Congestive Heart Failure Clinical Trial
Official title:
Morphodynamic Study of Left Ventricular Remodeling With Possible Mechanisms for Pharmacologic Therapy: Assessment by Real-time 3-dimensional Echocardiography and 2-dimensional Speck Tracking Imaging.
Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. The recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI. As a leading cause of heart failure, postinfarction LV remodeling represents an important target for therapeutic interventions. Within the ventricular mass, size, shape, connections and orientation in a three-dimensional space of every single constituent determine its functional behavior. The complex architecture of the ventricular mass creates multiple inhomogeneities of electrical and mechanical loads at the cellular and the microscopic tissue level, that cause cardiac function to be 'stochastic in nature'. The myocardial infarction will altered the ventricular shape and functional inhomogeneities carrying the morphodynamic advantages such as impaired suction for diastole after diminishing recoil relaxation with decreased twisting strain in systole. The alteration in contractile mechanics interacts with the intraventricular fluid dynamic filed that influence the regional myocardial shearing stress. Altered LV transmural wall strains have been proposed to cause infarct extension and may have an important role in propagating LV remodeling.
We are currently witnessing the advent of new diagnostic tools and therapies for heart
diseases, but,without serious scientific consensus on fundamental questions about normal and
diseased heart structure and function. During the last decade, three successive,
international, multidisciplinary symposia were organized in order to setup fundamental
research principles, which would allow us to make a significant step forward in
understanding heart structure and function. (Kocica MJ et al., 2006) Helical ventricular
myocardial band (HVMB, Figure 2-1) of Torrent-Guasp is the revolutionary new concept in
understanding global, three-dimensional, functional architecture of the ventricular
myocardium. This concept defines the principal, cumulative vectors, integrating the tissue
architecture (i.e. form) and net forces developed (i.e. function) within the ventricular
mass. Helical ventricular myocardial band of Torrent-Guasp may also, hopefully, allow
overcoming some difficulties encountered in contemporary efforts to create a comprehensive
mathematical model of the heart.
Within the ventricular mass, size, shape, connections and orientation in a three-dimensional
space of every single constituent determine its functional behavior. This kind of spatial
dependence allows the ventricular myocardial mass to be considered as the source of
interdependent vectorial forces (i.e.
electrical and mechanical), being generated on different length and time scales. The
ultimate net result of these vectorial forces is to translate uniaxial sarcomere shortening
into efficient three-dimensional deformation of the ventricular cavity. The complex
architecture of the ventricular mass creates multiple inhomogeneities of electrical and
mechanical loads at the cellular and the microscopic tissue level, that cause cardiac
function to be 'stochastic in nature'. However, at macroscopic (i.e. organ) level, these
stochastic events become average and appear consistent with a continuous medium. This
dialectic coexistence of complexity and simplicity, discreetness and continuity suggests the
existence of certain rule-based assignment, which 'may be applied equally well to all the
ventricular myocardial fibers', enabling the ventricular myocardial mass to assemble
abundant, dynamic, stochastic vectorial forces and produce apparently smooth, averaged,
continuous, global response.
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Observational Model: Case-Only, Time Perspective: Prospective
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