08-19-2018, 04:29 PM
Angina pectoris is pain caused by a decrease in myocardial perfusion that normally presents as tightness, squeezing, or heaviness in the chest area.
The pain episodes caused by angina pectoris normally lasts 5-10 minutes unless it has progressed to an ongoing infarction.
The three forms of angina pectoris are:
• Stable
• Unstable
• Variant (Prinzmetal)
Stable angina is chest pain precipitated by exertion (e.g. walking uphill, running, mowing lawn, cardiac stress test) where oxygen demand exceeds oxygen supply and is relieved by rest or the administration of nitrates.
In the case of stable angina pectoris the decreased ability to perfuse is due to fixed, high-grade stenosis of the coronary artery secondary to stable atherosclerotic plaque. Typically a 70% decrease in luminal area is necessary to cause stable angina pectoris.
During episodes of stable angina pectoris, ECG may show ST depression; however there is no elevation in troponin levels.
Unstable angina pectoris is described as chest pain increasing in severity, frequency, and duration that occurs at rest.
During an unstable angina pectoris episode, the ECG may or may not show ST depression and/or T-wave inversion but there will be no elevation in troponin levels.
Unstable angina pectoris episodes are triggered by situations in which there is an acute plaque disruption that leads to an acute thrombosis with mural (non-occlusive) thrombus formation. The decreased perfusion is due to fixed, high grade stenosis of coronary artery due to unstable atherosclerotic plaque.
Typically a 90% decrease in luminal area is necessary to cause unstable angina pectoris.
Any time there is acute thrombosis secondary to acute plaque disruption (e.g., unstable angina, NSTEMI, STEMI), there is the potential for thromboembolization. Thromboemboli (pieces of thrombus) can break off, travel downstream, and embolize in vessels distal to the primary plaque disruption, potentially causing microinfarctions.
Variant (Prinzmetal) angina pectoris is described as intermittent chest pain secondary to coronary artery vasospasms. Variant angina pectoris is unrelated to physical activity and episodes usually occur at rest, especially at night and early in the morning.
During an episode of variant (Prinzmetal) angina, the vasoconstriction and transmural ischemia generated lead to an ST elevation on ECG. Unlike a MI, there are no elevations in troponin levels during an episode of variant angina.
Even though patients presenting with variant (Prinzmetal) angina may have significant atherosclerosis, the coronary vasospasms causing the episodes are not related to atherosclerosis, thrombus formation, or physical activity.
Although the trigger of variant (Prinzmetal) angina is often unknown, known triggers include:
• Triptans (sumatriptan is contraindicated in these patients)
• Tobacco (smoking cessation should be encouraged)
• Cocaine
Note that these agents induce vasoconstriction, which could induce or potentiate a coronary artery vasospasm.
Women with variant (Prinzmetal) angina often have a history of migraine headaches; both conditions are associated with arterial vasospasms.
Ergonovine triggers vasospasm in susceptible patients including those with variant (Prinzmetal) angina.
The first-line treatment of variant (Prinzmetal) angina involves calcium channel blockers, such as diltiazem. Nitrates such as nitroglycerin can also be used to relieve symptoms.