There is considerable evidence suggesting that damage to the coronary endothelium results in diminished production of the vasodilator nitric oxide . The absence of nitric oxide leads to enhanced vasoconstrictor responses to sympathetic nerves innervating the coronary vessels, as well as to other vasoconstricting factors . Unstable angina is not necessarily associated with exercise or stress, and its onset is therefore unpredictable. It is generally thought to be due to spontaneous thrombus formation within a coronary artery and therefore is refractory to nitroglycerin. Endothelial dysfunction leads to reduced nitric oxide and prostacyclin production, both of which normally inhibit platelet adhesion and aggregation.
Unstable angina can be difficult to distinguish from acute myocardial infarction.
Angina may also be precipitated by a combination of supply and demand ischemia. A hemodynamic condition may exist that leads to coronary vascular steal . In this condition, multiple fixed stenotic lesions can lead to a redistribution of flow within the major supply arteries of the heart under conditions of exercise or vasodilator therapy. As blood flow increases in one region of the coronary vascular network, blood flow can reciprocally decrease in another leading to anginal pain.