Angina Pectoris

At a Glance

Ischemia of the myocardium results when coronary blood flow is reduced by stenosis of the coronary arteries, abnormal constriction of the coronary microcirculation, or reduced oxygen carrying capacity of the blood. When the delivery of oxygen is insufficient for demand, ischemia results and can present as angina pectoris (chest pain).

Angina presents with a wide assortment of symptoms, making delination of cause difficult in many cases. Typical presentation is substernal chest pressure that may radiate to the arms or jaw. Shortness of breath, nausea, and sweating are also present in some cases. Diagnostic tools, including biochemical measures, are limited in their capabilities to assist with diagnoses associated with angina pectoris.

Angina pectoris is classified into four different forms:

Stable angina (symptoms occur during or following exertion)

Unstable angina (symptoms occur more frequently or while at rest)

Prinzmetal angina (symptoms occur with exertion or while at rest, associated with coronary artery vasospasm)

Syndrome X (symptoms occur in patients without coronary artery diesease nor coronary artery vasospasm)

Adenosine is produced by the degradation of adenosine triphosphate (ATP) during ischemia and is thought to be the mediator of anginal pain.

Atherosclerosis and accompanying stenosis is the most common cause of anginal pain.

What Tests Should I Request to Confirm My Clinical Dx?

There are no biochemical measures available to confirm angina pectoris.

Patients with unstable angina, resulting from partial occlusion of the coronary vessels, may have elevated troponins.

The British Cardiovascular Society Working Group classified patients with angina pectoris and troponin T greater than 0.03 ng/mL or a troponin I greater than 0.06 ng/mL on 2 occasions more than 6 hours apart as having unstable angina. See the section on Acute Coronary Syndrome for more information.

Ischemia modified albumin (IMA) has been approved by the U.S. Federal Drug Adminstration (FDA) as a biomarker that can detect myocardial ischemia within minutes of presentation. IMA is released within minutes of ischemia, peaks at 2-4 hours, and is undetectable 6-12 hours post-ischemia. Several studies found the use of IMA, combined with troponins and electrocardiogram (ECG), provided a useful tool to rule out ischemia mediated angina with a high negative predictive value. However, increases in IMA have also been observed following ischemia of organs other than the heart. Clinical data is too limited to support its use at this time, and the test has been withdrawn from the commercial market.

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications – OTC drugs or Herbals – that might affect the lab results?

Several, but not all, troponin I assays have been found to have a positive interference from hemolysis of the sample. The currently available Troponin T assay is known to have a negative interference from hemolysis. Clinicians should contact their laboratory to understand criteria for accepting and/or rejecting samples with hemolysis and the potential impact on results.

What Lab Results may be useful to determine a cause of angina pectoris?

To determine if ischemia may be the result of reduced oxygen carrying capacity, clinicians should test for hemoglobin (<8 g/dL) and/or carboxyhemoglobin (elevated).

Prinzmetal angina has been associated with hyperinsulinemia, low intracellular magnesium levels, and cocaine use.

Will there be lab tests useful in diagnosing angina pectoris?

Several markers have been suggested as potential additions to the panel of available biomarkers. Most require further investigation before recommendation for use can be made. The potential markers include ischemia modified albumin, unbound free fatty acids, heart-type fatty acid binding protein (H-FABP), pregnancy-associated plasma protein A, and glycogen phosphorylase isoenzyme BB.