The initiation of angina emerges with the excitation of free nerve endings present within the myocardium with electrochemical firing caused by mechanical and chemical; mechanical stimulation may occur by way of ischemia-induced changes in the functionality of the ventricular; in addition, chemicals released from the cardiac myocytes in response to hypoxia can also be held accountable for nerve stimulation in this manner (Edelman and Tabibiazar, 2003). The impulses generated as a result this nerve stimulation propagate through the cardiac sympathetic nervous system to the thoracic sympathetic ganglia and then to the dorsal horn spinal neurons; they then reach the thalamus travelling along the spinothalamic tract and are finally transported by the thalamocortical tract to the cerebral cortex, where they are then perceived as pain or discomfort (Edelman and Tabibiazar, 2003). …show more content…
Episodes of silent ischemia may present as less severe or events of a shorter duration than those commonly associated with angina pectoris; in diabetic patients, it is hypothsised that partial or complete autonomic denervation through diabetic neuropathy may play a role in the prevalence of silent ischemia (Edelman and Tabibiazar,