The Washington Manual ACS.pdf

1 Cardiovascular Emergencies: Acute Coronary Syndrome Xiaowen Wang and Stacey House GENERAL PRINCIPLES Definition • Acute coronary syndrome (ACS) encompasses a spectrum of illnesses from ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI) to unstable angina...

1 Cardiovascular Emergencies: Acute Coronary Syndrome Xiaowen Wang and Stacey House GENERAL PRINCIPLES Definition • Acute coronary syndrome (ACS) encompasses a spectrum of illnesses from ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI) to unstable angina (UA). • STEMI: myocardial ischemia with persistent ST elevation on electrocardiogram (ECG) and release of biomarkers that indicate myocardial necrosis. • NSTEMI: myocardial ischemia without ST elevation and with positive myocardial biomarkers. • UA: patients with ACS but no ST elevation on ECG and no positive myocardial biomarkers that suggest myocardial damage. Epidemiology/Etiology • Chest pain accounts for 9% (or 8–10 million) of non-injurious ED visits annually in the United States. • In the United States, ~1.1 million patients are admitted annually to hospitals with NSTEMI/UA and ~300,000 patients with STEMI. • Traditional risk factors include diabetes, hypertension, tobacco use, hypercholesterolemia, and family history of cardiovascular disease, especially at a young age (<40 years). Pathophysiology • NSTEMI/UA usually happens with sudden imbalance between oxygen consumption and demand of the myocardium. This could be due to obstruction of coronary arteries but also could be due to vasospasm (Prinzmetal angina), myocardial injury due to non-ischemic causes, or increased oxygen demand without coronary obstruction. • In STEMI, obstruction is usually due to sudden plaque rupture and thrombotic occlusion of coronary arteries. DIAGNOSIS • STEMI or new LBBB with signs and symptoms of an acute ischemic event is an indication for immediate reperfusion therapy. Clinical Presentation History • The patient commonly presents with pressure-type chest pain, usually described as “heavy,” “squeezing,” or “crushing.” Pain can radiate to the arms and less commonly to the upper abdomen, back, jaw, and neck. 1 2 Chapter 1 • Cardiovascular Emergencies: Acute Coronary Syndrome • Chest pain can be accompanied by diaphoresis, weakness, light-headedness, dizziness, nausea, vomiting, or anxiety. • Pain usually lasts more than 10 minutes. For chest pain associated with STEMI, it can last more than 30 minutes. • Females, older patients (>75 years of age), patients with diabetes, renal insufficiency, or dementia may have atypical anginal symptoms. • Atypical presentations, such as stabbing/pleural pain, indigestion, epigastric pain, fatigue, or weakness can also represent ACS even in the absence of chest pain. • In unstable angina, symptoms occur at rest, are of new onset, or are more frequent or longer in duration than previous episodes of angina. Physical Examination • Heart sounds may have an S4, a paradoxical splitting of S2, or new mitral regurgitation murmurs. • The patient may have signs of heart failure or other vascular disease. Differential Diagnosis • Cardiovascular: aortic dissection, pericarditis, aortic aneurysm • Pulmonary: pulmonary embolism, pleuritis, pneumonia, pneumothorax • Gastrointestinal: esophageal spasm, gastroesophageal reflux disease (GERD), pancreatitis, peptic ulcer, hepatobiliary disease • Musculoskeletal: costochondritis, cervical radiculopathy • Skin: herpes zoster • Hematologic: sickle cell crisis/acute chest Diagnostic Criteria and Testing • Risk stratification: patients with TIMI score of 0 and negative high-sensitivity troponin after 2 hours of presentation can be ruled out for ACS using accelerated diagnostic protocols. Patients with TIMI score ≥ 3 should be considered for therapies such as low molecular weight heparin (Table 1.1). Laboratories • Troponin: serial troponin I or T levels should be measured at presentation and 3–6 hours after symptom onset. In a patient with initial normal serial troponin levels, additional troponin levels should be obtained beyond 6 hours if there is high clinical suspicion or if the patient has abnormal ECGs. With high-sensitivity troponin assays, patients with chronic elevations in troponin levels will be identified; thus, the serial changes of troponin levels are important. Patients with renal failure and some patients with heart failure are more likely to have chronic elevations of troponin. Delta troponin: It is defined as change in troponin concentration between two assays performed preferably 2 hours apart. A change of more than 20% signifies myocardial infarction in patients with baseline elevation in troponins. • Creatine kinase myocardial isoenzyme (CK-MB): with contemporary troponin assays, CK-MB is not useful for diagnosis of ACS. However, CK-MB is useful to estimate MI size and to screen for new ischemia in the case of a chronically elevated or decreasing troponin. Electrocardiography • A 12-lead ECG should be performed within 10 minutes of patient’s arrival. Diagnosis TABLE 1.1 1. 2. 3. 4. 5. 6. 7. 3 TIMI Risk Score (1 Point for Each) Age >65 y Known coronary artery disease (CAD) (stenosis >50%) 2+ episodes of chest pain in 24 h ST segment or T-wave changes Elevated cardiac biomarkers Acetylsalicylic acid in the last 7 d 3+ CAD risk factors Score interpretation: risk of 14-day all-cause mortality, new or recurrent MI, severe recurrent ischemia requiring revascularization: Score 0–1 = 4.7% Score 2 = 8.3% Score ≥3 = 13.2–40.9% Data from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/nonST elevation MI: a method for prognostication and therapeutic decision making. J Am Med Assoc 2000;284:835–42. • For NSTEMI and UA, ECG may show ST depression, T-wave inversions, or transient ST elevation. ECG can also be normal in 1–6% of patients, especially with occlusions in left circumflex and right coronary artery. • STEMI: ST elevation at the J point in at least two contiguous leads ≥1 mm in all leads other than V2 or V3. In leads V2–V3 elevation the cutoff point is ≥2.5 mm in men below 40 years of age and ≥2 mm in men >40 years of age or ≥1.5 mm in women. In early phases of STEMI, before ST elevation develops, tall T-waves (hyperacute T wave) may be observed. Reciprocal changes in lead I and aVL can appear earlier than ST-elevation in LCX and RCA involvement. New left bundle-branch block (LBBB) with features of acute coronary syndrome is considered as a STEMI equivalent. The ECG can be initially normal or nondiagnostic. If this is the case, the ECG should be repeated at 15–30 minute intervals during the first hour, especially if symptoms recur. ST depression in ≥2 precordial leads (V1–V4) may indicate STEMI of posterior wall. Multilead ST depression with coexistent ST elevation in lead aVR indicates left main or proximal left anterior descending artery occlusion. • Sgarbossa criteria – criteria to evaluate an acute infarction in the presence of a preexisting LBBB or ventricular paced rhythm. The criteria are given a point scale of 0–5 and three or more points is highly specific (with lower sensitivity) for an acute MI. ST segment elevation of 1 mm or more that is in the same direction (concordant) as the QRS complex in any lead –5 points. ST segment depression of 1 mm or more in any lead from V1 to V3 – 3 points. ST segment elevation of 5 mm or more that is discordant (opposite) with the QRS complex –2 points. 4 Chapter 1 • Cardiovascular Emergencies: Acute Coronary Syndrome • Modified Sgarbossa criteria: Discordant ST-elevation of 5 mm has been replaced by discordant ST/S ratio of ≤-0.25. The modified Sgarbossa criteria is more sensitive than Sgarbossa criteria for STEMI. Imaging • There is no radiographic study that is specific for diagnosing ACS. • Echocardiogram: can help to identify any regional wall motion abnormalities. Diagnostic Procedures • Coronary CT angiography: in patients who are low risk, coronary CT angiography can be more cost-effective and achieve more rapid diagnosis than stress myocardial perfusion imaging. • Stress test: for patients with possible ACS but normal ECG and serial cardiac markers, it is reasonable to have the patient undergo stress testing (treadmill ECG, stress echocardiography, or stress myocardial perfusion imaging) before discharge or within 72 hours after discharge. T R E AT M E N T • Treatment of STEMI and NSTEMI/UA is on similar lines except for the use of thrombolytics. Medications • Oxygen (if saturation <90%) • Antiplatelets Aspirin 325 mg to be chewed immediately on diagnosis. In addition to aspirin, administer one of the following P2Y12 receptor antagonists: QQ Clopidogrel: initial loading dose of 300 mg (if PCI is not planned) or 600 mg (if PCI is planned). Patients above 75 years should receive 75 mg/day without loading dose. QQ Prasugrel: initial loading dose of 60 mg. Avoid in patients with a history of transient ischemic attack or stroke; those above 75 years of age or those who weigh <60 kg. QQ Ticagrelor: initial loading dose of 180 mg. • Nitrates can reduce LV preload and increase blood flow to coronary arteries. They should be avoided in patients with hypotension, marked tachycardia or bradycardia, RV infarction, or phosphodiesterase -5 inhibitor use within 24–48 hours. • Morphine has potential beneficial effects by providing analgesic and anxiolytic effects, causing venodilation and modest reduction in heart rate. However, there are observational studies that have demonstrated increased adverse events in patients with ACS and acute decompensated heart failure. • Thrombolytics (fibrinolytics): Recombinant tissue plasminogen activator (rtPA or alteplase), tenecteplase, reteplase. Streptokinase and urokinase can be used if rtPA is not available. Initiate fibrinolytic therapy within 30 minutes (door-to-needle time or first medical contact-to-needle time). Indicated if primary PCI cannot be performed. Useful in STEMI patients with time to therapy 12 hours or less. Also, in presence of LBBB when it suggests acute MI (see above). Treatment 5 Streptokinase is used in a dose of 1.5 million units as an infusion over a period of 1 hour. In patients >65 kg, rtPA is given in a dose of 15 mg bolus followed by 50 mg over 30 minutes and 35 mg over the next 60 minutes. For patients <65 kg, dose is 15 mg bolus; then 0.75 mg/kg over 30 minutes and 0.5 mg/kg over the next 60 minutes. Signs of re-perfusion: QQ Sudden relief of chest pain. QQ Reduction by 50% of the initial ST-segment elevation within 60–90 minutes of fibrinolytic therapy. QQ Onset of re-perfusion arrhythmias (mainly accelerated idioventricular rhythm and frequent ventricular ectopics). QQ Early peaking of cardiac enzymes. Major contraindications include active bleeding (except menses), severe uncontrolled hypertension, history of hemorrhagic stroke, ischemic stroke within 3 months (except for acute ischemic stroke within 3–4.5 hours), suspected aortic dissection, known intracranial aneurysm or AV malformation, intracranial/ spinal surgery within last 3 months and significant cranial/spinal trauma in last 3 months. Also contraindicated in NSTEMI/UA. • Anticoagulants are required in patients receiving thrombolysis particularly with rt-PA or tenecteplase. Enoxaparin: 1 mg/kg subcutaneous every 12 hours or 1 mg/kg subcutaneous daily for patients with creatinine clearance <30 mL/min. Bivalirudin: 0.1 mg/kg loading dose followed by 0.25 mg/kg per hour. Fondaparinux: 2.5 mg subcutaneous daily (avoid if patient is likely to undergo primary PCI). Unfractionated heparin: loading dose of 60 IU/kg (maximum of 4000 IU) with initial infusion of 12 IU/kg/h (maximum of 1000 IU/h), adjusted to attain the activated partial thromboplastin time at 1.5–2 times control. Argatroban: used in patients with heparin-induced thrombocytopenia, with initial dose of 2 mcg/kg/min. • Beta-blockers can be initiated in the first 24 hours in STEMI patients who do not have contraindications (heart failure, low output state, cardiogenic shock, PR > 0.24 seconds, second- or third-degree heart block, active asthma/reactive airway disease). • Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) should be initiated within 24 hours in STEMI patients with heart failure, anterior infarction, or EF ≤ 0.4 unless contraindicated. ARBs should be given to patients who are intolerant of ACE inhibitors. • Statins (e.g., atorvastatin 40–80 mg) is initiated as early as possible but within 24 hours after hospital admission. Other Nonpharmacologic Therapies • Primary percutaneous coronary intervention (PCI) STEMI: QQ PCI-capable hospital: if patient is initially seen at a PCI-capable hospital, patient should be sent to the cath lab for primary PCI. The time between first medical contact (FMC) and device time should be within 90 minutes. 6 Chapter 1 • Cardiovascular Emergencies: Acute Coronary Syndrome QQ Non–PCI-capable hospital: the patient should be transferred to PCI-capable facility if the FMC to balloon time is expected to be <120 minutes. If FMC to balloon time is expected to be over 120 minutes, patients should be given fibrinolytic agent within 30 minutes of arrival, assuming no contraindications for fibrinolytic therapy. The patient should still be urgently transferred to PCI-capable facility if the patient develops evidence of failed reperfusion or re-occlusion. After thrombolysis, patients should still be transferred within 3–24 hours for angiography and revascularization as part of an invasive strategy. QQ For a patient with STEMI and cardiogenic shock or acute severe heart failure, primary PCI should still be performed. NSTEMI/UA: a patient who has failed medical therapy, has objective evidence of ischemia, or is very high risk should undergo early invasive testing (within 24 hours). S P E C I A L C O N S I D E R AT I O N S Disposition • For a low-risk patient (TIMI score of 0, normal ECG, normal high-sensitivity troponin at 0 and 2 hours), a 2-hour accelerated diagnostic protocol can be used if the patient has appropriate outpatient follow-up. The HEART score (Table 1.2) predicts adverse cardiac events, and low-risk patients with a score 0–3 have 1–1.7% risk of major adverse events at 6 weeks from incident. It is reasonable to discharge the patient with daily aspirin, short-acting nitroglycerin, with instructions of activity levels and appropriate outpatient follow-up for further testing. TABLE 1.2 HEART Score for Chest Pain Patients Score History Highly suspicious Moderately suspicious Slightly suspicious 2 1 0 ECG Significant ST depression Nonspecific repolarization disturbance Normal 2 1 0 Age ≤65 y 45–65 y <45 y 2 1 0 Risk factors ≥3 risk factors or history of atherosclerotic disease 1 or 2 risk factors No risk factors known 2 1 0 Troponin >2 × normal limit 1–2 × normal limit ≤normal limit 2 1 0 Total 0–3: 1.0–1.7% risk of adverse cardiac event. Patients can be discharged with follow-up. 4–6: 20.3% risk of adverse cardiac event. Patients should be admitted to the hospital for trending of troponin and provocative testing. ≥7: 72.7% risk of adverse cardiac event, suggesting early invasive measures with these patients and close coordination with inpatient cardiology. From Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Neth Heart J 2008;16(6):191–6, with permission. Special Considerations 7 For a patient with possible ACS but normal serial ECGs and cardiac troponins, a stress test should be performed before discharge or within 72 hours of discharge. For a patient with NSTEMI/UA and patients with recurrent symptoms, positive troponin, or ischemic ECG changes, admission is warranted. Patients with STEMI, continuing angina, hemodynamic instability, persistently uncontrolled arrhythmias, or large MI should be admitted to coronary care unit and for reperfusion therapy. Complications • Cardiac arrhythmias • Cardiogenic shock • Right ventricular infarction It leads to reduced right ventricular stroke volume producing hypotension, raised jugular venous pressure, and clear lungs on auscultation. Volume expansion is the initial treatment of choice for hemodynamically significant right ventricular infarction. Avoid diuretics, ACE inhibitors and nitrates. These patients should be routinely considered for re-perfusion therapy (fibrinolysis or PCI). SUGGESTED READINGS Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:e344–426. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018; 39:119–77. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61:e78–140. Pitts SR, Niska RW, Xu J, Burt CW. National Hospital Ambulatory Medical Care Survey: 2006 Emergency Department Summary. National Health Statistics Reports; No. 7. Hyattsville, MD: National Center for Health Statistics, 2008. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996;334:481. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Neth Heart J 2008;16(6):191–6. Smith SW, Dodd KW, Henry TD, et.al. Diagnosis of ST-elevation Myocardial Infarction in the presence of left bundle branch block using the ST elevation to S wave ratio in a modified Sgarbossa rule. Ann Emerg Med 2012;60:766–76. Tabas JA, Rodriguez RM, Seligman HK, Goldschlager NF. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a metaanalysis. Ann Emerg Med 2008;52:329.