Tumor Growth Ameliorates Cardiac Dysfunction.

Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling.

Evaluation of an Innovative Device for Mitral Valve Regurgitation: Experimental Acute In Vivo Results.

Currently, mitral prosthetic rings are intended only to reshape the annulus. We present in vivo results of an innovative device characterized by an intraventricular segment designed to enable artificial chordae implantation and simplify leaflets and subvalvular apparatus correction. Eight sheep were employed.

Usability, performance and safety of a new device for degenerative mitral regurgitation: in vivo chronic evaluation.

Objectives: This study aimed to evaluate the usability, performance and safety of an innovative mitral valve device in the chronic setting characterized by an intraventricular bridge, which enables artificial chordae anchoring and/or direct posterior leaflet fixation.

Methods: Ten female sheep were employed and underwent device implantation. Any interference of the device with leaflet motion, ease of device use, correct chordae length estimation and implantation were evaluated.

Early Cardiac Remodeling Promotes Tumor Growth and Metastasis.

Background: Recent evidence suggests that cancer and cardiovascular diseases are associated. Chemotherapy drugs are known to result in cardiotoxicity, and studies have shown that heart failure and stress correlate with poor cancer prognosis. However, whether cardiac remodeling in the absence of heart failure is sufficient to promote cancer is unknown.

JDP2 and ATF3 deficiencies dampen maladaptive cardiac remodeling and preserve cardiac function.

c-Jun dimerization protein (JDP2) and Activating Transcription Factor 3 (ATF3) are closely related basic leucine zipper proteins. Transgenic mice with cardiac expression of either JDP2 or ATF3 showed maladaptive remodeling and cardiac dysfunction. Surprisingly, JDP2 knockout (KO) did not protect the heart following transverse aortic constriction (TAC).