Introduction

Introduction

The most serious form of the acute coronary syndrome, ST segment elevation myocardial infarction, or STEMI, most often results from complete thrombotic occlusion of a major epicardial coronary artery.

STEMI is a life-threatening, time-sensitive emergency. Early accurate diagnosis and prompt treatment to restore coronary perfusion, usually by percutaneous coronary intervention (PCI), are critical to effective management.

As the term STEMI implies, the 12-lead ECG shows significant ST segment elevation during STEMI, unlike the ST depressions and ST-T wave changes seen during unstable angina and non-ST segment elevation MI. The Figure below illustrates the ECG during an anterior ST segment elevation MI with “tombstoning” on the ECG.

Enlarge 

With recent advances in interventional cardiology, the terms “transmural,” “non-transmural,” “Q wave MI,” and “non-Q wave MI” have fallen out of favor and are no longer recommended. The clinical differences between the types of acute coronary syndromes are discussed below.

Unstable Angina Pectoris

Three different presentations of angina qualify as “unstable”:

• New-onset exertional angina; angina is considered unstable when it first occurs.
• Previously stable exertional angina that now occurs with less physical exertion.
• Anginal symptoms at rest, occurring without physical exertion.

With unstable angina, cardiac enzymes remain normal or are very minimally elevated.

Non-ST segment elevation myocardial infarction

Anginal symptoms/chest pain at rest that are associated with acute myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) without ST segment elevations on the 12-lead ECG. ECG changes may include ST and T-wave abnormalities.

ST segment elevation myocardial infarction

Anginal symptoms/chest pain at rest associated with myocardial necrosis, indicated by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) and ST segment elevations on the 12-lead ECG.

Classification of Myocardial Infarction

According to the Fourth Universal Definition of Myocardial Infarction, a myocardial infarction (MI) is defined as an acute myocardial injury accompanied by symptoms of myocardial ischemia, signs of ischemia on an ECG, or evidence of a new regional wall motion abnormality. Type 1 and type 2 MIs are distinguished by pathophysiology. [DeFilippis 2019;2b-d(1662)] A type 1 MI is “caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (rupture or erosion)”, while a type 2 MI is “caused by a mismatch between oxygen supply and demand by a pathophysiological mechanism other than coronary atherothrombosis.” [DeFilippis 2019;2d(1662)]

Before the routine use of acute interventions, the Killip Classification was used to predict mortality during STEMI. This system focused on physical examination and the development of heart failure to predict risk, as described below.

Class I: No evidence of heart failure (HF): mortality 6%
Class II: Findings of mild to moderate HF (S3 gallop, rales < halfway up lung fields or elevated jugular venous pressure): mortality 17%
Class III: Pulmonary edema: mortality 38%
Class IV: Cardiogenic shock defined as systolic blood pressure (BP) < 90 mm Hg and signs of hypoperfusion such as oliguria, cyanosis and sweating: mortality 67%

The original data (from 1967) showed the mortality rates listed above for each class. With advances in therapy, mortality rates have declined about 30% to 50% in each class.

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