Unstable angina has a lower incidence of coronary thrombosis compared with non-STEMI or STEMI and is more often the result of fixed atherosclerotic stenosis. STEMI is most often from coronary thrombosis after plaque rupture and less often from fixed obstruction. Plaque rupture and plaque erosion (ulceration) can result in coronary thrombosis. A clinically-useful means to distinguish these types of plaque is not currently available.
Others are thin and considered vulnerable. Some atherosclerotic plaques have a more stable fibrous cap. Recall that stress testing detects flow-limiting stenosis of greater than 70%. This disruption of the fibrous cap is called “plaque rupture” or “plaque erosion.” Surprisingly, plaque rupture and thrombosis frequently occur at the site of modest coronary stenosis (< 50% luminal narrowing) therefore, even if stress test results are normal, the risk for an ACS is still present. Tissue factor is exposed when the fibrous cap that covers the plaque becomes disrupted or ulcerated. When exposed to the bloodstream, tissue factor activates the clotting cascade, and thrombosis occurs.
There are conditions that mimic STEMI, and distinguishing these can be difficult these are described in Diagnosis.Ī substance known as “tissue factor” is located within the necrotic core of the plaque. The “vulnerable” plaque that formed from the atherosclerotic process is responsible for acute coronary syndromes and, ultimately, coronary artery thrombosis see Atherosclerosis Topic Review. With advances in therapy, the mortality rates have declined about 30% to 50% in each class. This was before reperfusion therapy (thrombolytics and/or percutaneous coronary intervention). The original data from 1967 showed the above mortality rates in each class. This system focuses on physical examination and the development of heart failure to predict risk, as described below.Ĭlass I: No evidence of HF (mortality 6%)Ĭlass II: Findings of mild to moderate HF (S3 gallop, rales < halfway up lung fields or elevated jugular venous pressure (mortality 17%)Ĭlass III: Pulmonary edema (mortality 38%)Ĭlass IV: Cardiogenic shock defined as systolic blood pressure < 90 mm Hg and signs of hypoperfusion such as oliguria, cyanosis and sweating (mortality 67%) The Killip Classification is frequently used to predict mortality during STEMI. ST Segment Elevation Myocardial InfarctionĪnginal symptoms at rest that result in myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) with ST segment elevation on the 12-lead ECG.
Non-ST Segment Elevation Myocardial InfarctionĪnginal symptoms at rest that result in myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) with no ST segment elevation on the 12-lead ECG. In unstable angina, the cardiac enzymes remain normal or are only very minimally elevated. Anginal symptoms at rest without physical exertion.Exertional angina that was previously stable and now occurs with less physical exertion.Exertional angina of new onset (even if relieved with rest and requiring a consistent amount of exertion to procedure symptoms, angina is considered unstable when it first occurs).Three different presentations of unstable angina exist. The differences between the types of acute coronary syndromes are discussed below. The terms “transmural,” “non-transmural,” “Q wave MI” and “non-Q wave MI” are no longer recommended.