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Course Sample:

Acute Coronary Syndromes

Case study

Ms. Smith is a 65-year-old who presents with a 60-minute history of chest pain. She describes it as intermittent, crushing, substernal, and non-radiating. The pain occurs during exertion and at rest, and is accompanied by nausea and dyspnea. Ms. Smith has a history of hypertension, but denies diabetes mellitus, hyperlipidemia, or other risk factors for acute coronary syndrome (ACS).

On examination, Ms. Smith is in visible discomfort, and is slightly diaphoretic. A 12-lead EKG is done and shows ST-segment elevation in the anterior leads (V3 & V4). Cardiac enzymes are sent and she is prepared for thrombolytic therapy.

Ms. Smith is experiencing an acute coronary syndrome. She presented promptly to the Emergency Department, and will receive appropriate treatment for her ischemic myocardium. In this article we will discuss what caused Ms. Smith to develop acute coronary syndrome, how it presents, and the appropriate treatment strategies for ACS.

What causes ACS?

Acute coronary syndromes are the result of the atherosclerotic process. A plaque begins to form in early adult life from an injury to the blood vessel wall. As the injury begins to heal, it collects platelets and fibrin making the vessel wall rough. If fat molecules stick to it, a fatty streak is formed and the atherosclerotic process is begun. In the middle of the plaque, a necrotic core develops that keeps the inflammation going and produces a larger plaque. Eventually the plaque gets large enough that it occludes the vessel, causing ischemia, injury and necrosis of the distal tissue.

Atherosclerotic coronary disease is a very common problem that affects about 13 million people in the United States. In fact, cardiac disease ranks as the number one cause of death. For years the amount of fat in the American diet has been criticized and blamed on the high risk of cardiovascular disease, but that is only one part of the equation. The underlying vascular inflammation is also to blame. This is why some patients can be thin, eat well and exercise regularly and still develop ACS, but the precise way to use this information has not been determined.

What is ACS?

The term "Acute Coronary Syndrome" was coined to refer to the constellation of conditions that decrease blood flow to the heart. These include stable angina, unstable angina, and myocardial infarction. In the initial presentation these three problems can look very similar and EKG interpretation and diagnostic testing is needed to make the diagnosis. In the past, these patients were the ones admitted to our hospitals with the diagnosis of "rule-out MI."

Ischemia

Stable angina is the result of advanced atherosclerosis where the patient will have intermittent chest pain from narrowed arteries. The typical presentation is chest pain with exertion that is relieved by rest or nitroglycerine. Stable angina is a precursor for unstable angina and myocardial infarction.

Injury

Unstable angina is characterized by chest pain that is not relieved by rest and nitroglycerine. It is often difficult to differentiate between unstable angina and myocardial infarction due to the similarity in symptoms. Unstable angina can present with ST-segment depression and T-wave inversion on the EKG, and elevations in troponin levels.

Infarction

Myocardial infarction also presents with chest pain that is unrelieved by nitroglycerine and rest. The EKG changes are different with ST-segment elevation and Q-waves possibly being present and elevations in the troponin and CPK-MB enzymes. The specific characteristics of myocardial infarction are described by the EKG findings. For example: ST-segment elevation MI (STEMI), and Q-wave MI. Those infarctions lacking EKG changes are classified as non Q-wave, or non ST-segment elevation MI (NSTEMI).

How can you predict patterns of infarction?

If you know your patient has previous cardiovascular disease, you may be able to predict the pattern of infarction based on the affected vessels. For example, the right coronary artery (RCA) supplies blood flow to the right ventricle, atrioventricular (AV) node, and inferior left ventricle. Distal blockage of the RCA would cause inferior wall infarction, whereas proximal occlusion causes inferior wall, and right ventricular infarction, along with conduction disturbances in the AV node.

The left coronary artery (LCA) and circumflex supplies the left ventricle and atria. Distal blockage of the LCA would cause anterior wall and septal injury; distal blockage of the circumflex would affect the lateral and posterior walls. Proximal blockage of the LCA could affect the entire left ventricle and atria.

The location of the infarct is determined by the EKG changes; T-wave inversion indicates ischemia, ST-segment elevation indicates injury, and Q-waves indicate infarction. The pattern of infarction can be identified by using Table 1 below.

Table 1