"Unlike acute cardiac dilatation with failure, chronic dilatation is not associated with stretching or overstretching of cardiac muscle cells. Starling's law is not applicable for explaining heart failure in these chronic cases. Chronic dilatation is a structural dilatation (Gefugedilatation) produced by sliding displacements (slippage) of heart muscle cells leading to a decrease in the number of muscle layers in the ventricular wall." Linzbach AJ.Adv Cardiol. 1976;18(0):1-14.

The term 'harmonious hypertrophy' proposed by Linzbach  cannot be defined as a symmetric enlargement of all chambers. This term implies an exact correspondence of physiology between the cardiac hypertrophy and normal heart.  Physiological hypertrophy always remains within reasonable limits.  A loss of this physiological limitation leads to pathological hypertrophy. According Linzbach a pathological hypertrophy results from a "structural dilatation" (= Gefügedilatation), the precondition of heart failure.This structural modification will occur if the critical heart weight of 500g.

Disease-related left ventricular remodeling is a complex process involving cardiac myocyte growth and death, vascular rarefaction, fibrosis, inflammation, and electrophysiological remodeling. Specific hemodynamic can be demonstrated through application of physical principles in the context of known biological processes (such as molecular, cellular, and functional mechanisms that lead to cardic hypertrophy) - it is  Laplace relationship  α= pr/2h, where α is wall stress, p is intracavitary pressure, r is the internal radius of the chamber, and h is the thickness of the chamber walls. 

Dear Misses Vaikhanskaya. 

Thank you for your response. Interesting how easily you accept the concept of a layered gliding in the dilating heart such that the number of layers is reduced. Are you aware of the dense intruding and extruding transversal netting of the heart muscle which definitely makes any layered gliding impossible? This was always an argument against Linzbachs Gefügedilatation. Even W. Hort, his pupil, had problems with your explanation. Instead there are faint hints in which direction Linzbach might have thought. He speculated about some kind of cleaving process in length direction of individual long chains of myocytres. Unfortunately, nobody has ever seen that kind of structure in the hypertrophied heart.

Likewise I essentially disagree about the applicability of Laplaces law in that simple way you suggest it and as it is documented in classical textbooks.. The concept would apply, if all forces engendered by the myocardium  were acting in centripetal direction., This is old Physiology postulated by Otto Frank. Meanwhile we know from direct measurements with needle force probes, that 30- 40 % of forces generated are auxotonic forces and not unloading forces hence they do not folliw Laplace law and they are acting in the direction of ventricular dilatation. The heart muscle is organized in structure and function in a strongly antagonistic fashion.

Perhaps Linzbach's ideas were embodied to Speckle Tracking Echocardiography by assessment of  these  dysfunctions by value of global longitudinal strain (GLS), subendocardial and subepicardial longitudinal strain (EndLS and EpiLS, respectively). What do you think?

Dear Misses Waikhanskaya

Linzbach died in the early 60ies. At that time, none of l the new imaging techniques existed. Linzbach was an extremely ingenious and sorrowly observing pathologist. By the way, referring to your suggestion about a layered gliding: Disruption of transversal linkages have never been observed  in those patients, which, houwever would be necessary for enhanced gliding. However, what we have observed is that in extreme hypertrophic hearts the transversal bending in intruding and extruding direction increases critically, so that antagonistic forces might exceed constrictive forces. After late dilation this transversal bending is corrected, transversal netting errects hence antagonistic forces are temperred. So we see a rescue process in this event.

Dear Dr. Paul Peter Lunkenheimer. It was interesting to learn about the original hypotheses of your compatriot as well as the morphofunctional model that is remarkably presented in your article "Models of Ventricular Structure and Function Reviewed for Clinical Cardiologists". Thanks