The Titan can help titin: from micro to macro myocardial elasticity.
Heart failure of different etiologies is due to changes in cardiac structure and function. During normal diastolic filling, the passive stretch of the ventricular myocardium is modulated by titin, a giant elastic protein that acts as a molecular spring and leads to the recapitulation of single cell mechanics at global ventricular level. The mechanics of a dilated failing heart are at least partially determined by variations in the passive filling properties of the myocardium that impair contraction. Current volume reduction surgery is based on Laplace's law and obtained by rigid means that may impair diastolic function. We postulate that inserting one or more elastic elements at different levels of a failing ventricle (the mitral annulus, equator and apex) could improve cardiac performance. We describe our invention for the first time by presenting the results of two animal experiments.
Ferrazzi
Paolo
P
Dipartimento Cardiovascolare Clinico e di Ricerca, Ospedali Riuniti, Bergamo, Italy.
Iascone
Maria R
MR
Senni
Michele
M
Quaini
Eugenio
E
D000818:Animals; D001696:Biomechanical Phenomena; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology* / Q000601:surgery / Q000628:therapy*; D064211:Connectin; D004195:Disease Models, Animal; D004548:Elasticity; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009124:Muscle Proteins / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D019736:Prostheses and Implants; D011474:Prosthesis Design; D011494:Protein Kinases / Q000502:physiology*; D012756:Sheep; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology* / Q000601:surgery / Q000628:therapy*
D064211:Connectin; D009124:Muscle Proteins; C577285:TTN protein, human; D011494:Protein Kinases