To optimize Laplace s law dynamic

To optimize Laplace’s law, dynamic cardiomyoplasty (DCMP) is applied to reduce wall stress by wrapping the latissimus dorsi muscle around the heart. The latissimus dorsi muscle is stimulated to contract in synchrony with the heart via an electromyostimulator. Because of the absence of data on hemodynamic or survival improvement, the DCMP is available only in Russia, Europe, Asia and the Caribbean at present. The DCMP concept stimulated the development of passive cardiac support devices, including the Acorn Cardiac Support Device (ACSD; Acorn Medical, Minneapolis, MN, USA) and the Myocor Myosplint (Myocor Medical, St Paul, MN, USA). The ACSD, which is made of polyester mesh fabric, is placed outside the ventricles in a posteroanterior orientation. Similar to the DCMP, the ACSD was proved to support the dilated ventricles passively, reduce ventricular wall stress, and prevent further dilation by girdling compression. The Myocor Myosplint directly alters cardiac geometry and reduces ventricular wall stress. Under the hypothesis of optimization of the law of Laplace, the Myocor Myosplint is placed through the right and left ventricular walls to achieve a 20% reduction in wall stress. The ACSD and Myocor Myosplint have been proven to suppress further ventricular dilation and to improve ejection fraction in investigational clinical studies. In the future, further studies will be needed to show the safety and long-term efficacy of this kind of device.
Stem-cell regeneration of myocardium Stem-cell regeneration of the myocardium, which replaces myocytes lost from the injured cardiac region, is another alternative nontransplant treatment for end-stage heart failure. The myocardium could be regenerated by injecting stem SW033291 Supplier into the damaged heart. The ideal cell types include skeletal myoblasts, peripheral blood stem cells, and bone marrow stem cells. The major modes of delivery consist of direct epicardial injection, percutaneous catheter-based endocardial injection, and percutaneous transluminal coronary injection. Possible mechanisms of myocardial regeneration involve transdifferentiation of stem cells into cardiomyocytes, cytokine- and growth factor-mediated endogenous stem cell mobilization, improved homing of stem cells to sites of injury, and induction of antiapoptotic pathways. The paracrine hypothesis has been emphasized recently. Indeed, the ideal stem cell would secrete a broad variety of cytokines, chemokines and growth factors that are beneficial for cardiac repair, providing cytoprotection of resident myocytes, upregulation of angiogenesis, and modulation of inflammatory process. And these synergistic effects will promote re-entry of cardiomyocyte sell cycle, recruit endogenous stem cells, and induct secondary humoral effects in the host tissue. All the above-mentioned mechanisms may contribute to neomyogenesis, neoangiogenesis, and alteration of ventricular remodeling. Neomyogenesis results in an overall increase in functional myocardial mass, whereas the neoangiogenesis results in increased capillary density, improving myocardial perfusion and recruiting the hibernating myocardium. In the early 2000s, Menasché et al published a series on autologous skeletal myoblast transplantation concomitant with CABG in patients with severe heart failure. He demonstrated improvement in NYHA functional class and left ventricular ejection fraction 11 months after the CABG. Other studies also showed improved myocardial wall thickening within the injection region and overall improvement in LVEF. At the same time as Menasché’s publications, Hamano reported autologous bone marrow cell transplantation concomitant with CABG in patients with ischemic heart disease. In 2004, Wollert’s randomized controlled trial demonstrated the safety and efficacy of bone marrow-derived cell therapy for acute ST-elevation MI. In his BOOST trial (bone marrow transfer to enhance ST-elevation infarct regeneration), 60 patients were randomized to primary percutaneous intervention with or without intracoronary infusion of autologous bone marrow cells. At the 6-month follow-up, the group with cell therapy showed significant improvement in LVEF (from 50% to 56.7%) as compared with the group that did not receive cell therapy (from 51.3% to 52%). Chen’s randomized trial also showed improvement in LVEF, myocardial perfusion, and wall motion in acute-MI patients (n = 69) who underwent primary percutaneous coronary intervention concomitant with intracoronary infusion of autologous bone marrow-derived mesenchymal stem cells.