Pathophysiology of Angina

Pathophysiology of Angina

An important feature is that ischemia reduces the formation of adenosine triphosphate (ATP), resulting in the development of acidosis, the loss of the normal ATP sodium-potassium pump, the loss of myocardial membrane integrity, and the release of chemical substances that stimulate chemosensitive and mechanoreceptive receptors innervated by unmyelinated nerve cells found within cardiac muscle fibers and around the coronary vessel . The substances that are released include lactate, serotonin, bradykinin, histamine, reactive oxygen species, and adenosine . In addition there are substances released from platelets, which often spontaneously aggregate in the area of a coronary artery stenosis, which may also be responsible for myocardial ischemia and angina. These include serotonin, thromboxane A2, and 5-hydroxytyrptamine .
There is substantial evidence that the primary mediator of angina is adenosine, via stimulation of the A1 adenosine receptor . It is also possible that venodilation as a response to ischemia can activate these receptors. The nerve fibers travels along the sympathetic afferent pathways from the heart and enter the sympathetic ganglia in lower cervical and upper thoracic spinal cord . Impulses are then transmitted via the ascending spinothoracic pathways to the medial and lateral thalamus and ultimately activate several areas of the cerebral cortex .