Passive ventricular constraint prevents transmural shear strain progression in left ventricle remodeling.
BACKGROUND
Passive ventricular constraint provides external cardiac support to reduce left ventricular (LV) wall stress and myocardial stretch, which are primary determinants of LV remodeling. Altered wall strain results in cytokine and reactive oxygen species production, which, in turn, stimulates apoptosis and extracellular matrix disruption and could be an important trigger for adverse global LV dilatation and remodeling. The effects of the Acorn cardiac support device (CSD) on regional transmural LV wall strains, however, remain unknown.


RESULTS
Thirty-three sheep had transmural radiopaque beadsets surgically inserted into the anterior basal and lateral equatorial LV walls, with additional markers silhouetting the left ventricle. Eight animals had CSD implanted (myocardial infarction [MI]+CSD). One week thereafter, the MI+CSD group and 10 animals without CSD (MI) underwent posterior LV infarction by snaring obtuse marginal coronary arteries. Fifteen animals (Sham) had no infarction or CSD. 4D marker dynamics were measured with biplane videofluoroscopy 1 and 8 weeks postoperatively. LV volumes, sphericity index, and transmural circumferential, longitudinal, and radial systolic strains were analyzed. Compared with Sham, infarction (MI) dilated the heart, reduced sphericity index (LV length/width), and increased longitudinal-radial shear strains in the inner half of both the anterior and lateral LV walls. CSD prevented this shear strain perturbation, minimized LV end diastolic volume increase, and augmented the LV sphericity index.


CONCLUSIONS
Prophylactic CSD prevented infarct-induced shear strain progression not only in myocardium adjacent to, but also remote from, the infarct. CSD also prevented LV dilatation and sphericalization. By attenuating shear strain abnormalities, CSD could prevent the heart from entering into a positive feedback loop of further LV dilatation and exaggeration of LV wall stress and may reduce biochemical triggers portending adverse LV remodeling.
Cheng
Allen
A
Department of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, California 94305-5247, USA.
Nguyen
Tom C
TC
Malinowski
Marcin
M
Langer
Frank
F
Liang
David
D
Daughters
George T
GT
Ingels
Neil B
NB
Miller
D Craig
DC
D000818:Animals; D001458:Bandages; D003971:Diastole; D018450:Disease Progression; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology; D008863:Microspheres; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D009929:Organ Size; D011312:Pressure; D017382:Reactive Oxygen Species; D033081:Shear Strength; D012756:Sheep; D013526:Surgical Mesh; D013599:Systole; D014463:Ultrasonography; D020257:Ventricular Remodeling / Q000502:physiology*
D017382:Reactive Oxygen Species