Acute Coronary Syndrome
Myocardial infarction, Unstable angina
ST-elevation myocardial infarction
Non-ST-elevation myocardial infarction
1. Description of the problem
Acute coronary syndromes (ACS) represent a continuum of interrelated diseases including unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Each year, there are over 1.5 million hospitalizations for ACS in the United States alone, and nearly one out of every three admitted patients will die from their disease.
These interrelated diseases all share a common pathophysiology. In all cases, a vulnerable coronary atherosclerotic plaque ruptures, exposing the circulating blood to the thrombogenic components of the plaque and the underlying, damaged coronary endothelium. As a result, platelet activation and aggregation ensues, forming a potent “scaffold” for additional platelet and fibrin deposition. 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.
In both unstable angina and NSTEMI, the body’s natural fibrinolytic system prevents complete and sustained coronary occlusion; in many cases occlusion and reperfusion continuously occur. In the simplest sense, UA and NSTEMI are caused by a partially occlusive thrombus. While ischemia results in both instances, true subendocardial infarction/myocardial necrosis occurs only during NSTEMI. As a result, cardiac biomarker elevation (CK-MB, cardiac troponin) is present only with NSTEMI.
In STEMI, complete and sustained coronary occlusion occurs. As a result, perfusion to the myocardium supplied by the affected coronary artery is lost. Transmural infarction ensues, myocardial necrosis occurs, cardiac biomarker elevation can be detected, and ST-segment elevations indicating acute injury are seen with electrocardiography.
It is important to differentiate STEMI from the other acute coronary syndromes. With STEMI, rapid restoration of epicardial coronary blood flow is paramount. An ECG demonstrating ST-segment elevation ≥1mm in contiguous limb leads or ≥2mm in contiguous precordial leads, or new left bundle branch block should prompt the treating clinician to identify and initiate appropriate reperfusion strategies in an effort to limit myocardial damage.
In non-ST-elevation acute coronary syndromes (i.e. UA and NSTEMI), other high-risk factors should be identified; these 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 ACS should focus on hemodynamic and electrical stabilization. Upon presentation, a 12-lead ECG should be obtained in order to identify the patient with an ST-elevation MI who requires emergency revascularization.
All patients with ACS should receive antiplatelet therapy with aspirin. Aspirin inhibits platelet synthesis of thromboxane A2 and has been shown to dramatically reduce mortality in patients with all types of acute coronary syndromes. Consideration should also be given to instituting 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 achieved 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 ACS is the 12-lead ECG. In non-ST-elevation ACS patients, electrocardiographic 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 ST-elevation MI, the ECG will reveal ST-segment elevation in 2 or more contiguous leads ( ≥1mm in contiguous limb leads or ≥2mm 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 for the biomarker results. In non-ST-elevation ACS 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 troponins (TnI or TnT). Given their high sensitivity and specificity, the cardiac troponins are the preferred biomarker for the detection of myocardial injury in ACS.
In some cases, bedside transthoracic echocardiography may help in evaluating the patient with chest pain. Echocardiography can identify segmental wall motion abnormalities that might result from acute ischemia/infarction. This imaging modality can also help determine if other structural disease is present, including valvular heart disease, pericardial disease, aortic dissection, ventricular septal defects, or free wall rupture.
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.
Patients classically present with signs and symptoms of myocardial ischemia, including chest pain, dyspnea, nausea/vomiting, and diaphoresis. ST-segment elevation in contiguous leads suggests the presence of STEMI. ST-segment depression and/or T-wave inversions may suggest a non-ST-elevation ACS (either NSTEMI or UA). In the absence of classic ECG changes, cardiac biomarker elevation can identify patients with myocardial necrosis.
Conditions that can be confused with ACS might include pericarditis, aortic dissection, pneumonia, pneumothorax, acute pulmonary embolism, gastroesophageal reflux, esophageal spasm, and musculoskeletal injury, to name a few.
Obtaining a 12-lead ECG at presentation, serially, and with each episode of chest pain is vital. Additionally, cardiac biomarkers (CK, CKMB, and cardiac troponin) should be obtained serially. Given that traditional biomarkers tend to rise 3-8 hours following infarction, and peak at about 24 hours, laboratory evaluation of biomarker elevation should continue for at least 9 hours after presentation.
4. Specific Treatment
All patients with presumed ACS should receive an aspirin, 162mg to 325mg, 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 ACS patients.
Clopidogrel, a potent ADP receptor antagonist, should be given to all STEMI patients. For NSTE-ACS (NSTEMI or UA) 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 ACS patients who have an aspirin allergy.
Glycoprotein IIb/IIIa antagonists are often given to high-risk ACS patients, but are usually administered during PCI.
Statins, particularly high-dose (80mg) atorvastatin, improve short- and long-term outcomes for patients with ACS.
Drugs and dosages
Aspirin – chewed – 162 to 325mg
Clopidogrel – 300-600mg orally administered
Prasugrel – alternative ADP receptor blocker particularly for clopidogrel non-responders; 60mg loading dose, then 10mg 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 – 80mg, orally administered for all patients with ACS
Patients with refractory symptoms should be taken to the cardiac catheterization laboratory in order to define the 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 successfully 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 acute coronary syndromes – 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 or fibrinolysis) should decrease myocardial necrosis and alleviate the symptoms associated with ACS. Preservation of myocardial contractile function is paramount, and left ventricular 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 ACS. 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 ACS and risk factors for ACS (e.g. hypertension, vascular disease, hyperlipidemia, advanced age, diabetes, etc.) is truly suffering from one of the acute coronary syndromes. 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 infarction. 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 favor alternative diagnoses.
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 considered in the outpatient arena – therapies that depend a lot on the type of ACS presentation, the type of PCI performed (i.e. drug-eluting stent vs. bare metal stent implantation), the extent of coronary disease, patient comorbidities, etc.
In patients with left ventricular contractile dysfunction, follow-up imaging with echocardiography is usually appropriate to monitor for progression or improvement.
The majority of acute coronary syndromes result from disruption of a vulnerable atherosclerotic plaque within an epicardial coronary artery. Exposure of constituents of these lipid-rich plaques, along with the exposed coronary endothelium, to circulating blood promotes a rapid and robust thrombotic process that primarily involves platelet activation and aggregation.
In STEMI, complete occlusion of an epicardial coronary artery occurs.
In NSTEMI, partial occlusion of an epicardial coronary artery usually occurs. In other cases, there may be transient complete occlusion that improves via the effects of endogenous fibrinolysis. The pathophysiology is similar in patients with UA; the difference is that in NSTEMI, myocardial necrosis occurs and cardiac biomarkers are elevated, while in UA true necrosis and infarction does not occur.
In true myocardial infarction, irreversible cell injury begins to occur 20 or more minutes following cessation of myocardial perfusion. The benefit of reperfusion strategies dramatically diminishes with time and, in the absence of ongoing symptoms or shock, percutaneous intervention is unlikely to provide significant improvements in contractile function, morbidity, or mortality. Most authorities suggest that there is little benefit to PCI when intervention is attempted >12 hours after symptom onset.
The total process of ventricular remodeling, fibrosis, and scarring takes several weeks to complete.
There are a number of risk factors for ACS. These include advanced age, diabetes mellitus, hypertension, hyperlipidemia, tobacco abuse, family history, and male sex.
Patients who present to the hospital with an ACS 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 is actually highest for patients with NSTEMI, followed by those with STEMI, and those who present with UA. If contractile dysfunction results from an ACS presentation, morbidity and mortality are significantly increased.
Patients should be monitored for potential mechanical complications of their ACS. 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 ACS 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 following ACS presentation, particularly in patients with acute myocardial infarction. Often 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 intervention: 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?