher than remaining active fiber force, corresponding to a negative transmural pressure.

Abstract 4732: Determinants of Left Ventricular Early Diastolic Lengthening Velocities

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Espen W Remme ◽  
Anders Opdahl ◽  
Otto A Smiseth
Keyword(s):  
Mathematical Model ◽  
Left Ventricular ◽  
Lumped Parameter Model ◽  
Passive Stiffness ◽  
Fiber Stress ◽  
Active Fiber ◽  
Wall Stiffness ◽  
Restoring Forces ◽  
The Individual ◽  
Early Filling

The proposed determinants of the LV wall early diastolic lengthening velocity (E′) are: relaxation rate of active fiber stress ( tau ), LV pressure during early filling, restoring forces, and passive elastic wall stiffness. In experimental and clinical studies the individual determinants are difficult to alter and investigate separately due to their inter-dependency. The purpose of this study was to develop a mathematical model that provided a physical basis for the determinants and to validate their individual effect on E′. The LV wall was represented by a lumped parameter model consisting of two elements in parallel (Fig. a ): one representing the active fiber stress (Sa) and the other the passive elastic stress (Sp) represented by an elastic spring with stiffness K and resting length L 0 . The sum of active and passive wall stresses was set to equal LV pressure (LVP). Active stress was prescribed to decay exponentially. E′ was assessed during a simulation with baseline model parameter values and a higher value of each parameter in turn. At baseline E′ was 6.2 cm/s. E′ was decreased to 4.1 cm/s and delayed by prolonging relaxation from tau = 40 to 60 ms (Fig. b ). Increasing LVP during early filling by 5 mmHg increased E′ to 10.6 cm/s (Fig. c ). Decreasing restoring forces by increasing end systolic length from 57 to 60 mm decreased E′ to 2.6 cm/s (Fig. d ). Increasing passive stiffness from K=1500 to 3000 mmHg/m decreased E′ to 5.1 cm/s (Fig. e ). The mathematical model validated former experimental results and confirmed that E′ increases with shortening of tau , increase of diastolic LVP, decreased end systolic length, and decreased passive stiffness.

scholarly journals Ejection timing as a major determinant of left ventricular relaxation rate in isolated perfused canine heart.

1984 ◽  
Vol 55 (1) ◽  
pp. 31-38 ◽  
Author(s):  
M Hori ◽  
M Inoue ◽  
M Kitakaze ◽  
K Tsujioka ◽  
Y Ishida ◽  
...  
Keyword(s):  
Relaxation Rate ◽  
Left Ventricular ◽  
Major Determinant ◽  
Canine Heart ◽  
Left Ventricular Relaxation ◽  
Ventricular Relaxation

scholarly journals Effects of myocardial function and systemic circulation on regional coronary perfusion

2020 ◽  
Vol 128 (5) ◽  
pp. 1106-1122 ◽  
Author(s):  
Ravi Namani ◽  
Lik C. Lee ◽  
Yoram Lanir ◽  
Benjamin Kaimovitz ◽  
Sheikh M. Shavik ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Relaxation Rate ◽  
Coronary Flow ◽  
Myocardial Function ◽  
Regional Distribution ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Tree Structure ◽  
Coronary Perfusion ◽  
Ventricular Relaxation

We present a model of left ventricle perfusion based on an anatomically realistic coronary tree structure that includes its interaction with the systemic circulation. Left ventricular relaxation rate has a significant effect on the regional distribution of coronary flow and myocardial work.

Cardiac Contractile Reserve in Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 365s-368s ◽  
Author(s):  
M. A. Saragoca ◽  
R. C. Tarazi
Keyword(s):  
Relaxation Rate ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Left Ventricular ◽  
Contractile Reserve ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ventricular Relaxation ◽  
Cardiac Contractile ◽  
Response To Stress

1. In response to graded infusions of isoprenaline, adult spontaneously hypertensive rats (20-24 weeks old) showed diminished responses of left ventricular contractile indices, diminished chronotropic responses and impairment of left ventricular relaxation rate as compared with matched Kyoto-Wistar rats. 2. These findings suggest reduced capacity to increase contractility in response to stress.

scholarly journals Cardiotoxic effects and myocardial injury: the search for a more precise definition of drug cardiotoxicity

2021 ◽  
Vol 59 (1) ◽  
pp. 51-57
Author(s):  
Daniela Maria Cardinale ◽  
Martina Zaninotto ◽  
Carlo Maria Cipolla ◽  
Claudio Passino ◽  
Mario Plebani ◽  
...  
Keyword(s):  
Early Detection ◽  
Myocardial Injury ◽  
Randomized Clinical Trials ◽  
Imaging Techniques ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Imaging Techniques ◽  
Ventricular Ejection Fraction ◽  
Early Evaluation ◽  
Definition Of

AbstractDrug-induced cardiotoxicity is a major clinical problem; cardiotoxic drugs may induce both cardiac dysfunction and myocardial injury. Several recent studies reported that cardiac troponins measured with high-sensitivity methods (hs-cTn) can enable the early detection of myocardial injury related to chemotherapy or abuse of drugs that are potentially cardiotoxic. Several authors have some concerns about the standard definition of cardiotoxicity, in particular, regarding the early evaluation of chemotherapy cardiotoxicity in cancer patients. Several recent studies using the hs-cTn assay indicate that myocardial injury may precede by some months or years the diagnosis of heart failure (HF) based on the evaluation of left ventricular ejection fraction (LVEF). Accordingly, hs-cTn assay should considered to be a reliable laboratory test for the early detection of asymptomatic or subclinical cardiotoxic damage in patients undergoing cancer chemotherapy. In accordance with the Fourth Universal Definition of Myocardial Infarction and also taking into account the recent experimental and clinical evidences, the definition of drug-cardiotoxicity should be updated considering the early evaluation of myocardial injury by means of hs-cTn assay. It is conceivable that the combined use of hs-cTn assay and cardiac imaging techniques for the evaluation of cardiotoxicity will significantly increase both diagnostic sensitivity and specificity, and also better prevent chemotherapy-related left ventricular (LV) dysfunction and other adverse cardiac events. However, large randomized clinical trials are needed to evaluate the cost/benefit ratio of standardized protocols for the early detection of cardiotoxicity using hs-cTn assay in patients receiving chemotherapy for malignant diseases.

Estimation of Left Ventricular Wall Stiffness by Analysis of Late Diastolic Pressure Components

2011 ◽  
Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Ventricular Relaxation ◽  
Wall Stiffness ◽  
Ventricular Diastolic Dysfunction

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.

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