심근허혈에 의한 심근괴사의 증거가 있고, 이에 대해서 심근특이효소의 증가와 감소, 허혈성 증상, ECG 의 심근손상 소견(ST-T 변화, 새로운 LBBB), 새로 발견 된 국소벽운동장애, 관상동맥내 혈전, 심근허혈유발 급사, PCI나 CABG 관련 심근손상의 증거, stent thrombosis 중 어느 하나만 있으면 급성 심근경색증으로 정의한다.
Patients who are experiencing an acute STEMI are classically described as presenting with chest pressure or crushing chest pain associated with shortness of breath, nausea/vomiting, or diaphoresis. The chest pain might be described as radiating into the patient’s neck, left arm, or jaw. Often times, they will appear visibly uncomfortable and may have a fist clutching the center of their chest. This classic finding of angina is known as the Levine’s sign.
ECG
ECGs are the mainstay in diagnosing STEMIs, as there are characteristic ECG findings that help diagnose a STEMI. Physicians should not wait for a troponin level to return before activating the cath lab, as the diagnosis should be made on ECG alone and, as mentioned before, “time is muscle.” Given the importance of rapid recognition of STEMIs to reduce patient’s mortality and morbidity, it is recommended that all patients with chest pain have a Door to ECG time of 10 minutes or less.
Evolution of ECG Changes in STEMI
The ECG in STEMI changes over time.
This is important to note, as when the diagnosis is unclear, repeating ECGs can be helpful in making the diagnosis.
The general progression of the ECG changes in a STEMI follows:
- Acute, hyperacute T waves form. These form in the first minutes to hours of a STEMI.
A hyperacute T wave is characterized by an increase in the amplitude and the width of the T wave. - Next, ST elevations will develop.
- Followed by the development of Q waves.
- Later, the T wave will invert
STEMI Territories
STEMIs are classically categorized by the portion of the heart that is affected by the myocardial infarction: anterior, posterior, lateral and inferior. By understanding which portion of the heart is affected, you also begin to determine which coronary artery is occluded. Please refer to the figure below for the territories.
The coronary arteries and their relation to the ECG leads.
Localization of myocardial infarction / ischemia is done by using ECG changes to determine the affected area and subsequently the occluded coronary artery (culprit).
Reciprocal Changes
Reciprocal changes in STEMIs are the ST depressions found on the ECG that are on the opposite side of the heart of the myocardial infarction. It is important to note that the absence of reciprocal changes does not preclude the presence of a STEMI, but the presence of reciprocal changes makes it more likely.
Cardiac Enzymes (Cardiac Biomarkers)
Cardiac biomarkers are released in the circulation due to damage or death of cardiac myocytes, and measuring these biomarkers in serum or plasma is useful in the diagnosis of myocardial infarction.
Cardiac Marker | Increases | Peak | Return to Baseline |
Comments |
Myoglobin | 1–4 h | 4–12 h | 24–36 h | Earliest marker, but non-specific with negative predictive value. |
CK-MB | 4–9 h | 24 h | 48–72 h | Gold standard before troponin was introduced. |
Troponin I/T | 4–9 h | 12–24 h | 7–14 days | Most specific marker. Troponin T is less specific than troponin I because troponin T is also found in muscle. |
Cardiac markers are not necessary for the diagnosis of patients who present with ischemic chest pain and diagnostic EKGs with ST-segment elevation. These patients may be candidates for thrombolytic therapy or primary angioplasty.
Treatment should not be delayed to wait for cardiac marker results, especially since the sensitivity is low in the first 6 hours after onset of initial symptoms.
General principles of treatment
STEMI is treated with anti-ischemic agents, anti-thrombotic agents, anticoagulants, and reperfusion (PCI or fibrinolysis). Reperfusion therapy is immediately needed because patients with acute STEMI have complete arterial occlusions which require reperfusion to restore patency. Virtually all patients with acute STEMI should be referred to the catheterization laboratory for angiography with the intention to perform PCI (percutaneous coronary intervention). Anti-thrombotic medications, anticoagulants, and reperfusion reduce mortality by counteracting thrombus formation and restoring coronary blood flow.
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