The effect of distension of the left ventricle of the heart on the length of the individual myocardial fibers

Based on the ellipsoid model of the left ventricle and the helicoidal course of the left ventricular myocardial fibers, a theory has been developed for calculating the length of the individual myocardial fibers. Numerical solutions of the final equation show that when the left ventricle is distended, the increase in length of the myocardial fibers is not uniform throughout the thickness of the myocardial wall. It was shown that with increasing dimensions of the left ventricle, the distension of the myocardial fibers becomes smaller as one advances from the endocardium to the middle layer of fibers, whereas it increases as one advances from the middle layer to the epicardial layer. The mechanism by which this effect is brought about as well as its physiological implications are discussed.     

The preload of individual myocardial fibers

The preload of the indiviuual myocardial fibers of the left ventricle, that is, the stress exerted upon the myocardial fibers at end-diastole, is calculated by means of a set of equations. The development of the equations was based on anatomical data referring to the shape of the left ventricle and the orientation of the myocardial fibers, as well as some assumptions of minor importance. Numerical solution of the equations shows that in general, the preload increases as one advances from the apex to the equator of the left ventricle and then it decreases as one advances toward the base. The preload also changes as one advances from the epicardium to the endocardium in such a way that one can distinguish three zones: one outer, or epicardial, with low preloads, one middle with high preloads and one inner, or endocardial, with low preloads. The physiological significance of the findings as well as the validity of the assumptions on which the theory was based are discussed.     

Flow dynamics and energy efficiency of flow in the left ventricle during myocardial infarction

Cardiovascular disease is a leading cause of death worldwide, where myocardial infarction (MI) is a major category. After infarction, the heart has difficulty providing sufficient energy for circulation, and thus, understanding the heart’s energy efficiency is important. We induced MI in a porcine animal model via circumflex ligation and acquired multiple-slice cine magnetic resonance (MR) images in a longitudinal manner—before infarction, and 1 week (acute) and 4 weeks (chronic) after infarction. Computational fluid dynamic simulations were performed based on MR images to obtain detailed fluid dynamics and energy dynamics of the left ventricles. Results showed that energy efficiency flow through the heart decreased at the acute time point. Since the heart was observed to experience changes in heart rate, stroke volume and chamber size over the two post-infarction time points, simulations were performed to test the effect of each of the three parameters. Increasing heart rate and stroke volume were found to significantly decrease flow energy efficiency, but the effect of chamber size was inconsistent. Strong complex interplay was observed between the three parameters, necessitating the use of non-dimensional parameterization to characterize flow energy efficiency. The ratio of Reynolds to Strouhal number, which is a form of Womersley number, was found to be the most effective non-dimensional parameter to represent energy efficiency of flow in the heart. We believe that this non-dimensional number can be computed for clinical cases via ultrasound and hypothesize that it can serve as a biomarker for clinical evaluations.     

Assessment of human left ventricle flow using statistical shape modelling and computational fluid dynamics

Blood flow patterns in the human left ventricle (LV) have shown relation to cardiac health. However, most studies in the literature are limited to a few patients and results are hard to generalize. This study aims to provide a new framework to generate more generalized insights into LV blood flow as a function of changes in anatomy and wall motion. In this framework, we studied the four-dimensional blood flow in LV via computational fluid dynamics (CFD) in conjunction with a statistical shape model (SSM), built from segmented LV shapes of 150 subjects. We validated results in an in-vitro dynamic phantom via time-resolved optical particle image velocimetry (PIV) measurements. This combination of CFD and the SSM may be useful for systematically assessing blood flow patterns in the LV as a function of varying anatomy and has the potential to provide valuable data for diagnosis of LV functionality.     

The motion of the left ventricle: II

We use the dimensional parameters previously derived (Bull. Math. Biophysics,28, 355–362, 1966), the ventricular pressure expressed as a Fourier series, and several additional assumptions to derive expressions for the mechanical parameters of the ventricle: flow, muscle segment length, surface area, transmural force, wall tension and work. The wall of the ventricle is assumed to consist of three layers of muscle. Each of the mechanical parameters is expressed in terms of Fourier series.     

Dynamics of the strength of the rat left ventricle wall in experimental uncomplicated myocardial infarction

Left ventricular wall stability was studied in 131 normal rats at different terms of uncomplicated experimental myocardial infarction. Left ventricular wall stability was estimated by the normal effort required for its destruction. Normal left ventricular wall could stand the pressure of 1.1 X 10(5) Pa. During ischemic phase of myocardial infarction the wall stability in the infarction area increased up to 1.5 X 10(5) Pa. It diminished during necrotic phase, however timely started repair processes did not let it drop lower than 1.0 X 10(5) Pa. The mechanisms of preserving ventricular wall stability in the infarction area were studied in detail.     

Intraventricular vortex flow changes in the infarcted left ventricle: numerical results in an idealised 3D shape

The cardiac diagnostic process is primarily based on the evaluation of myocardial mechanics whereas little is known about blood dynamics that is rarely considered to this purpose. The intraventricular blood flow is analysed here for akinetic and dyskinetic myocardial motion corresponding to the presence of an ischaemic pathology. This study is performed through a 3D numerical model of the left ventricular flow. Results show that the presence of an anterior-inferior wall infarction leads to the shortening and weakening of the diastolic mitral jet. A region of stagnating flow is found near the apex and close to the ischaemic wall. These results are in agreement with previous clinical findings based on echographic imaging. The described phenomena are also noticed for moderate degrees of the ischaemic pathology and suggest a potential value of the study of the intraventricular flow to develop early diagnostic indicators.     

Clinical observations and echocardiographic features of mural thrombi in the left ventricle during myocardial infarction]

The incidence and changes in the mural thrombi in left ventricle in ECHO-2D in the acute myocardial infarction as well as relationship between clinical parameters and echocardiographic indices of the left cardiac ventricle contractability asynergy and dynamics of changes in mural thrombi have been investigated. The studies included 137 consecutive patients (98 males and 39 females) treated for the acute myocardial infarction. Patients' age ranged from 35 to 87 years (mean 62 years). Infarction of the anterior and/or lateral wall was diagnosed in 67 patients, and infarction of the inferior and/or posterior wall in 70 patients. Mural thrombi were diagnosed in 42 (31%) patients. Eighteen thrombi (43%) were liquefied during hospitalization. Comparative analysis of patients in whom mural thrombi underwent liquefaction in the hospital and a group of patients with myocardial infarction and persisting mural thrombi showed that return of left ventricle movements with subsequent contractability facilitate liquefaction of mural thrombi. Higher mortality rate in the group of patients with myocardial infarction with mural thrombi is due to extension of the infarction accompanied by marked asynergy of left ventricular contractions which does not decrease in sequential examinations, and increasing congestive heart failure.