Three dimensional modeling of atrioventricular valves provides predictive guides for optimal choice of prosthesis.

Inaccuracies in intraoperative and preoperative measurements and estimations may lead to adverse outcomes such as patient-prosthesis mismatch. We aim to measure the relation between different dimensions of the atrioventricular valve complex in explanted porcine heart models. After a detailed physical morphology study, a cast of the explanted heart models was made using silicon-based materials. Digital models were obtained from three-dimensional scanning of the casts, showing the measured annulopapillary distance was 2.50 ± 0.18 cm, and 2.75 ± 0.36 cm for anterior and posterior papillary muscles of left ventricle, respectively. There was a significant linear association between the mitral annular circumference to anterior-posterior distance (p = 0.003, 95% CI 0.78-3.06), mitral annular circumference to interpapillary distance (p = 0.009, 95% CI 0.38-2.20), anterior-posterior distance to interpapillary distance (p = 0.02, 95% CI 0.10-0.78). Anterior-posterior distance appeared to be the most important predictor of mitral annular circumference compared to other measured distances. The mean length of the perpendicular distance of the tricuspid annulus, a, was 2.65 ± 0.54 cm; b was 1.77 ± 0.60 cm, and c was 3.06 ± 0.55 cm. Distance c was the most significant predictor for tricuspid annular circumference (p = 0.006, 95% CI 0.28-2.84). The anterior-posterior distance measured by three-dimensional scanning can safely be used to predict the annular circumference of the mitral valve. For the tricuspid valve, the strongest predictor for the circumference is the c-distance. Other measurements made from the positively correlated parameters may be extrapolated to their respective correlated parameters. They can aid surgeons in selecting the optimal prosthesis for the patients and improve procedural planning.

Identification and characterization of uncoupling protein in heart and muscle mitochondria of canary birds.

An uncoupling protein (cUCP) was identified in heart and skeletal muscle mitochondria of canary birds. cUCP was immunodetected using polyclonal antibodies raised against murine UCP2. Its molecular mass was similar to those of mammalian UCPs (32 kDa). The activity of cUCP was stimulated by palmitic acid (PA) and inhibited by GTP mainly in state 3 respiration. Additions of PA augmented state 4 respiration and lowered the ADP/O ratio. Thus, the activity of cUCP diverted energy from oxidative phosphorylation in state 3 respiration. cUCP in heart and skeletal muscles of canary birds might have implications in thermogenesis as well as protection against free radical production.

Myocardial infarction in the C57BL/6J mouse: a quantifiable and highly reproducible experimental model.

INTRODUCTION: The laboratory mouse is a powerful tool in cardiovascular research. In this report, we describe a method for a reproducible mouse myocardial infarction model that would allow subsequent comparative and quantitative studies on molecular and pathophysiological variables. METHODS: (A) The distribution of the major coronary arteries including the septal artery in the left ventricle of the C57BL/6J mice (n=20) was mapped by perfusion of latex dye or fluorescent beads through the aorta. (B) The territory of myocardial infarction after the ligation of the most proximal aspect of the left anterior descending (LAD) coronary artery was quantified. (C) The consistency in the histological changes parallel to the infarction at different time points was analyzed. RESULTS: (A) The coronary artery tree of the mouse is different from human and, particularly, in regard to the blood supply of the septum. (B) Contrary to previous belief, the septal coronary artery in the mouse is variable in origin. (C) A constant ligation of the LAD immediately below the left auricular level ensures a statistically significant reproducible infarct size. (D) The ischemic changes can be monitored at a histological level in a way similar to what is described in the human. CONCLUSION: We illustrate a method for maximal reproducibility of experimental acute myocardial infarction in the mouse model, due to a consistent loss of perfusion in the lower half of the left ventricle. This will allow the study of molecular and physiological variables in a controlled and quantifiable experimental model environment.