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An Alternative Non-Invasive Therapy for Refractory Angina

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An Alternative Non-Invasive Therapy for Refractory Angina European Review for Medical and Pharmacological Sciences 2018; 22: 5402-5410 Cardiac shock wave therapy: an alternative non-invasive therapy for refractory angina H. LI, M.-L. LIU Peking University First Hospital, Beijing, People’s Republic of China Abstract. – OBJECTIVE: Refractory angina “the myocardial ischemia must be clinically es- (RFA), known as “no option angina” before, is tablished to be the root cause”2. RFA patients increasing worldwide. The prognosis for RFA suffer with psychological distress, activity re- patients still remains poor due to the lack of striction, and impaired health-related quality of effective treatments. The potential of cardiac 3 shock wave therapy (CSWT) to treat RFA by pro- life . Meanwhile, the incidence and prevalence of moting angiogenesis was first shown by Nishi- RFA is increasing with the improving coronary da et al in a porcine model of chronic ischemic artery disease (CAD) related survival rate and the cardiomyopathy. The main objective of this pa- aging society4. It is therefore crucial to develop per is to review the mechanisms of its action, in- effective therapeutic strategies for RFA patients. fluence on the cardiac tissue, and also clinical studies demonstrating its efficacy. Transmyocardial laser revascularization (TM- MATERIALS AND METHODS: This is a litera- LR), the mostly studied alternative therapy, is as- ture review of recent articles published on MED- sociated with significant early postoperative mor- LINE and SciELO databases in English. tality risk5. Other invasive therapies like percuta- RESULTS: Researchers found that CSWT neous laser revascularization (PMLR) and spinal leads to multiple biochemical effects, such as cord stimulation (SCS) are not suitable for every angiogenesis, inflammatory response modula- 6-9 tion, ameliorate myocardial fibrosis, and so on. RFA patient (because of the complications) . Based on the promising results above, a series Enhanced external counter-pulsation (EECP) is of clinical studies have been performed. And a noninvasive therapy that improves symptoms the studies demonstrated that CSWT is asso- by its hemodynamic effect and has numerous ciated with the improvement of angina symp- contraindications, such as arrhythmias, periph- toms, heart function, and myocardial perfusion eral vascular disease, and bleeding diathesis, for patients with refractory angina. No procedur- 10,11 al complications or adverse effects were noted which occurs commonly in patients with RFA . in these studies. Emerging therapies such as coronary sinus reduc- CONCLUSIONS: CSWT appears to be an effec- tion and myocardial cryotherapy are limited by tive, safe, and non-invasive approach to treat RFA. their complicated operation procedure12,13. Key Words: Consequently, cardiac shock wave therapy Non-invasive, Shock Wave, Refractory angina. (CSWT), an application of therapeutic ultrasound, has advanced to eliminate such shortcomings. In this paper, we will review the mechanisms Introduction of CSWT, the influence on the cardiac tissue, and clinical studies demonstrating its efficacy. Although the current management of isch- Furthermore, we will discuss the advantages of emic heart diseases has been advanced, numer- CSWT and areas in which future research is ous patients remain symptomatic. The concept needed. of refractory angina (RFA) has been put forward to describe these patients centuries ago1. Accord- ing to the guideline of Canadian Cardiovascular Materials and Methods Society (CCS) in 2012, RFA was defined as “a persistent, painful condition which cannot be Mechanisms controlled by a combination of medication, angio- Although CSWT has been proven to be ef- plasty/percutaneous coronary intervention (PCI), fective in preliminary clinical research14, the or coronary artery bypass grafting (CABG)” and precise biomechanical effects of CSWT and its 5402 Corresponding Author: Meilin Liu, MD; e-mail [email protected] Cardiac shock wave therapy: an alternative non-invasive therapy for refractory angina therapeutic mechanisms remain obscure. When system contains angiopoietin 1 that protects a mismatch arises between myocardial oxygen cells from excessive vascular leakage and an- needs and myocardial oxygen supply, ischemia, giopoietin 2 that inhibits Tie2 signaling). inflammation, cell apoptosis/necrosis, and car- diac remodeling can manifest in succession. VEGF CSWT may influence these processes, improv- VEGF has been proven to be essential in the ing prognosis of RFA. When a shock wave initiation of angiogenesis22. A relative study (SW) with relatively high acoustic amplitude demonstrated the mRNA expression and the (up to about 100MPa) hits tissue, acoustic protein levels of fms-like tyrosine kinase (Flt-1) cavitation and a violent collapse of small gas and foetal liver kinase-1(Flk-1) were up-regulat- bubbles in the blood via transmission of SW ed in HUVECs as well as direct VEGF receptors energy generates localized shear stress on cell (VEGFR) stimulation. This then leads to the membranes15,16. This procedure leads to posi- phosphorylation of VEGFR and downstream tive biochemical effects, such as up-regulation effects23,24. In this study, quantification of rel- of vascular endothelial growth factor (VEGF), ative VEGFR phosphorylation revealed a two- activation of Toll-like receptor 3 (TLR3) path- fold increase in VEGFR1 and a nearly four-fold way, and so on17-20. These effects are described increase in VEGFR2 compared to untreated below (Figure 1). controls. And SW treatment induced VEGF expression in endothelial cells in a hypoxia-in- Vascular Permeability duced factor 1-independent manner. The con- Vascular permeability increasing, the first clusion that CSWT could enhance angiogenesis step of angiogenesis, allows for extravasation by up-regulating of VEGF and its receptors also of plasma proteins, which lays down a provi- has recently been suggested in some in vivo ex- sional scaffolding for migrating endothelial periments17,23,25. cells. When Shock wave (SW) hits cells, per- meability may also be enhanced by the ex- PlGF panding and compressing ultrasound-activated Placental growth factor (PlGF) could amplify micro-bubbles21. Meanwhile, the endothelial the angiogenesis effect of VEGF by increasing cell-specific receptor, Tie-2 mRNA, is highly the responsiveness of VEGFR2 to VEGF and increased in the endothelial cells20. It indi- inducing further VEGF release. Zimpfer et al26 cates that the angiopoietin/Tie-2 system, are have shown that higher protein levels of PlGF involved in CSWT-induced angiogenesis (the could be found in HUVECs and the extracellular Figure 1. Mechanism of CSWT. 5403 H. Li, M.-L. Liu matrix after Shock wave treatment. In addition, promotion of angiogenesis. Endothelial apoptosis Holfeld et al23 verified that PlGF mRNA was is a natural mechanism and prominent inhibitor highly up-regulated in SW-treated mice myocar- of angiogenesis29. An in vitro study30 demonstrat- dium in vivo. ed that apoptosis could be induced by ischemia/ hypoxia in H9c2 cells, and CSWT suppresses the Endothelial Cell Proliferation expression of apoptosis molecules by activating and Differentiation of the PI3K (Phosphoinositide 3-kinase)-AKT Endothelial cell proliferation and differentia- (Protein kinase B) pathway. Fas/FasL is an im- tion play key roles in angiogenesis. Scholars have portant signaling pathway that induces myocar- confirmed that SW have positive influence on the dial cell apoptosis that may related to CSWT31. proliferation and differentiation of cardiomyo- However, the effects of CSWT in vivo require cytes, smooth muscle, and endothelial cells pre- future investigations. cursors27. Researchers also found that the prolif- eration of HUVECs is associated with high level Endothelial Progenitor Cell Homing of extracellular signal-regulated kinase (ERK). Regenerative medicine has applied in ischemic And the significant increase in phosphorylation heart disease increasingly32. Based on the previ- of extracellular signal-regulated kinase (ERK) ous discovery that there is enhanced recruitment after SW treatment can then be suppressed by of intravenously injected endogenous endothelial anti-VEGF neutralizing antibodies19. The results progenitor cells (EPCs) to shock wave-treated indicate that the positive influence may rely on ischemic hind limbs in rats33, Tepekoylu et al34 VEGF/ERK/MAPK (mitogen-activated protein found expression of hypoxia-inducible factor 1α kinase) pathway. (HIF-1α) regulating stromal cell-derived factor-1 (SDF-1) significantly elevated after SW therapy. Inflammation SDF-1 serves as a chemo-attractants for recruit- Inflammatory processes play an important role ment of EPCs from bone marrow, and HIF-1α in ischemic myocardial pathophysiology. Exces- plays a crucial role in the regulation of SDF-1. sive inflammatory response will hinder the initi- In line with this finding, significantly greater ation of angiogenesis, while a deficient inflamma- numbers of proliferating endothelial cells were tory response will disturb the process of replacing found in the treatment group35. Di Meglio et al18 necrotic tissue. SW treatment modulates inflam- confirmed the conclusion that SW facilitates re- mation via the Toll-like receptor 3 (TLR3) path- cruitment of endothelial progenitor cells in vivo. way. TLR3 activation is characterized by an early Zhang et al36 found that TGF-β1 regulates the pro-inflammatory phase and a late anti-inflamma- SDF-1/CXCR4 axis-induced cells homing in in- tory response. The interaction between interleukin jured myocardial.
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