Myocardial stunning or  transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow. In this situation, even after ischemia has been relieved (by for instance angioplasty or coronary artery bypass surgery) and myocardial blood flow (MBF) returns to normal, myocardial function is still depressed for a variable period of time, usually days to weeks. This reversible reduction of function of heart contraction after reperfusion is not accounted for by tissue damage or reduced blood flow, but rather, its thought to represent a perfusion-contraction "mismatch". Myocardial stunning was first described in laboratory canine experiments in the 1970s where LV wall abnormalities were observed following coronary artery occlusion and subsequent reperfusion. Cause
Clinical situations associated with myocardial stunning include:
acute myocardial infarction (AMI) with early reperfusion
unstable angina
after percutaneous transluminal coronary angioplasty (PTCA)
after cardiac surgery
neurogenic stunned myocardium following an acute cerebrovascular event such as a subarachnoid hemorrhage
in patients undergoing chronic hemodialysis, chronic myocardial stunning may lead to heart failureMyocardial stunning has been implicated in the development of Takotsubo (Stress) cardiomyopathy. Pathophysiology
The underlying mechanisms of myocardial stunning have remained the subject of debate for several decades. Two leading hypotheses implicate reperfusion-induced oxygen free-radical damage and altered calcium flux resulting in intracellular hypercalcemia and desensitization of myofilaments.
Management
Treatment considerations for myocardial stunning should be determined based on the clinical judgment of the cardiologist or physician, the degree of LV impairment and symptoms, and the wishes of the person.Some evidence supports the use of inotropic drugs in the case of severe myocardial dysfunction.Results from canine experimental trials investigating the oxygen free-radical hypothesis for myocardial stunning have shown a reduction in free radical generation and improvement in myocardial function following anti-oxidant infusion. References
Further reading
"Myocardial “stunning” in man"
Baker C, Rimoldi O, Camici P, Barnes E, Chacon M, Huehns T, Haskard D, Polak J, Hall R (1999). "Repetitive myocardial stunning in pigs is associated with the increased expression of inducible and constitutive nitric oxide synthases". Cardiovasc. Res. 43 (3): 685–97. doi:10.1016/S0008-6363(99)00149-2. PMID 10690340. Wittstein IS, Thiemann DR, Lima JA,  et al. (February 2005). "Neurohumoral features of myocardial stunning due to sudden emotional stress". N. Engl. J. Med. 352 (6): 539–48. doi:10.1056/NEJMoa043046. PMID 15703419. == External links ==