Autologous cardiomyotissue implantation promotes myocardial regeneration, decreases infarct size, and improves left ventricular function.

BACKGROUND: Cell therapy for myocardial infarction (MI) may be limited by poor cell survival and lack of transdifferentiation. We report a novel technique of implanting whole autologous myocardial tissue from preserved myocardial regions into infarcted regions. METHODS AND RESULTS: Fourteen rats were used to optimize cardiomyotissue size with peritoneal wall implantation (300 µm identified as optimal size). Thirty-nine pigs were used to investigate cardiomyotissue implantation in MI induced by left anterior descending balloon occlusion (10 animals died; male-to-female transplantation for tracking with in situ hybridization for Y chromosome, n=4 [2 donors and 2 MI animals]; acute MI implantation cohort at 1 hour, n=13; and healed MI implantation at 2 weeks, n=12). Assessment included echocardiography, magnetic resonance imaging, hemodynamics, triphenyltetrazolium chloride staining, and histological and molecular analyses. Tracking studies demonstrated viable implants with donor cells interspersed in the adjacent myocardium with gap junctions and desmosomes. In the acute MI cohort, treated animals compared with controls had improved perfusion by magnetic resonance imaging (1.2±0.01 versus 0.86±0.05; P<0.01), decreased MI size (magnetic resonance imaging: left ventricle, 2.2±0.5% versus 5.4±1.5%, P=0.04; triphenyltetrazolium chloride: anterior wall, 10.3±4.6% versus 28.9±5.8%, P<0.03), and improved contractility (dP/dt, 1235±215 versus 817±817; P<0.05). In the healed MI cohort, treated animals had less decline in ejection fraction between 2 and 4 week assessment (-3±4% versus -13±-4%; P<0.05), less decline in ±dP/dt, and smaller MI (triphenyltetrazolium chloride, 21±11% versus 3±8%; P=0.006) than control animals. Infarcts in the treated animals contained more mdr-1(+) cells and fewer c-kit(+) cells with a trend for decreased expression of matrix metalloproteinase-2 and increased expression of tissue inhibitor of metalloproteinase-2. CONCLUSION: Autologous cardiomyotissue implanted in an MI area remains viable, exhibits electromechanical coupling, decreases infarct size, and improves left ventricular function.

[Instrument for the plastic repair of large defects in the interventricular septum of the heart]. / Instrument dlia plastiki bol'shikh defektov mezhzheludochkovoi peregorodki serdtsa.

By taking advantage of an experience gained during 81 radical operations performed in connection with a defect in the interventricular septum of the heart at an early age the authors have worked out a new procedure for the plastic operation--closure of the defect with a transplant. A special instrument used for this purpose is described.

A new approach to total repair of transposition of the great vessels: a technique for atrial autotransplantation.

We have devised a new operative procedure called atrial autotransplantation for transposition of the great vessels and applied it in 7 cases. Results were satisfactory except for one death. The bais of this technique was the experiment, using 70 dogs, in which the relationship of separation of the atrial wall and atrial septum to the development of arrhythmia was studied. It was found that reservation of the upper one sixth of the right atrial wall and the upper one third of the left atrial wall developed almost no significant arrhythmia with slow rate. By this concept and method, the left and right atria are almost completely separated, and a complete intraventricular and intra-atrial repair is made in a satisfactory operative field. Since there is no surgical intervention in the ventricular wall, postoperative cardiac function can be satisfactorily maintained. With this procedure intr-atrial conversion was performed in four cases and intraventricular conversion in three cases-the former for type I of uncomplicated transposition and type III of combined pulmonary stenosis, with or without VSD, and the latter for type II of combined large VSD. Only one patient with intraventricular conversion died of low cardiac output syndrome, probably due to incomplete relief of combined pulmonary stenosis.