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

1970 ◽  
Vol 32 (1) ◽  
pp. 45-58 ◽  
Author(s):  
Panagiotis C. Voukydis
Keyword(s):  
Left Ventricle ◽  
Myocardial Fibers ◽  
The Individual

Absence of the left ventricular myocardium in a newborn

1996 ◽  
Vol 6 (4) ◽  
pp. 344-347 ◽  
Author(s):  
Angelika Lindinger ◽  
Yvonne Masur ◽  
Hans-Gerhard Limbach
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Ventricular Myocardium ◽  
Arrhythmogenic Right Ventricular Dysplasia ◽  
Left Ventricular ◽  
Adolescent And Young Adult ◽  
Left Ventricular Myocardium ◽  
Fatty Replacement ◽  
Myocardial Fibers ◽  
The Right

SummaryAbsence of myocardial fibers in the right ventricle is the essence of so-called Uhl's anomaly, which should be distinguished from the fatty replacement producing arrhythmogenic right ventricular dysplasia of the adolescent and young adult. In this report, we describe a newborn with nearly complete absence of the myocardium of the left ventricle. The infant died on the seventh day because of myocardial incompetence of the left ventricle, which was unable to open the aortic valve.

Mechanical Effects of Myofibril Disarray on Cardiac Function

2013 ◽  
Author(s):  
A. I. Veress ◽  
A. Giannakidis ◽  
G. T. Gullberg
Keyword(s):  
Left Ventricle ◽  
Cardiac Function ◽  
Normal Myocardium ◽  
Fiber Distribution ◽  
Mechanical Effects ◽  
Myocardial Fibers

Myocardial disarray is a fiber distribution that deviates away from the tightly organized, parallel alignment of myocardial fibers that characterizes the normal myocardium. This coherently-organized distribution of the myofibers results in the twisting contraction of the normal left ventricle (LV). With myofiber disarray, the fibers have random directionality, either locally or globally, within the LV.

Double inlet left ventricle associated with a subpulmonary tissue tag, dissection of the pulmonary trunk and pheochromocytoma

1997 ◽  
Vol 7 (3) ◽  
pp. 334-336 ◽  
Author(s):  
Shaun A.C. Medlicott ◽  
Joyce R. Harder ◽  
Lloyd N. Denmark
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Left Ventricle ◽  
Congenital Heart ◽  
Pulmonary Trunk ◽  
Primitive Neuroectodermal Tumors ◽  
Neuroectodermal Tumors ◽  
The Individual ◽  
Double Inlet Left Ventricle

AbstractPrevious studies have demonstrated the individual association of subpulmonary tissue tags, dissection of the pulmonary trunk and primitive neuroectodermal tumors with congenital heart disease. We are reporting a case of double inlet left ventricle with all these associations as it is exceptionally rare for all features to be manifest in one individual.

Unique strain history during ejection in canine left ventricle

1991 ◽  
Vol 260 (5) ◽  
pp. H1596-H1611 ◽  
Author(s):  
A. S. Douglas ◽  
E. K. Rodriguez ◽  
W. O'Dell ◽  
W. C. Hunter
Keyword(s):  
Left Ventricle ◽  
Ejection Fraction ◽  
Volume Fraction ◽  
Three Dimensional ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Strain History ◽  
Canine Heart ◽  
The Individual ◽  
The Relationship

Understanding the relationship between structure and function in the heart requires a knowledge of the connection between the local behavior of the myocardium (e.g., shortening) and the pumping action of the left ventricle. We asked the question, how do changes in preload and afterload affect the relationship between local myocardial deformation and ventricular volume? To study this, a set of small radiopaque beads was implanted in approximately 1 cm3 of the isolated canine heart left ventricular free wall. Using biplane cineradiography, we tracked the motion of these markers through various cardiac cycles (controlling pre- and afterload) using the relative motion of six markers to quantify the local three dimensional Lagrangian strain. Two different reference states (used to define the strains) were considered. First, we used the configuration of the heart at end diastole for that particular cardiac cycle to define the individual strains (which gave the local “shortening fraction”) and the ejection fraction. Second, we used a single reference state for all cardiac cycles i.e., the end-diastolic state at maximum volume, to define absolute strains (which gave local fractional length) and the volume fraction. The individual strain versus ejection fraction trajectories were dependent on preload and afterload. For any one heart, however, each component of absolute strain was more tightly correlated to volume fraction. Around each linear regression, the individual measurements of absolute strain scattered with standard errors that averaged less than 7% of their range. Thus the canine hearts examined had a preferred kinematic (shape) history during ejection, different from the kinematics of filling and independent or pre-or afterload and of stroke volume.

scholarly journals Regulation of Cardiac Muscle Contractility

1967 ◽  
Vol 50 (6) ◽  
pp. 185-196 ◽  
Author(s):  
Arnold M. Katz
Keyword(s):  
Myocardial Contractility ◽  
Myocardial Contraction ◽  
Cardiac Myosin ◽  
Shortening Velocity ◽  
Cardiac Contractile ◽  
Myocardial Fibers ◽  
Cardiac Contractile Proteins ◽  
The Individual ◽  
Intact Heart

The heart's physiological performance, unlike that of skeletal muscle, is regulated primarily by variations in the contractile force developed by the individual myocardial fibers. In an attempt to identify the basis for the characteristic properties of myocardial contraction, the individual cardiac contractile proteins and their behavior in contractile models in vitro have been examined. The low shortening velocity of heart muscle appears to reflect the weak ATPase activity of cardiac myosin, but this enzymatic activity probably does not determine active state intensity. Quantification of the effects of Ca++ upon cardiac actomyosin supports the view that myocardial contractility can be modified by changes in the amount of calcium released during excitation-contraction coupling. Exchange of intracellular K+ with Na+ derived from the extracellular space also could enhance myocardial contractility directly, as highly purified cardiac actomyosin is stimulated when K+ is replaced by an equimolar amount of Na+. On the other hand, cardiac glycosides and catecholamines, agents which greatly increase the contractility of the intact heart, were found to be without significant actions upon highly purified reconstituted cardiac actomyosin.

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