Acute myocardial infarction is one of the leading causes of death in the developed world. The prevalence of the disease approaches three million people worldwide with more than one million deaths in the United States, annually. Acute myocardial infarction can be divided into two categories, non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is similar to NSTEMI. However, cardiac markers are not elevated.
The etiology of acute myocardial infarction is decreased coronary blood flow. The available oxygen supply cannot meet oxygen demand, resulting in cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acute decreased blood flow in the coronary. Other etiologies of decreased oxygenation/myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.
Among patients suffering from acute myocardial infarction, 70% of fatal events are due to occlusion from atherosclerotic plaques. As atherosclerosis is the predominant cause of acute myocardial infarction, risk-factors for the atherosclerotic disease are often mitigated in the prevention of disease. Modifiable risk factors account for 90% (men) and 94% (female) of myocardial infarctions. Modifiable risk factors include cigarette smoking, exercise, hypertension, obesity, cholesterol, LDL, and triglyceride levels. In contrast, age, sex, and family history are non-modifiable risk factors for atherosclerosis.
Atherosclerotic rupture leads to an inflammatory cascade of monocytes and macrophages, thrombus formation, and platelet aggregation. This leads to the decreased oxygen delivery through the coronary artery resulting in decreased oxygenation of the myocardium. Inability to produce ATP in the mitochondria leads to the ischemic cascade, and therefore apoptosis (cell death) of the endocardium, or myocardial infarction.
With some exception due to genetic variation, coronary arteries have unique and diagnostic territorial distributions. For example, the left anterior descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall, and ventricular apex. The left circumflex artery supplies blood to the posterolateral wall. The right coronary artery supplies the right ventricle. The inferior wall is supplied either by the left circumflex or right coronary artery. 
The histology of myocardial infarction changes over the time-course of the disease. At time 0, there are no microscopic histologic changes. Under light microscopy, within 0.5 to 4 hours, waviness of fibers at the periphery of the tissue is seen. Glycogen is depleted. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema. At 12 to 24 hours, the gross specimen becomes dark and mottled. There are contraction band necrosis and neutrophil predominance on histopathology. At 1 to 3 days, there is a loss of nuclei, and at 3 to 7 days, macrophages appear to remove apoptosis cells. At 7 to10 days, granulation tissue appears. At 10 days and onward, there is collagen one deposition. After 2 months, the myocardium is scarred.
Cardiac biomarkers are useful in the diagnosis of acute myocardial infarction, specifically non-ST-elevation MI. Troponin is the most specific lab test and has two isoforms, I and T. Troponins peak at 12 hours and persist for seven days. Creatinine Kinase, MB is also specific to the myocardium. It peaks at ten hours, however, normalizes within two to three days. LDH peaks over 72 hours and normalizes over ten to 14 hours. In clinical practice, LDH is not used to diagnose acute MI. Finally, MB has very low specificity for myocardium and is not used clinically; it quickly rises and normalizes. High-sensitivity troponin has recently been approved for use in the United States after having been heavily studied and utilized in Europe. Although it is more sensitive than conventional troponin, it is also less specific. Thus, potential challenges include numerous false-positive interpretations.
The history of and physical exam is often inconsistent when evaluating for acute myocardial infarction. The history should focus on the onset, quality, and associated symptoms. Recent studies have found that diaphoresis and bilateral arm radiating pain most often are associated with myocardial infarction in men. Physical exam most importantly should note vital signs and patient’s appearance, including diaphoresis, as well as lung findings and cardiac auscultation.
Early and rapid ECG testing should be employed in all patients presenting with chest pain. Women often have atypical symptoms such as abdominal pain or dizziness and may present without chest pain at all. Elderly patients more often have shortness of breath as their presenting symptom for myocardial infarction. All of these presentations should prompt ECG testing, as well.
The ECG is highly specific for MI (95% to 97%), yet not sensitive (approximately 30%). Right-sided, posterior lead placement, and repeat ECG testing can increase ECG sensitivity. For example, peaked T-waves on ECG, known as “hyperacute T waves,” often indicate early ischemia and will progress to ST elevation. When present, findings of ST-elevations greater than 2 mm in two contiguous leads on ECG (Inferior: leads II, III, aVF; Septal equal V1, V2; Anterior: V3, V4; Lateral: I, aVL, V5, V6) are indicative of an ST-elevation myocardial infarction. Often, there are ST depressions that are visualized in opposite anatomical regions of the myocardium.
ECG diagnosis of STEMI can be difficult, particularly in patients with a left bundle branch block and pacemakers. Sgarbosa described criteria that can assist the physician or practitioner in diagnosing STEMI in these patients. Isolated ST-elevations in aVR are indicative of left main coronary artery occlusion in the appropriate clinical setting. Wellens noted deeply biphasic T waves in V2, V3, and found they are often predictive of an impending proximal left anterior descending artery occlusion which may lead to devastating anterior wall myocardial infarction.
Patients that present with myocardial infarction may not have diagnostic ST-elevation ECG abnormalities. Patients with typical chest pain should be investigated for NSTEMI with subtle abnormalities on ECG, including ST-depressions and T wave changes. Serial ECGs can be helpful here as well to look for dynamic changes. ECG without acute changes or any abnormalities is common in NSTEMI.
There are diagnostic guidelines that can assist the practitioner in determining whether further testing is useful in identifying patients with NSTEMI. Given the poor sensitivity of ECG for STEMI, troponins are almost universally used for patients with a suspicious clinical history. The HEART score has been validated and popularized. It utilizes clinician’s suspicion, patient risk factors, ECG diagnostics, and troponin level to determine the “risk level” of the patient.
All patients with STEMI and NSTEMI require immediately chewed aspirin 160 mg to 325 mg. Furthermore, the patient should have intravenous access and oxygen supplementation if hypoxic less than 91%. Opioids may be used for pain control in addition to sublingual nitroglycerin if the blood pressure is adequate.
Treatment for STEMI includes immediate reperfusion. Preference is for emergent percutaneous coronary intervention (PCI). Before PCI, patients should receive dual antiplatelet agents, including intravenous heparin infusion as well as an adenosine diphosphate inhibitor receptor (P2Y2 inhibitor), most commonly ticagrelor. Furthermore, Glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may be given at the time of percutaneous intervention.
If percutaneous intervention is unavailable within 90 minutes of diagnosis of STEMI, reperfusion should be attempted with an intravenous thrombolytic agent.
NSTEMI in a stable asymptomatic patient may not benefit from emergent percutaneous coronary intervention and should be managed medically with antiplatelet agents. Percutaneous coronary intervention can be done within 48 hours of admission and may lead to improved in-hospital mortality and decreased the length of stay. In NSTEMI patients with refractory ischemia or ischemia with hemodynamic or electrical instability, PCI should be performed emergently
Before discharge for acute MI, patients may routinely be given aspirin, high-dose statin, beta-blocker, and/or ACE-inhibitor.
Acute myocardial infarction in the US is managed by a health team that is solely dedicated to heart disease. Besides the cardiologist, the team usually consists of a cardiac surgeon, an interventional cardiologist, intensivist, cardiac rehabilitation specialist, critical care nurses and physical therapists. Because many patients die before even reaching the hospital, the key is to educate the patient on symptoms and early arrival to the emergency department. Patients should be educated on how to take nitroglycerin, and if there is no relief after three doses, then 911 should be called. After discharge, the patient needs to enter a cardiac rehabilitation program, eat a healthy diet, discontinue smoking, abstain from alcohol, reduce body weight and lower cholesterol and blood glucose levels. The patient should be educated on the importance of compliance with medications to lower blood pressure and blood cholesterol. (Level II)
Acute myocardial infarction continues to have a high mortality out of the hospital. Data indicate that at least one-third of patients die before coming to the hospital and another 40-50% are dead upon arrival. Another 5-10% of patients will die within the first 12 months after their myocardial infarction. Readmission is common in about 50% of patients within the first 12 months after the initial MI. The overall prognosis depends on the ejection fraction, age, and other associated comorbidity. Those who do not undergo any type of revascularization will have a poorer outcome compared to patients who undergo revascularization. The best prognosis is in patients with early and successful reperfusion and preserved left the ventricular function. (Level II)