Shock wave therapy in cardiology: a commentary

Abstract

The evidences in favor of efficiency of shock-wave in ischemic heart disease therapy are originated mainly from small, uncontrolled observational studies. The experiments have relatively short duration. The shock-wave therapy benefits for ischemic heart disease have been explained by heightened myocardial perfusion and angiogenesis attributed among others to activation of vascular endothelial growth factors of the VEGF group. The role of VEGF in heart diseases and atherosclerosis is ambivalent; along with potential benefit it may contribute to fibrosis. A shock wave induces tissue cavitation and shear stress to membranes. The vulnerability of cardiac muscle cells under conditions of ischemia is increased. Additional damage may contribute to the cell loss. Reported effects of shock-wave treatment may be transient and reactive in their nature. Clinical improvements in humans are caused, at least in part, by the placebo effect. Placebo therapy is beneficial for some patients; however, placebo must be harmless by definition. In conclusion, animal experiments with a longer follow-up are needed prior to the initiation of clinical research with large cohorts of patients. However, some possible late outcomes such as increased vascularization of atherosclerotic plaques and their instability cannot be reliably reproduced in experiments. A promising approach to the evaluation of net harm or benefit could be lifelong animal experiments with comparisons of average life span between test and control groups.

Keywords

• shock wave therapy
• ischemic heart disease
• angina pectoris