Acute coronary syndromes

See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/236636376 Acute coronary syndromes ARTICLE in DISEASE-A-MONTH: DM · MAY 2013 Impact Factor: 0.95 · DOI: 10.1016/j.disamonth.2013.03.006 · Source: PubMed CITATIONS READS 15 49 6 AUTHORS, INCLUDING: Ernest Wang NorthShore University Hea… 74 PUBLICATIONS 632 CITATIONS SEE PROFILE Available from: Ernest Wang Retrieved on: 04 February 2016 Disease-a-Month 59 (2013) 202–209 Contents lists available at SciVerse ScienceDirect Disease-a-Month journal homepage: www.elsevier.com/locate/disamonth Acute coronary syndromes Constantine Karras, BA, Sarah M. Donlan, MD, FACEP, Robert Aitchison, BA, Pamela Aitchison, BSN, RN, Ernest Wang, MD, FACEP, Morris Kharasch, MD, FACEP Acute coronary syndrome (ACS) is a spectrum of disease ranging from undifferentiated chest pain to unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) to STsegment elevation myocardial infarction (STEMI) (see Table 1). The management goal of acute coronary syndrome is to identify where the patient falls on the ACS spectrum to guide treatment and testing to reduce the amount of myocardial necrosis and thus preserve left ventricle function and to prevent and manage major adverse cardiac events: ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), decompensated heart failure, and cardiogenic shock. 1. Prehospital management In the prehospital setting, time identification and rapid transport by emergency medical services (EMS) is of primary importance. For patients with STEMI, prompt diagnosis and treatment leads to increased myocardial salvage. For NSTEMI or unstable angina (UA) early management improves outcomes. For patients at risk for ACS, primary care physicians and other healthcare providers should discuss the signs and symptoms of ACS, appropriate use of aspirin, activation of the EMS system, and locations of nearby emergency departments. Symptoms of ACS include the following: chest discomfort (angina), discomfort of upper body, loss of breath, sweat, dizziness, and vomiting. Atypical symptoms are common in women, elderly, and diabetic patients. EMS responders should be well trained in the presentation of management of ACS, CPR, and defibrillation. EMS providers should administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence of the role of supplemental oxygen in patients without hypoxia. An oxygen saturation of 494% should be maintained if the patient demonstrates hypoxia or dyspnea. EMS providers should obtain a 12-lead ECG and have the capabilities of identifying STEMI and life-threatening arrhythmias. If possible, the ECG should be transmitted to the emergency department for physician interpretation. EMS providers should administer 160–325 mg of nonenteric chewable aspirin, assuming there is no aspirin allergy and/or signs of active or recent gastrointestinal bleeding. If pain is present, EMS providers should administer up to 3 nitroglycerin doses (tablet or spray) 0011-5029/$ - see front matter & 2013 Published by Mosby, Inc. http://dx.doi.org/10.1016/j.disamonth.2013.03.006 C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 203 Table 1 The spectrum of acute coronary syndromes. Unstable angina Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) Anginal pain with at least one of the following features: Characterized by clinical features of unstable angina in addition to elevated cardiac markers. Cardiac markers are elevated as a result of myocardial necrosis  Is of new onset and severe  Occurs at rest or with minimal exertion ST-Segment Elevation Myocardial Infarction (STEMI) Characterized by clinical features of myocardial infarction in addition to ST-segment elevation on a 12-lead EKG  Pain is worsening in the severity and length of each episode (i.e. occurring in a crescendo pattern) Source: Boateng S and Sanborn T1 every 3–5 min; however, nitrates in all forms are contraindicated in patients with initial systolic blood pressure o90 mmHg and in patients with suspected infarctions of the right ventricle. Morphine may be used when chest discomfort is unresponsive to nitrates. Providers should monitor vitals and cardiac rhythm while transporting patient. EMS transport times of less than 30 min to hospital significantly reduce mortality. At times, direct triage of STEMI to a PCI-capable hospital is recommended, even bypassing some EDs if contact-balloon times are o 90 min. PCI hospitals have ‘‘STEMI alert’’ systems, which are composed of prehospital ECGs, EMS notification of receiving hospital, and activation of the cardiac catherization team to shorten reperfusion time. If the emergency physician activates the STEMI protocol, the rate of ‘false-positive’ activations are infrequent. 2. ED evaluation For all patients with suspected ACS in the emergency department setting, the following rapid assessment should be performed. Within 10 min of ED arrival, providers should obtain an ECG, a complete set of vital signs with frequent vital updates, and place the patient on a continuous cardiac monitor. It is important for the clinician to obtain serial ECGs especially if the patient’s symptoms or vital signs change. The history should focus on chest pain, associated signs and symptoms, prior cardiac history, quick assessment of other life-threatening causes of chest pain such as aortic dissection, pulmonary embolus, pericarditis, risk factors for ACS, and historical features that may preclude the use of PCI, anticoagulation, antiplatelet therapies, and fibrinolytics. Cardiac biomarkers should be obtained during the evaluation of patients with suspected ACS. Troponin I and T are preferred and more sensitive and specific than creatinine kinase isoenzyme (CK-MB). Serial cardiac enzymes should be obtained regardless of initial results. Clinicians should not wait for biomarker results with STEMI patients before initiating reperfusion therapy. 3. Interpretation of the 12-lead ECG  Diagnosis of ST-segment elevation myocardial infarction (STEMI) is established by ECG findings revealing greater than 1-mm J point (junction of the ST segment and QRS complex) elevation in two or more contiguous limb leads or precordial leads V4–V6 or greater than 2 mm in two or more precordial leads V1–V3. Development of a new left bundle branch 204   C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 block should be considered as a STEMI equivalent until proven otherwise. The goal of treatment is early reperfusion therapy through PCI and less commonly fibrinolysis when PCI capabilities are not available. NSTEMI or unstable angina (UA) are initially difficult to distinguish between as ECG findings can be similar. Elevated cardiac biomarkers (troponin) differentiates NSTEMI from UA, troponin being 4 0.5. Non-emergent PCI is the treatment of choice. Thrombolytics should not be administered for UA/NSTEMI. Nondiagnostic ECG—Many patients presenting to the ED will have normal or nondiagnostic ECGs, (nonspecific ST or T wave changes). Physicians should use risk stratification criteria to target those at higher risk for whom treatment would be beneficial while simultaneously avoiding risky therapies and testing complications (e.g. anticoagulation and invasive cardiac catheterization) in low-risk patients. 4. Reperfusion therapy Diagnosis of STEMI requires emergent reperfusion therapy to restore normal blood flow through coronary arteries and limit infarct size. Randomized trials performed at high-volume institutions compared fibrinolysis therapy to percutaneous intervention (PCI) for STEMI. PCI is associated with reduced mortality (30%) and reinfarction rates compared to fibrinolytic drug therapy and decreased risk of intracranial hemorrhage and stroke, which makes it the best choice for elderly and those at risk for bleeding. In optimal circumstances, the usage of PCI is able to achieve restored coronary artery flow in 490% of subjects. Fibrinolytics restores normal coronary artery flow in 50–60% of subjects. PCI is treatment of choice for STEMI when door-to-balloon time is o 90 min by skilled provider in a skilled facility. PCI may also be an option for patients who arrive at a non-PCI hospital and transfer time to a PCI hospital with effective balloon time of o90 min. Transferring patients instead of more immediate fibrinolytic therapy has the combined death rate, nonfatal MI, and stroke rates reduced by 42% when the mean transfer to PCI time is less than 80–122 min. When delays are expected, the physician must consider fibrinolytics if the patient is an appropriate candidate, because delays negate the benefit of PCI over immediate fibrinolytics. The use of fibrinolytics is well established in STEMI patients who have had symptoms for less than 12 h and cannot receive PCI within 90 min of first medical contact and lack contraindications to its use. Proper usage of fibrinolytics has a 47% reduction in mortality when it is provided within the first hour after the onset of symptoms. Absolute contraindications to fibrinolytics include the following: prior intracranial hemorrhage, known structural cerebral vascular lesion, known malignant intracranial neoplasm, ischemic stroke within 3 months (except acute ischemic stroke within 3 h), suspected aortic dissection, active bleeding (excluding menses), and significant head or facial trauma within 3 months. Relative contraindications to fibrinolytics include the following: history of poorly controlled hypertension, severe uncontrolled hypertension (systolic 4 180 mmHg or diastolic 4 110 mmHg), prolonged CPR ( 410 min), major surgery within 3 weeks, noncompressible vascular punctures, streptokinase/anistreplase exposure 4 5 days ago or known allergy, pregnancy, active peptic ulcer, current use of anticoagulants (the higher the international normalized ratio (INR), the higher the risk), prior ischemic stroke 4 3 months ago, dementia, or other known intracranial pathology. Fibrinolytics should be administered within 12 h of the onset of symptoms, but the sooner the fibrinolytic therapy is initiated the better the outcomes. Emergency department physicians should, after evaluation and determination that fibrinolytic therapy is appropriate, administer fibrinolytics within 30 min of emergency department arrival (door-to-needle time). Fibrinolytic therapy is generally not recommended for patients who present symptoms between 12 and 24 h from initial onset, unless continued ischemic pain and continued ST-segment elevation are present. C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 205 5. Adjunctive acute coronary syndrome therapies 5.1. Oxygen Supplemental oxygen should be given to patients with signs of breathlessness, heart failure, shock, or an arterial oxyhemoglobin saturation o94%. There is insufficient evidence to support the use of supplemental oxygen without the signs of hypoxemia or heart failure. 5.2. Nitroglycerin Nitroglycerin has beneficial effects during suspected cases of ACS. It dilates the coronary arteries, peripheral arterial bed, and venous capacitance vessels. However, the benefits of nitroglycerin are limited and there is no conclusive evidence to support routine use in cases of ACS. The administration of nitroglycerin should be carefully considered in cases when administration would exclude the use of other helpful medications (beta blockers), and especially in patients with low blood pressures (o 90 mmHg systolic or Z30 mmHg below baseline). Patients with ischemic discomfort receive up to 3 doses (0.4 mg) over 3–5 min intervals, until chest discomfort is relieved or low blood pressure limits its use. Nitroglycerin may be administered intravenously, orally, or topically. Clinicians should be cautious in cases of known inferior wall STEMI and suspected right ventricular involvement because patients require adequate right ventricle preload. A right-sided ECG should be performed to rule out right ventricular ischemia. Patients who have taken a phosphodiesterase inhibitor within the last 24 h to treat erectile dysfunction should not receive nitroglycerin; the contraindication time is extended to 48 h if tadalafil was taken. 5.3. Analgesia Clinicians should administer analgesics when chest discomfort is unresponsive to nitroglycerine. Morphine is the preferred analgesic. Known side effects are respiratory depression and hypotension. 5.4. Antiplatelet therapy 1. Aspirin—Early administration of aspirin is associated with decreased mortality rates. Aspirin administration in cases of suspected ACS has been shown to be safe, except in cases when there is a known aspirin allergy or active gastrointestinal hemorrhage. Aspirin causes a rapid antiplatelet effect and the inhibition of thromboxane A2 production. It reduces coronary occlusion and recurrent ischemia after fibrinolytic therapy. Aspirin is effective in patients with both STEMI and NSTEMI. The recommended dose is 160–325 mg of nonenteric aspirin. Patients should chew the medication for quicker absorption. Aspirin suppositories of 300 mg can be considered for patients when oral medication is contraindicated. Other nonsteriodal anti-inflammatory medications (NSAIDS) are not recommended in suspected cases of ACS. 2. Thienopyridine—Clopidogrel reduces platelet aggregation by irreversibly inhibiting adenosine diphospate receptors on platelets. Recent studies have documented its efficacy in NSTEMI and STEMI patients. The risks for bleeding are minimal. In patients o75 years of age with ACS, it is reasonable to give patient a 300 mg oral dose. There has been little study on the effects of clopidogrel on patients Z75 years of age. Prasugrel also inhibits platelet aggregation through the same mechanism as clopidogrel. Prasugrel may be associated with a reduction in combined event rate with no benefit in mortality compared to clopidogrel, but there is an increase in major bleeding when prasugrel is administered to NSTEMI patients after angiography and who are about to undergo PCI. 3. Glycoprotein IIb/IIIa inhibitors block the IIb/IIIa receptors that activate fibrinogen. Studies investigating the role of this class of drugs in STEMI have demonstrated a reduction in the 206 C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 composite end point of death, MI, and target revascularization in patients treated with PCI. The use of IIb/IIIa inhibitors are contraindicated in patients receiving fibrinolytics. 5.5. Beta blockers b-Adrenergic receptor blockers have shown to reduce mortality and decrease infarct size with early intravenous usage and can prevent arrhythmias. b-Blockers reduce myocardial workload and oxygen demand by reducing contractility, heart rate, and arterial blood pressure. Contraindications are moderate to severe left ventricle failure, pulmonary edema, bradycardia, hypotension (systolic blood pressure o100 mmHg), signs of poor peripheral perfusion, secondor third-degree heart block, or reactive airway disease. 5.6. Anticoagulation Anticoagulant medications such as unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), or less commonly bivalirudin have been shown to decrease reinfarction following reperfusion therapy and are commonly administered in the spectrum of Acute Coronary Syndrome (ACS) unless contraindicated. Unfractionated heparin (UHF) is an indirect inhibitor of thrombin and can be used as an adjunctive therapy for PCI and fibrinolysis and in combination with aspirin and other platelet inhibitors. It works fast, can be shut off quickly, and can be reversed with protamine sulfate. There are several disadvantages of using UHF: it must be given intravenously, it requires close monitoring of the activated partial thromboplastin time due to unpredictable anticoagulant response in patients, and it can induce thrombocytopenia. UFH is used in patients presenting with STEMI until the coronary anatomy can be determined. Because of these limitations, the use of low-molecular-weight heparins (LMWH) is more common in NSTEMI/UA patients. It is not given in routine STEMI patients because the extent of coronary artery disease is not known and the patient might need a CABG. For in-hospital patients with NSTEMI managed with a planned initial conservative approach, either fondaparinux or enoxaparin are reasonable alternatives to UFH. 5.7. ACE inhibitors/angiotensin II receptor blockers ACE inhibitor therapy improves survival rates in patients with STEMI. The beneficial effects are most apparent in patients with anterior infarctions, pulmonary congestion, or a left ventricle ejection fraction of o40%. Administration of an oral ACE inhibitor is recommended within the first 24 h after onset of symptoms in the absence of hypotension (systolic blood pressure o100 mmHg). Although ACE inhibitors have been shown to reduce long-term mortality in STEMI patients, there is insufficient evidence to support routine use in the prehospital or emergency department setting. ARBs can be used if there is an allergy to an ACE inhibitor. 5.8. Statin therapy HMG coenzyme A reductase inhibitors (statins) have been shown to reduce complications when statin treatment is initiated within a few days of ACS symptoms. Mechanism of action in the acute setting is thought to promote plaque stabilization and reverse endothelial dysfunction. There is little data to suggest this therapy should be initiated in the emergency department. Initiation within 24 h of presentation is recommended in patients with ACS, unless contraindicated. 6. Management of arrhythmias Treatment of ventricular arrhythmias during and after STEMI/NSTEMI continues to be controversial. Recent studies have shown many prophylactic antiarrhythmic drugs to be of C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 207 little benefit and are not recommended for patients with suspected ACS or myocardial infarction in the prehospital or emergency department. Clinicians should aggressively monitor potassium and magnesium levels to maximize prevention of arrhythmias (potassium 44 mEq/L and magnesium 4 2 mEq/L). Fig. 1. ACS algorithm with permission from ACLS advisor by CCS publishing.2 208 C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 7. Risk stratification/disposition The goal of risk stratification is to identify where a patient falls on the acute coronary syndrome spectrum to determine who would benefit from ACS therapies and also avoid unnecessary drug and procedural risks when patients are at low risk for immediate major cardiac events (see Fig. 1). Recognition of STEMI allows prompt transfer to the cardiac catherization lab for emergency PCI treatment. Urgent but not emergent PCI is preferred in NSTEMI and patients deemed to be high risk for ACS such as patients with symptoms of recurrent angina or ischemia at rest despite intensive medical therapies, elevated troponins, new ST-segment depression, signs of symptoms of heart failure, worsening mitral regurgitation, high-risk findings from noninvasive testing, hemodynamic instability, ventricular tachycardia, PCI within 6 months, prior coronary artery bypass graft surgery, high-risk TIMI scores (see Table 2), and reduced left ventricular function. Conservative treatments are generally preferred when patients present with low-risk TIMI scores or patients who are too high risk for PCI morbidity and mortality. The standard of care in a patient presenting with suspected ACS with a normal or nondiagnostic ECG who is deemed low or intermediate risk includes a history and physical examination, a period of observation, serial ECG, and serial measurement of cardiac markers and provocative testing. This can occur entirely in the ED or during an inpatient observation admission. The provocative testing can occur during this time or when appropriate outpatient testing can be arranged within 72 h. Discharging clinicians should consider nonmedical barriers to follow-up care prior to discharge that may require inpatient admission. Provocative testing encompasses the following noninvasive tests for inducible myocardial ischemia or evaluation of coronary arteries. These patients need to be chest pain free and have negative serial cardiac markers.    An exercise stress test is appropriate for patients with an interpretable ECG and who are able to run on a treadmill. Pharmacological stress test with imaging (dobutamine stress echocardiography or vasodilator stress rMPI) is appropriate for patients who are unable to exercise or have an uninterpretable ECG for ischemia (e.g. LBBB, ventricular paced rhythm, LVH with strain pattern, or Digoxin therapy). Multidetector computed tomography (MDCT) angiography has demonstrated a high sensitivity and specificity for CAD and ACS. This is best used with low-risk patients. 8. Summary There has been much progress in the treatment of ACS, but there are still improvements to be made. Early recognition of symptoms and determining where the patient falls on the acute coronary spectrum allows prompt and accurate treatment. Table 2 TIMI risk score for ST-elevation myocardial infarction. Risk factor Points Risk score 30-Day mortality (%) Age Z 75 yr Age 65–74 yr Diabetes or hypertension Systolic BP o 100 mmHg Heart rate 4100/min Killip class II–IV Anterior MI or LBBB Weight o67 kg Time to treatment 4 4 h 3 2 1 3 2 2 1 1 1 0 1 2 3 4 5 6 7 8 48 0.8 1.6 2.2 4.4 7.3 12.4 16.1 23.4 26.8 35.9 Data from Morrow et al.3 Abbreviations: BP ¼ blood pressure; TIMI ¼ Thombolysis in Myocardial Infarction (trial). C. Karras, et al. / Disease-a-Month 59 (2013) 202–209 209 References 1. Boateng S, Sanborn T. Acute myocardial infarction. Dis Mon. 2013;59:83–96. 2. Current clinical strategies publishing (ACLS advisor) [Apple i-device application]. Current clinical strategies; Ver.2013.1. 3. Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation: an intravenous nPA for treatment of infracting myocardium early II trial substudy. Circulation. 2000;102:2031–2037. Suggested reading O’Connor RE, Brady W, Brooks SC, et al. Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(suppl 3): S787–S817.