Swine (Sus scrofa) as a Model of Postinfarction Mitral Regurgitation and Techniques to Accommodate Its Effects during Surgical Repair.

Mitral regurgitation (MR) is a common heart-valve lesion after myocardial infarction in humans. Because it is considered a risk factor for accelerated heart failure and death, various surgical approaches and catheter-based devices to correct it are in development. Lack of a reproducible animal model of MR after myocardial infarction and reliable techniques to perform open-heart surgery in these diseased models led to the use of healthy animals to test new devices. Thus, most devices that are deemed safe in healthy animals have shown poor results in human efficacy studies, hampering progress in this area of research. Here we report our experience with a swine model of postinfarction MR, describe techniques to induce regurgitation and perform open-heart surgery in these diseased animals, and discuss our outcomes, complications, and solutions.

The Impact of Intimal Tear Location and Partial False Lumen Thrombosis in Acute Type B Aortic Dissection.

BACKGROUND: Partial false lumen (FL) thrombosis is a risk factor for long-term mortality in acute type B aortic dissection (ATBAD). This study investigates FL pressures in models of ATBAD with patent and partially thrombosed FL. METHODS: Twenty-five porcine aortas were used to create five models of ATBAD that were connected to a pulsatile flow loop. Models A through C had a patent FL with the following morphologies: model A, single proximal tear; model B, single distal tear; and model C, single proximal and single distal tear. Models D and E had a single proximal and a single distal tear, with partial FL thrombosis. Model D had FL occlusion of the proximal tear, and model D had FL occlusion of the distal tear. True lumen (TL) and FL pressures were measured at 90 to 150 mm Hg. RESULTS: In model A, FL pressures were 6 mm Hg higher than TL pressures (p < 0.01). In model B, FL pressures were 10 mm Hg lower than TL pressures (p ≤ 0.01). In model C, TL and FL pressures were equivalent. In model D, FL pressures were 40 mm Hg lower than TL pressures (p < 0.001). In model E, FL pressures were 10 mm Hg higher than TL pressures (p < 0.01). CONCLUSIONS: In a biologic model of ATBAD, the number, location, and FL thrombosis status determine FL pressure. In the setting of partial FL thrombosis, the FL pressure is reduced with proximal tear occlusion and increased with distal tear occlusion. Reduced FL pressure is related to retrograde flow.