Also known as a heart attack, myocardial infarction (MI) is a necrosis of the heart muscle that originates from an acute obstruction of a coronary artery. It decreases blood flow and leads to irreversible damage to the heart due to myocardial ischaemiaLoad more
What is Myocardial Infarction?
Also known as a heart attack, myocardial infarction (MI) is a necrosis of the heart muscle that originates from an acute obstruction of a coronary artery. It decreases blood flow and leads to irreversible damage to the heart due to myocardial ischaemia1,2.
There are two categories of MI:
- Non-ST-segment elevation MI (NSTEMI)
- ST-segment elevation MI (STEMI)
Unstable angina looks like NSTEMI, but cardiac markers are not elevated2.
Causes of MI include atherosclerotic plaques rupturing and leading to thrombosis (majority), coronary artery embolism, cocaine-induced ischaemia, coronary dissection, trauma, and coronary vasospasm2.
Nonmodifiable risk factors: sex, age, family history, and male pattern baldness.
Modifiable risk factors: tobacco use, diabetes, high blood pressure, obesity, dyslipidemia, sedentarism, poor oral hygiene, peripheral vascular disease (PVD), and high levels of homocysteine2.
Signs & Symptoms
Chest pain and dyspnea are the most common symptoms, with other symptoms including:
- pressure or tightness in the chest
- pain in the chest, back, jaw, and other areas of the upper body that lasts more than a few minutes or that goes away and comes back
- sweating, nausea and vomiting
- tachycardia and tachypnea3
Typical chest pain:
- Intense and unremitting for 30-60 minutes
- Substernal, usually radiating up to the neck, shoulder, and jaw, and down the left arm
- Can be characterised as a substernal pressure sensation that is also described as squeezing, aching, burning, or even sharp
- In some cases, the symptom is epigastric, with a feeling of indigestion or fullness and gas4
Diagnosis of myocardial infarction is made through ECG and cardiac biomarkers.
Cardiac troponin (cTn): detection of an elevated cTn value above the 99th percentile of the upper reference limit characterises MI. When it is acute, there is a rise or fall of cTn levels5.
MI is also characterised when an elevated cTn is noted in addition to at least one of the following:
- Symptoms of ischaemia
- New ST-segment changes or a left bundle branch block (LBBB)
- Presence of pathological Q waves on the ECG
- Imaging study showing new regional wall motion abnormality
- Presence of an intracoronary thrombus at autopsy or angiography1,2
The American College of Cardiology/American Heart Association (ACC/AHA) and European Society of Cardiology (ESC) guidelines recommend that, in case of suspicion of MI, cardiac biomarkers (cardiac troponin) should be measured at the patient’s presentation. An ECG confirms the diagnosis of MI in approximately 80% of cases4.
- Type 1: Spontaneous MI caused by ischaemia due to a primary coronary event (e.g. plaque rupture, erosion, or fissuring; coronary dissection)
- Type 2: ischaemia due to increased oxygen demand (e.g. hypertension), or decreased supply (e.g. coronary artery spasm or embolism, arrhythmia, hypotension)
- Type 3: Related to sudden unexpected cardiac death
- Type 4a: Associated with a percutaneous coronary intervention (signs and symptoms of MI with cTn values > 5 × 99th percentile URL)
- Type 4b: Associated with documented stent thrombosis
- Type 5: Associated with coronary artery bypass grafting (signs and symptoms of MI with cTn values >10 × 99th percentile URL)1
MI affects predominantly the left ventricle (LV), but the damage may extend into the right ventricle (RV) or the atria. Depending on the coronary affected, it can be classified as right ventricular infarction, inferoposterior infarction, or anterior infarct1.
Transmural: affects the whole thickness of myocardium from epicardium to endocardium. Abnormal Q waves on ECG. It cannot be precisely determined clinically.
Nontransmural: does not extend through the whole ventricular wall and causes only ST-segment and T-wave (ST-T) abnormalities.
Presence or absence of ST-segment elevation or Q waves on the ECG:
Non–ST-segment elevation myocardial infarction (NSTEMI, subendocardial MI): myocardial necrosis (troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ST-segment depression, T-wave inversion, or both may be present on ECG.
ST-segment elevation myocardial infarction (STEMI, transmural MI): myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin. Elevation of troponin I or troponin T and CK levels1.
Management and treatment
- Intravenous (IV) access, supplemental oxygen if SaO2 < 90%, pulse oximetry
- Immediate administration of nonenteric-coated chewable aspirin
- Nitroglycerin for active chest pain
- ECG, if available1
Emergency department and inpatient care
- STEMI treatment includes immediate reperfusion. Emergent percutaneous coronary intervention (PCI) is preferred. Previously, patients should receive dual antiplatelet agents (IV heparin infusion and adenosine diphosphate inhibitor receptor). Furthermore, glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may be given at the time of PCI.
- If PCI is unavailable within 90 minutes of the diagnosis of STEMI, a reperfusion with IV thrombolytic agent is the adequate treatment.
- In the case of NSTEMI in a stable asymptomatic patient: antiplatelet agents.
- PCI can be done <48 hours of admission and results in reduced mortality and decreased length of hospitalisation.
- In case of NSTEMI patients with refractory ischaemia or ischaemia with haemodynamic or electrical instability, PCI needs to be done emergently.
- Patients may routinely be given aspirin, high-dose statin, beta-blocker, and/or ACE-inhibitor.
- PCI: to be done within 12 hours. Fibrinolytic therapy: should be done within 2 hours.
- Parenteral anticoagulation, in addition to antiplatelet therapy, is always recommended2
MI may lead to impairment in diastolic and systolic function, resulting in long-term arrhythmias1. Even with the evolution of management, acute MI has a high mortality rate and most of the deaths occur before arrival to the hospital. 5%-10% of survivors die and approximately 50% need hospitalisation within the first year after the MI2.
The earlier the treatment (< 6 hours from symptom onset), the better the prognosis1. Prognosis depends on the extent of muscle damage. Better outcomes are related to early perfusion-thrombolytic therapy within 30 minutes of arrival or PCI within 90 minutes; ejection fraction (EF) preserved, and whether the patient is started on aspirin, beta-blockers, and ACE inhibitors.
Factors that negatively affect prognosis include: diminished EF (the strongest predictor), diabetes mellitus (DM), an elderly age, a prior cardiovascular event, delayed reperfusion, congestive heart failure (CHF), elevated C-reactive protein and BNP levels, and depression2.
- https://www.msdmanuals.com/professional/cardiovascular-disorders/coronar.... Ischemic cardiomyopathy: Treatment and prognosis Literature review current through: May 2020. | This topic last updated: Jul 11, 2018.
- Mechanic OJ, Grossman SA. Acute Myocardial Infarction. [Updated 2019 Dec 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459269/.
- A Maziar Zafari, Medscape, Myocardial Infarction, 2019. https://emedicine.medscape.com/article/155919-overview.
- Kristian Thygesen, Joseph S Alpert, Allan S Jaffe, Bernard R Chaitman, Jeroen J Bax, David A Morrow, Harvey D White, ESC Scientific Document Group, Fourth universal definition of myocardial infarction (2018), European Heart Journal, Volume 40, Issue 3, 14 January 2019, Pages 237–269.
Tamara García Camarero, Jose M de la Torre HernandezEuropean Cardiology Review 2020;15:e07.DOI: https://doi.org/10.15420/ecr.2019.25.2
Alberto Lorenzatti, Peter P TothEuropean Cardiology Review 2020;15:e04.DOI: https://doi.org/10.15420/ecr.2019.06
Muhammad Shahzeb Khan, Javed ButlerCardiac Failure Review 2019;5(3):169–72.DOI: https://doi.org/10.15420/cfr.2019.06.R1
Michael G Kirby, Geoffrey Hackett, Sudarshan Ramachandran, et alEuropean Cardiology Review 2019;14(2):103–10DOI: https://doi.org/10.15420/ecr.2019.13.1