* This is the Professional Version. *
- Symptoms and Signs
- Rehabilitation and Postdischarge Treatment
- Key Points
- Resources In This Article
Overview of Acute Coronary Syndromes (ACS)
(Unstable Angina; Acute MI; Myocardial Infarction)
Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and sudden cardiac death. Symptoms are similar in each of these syndromes (except sudden death) and include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by ECG and the presence or absence of serologic markers. Treatment is antiplatelet drugs, anticoagulants, nitrates, beta-blockers, and, for STEMI, emergency reperfusion via fibrinolytic drugs, percutaneous intervention, or, occasionally, coronary artery bypass graft surgery.
(See also Overview of Coronary Artery Disease.)
Acute coronary syndromes include
These syndromes all involve acute coronary ischemia and are distinguished based on symptoms, ECG findings, and cardiac marker levels. It is helpful to distinguish the syndromes because prognosis and treatment vary.
Unstable angina (acute coronary insufficiency, preinfarction angina, intermediate syndrome) is defined as one or more of the following in patients whose cardiac biomarkers do not meet criteria for MI:
Rest angina that is prolonged (usually > 20 min)
New-onset angina of at least class 3 severity in the Canadian Cardiovascular Society (CCS) classification (see Table: Canadian Cardiovascular Society Classification System of Angina Pectoris)
Increasing angina, ie, previously diagnosed angina that has become distinctly more frequent, more severe, longer in duration, or lower in threshold (eg, increased by ≥ 1 CCS class or to at least CCS class 3)
ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina but they are transient. Of cardiac markers, CK is not elevated but cardiac troponin, particularly when measured using high-sensitivity troponin tests (hs-cTn), may be slightly increased. Unstable angina is clinically unstable and often a prelude to MI or arrhythmias or, less commonly, to sudden death.
Non–ST-segment elevation MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
ST-segment elevation MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin or showing new left bundle branch block. Cardiac markers, troponin I or troponin T, and CK are elevated.
Both types of MI may or may not produce Q waves on the ECG (Q wave MI, non-Q wave MI).
The most common cause of acute coronary syndromes is
Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheromas causing minimal obstruction can rupture and result in thrombosis; in > 50% of cases, pre-event stenosis is <40%. Thus, although the severity of stenosis helps predict symptoms, it does not always predict acute thrombotic events. The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about two thirds of patients; 24 h later, thrombotic obstruction is found in only about 30%. However, in virtually all cases, obstruction lasts long enough to cause tissue necrosis.
Rarer causes of acute coronary syndromes are
Coronary arterial embolism can occur in mitral or aortic stenosis, infective endocarditis, or marantic endocarditis. Cocaine use and other causes of coronary spasm can sometimes result in MI. Spasm-induced MI may occur in normal or atherosclerotic coronary arteries.
Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted.
Ischemic (but not infarcted) tissue has impaired contractility and relaxation, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock; usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Some degree of heart failure occurs in about two thirds of hospitalized patients with acute myocardial infarction. It is termed ischemic cardiomyopathy if low cardiac output and heart failure persist. Ischemia involving the papillary muscle may lead to mitral valve regurgitation. Dysfunctional wall motion can allow mural thrombus formation.
Myocardial infarction is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue. MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria.
Infarction may be transmural or nontransmural. Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG. Nontransmural or subendocardial infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG.
Necrosis of a significant portion of the interventricular septum or ventricular wall may rupture, with dire consequences. A ventricular aneurysm or pseudoaneurysm may form,
Electrical dysfunction can be significant in any form of ACS. Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T abnormalities), arrhythmias, and conduction disturbances. ST-T abnormalities of ischemia include ST-segment depression (often downsloping from the J point), T-wave inversion, ST-segment elevation (often referred to as injury current), and peaked T waves in the hyperacute phase of infarction. Conduction disturbances can reflect damage to the sinus node, the atrioventricular (AV) node, or specialized conduction tissues. Most changes are transient; some are permanent.
Symptoms of ACS depend somewhat on the extent and location of obstruction and are quite variable. Painful stimuli from thoracic organs, including the heart, can cause discomfort described as pressure, tearing, gas with the urge to eructate, indigestion, burning, aching, stabbing, and sometimes sharp needle-like pain. Many patients deny they are having pain and insist it is merely “discomfort.” Except when infarction is massive, recognizing the amount of ischemia by symptoms alone is difficult.
After the acute event, many complications can occur. They usually involve
Electrical dysfunction can be significant in any form of ACS, but usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Other complications of ACS include recurrent ischemia and pericarditis. Pericarditis that occurs 2 to 10 wk after an MI is known as post-MI syndrome or Dressler syndrome.
Serial cardiac markers
Immediate coronary angiography for patients with STEMI or complications (eg, persistent chest pain, hypotension, markedly elevated cardiac markers, unstable arrhythmias)
Delayed angiography (24 to 48 h) for patients with NSTEMI or unstable angina without complications noted above
ACS should be considered in men > 30 yr and women > 40 yr (younger in patients with diabetes) whose main symptom is chest pain or discomfort. Pain must be differentiated from the pain of pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral separation, esophageal spasm, acute aortic dissection, renal calculus, splenic infarction, or various abdominal disorders. In patients with previously diagnosed hiatus hernia, peptic ulcer, or a gallbladder disorder, the clinician must be wary of attributing new symptoms to these disorders. (For approach to diagnosis, see also Chest Pain.)
The approach is the same when any ACS is suspected: initial and serial ECG and serial cardiac marker measurements, which distinguish among unstable angina, NSTEMI, and STEMI. Every emergency department should have a triage system to immediately identify patients with chest pain for rapid assessment and ECG. Pulse oximetry and chest x-ray (particularly to look for mediastinal widening, which suggests aortic dissection) is also done.
ECG is the most important test and should be done within 10 min of presentation. It is the center of the decision pathway because fibrinolytics benefit patients with STEMI but may increase risk for those with NSTEMI. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not for those with NSTEMI.
For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area (see Figure: Acute anterior left ventricular infarction (tracing obtained within a few hours of onset of illness).,).
Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader’s attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI. Serial tracings (obtained every 8 h for 1 day, then daily) showing a gradual evolution toward a stable, more normal pattern or development of abnormal Q waves over a few days (see Figure: Inferior (diaphragmatic) left ventricular infarction (after the first 24 h).) tends to confirm the diagnosis.
Because nontransmural (non–Q wave) infarcts are usually in the subendocardial or midmyocardial layers, they do not produce diagnostic Q waves or distinct ST-segment elevation on the ECG. Instead, they commonly produce only varying degrees of ST-T abnormalities that are less striking, variable, or nonspecific and sometimes difficult to interpret (NSTEMI). If such abnormalities resolve (or worsen) on repeat ECGs, ischemia is very likely. However, when repeat ECGs are unchanged, acute MI is unlikely and, if still suspected clinically, requires other evidence to make the diagnosis. A normal ECG taken when a patient is pain free does not rule out unstable angina; a normal ECG taken during pain, although it does not rule out angina, suggests that the pain is not ischemic.
If right ventricular (RV) infarction is suspected, a 15-lead ECG is usually recorded; additional leads are placed at V4R, and, to detect posterior infarction, V8 and V9.
ECG diagnosis of MI is more difficult when a left bundle branch block configuration is present because it resembles STEMI changes (see Figure: Left bundle branch block.). ST-segment elevation concordant with the QRS complex strongly suggests MI as does > 5-mm ST-segment elevation in at least 2 precordial leads. But generally, any patient with suggestive symptoms and new-onset (or not known to be old) left bundle branch block is treated as for STEMI.
Cardiac markers (serum markers of myocardial cell injury) are
These markers are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and specific and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure Tn levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL).
Previous, less sensitive cTn tests were unlikely to detect Tn except in patients who had an acute cardiac disorder. Thus, a "positive" Tn (ie, above the limit of detection) was very specific. However, the new hs-cTn tests can detect small amounts of Tn in many healthy people. Thus, hs-cTn levels need to be referenced to the normal range, and are defined as "elevated" only when higher than 99% of the reference population. Furthermore, although an elevated troponin level indicates myocardial cell injury, it does not indicate the cause of the damage (although any troponin elevation increases the risk of adverse outcomes in many disorders). In addition to ACS, many other cardiac and non-cardiac disorders can elevate hs-cTn levels (see Table: Causes of Elevated Troponin); not all elevated hs-cTn levels represent MI, and not all myocardial necrosis results from an acute coronary syndrome event even when the etiology is ischemic. However, by detecting lower levels of Tn, hs-cTn assays enable earlier identification of MI than other assays, and have replaced other cardiac marker tests in many centers.
Patients suspected of having an ACS should have an hs-cTn level done on presentation and 3 h later (at 0 and 6 h if using a standard Tn assay).
An hs-cTn level must be interpreted based on the patient's pre-test probability of disease, which is estimated clinically based on:
A high pre-test probability plus an elevated hs-cTn level is highly suggestive of ACS, whereas a low pre-test probability plus a normal hs-cTn is unlikely to represent ACS. Diagnosis is more challenging when test results are discordant with pre-test probability, in which case serial hs-cTn levels often help. A patient with low pre-test probability and an initially slightly elevated hs-cTn that remains stable on repeat testing probably has non-ACS cardiac disease (eg, heart failure, stable coronary artery disease). However, if the repeat level rises significantly (ie, > 20 to 50%) the likelihood of ACS becomes much higher. If a patient with high pre-test probability has a normal hs-cTn level that rises > 50% on repeat, ACS is likely; continued normal levels (often including at 6 h and beyond when suspicion is high) suggest need to pursue an alternate diagnosis.
Causes of Elevated Troponin
Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie, angioplasty, stent placement). When possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute MI (primary PCI). In many tertiary centers, this approach has significantly lowered morbidity and mortality and improved long-term outcomes. Frequently, the infarction is actually aborted when the time from pain to PCI is short (< 3 to 4 h).
Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients with uncomplicated NSTEMI or unstable angina whose symptoms have resolved typically undergo angiography within the first 24 to 48 h of hospitalization to detect lesions that may require treatment.
After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that angiography be done before hospital discharge in STEMI patients with inducible ischemia on stress imaging or an ejection fraction < 40%.
Routine laboratory tests are nondiagnostic but, if obtained, show nonspecific abnormalities compatible with tissue necrosis (eg, increased ESR, moderately elevated WBC count with a shift to the left). A fasting lipid profile should be obtained within the first 24 h for all patients hospitalized with ACS.
Myocardial imaging (see also Cardiac Imaging Tests) is not needed to make the diagnosis if cardiac markers or ECG is positive. However, in patients with MI, bedside echocardiography is invaluable for detecting mechanical complications. Before or shortly after discharge, patients with symptoms suggesting an ACS but nondiagnostic ECGs and normal cardiac markers should have a stress imaging test (radionuclide or echocardiographic imaging with pharmacologic or exercise stress). Imaging abnormalities in such patients indicate increased risk of complications in the next 3 to 6 mo and suggest need for angiography, which should be done before discharge or soon thereafter, with PCI or CABG done as necessary.
Right heart catheterization using a balloon-tipped pulmonary artery catheter can be used to measure right heart, pulmonary artery, and pulmonary artery occlusion pressures and cardiac output. This test is not routinely recommended and should be done only if patients have significant complications (eg, severe heart failure, hypoxia, hypotension) and by doctors experienced with catheter placement and management protocols.
Global risk should be estimated via formal clinical risk scores (Thrombosis in Myocardial Infarction [TIMI], Global Registry of Acute Coronary Events [GRACE], Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy [PURSUIT]) or a combination of the following high-risk features:
Recurrent angina/ischemia at rest or during low-level activity
Worsening mitral regurgitation
High-risk stress test result (test stopped in ≤ 5 min due to symptoms, marked ECG abnormalities, hypotension, or complex ventricular arrhythmias)
Sustained ventricular tachycardia
PCI within past 6 mo
LV ejection fraction < 0.40
Prehospital care: Oxygen, aspirin, nitrates and/or opioids for pain, and triage to an appropriate medical center
Drug treatment: Antiplatelet drugs, antianginal drugs, anticoagulants, and in some cases other drugs
Often, angiography to assess coronary artery anatomy
Often, reperfusion therapy: Fibrinolytics, percutaneous coronary intervention or coronary artery bypass surgery
Post discharge rehabilitation and chronic management of coronary artery disease
Treatment, including drug treatment, is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications. An ACS is a medical emergency; outcome is greatly influenced by rapid diagnosis and treatment.
Treatment occurs simultaneously with diagnosis.
Contributing disorders (eg, anemia, heart failure) are aggressively treated.
Because the chest pain of MI usually subsides within 12 to 24 h, any chest pain that remains or recurs later is investigated. It may indicate such complications as recurrent ischemia, pericarditis, pulmonary embolism, pneumonia, gastritis, or ulcer.
A reliable IV route must be established, oxygen given (typically 2 L by nasal cannula), and continuous single-lead ECG monitoring started. Prehospital interventions by emergency medical personnel—including ECG, chewed aspirin [325 mg], pain management with nitrates or opioids (see Table: Drugs for Coronary Artery Disease*), early thrombolysis when indicated and possible, and triage to the appropriate hospital where primary PCI is available—can reduce risk of mortality and complications. Early diagnostic data and response to treatment can help determine the need for and timing of revascularization when primary percutaneous coronary intervention is not possible.
Drug therapy with antiplatelet drugs, anticoagulants, and other drugs based on reperfusion strategy
Risk-stratify patient and choose a reperfusion strategy (fibrinolytics or cardiac angiography with PCI or CABG for patients with STEMI and cardiac angiography with PCI or CABG for patients with unstable angina or NSTEMI
On arrival to the emergency room, the patient's diagnosis is confirmed. Drug therapy and choice of revascularization depend on the type of acute coronary syndrome as well as the clinical picture (see Figure: Approach to acute coronary syndromes.). Choice of drug therapy is discussed in Drugs for Acute Coronary Syndrome, and choice of reperfusion strategy is further discussed in Revascularization for Acute Coronary Syndromes.
Approach to acute coronary syndromes.
When the diagnosis is unclear, bedside cardiac marker tests can help identify low-risk patients with a suspected ACS (eg, those with initially negative cardiac markers and nondiagnostic ECGs), who can be managed in 24-h observation units or chest pain centers. Higher-risk patients should be admitted to a monitored inpatient unit or coronary care unit (CCU). Several validated tools can help stratify risk. Thrombolysis in MI (TIMI) risk scores may be the most widely used.
Patients with suspected NSTEMI and intermediate or high risk should be admitted to an inpatient care unit or CCU. Those with STEMI should be admitted to a CCU.
Only heart rate and rhythm recorded by single-lead ECG are consistently useful for routine, continuous monitoring. However, some clinicians recommend routine multilead monitoring with continuous ST-segment recording to identify transient, recurrent ST-segment elevations or depressions. Such findings, even in patients without symptoms, suggest ischemia and identify higher-risk patients who may require more aggressive evaluation and treatment.
Qualified nurses can interpret the ECG for arrhythmia and initiate protocols for its treatment. All staff members should know how to do CPR.
The care unit should be a quiet, calm, restful area. Single rooms are preferred; privacy consistent with monitoring should be ensured. Usually, visitors and telephone calls are restricted to family members during the first few days. A wall clock, a calendar, and an outside window help orient the patient and prevent a sense of isolation, as can access to a radio, television, and newspaper.
Bed rest is mandatory for the first 24 h. On day 1, patients without complications (eg, hemodynamic instability, ongoing ischemia), including those in whom reperfusion with fibrinolytics or PCI is successful, can sit in a chair, begin passive exercises, and use a commode. Walking to the bathroom and doing nonstressful paperwork are allowed shortly thereafter. Recent studies have shown that patients with successful, uncomplicated primary PCI for acute MI may be ambulated quickly and be safely discharged in 3 to 4 days.
If reperfusion is not successful or complications are present, patients require longer bed rest, but they (particularly elderly patients) are mobilized as soon as possible. Prolonged bed rest results in rapid physical deconditioning, with development of orthostatic hypotension, decreased work capacity, increased heart rate during exertion, and increased risk of deep venous thrombosis. Prolonged bed rest also intensifies feelings of depression and helplessness.
Anxiety, mood changes, and denial are common. A mild tranquilizer (usually a benzodiazepine) is often given, but many experts believe such drugs are rarely needed.
Reactive depression is common by the 3rd day of illness and is almost universal at some time during recovery. After the acute phase of illness, the most important tasks are often management of depression, rehabilitation, and institution of long-term preventive programs. Overemphasis on bed rest, inactivity, and the seriousness of the disorder reinforces anxiety and depressive tendencies, so patients are encouraged to sit up, get out of bed, and engage in appropriate activities as soon as possible. The effects of the disorder, prognosis, and individualized rehabilitation program should be explained to the patient.
Maintaining normal bowel function with stool softeners (eg, docusate) to prevent straining is important. Urinary retention is common among elderly patients, especially after several days of bed rest or if atropine was given. A catheter may be required but can usually be removed when the patient can stand or sit to void.
Because smoking is prohibited, a hospital stay should be used to encourage smoking cessation. All caregivers should devote considerable effort to making smoking cessation permanent.
Although acutely ill patients have little appetite, tasty food in modest amounts is good for morale. Patients are usually offered a soft diet of 1500 to 1800 kcal/day with sodium reduction to 2 to 3 g. Sodium reduction is not required after the first 2 or 3 days if there is no evidence of heart failure. Patients are given a diet low in cholesterol and saturated fats, which is used to teach healthy eating.
For patients with diabetes and STEMI, intensive glucose control is no longer recommended; guidelines call for an insulin-based regimen to achieve and maintain glucose levels <180 mg/dL while avoiding hypoglycemia.
Patients who did not have coronary angiography during admission, have no high-risk features (eg, heart failure, recurrent angina, VT or VF after 24 h, mechanical complications such as new murmurs, shock), and have an ejection fraction > 40% whether or not they received fibrinolytics usually should have stress testing of some sort before or shortly after discharge (see Table: Functional Evaluation After MI).
Functional Evaluation After MI
Physical activity is gradually increased during the first 3 to 6 wk after discharge. Resumption of sexual activity, often of great concern to the patient and partner, and other moderate physical activities may be encouraged. If good cardiac function is maintained 6 wk after acute MI, most patients can return to all their normal activities. A regular exercise program consistent with lifestyle, age, and cardiac status reduces risk of ischemic events and enhances general well-being.
The acute illness and treatment of ACS should be used to strongly motivate the patient to modify risk factors. Evaluating the patient’s physical and emotional status and discussing them with the patient, advising about lifestyle (eg, smoking, diet, work and play habits, exercise), and aggressively managing risk factors may improve prognosis.
Several drugs clearly reduce mortality risk post-MI and are used unless contraindicated or not tolerated:
Aspirin and other antiplatelet drugs reduce mortality and reinfarction rates in post-MI patients. Enteric-coated aspirin 81 mg once/day is recommended long-term. Data suggest that warfarin with or without aspirin reduces mortality and reinfarction rates.
Beta-blockers are considered standard therapy. Most available beta-blockers (eg, acebutolol, atenolol, metoprolol, propranolol, timolol) reduce post-MI mortality rate by about 25% for at least 7 yr.
ACE inhibitors are also considered standard therapy and are given to all post-MI patients if possible. These drugs may provide long-term cardioprotection by improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not angioedema or renal dysfunction), an angiotensin II receptor blocker may be substituted.
Statins are also standard therapy and are routinely prescribed. Reducing cholesterol levels after MI reduces rates of recurrent ischemic events and mortality in patients with elevated or normal cholesterol levels. Statins appear to benefit post-MI patients regardless of their initial cholesterol level. Post-MI patients whose primary problem is a low HDL level or an elevated triglyceride level may benefit from a fibrate, but evidence of benefit is less clear. A lipid-lowering drug should be continued indefinitely, unless significant adverse effects occur, and dose should be increased to achieve an LDL level of 70 to 80 mg/dL (1.81 to 2.07 mmol/L).
Unstable angina, NSTEMI, and STEMI represent worsening degrees of myocardial ischemia and necrosis; the distinctions help differentiate prognosis and guide treatment.
Diagnosis is based on serial ECG and cardiac marker levels, particularly using new, highly sensitive troponin T tests.
Immediate medical treatment depends on the specific syndrome and patient characteristics but typically involves antiplatelet drugs, anticoagulants, beta-blockers, and nitrates as needed (eg, for chest pain, hypertension, pulmonary edema), and a statin to improve prognosis.
For unstable angina and NSTEMI, do angiography within 24 to 48 h of hospitalization to identify coronary lesions requiring PCI or CABG; fibrinolysis is not helpful.
For STEMI, do emergency PCI when door to balloon-inflation time is < 90 min; do fibrinolysis if such timely PCI is not available.
Following recovery, initiate or continue aspirin and other antiplatelet drugs, beta-blockers, ACE inhibitors, and statins in most cases unless contraindicated.
* This is the Professional Version. *