ST-Elevation Myocardial Infarction (STEMI)
Non-ST-Elevation Myocardial Infarction (NSTEMI)
Acute Coronary Syndrome
1. Description of the problem
Myocardial infarction results when coronary blood flow is compromised, resulting in myocardial necrosis. Pathologically speaking, a transmural infarct results when myocardial necrosis extends throughout the entire thickness of the myocardium – this is due to complete occlusion of an epicardial coronary artery (i.e. STEMI). A subendocardial infarct results in necrosis exclusively inolving the innermost aspect of the myocardium. Usually a subendocardial infarct is the result of a partially occluded epicardial coronary artery (i.e. NSTEMI).
Both STEMI and NSTEMI result from rupture of a vulnerable atherosclerotic plaque. This ruptured plaque exposes the circulating blood to highly thrombogenic substances, which propogates clot formation. At the same time, endothelial dysfunction contributes to additional thrombosis and ineffective vasodilatation. Ultimately, the lumen of the affected coronary artery gets occluded by thrombus, thereby limiting effective blood flow and consequently depriving the myocardium of effective oxygen delivery
Key management points
It is important to differentiate STEMI from NSTEMI. With STEMI, rapid restoration of epicardial coronary blood flow is paramount. An ECG demonstrating ST-segment elevation ≥1 mm in contiguous limb leads or ≥2 mm in contiguous precordial leads, or new left bundle branch block should prompt the clinician to identify and initiate appropriate reperfusion strategies in an effort to limit myocardial damage.
In NSTEMI, other high-risk factors should be identified to risk-stratify patients and to determine the most appropriate plan of care. These high-risk features include: advanced age, recent antiplatelet (aspirin) use, recurrent/refractory chest pain, ST-segment depression on ECG, and elevated cardiac biomarkers, to name a few. Among high-risk patients, an early invasive strategy to define the coronary anatomy and mechanically reperfuse the ischemic myocardium should be considered.
2. Emergency Management
Initial management of the patient with MI should focus on hemodynamic and electrical stabilization. Upon presentation, a 12-lead ECG should be obtained in order to identify the patient with an STEMI who requires emergency revascularization.
All patients with myocardial infarction should receive antiplatelet therapy with aspirin. Aspirin inhibits platelet synthesis of thromboxane A2, and has been shown to dramatically reduce mortality in patients with both types of MI. Consideration should also be given to the institution of antithrombotic therapy with either unfractionated or low-molecular-weight heparin.
In the STEMI patient, an optimal strategy for rapid reperfusion should be devised. Reperfusion should be obtained quickly and, if available, patients should be taken emergently to a capable cardiac catheterization laboratory for percutaneous intervention. The goal for percutaneous intervention should be a door-to-balloon time within 90 minutes of hospital presentation. Percutaneous coronary intervention (PCI) should also be considered for patients with a contraindication to fibrinolytic therapy, for those who present to the hospital late (>3 hours from symptom onset), or those with ongoing cardiogenic shock. In all other patients, in whom PCI cannot be acheived within 90 minutes of hospital presentation, fibrinolytic therapy should be employed.
– Ensure hemodynamic and electrical stabilization for the ACS patient who presents to the hospital.
– Must obtain rapid 12-lead ECG specifically looking for ST-segment elevation, which would prompt a rapid reperfusion management strategy
– All patients should receive aspirin; consideration should also be given to the initiation of heparin.
– PCI should be performed within 90 minutes of hospital presentation, or else fibrinolytic therapy should be considered.
– PCI is also indicated for patients with delayed presentations, fibrinolytic contraindications, or ongoing shock.
The hallmark diagnostic tool in the management of patients with MI is the 12-lead ECG. In NSTEMI, ECG manifestations might include ST-segment depression and/or T-wave inversions – these findings are often transient, and tend to parallel the development of symptoms (chest pain, dyspnea, nausea, diaphoresis). In STEMI, the ECG will reveal ST-segment elevation in 2 or more contiguous leads ( ≥1 mm in contiguous limb leads or ≥2 mm in contiguous precordial leads); initially, ST elevations will occur in the setting of peaked (hyperacute) T-waves. As the injury progresses and myocardial necrosis ensues, the amplitude of the R-waves will diminish, and Q-waves will begin to develop. Ultimately, the ST segment begins to fall and the T-wave inverts.
Cardiac biomarkers associated with myocardial necrosis can also be checked. In patients with ST-segment elevations on the ECG, delay to reperfusion should be avoided and the treating clinician should not wait on the biomarker results. In NSTEMI patients, biomarker elevation will help determine whether the patient is having a myocardial infarction (NSTEMI) or rather unstable angina without myocardial necrosis. Cardiac biomarkers include creatine kinase (CK), the creatine kinase MB isoenzyme (CKMB), and the cardiac-specific troponines (TnI or TnT). Given their high sensitivity and specificity, the cardiac troponins are the preserved biomarker for the detection of myocardial injury in ACS.
Normal lab values
Typical ECG for a patient with an inferior STEMI is shown in Figure 1.
Figure 2 provides details on localization of myocardial injury in STEMI based upon ECG patterns of ST-segment elevation.
How do I know this is what the patient has?
A STEMI is an ECG diagnosis. If, in the setting of a suggestive history and exam, there are ST-segment elevations in contiguous leads or new left bundle-branch block, a STEMI is present. In the absence of ST elevations, but with supportive history and elevated cardiac biomarkers (i.e. CK-MB or cardiac troponin), a NSTEMI is present.
Mimics of acute MI can include pericarditis, unstable angina, acute pulmonary embolism, pneumonia, and pneumothorax, to name a few.
All patients with presumed MI should have a 12-lead ECG. For patients with inferior ST-segment elevations, one should usually get a right-sided ECG to evaluate for the presence or absence of RV involvement. In a right-sided ECG, if there is ST-segment elevation in lead V4R, RV involvement is suggested. Elevations in cardiac biomarkers (i.e. CK-MB and cardiac troponins) can also confirm a diagnosis of MI. It should be noted, however, that while these markers are sensitive for myocardial necrosis, they may be elevated in non-coronary conditions (e.g. acute heart failure, myopericarditis, myocarditis, acute pulmonary embolism, etc.).
4. Specific Treatment
All patients with presumed MI should receive an aspirin – 162 mg to 325 mg chewed for rapid buccal absorption. All patients should get supplemental oxygen.
Provided patients do not have evidence of RV infarction (and hence are not preload-sensitive), sublingual and intravenous nitrates (nitroglycerin) can be administered for symptom relief.
Heparin – either unfractionated or low-molecular-weight – should be considered as an antithrombotic strategy for all MI patients.
Clopidogrel, a potent ADP receptor antagonist, should be given to all STEMI patients. For NSTEMI patients, clopidogrel should be considered in addition to aspirin. The risk of needing surgical revascularization (i.e. coronary artery bypass surgery) should be considered before using clopidogrel, given its long half-life and the potential need to delay surgery in order to avoid bleeding complications. Clopidogrel should also be administered to all MI patients who have an aspirin allergy.
Glycoprotein IIb/IIIa antagonists are often given to high-risk NSTEMI patients, but are more commonly administered as an adjunct to percutaneous coronary intervention (PCI).
Statins, particularly high-dose (80 mg) atorvastatin, improve short- and long-term outcomes for patients with MI.
Drugs and dosages
Aspirin – chewed – 162 to 325 mg
Clopidogrel – 300-600 mg orally administered
Prasugrel – alternative ADP receptor blocker particularly for clopidogrel non-responders; 60 mg loading dose, then 10 mg daily, orally administered
Unfractionated heparin – per institutional protocol, adjusted to achieve therapeutic aPTT
Low-molecular-weight heparin – prescribed as one or two daily subcutaneous dosages depending upon patient body weight and renal function
Nitroglycerin – given sublingual or IV and titrated to effect
Beta blockers – initiated within the first 24 hours of hospitalization, orally administered
Fondaparinux – factor Xa inhibitor
Bivalirudin – intravenous direct thrombin inhibitor; used in conjunction with planned PCI
GP IIb/IIIa Inhibitors – abciximab, eptifibatide, tirofiban – administered as adjunctive therapy for patients during PCI
Atorvastatin – 80 mg, orally administered for all patients with MI
Patients with refractory symptoms should be taken to the cardiac catheterization laboratory in order to define their coronary anatomy and revascularize high-grade, stenotic lesions. The use of an intra-aortic balloon pump should be considered for refractory angina/ischemia. If percutaneous intervention cannot restore blood flow to injured myocardium, surgical revascularization should be considered.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
Given the underlying pathophysiology contributing to the development of MI, particularly those pathways involving enhanced platelet activation and aggregation, along with thrombosis, the use of antiplatelet and antithrombotic therapies should decrease atherothrombotic sequelae. As a result, coronary reperfusion and myocardial oxygen delivery should be enhanced. This, along with appropriate revascularization strategies (i.e. PCI, CABG, or fibrinolysis), should decrease myocardial necrosis and alleviate the symptoms associated with MI. Preservation of myocardial contractile function is paramount, and left venticular ejection fraction should be monitored with short-term and long-term echocardiographic evaluation. If substantial injury/necrosis occurs, contractile function will suffer, and morbidity and mortality will increase.
In addition, vasodilators should improve coronary perfusion and reduce ischemic symptoms when given to patients with MI. Beta blockers decrease the sympathetic stimulation that contributes to myocardial oxygen supply-demand mismatch. These agents may improve symptoms, but also have been shown to improve both short- and longer-term mortality.
It is usually prudent to consider that a patient presenting with symptoms of MI and risk factors for MI (e.g. hypertension, vascular disease, hyperlipidemia, advanced age, diabetes, etc.) is truly suffering from an MI. In the absence of acute ST-segment elevations on the presenting ECG, the clinician often has time for further evaluation and consideration of alternative diagnoses. Normal cardiac biomarkers are certainly reassuring, and rule out the presence of true myocardial necrosis. If an invasive management approach is pursued (i.e. early cardiac catheterization), and no obstructive coronary disease is seen, one should consider alternative diagnoses. When a more conservative/non-invasive management approach is considered, stress testing may help determine if coronary ischemia/infarction is the primary mechanism behind a patient’s symptoms.
All patients should follow up with a cardiologist after hospital discharge. Careful evaluation and management of cardiovascular risk factors (i.e. secondary prevention) should be a focus of follow-up clinical visits in order to reduce the risk for future cardiovascular events. Beta blockers, statins, and ACE inhibitors (particularly for patients with systolic dysfunction) should be carefully titrated. The appropriate dosage and duration of antiplatelet therapies should be addressed during follow-up as well.
In patients with left ventricular contractile dysfunction, follow-up imaging with echocardiography is usually appropriate to monitor for progression or improvement. Evidence-based heart failure therapies (including ACE inhibitors, beta blockers, aldosterone antagonists, etc.) should be employed.
MI results from the disruption of a vulnerable atherosclerotic plaque within an epicardial coronary artery. Exposure of constituents of these lipid-rich plaques to circulating blood promotes a rapid and robust thrombotic process that primarily involves platelet activation and aggregation. In addition, endothelial dysfunction contributes to further platelet activation and diminished vasodilatation.
There are a number of risk factors for MI. These include advanced age, diabetes mellitus, hypertension, hyperlipidemia, tobacco abuse, family history, and male sex.
Patients who present to the hospital with an MI have substantial morbidity and mortality. Over 1/3 of all patients will die as a result of their disease, though mortality rates have been substantially declining over time. Short- and longer-term mortality rates are actually highest for patients with NSTEMI, followed by those with STEMI. If contractile dysfunction results from MI, morbidity and mortality are significantly increased.
Patients should be monitored for potential mechanical complications of their acute MI. These include congestive heart failure, cardiogenic shock, acute mitral valve insufficiency (due to papillary muscle ischemia, infarction, or rupture), ventricular free wall rupture, ventricular septal rupture, left ventricular aneurysm or pseudoaneurysm, and cardiac tamponade.
In addition, patients with MI are at risk for the development of both atrial and ventricular arrhythmias. Episodes of ventricular arrhythmias that develop within the first 48 hours of presentation are more commonly related to transient electrical instability, and are usually not chronic problems. Episodes that develop >48 hours following hospital presentation are likely to be the result of scar formation and re-entrant mechanisms; these arrhythmias place patients at high risk for future arrhythmic events and sudden cardiac death, and are considered an indication for implantable cardioverter-defibrillator (ICD) therapy. Conduction disease can also occur during and after acute MI. Often times conduction blocks are transient and related to acute ischemia; however, advanced conduction disease (e.g. third-degree atrioventricular block, Mobitz II second-degree AV block) could require permanent pacing.
Special considerations for nursing and allied health professionals.
What's the evidence?
Anderson, JL. “ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines”. Circulation. vol. 116. 2007. pp. 803-77. Guideline recommendations for the management of patients with non-ST-elevation ACS
Kushner, FG. “Focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infaction and ACC/AHA/SCAI guidelines on percutaneous coronary intervetion: a report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines”. Circulation. vol. 120. 2009. pp. 2271-2306. Guideline recommendations for the management of patients with STEMI
Mehta, SR. “Early versus delayed invasive intervention in acute coronary syndromes”. NEJM. vol. 360. 2009. pp. 2165-75. Randomized controlled trial evaluating outcomes in patients with ACS managed with early versus delayed/conservative intervention strategies; results favor early invasive strategy for reduction in outcomes, particularly in high-risk patients.
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- Special considerations for nursing and allied health professionals.
- What's the evidence?