Topic Editor: Becky Box, MBBS
Review Date: 11/24/2012
Definition 
Acute Coronary Syndrome (ACS) includes aspectrum of coronary artery disease(CAD) in which blood supply to the myocardium is compromised. The degree of myocardial ischemia determines the extent of myocardial damage and the severity of disease. The spectrum of disease includes unstable angina (UA), ST-elevation myocardial infarction (STEMI),and non-STEMI (NSTEMI).
Although, the underlying etiology, investigations and basic management of these clinical entities is similar, paramount importance is placed on differentiating between them in order to identify high risk patients, including those requiring prompt revascularization.
Description
- The underlying pathophysiological substrate that is responsible for causing the clinical spectrum of ACS is the development of atherosclerotic plaque rupture. Plaque rupture starts a process of platelet aggregation which leads to thrombus formation, with or without embolization, leading to partial or complete occlusion of coronary arteries
- The clinical presentation of patients with ACS varies extensively with typical symptoms including progressive or sudden onset chest pain, exertional dyspnoea, diaphoresis, pre-syncope or palpitations. Atypical presentations may include syncope, fatigue, lethargy, indigestion, nausea/vomiting, epigastric/thoracic or pleuritic chest pain, or even silent (asymptomatic) myocardial infarctions (MI)
- Myocardial infarction presents without chest pain in 42% of women and 31% of men. Presentation without chest pain is associated with higher mortality. Painless presentations are less common in the young (In age <45 years, 18.5% of females and 13% of males) than the elderly (>75 years had 50% of both genders)
- Chest pain syndromes are the second most common presentation to the emergency department, but only 10-15% of these patients are eventually diagnosed with ACS.Results from the Framingham heart study found that upto 50% of patients diagnosed with MI experienced either silent ischemia or presented with atypical symptoms
- Primary evaluation of patients with suspected ACS requires acquisition of a detailed history, along with investigation of risk factors, physical examination, an electrocardiogram (ECG), and cardiac biomarkers. Analysis of the above information enables the treating physician to risk stratify the patient and determine those patients at low, intermediate and high risk for ACS
- Risk stratification assists in identifying patients that require both invasive/non-invasive inpatient diagnostic testing and management versus patients who can be safely managed in the community with outpatient investigations
- Prompt management of ACS depends on features of the presenting ECG, especially the presence or absence of ST elevation
Epidemiology
Incidence/Prevalence
- CAD is currently the most common cause of death in developed countries among both genders and is expected to also become the most common cause of death in emerging countries within the next ten years
- The annual incidence varies between countries, but is documented at approximately 3 per 1000 inhabitants
- American Heart Association (AHA) reports a conservative estimate of 683,000ACS discharges from US hospitals in 2009, although the figure may be as high as 1,190,000 unique hospitalizations whensecondary discharge diagnoses are included
- Australian data from 2010 showed that 17% of all deaths occurred from ACS
Age
- Risk becomes substantial in men aged>45 years, and women aged >55 years
- The prevalence of risk factors for ACS varies with age. The predominant risk factors in younger patients include obesity, smoking and family history, whereas elderly patients have greater incidence of diabetes, hypertension or prior history of CAD
Gender
- Men have a higher risk than women at any given age
- Cardiac mortality in men is declining, but in women the rate has remained constant
Genetics
- Inflammatory mechanisms play a crucial role in the development of atherosclerotic plaques
- Recent studies of younger patients with ACS indicate that polymorphisms exist in expression and alleles of particular inflammatory proteinswithin this population
- Further studies are required to establish a firm link between these genetic polymorphisms and ACS
Risk factors
- Anemia
- Cigarette smoking
- Depression/Social isolation
- Diabetes and metabolic syndromeFamily history of coronary heart disease: Patients with a first-degree male/female relative who developed CAD<55 or <65, respectively, are at increased risk
- High levels of serum cholesterol [primarily Low Density Lipoprotein (LDL)] cholesterol, and less significantly, increased triglyceride (TG) levels
- Hypertension
- Lowlevels of High Density Lipoprotein (HDL) cholesterol
- Obesity
- Old age
- Male gender
- Sedentary lifestyle
- Stress
Etiology
- ACS depicts a lifethreatening presentation of atherosclerosis. Acute plaque rupture leads to thrombosis, with or without vasoconstriction, resulting in a sudden, critical reduction of blood flow
- Endothelial dysfunction plays a pivotal role in the initiation and progression/rupture of the atherosclerotic plaques. Factors that impair endothelial dysfunctioninclude, but are not limited to, smoking, hypercholesterolemia, hypertension and diabetes. Endothelial dysfunction leads to excess production of endothelin 1 and reduced availability of nitric oxide
- Endothelial dysfunction results in impaired vascular hemostasis with increased expression of cell adhesionmolecules and production of pro-thrombotic substances. The end result is platelet aggregation, adhesion and formation of an intracoronary thrombus
- Both the risk of plaque rupture and the degree of thrombus formation depend on multiple factors including: content of the plaque itself (lipid and tissue factor); degree of inflammation and blood flow at the site and also the patient's balance of pro-thrombotic/anti-thrombotic mediators. It is this interplay, between endothelial properties, inflammatory proteins and thrombogenicity which determine the presence and severity of ACS.
- Autopsy findings have established the etiology of coronary artery occlusion in fatal MIs to be 75% from acute plaque rupture and 25% due to endothelial erosion
- A less common cause for ACS occurs when a patient has a high-grade, fixed coronary obstruction without the ability to increase the myocardial oxygen/nutritional supply at times of increased physiological demands. This is more common in patients with unstable angina.
- Uncommon etiologies of ACS may include arteritis, traumatic injury, dissection, thromboembolism, congenital abnormalities, cocaine or amphetamine use, or complications following cardiac catheterization
[Outline]
History
- The classic symptoms of ACS are central chest pain orleft arm pain/discomfort. The nerves responsible for mediating chest pain are a part of the cardiac plexus (inferior cervical cardiac nerve), consequently the pain can be localized to anywhere within the C8-T10 dermatome. This includes anywhere from the angle of the jaw/nape of neck down to the umbilicus and across the entire precordium, including the medial aspectof the upper arm/forearm. It is critically important that clinicians understand that chest pain is often absent in ACS
- Ischemic chest pain is typically described as tight, pressing or band like that is poorly localized; however, any discomfort of any description in the chest, arms or upper abdomen may be due to cardiac ischemia
- The duration of the painmay relate to the duration of ischemia. However, the severity of the pain in no way relates to the degree of ischemia or infarction. There is no relationship with severity of pain an degree of myocardial ischemia/infarction
- Patients with stable angina report pain with exertion only, whereas in unstable anginapain may occur at rest
- Additional symptoms can include dyspnoea, diaphoresis, palpitations, nausea, vomiting, and lightheadedness
- Of note, at least 20% of MIs occur without significant pain anywhere
- Myocardial infarction presents without chest pain in 42% of women and 31% of men. Presentation without chest pain is associated with higher mortality. Painless presentations are less common in the young (In age <45 years, 18.5% of females and 13% of males) than the elderly (>75 years had 50% of both genders)
- Referred pain from myocardial ischemia may occur in the arm, neck, back, jaw or epigastric area
- Atypical presentations are more likely among women and elderly patients
- Atypical symptomsthat may not be recognized as ACSincludeshortness of breath, fatigue, lethargy, indigestion, epigastric or back pain,abdominal bloatingand anxiety
- The pain itself can be also be atypical in nature, described as tingling, burning, pleuritic,or stabbing, particularly in women
- Ischemia can occur with no obvious signs or symptoms("silent ischemia" or "silent MI"), occurring more commonly in the elderly and diabetic population
Physical findings on examination
- Physical examination of patients with ACS is often unremarkable
- Physical findings which may give evidence of underlying atherosclerosis include:
- Signs of peripheral vascular disease: poor peripheral pulses, smooth shiny skin, hair loss on extremities and non-healing ulcers
- Nicotine staining on finger tips
- Physical findings which may indicate a large area of ischemia with subsequent cardiac pump failure include:
- Diaphoresis
- Hypotension
- Peripheral vasoconstriction with cold/clammy skin
- Third-heart sound (S3 gallop), and possibly a fourth heart sound
- Jugular venous distension
- Pulmonary edema with coarse crepitationson lung auscultation
- Sinus tachycardia
- Physical findings which may help to differentiate alternate causes for chest pain include:
- Aortic dissection-Unequal pulses or new diastolic murmur (Aortic regurgitation)
- Musculoskeletal pain-Reproducible chest wall pain with particular movements or on palpation of thoracic facet joints. Note that a small percent of patients with ACS have chest wall tenderness, so its presence does not rule out ACS
- Pericarditis-pericardial friction rub
- Epigastric pain-pain reproducible in epigastric region and on stooping/bending forward
[Outline]
Blood test findings
- Complete blood count (CBC): To evaluate for anemia as a secondary cause for ACS, and also to evaluate for thrombocytopenia, which can be a contraindication for thrombolysis and hepain/heparinoid use
- Basic metabolic panel: Serum creatinine, and electrolytes. Elevation in creatinine may be first sign of acute renal failure secondary to pump failure
- Where indicated, lipase, liver enzymes and/or magnesium level may be useful
- B-natriuretic peptide (BNP), N-terminal (NT-ProBNP): Elevated levels may be associated with an increased mortality risk in NSTEMI patients
- Determination of serum cardiac markers plays a vital role in the diagnosis of acute MI:
Troponin I and Troponin T: - Preferred markers due to sensitivity to myocardial injury
- Both Troponin I and T increase within 4-6hrs of acute injury
- Troponin I elevated for 4-7 days; Troponin T elevated for 10-14 days
- May not detect re-infarction in patients with acute MI
- Typically in patients being investigated for ACS, cardiac enzymes are measured on arrival in the Emergency department and again in 6-12 hours. Some early rule out protocols with high sensitivity troponin obtain initial troponin and repeat in 2 hours from the initial test
- Recent development of high-sensitivity assays, with a 10 to 100 fold increase in the lower limit of detection is reducing the length of stay for serial assays. The negative predictive value for MI on admission with a negative high-sensitivity troponin is 95%, which approaches 100% when a serial measurement is taken at just 2-3 hours after the first level
- These markers cannot be relied on in isolation as patients with unstable angina may have normal cardiac markers on presentation but are still at a high risk of a future cardiac event
- It is important to note that elevated troponin levels can occur in some chronic disease states including; congestive cardiac failure, and chronic renal failure, and can elevate in acute conditions such as sepsis and acute pulmonary embolism
CK-MB
- This test may be reasonable alternative in the rare situation where troponin is unavailable. Unfortunately, it is not as sensitive as a troponin level.
- Rises within 4-6 hours of acute MI and peaks within 12-24 hours
- Return to baseline occurs within a couple of days, allowing serial measurements to detect reinfarction.
- Two consecutive levels of CK-MB greater than the 99th percentile are indicative of acute MI
Myoglobin
- Though not cardiospecific, serum myoglobin can be elevated as early as two hours following onset of myocardial necrosis
Radiographic findings
- Chest x-ray: Usually normal, but may show cardiomegaly, pulmonary edema/congestion or may identify other etiologies of chest pain such as pneumonia or pneumothorax to aid evaluating chest pain
- Echocardiogram: Is useful in a range of clinical scenarios including;
- Risk assessment assessing LV wall function and in stress testing for changes in wall function
- To assess degree of abnormal myocardial wall motion and ejection fraction in the post-infarction period and to optimise medical therapy based on these results
- To assess a patient with acute deterioration post MI to identify complications including valvular rupture/dysfunction, LV wall aneurysm or extension of infarction
- Myocardial Perfusion Scan (using technetium Tc99 / sestamibi)
- Radionuclide taken up by the myocardium in varying amounts depending on perfusion
- Allows assessment of perfusion during symptomatic episodes to rule out myocardial ischemia
- CT (computed tomography) coronary angiogram
- A 64-slice CT coronary angiography can be a valuable non-invasive diagnostic technique for detection of coronary artery stenosis (100% sensitivity, 75% specificity) as well as non-obstructive atherosclerotic plaques
- Recent studies suggest that CTCA will be a useful tool to exclude coronary artery disease in low to intermediate risk patients (accounting for 50-70% of presentations with possible ACS). One study showed a 50% improvement in discharge rates from the emergency department when using CTCA as a risk stratification tool
Other diagnostic test findings
- Electrocardiogram (ECG): The AHA and American College of Cardiology (ACC) recommend a 12-lead ECG in patients with suspected ACS within 10 minutes of ED arrival, and results interpreted by an experienced physician
- The ECG is valuable both to support the clinical diagnosis and also to use as part of risk stratification for the patient
- ECG findings are more likely to be useful when obtained in patients with ongoing chest pain, with serial ECGs able to identify dynamic changes in perfusion
- ECG findings can help differentiate between myocardial ischemia, injury, and STEMI
- ECG can localize the affected area in many cases, and also assess related conduction abnormalities
- ECG findings in unstable angina/NSTEMI include:
- ST segment depression or transient ST segment elevation
- ST segment depression may resolve when ischemia or pain resolves, however T-wave inversion often persists for days to weeks
- T-wave inversion alone is sensitive for ischemia but lacks specificity
- ECG findings in MI include:
- Hyperacute T waves - seen within minutes of onset
- ST segment elevation - "current of irreversible injury"
- Deep Q waves - occurs hours to days after injury, and signifies myocardial cell death
- T-wave inversion - lasts days to weeks
- New Left bundle branch block may be the presenting ECG finding in acute MI and is managed identically to a STEMI
- Abnormal Q waves occurring on ECG often indicates previous MI
- The site of myocardial infarction is defined as:
- Anteroseptal: V1-V3
- Anterolateral: V1-V6
- Inferior: II, III, aVF
- Lateral: I, aVL, V4-V6
- Right ventricular: RV4, RV5 (right-sided ECG)
- Posterior wall: Upright T waves in V1, V8/V9, R/S ratio >1 in V1/V2 (Posterior ECG)
- Limitations of the ECG include the inability to adequately represent the posterior, lateral and apical walls of the left ventricle. In addition, a normal ECG does not exclude ACS
- Right sided and posterior leads can be taken to give better view of poorly represented areas of myocardium
- Cardiac angiography:
- Early coronary angiography and intervention for NSTEMI acute coronary syndromes (NSTE-ACS) is associated with a lower risk of ischemia recurrence and shorter hospital stays
- Angiography with glycoprotein IIb/IIIa inhibition recommended in high-risk ACS patients without persistent ST elevation
- Indications for immediate cardiac catheterization:
- Cardiogenic shock
- Intractable angina (despite medication)
- Severe pulmonary edema or right ventricular (RV) infarction
[Outline]
General treatment items
- Immediate identification of patients with either unstable angina/NSTEMI versus STEMI is required to direct initial management of the patient. STEMI patients require either urgent invasive catheterization or thrombolysis depending on access to invasive management. Expedient transfer of the patient, either for primary percutaneous intervention or post-thrombolysis to a facility with catheterization facilities is recommended
- Initial assessment should identify those patients with ACS and signs of hemodynamic instability or cardiogenic shock. In this case, treatment will require acute resuscitation and management of failure. This may require non-invasive ventilation or inotrope administration depending on clinical findings
- Bed rest is recommended for all patients to reduce myocardial work load
- Patients with persistent pain or evidence of dynamic ECG changes or arrhythmia require continuous ECG monitoring
- Recent evidence suggests supplemental oxygen should only be administered in cases of low SpO2 (93%) and in such cases, only enough oxygen to maintain 93-94% is recommended. Hyperoxia may worsen cardiac outcomes
- Supplemental oxygen is however recommended in cases of cardiogenic shock (based on expert opinion)
- Medical treatment involves a multifaceted approach including; analgesia, anti-platelet therapy, anti-ischemic therapy, anti-coagulant therapy, optimization of cardiac function in all patients, along with reperfusion therapy in patients with STEMI
ANTI-PLATELET THERAPY
- All patients presenting with suspected ACS without contra-indications should be treated with immediate administration of 300-325 mg of aspirin. Studies of aspirin versus placebo have shown a 50% reduction in mortality rate in patients presenting with ACS that receive aspirin. A daily dose between 75-162 mg is recommended as long-term secondary prevention
- The 2012 ACCF/AHA guidelines recommend clopidogrel plus aspirin in patients with unstable angina/NSTEMI. Clopidogrel is given as a 300-600mg loading dose, followed by 75mg daily.
- Prasugrel and ticagrelor are considered suitable alternatives to clopidogrel in all patients with unstable angina/NSTEMI, especially those undergoing planned PCI
- The TRITON-TIMI 38 study demonstrated a greater benefit of prasugrel in ACS patients with a high risk for stent thrombosis, those with longer stents or bifurcated stents, renal dysfunction, and/or diabetes. However, prasugrel has been linked with increased risk of bleeding in certain patient populations
- The PLATO trial demonstrated a lower risk of ischemic events and mortality with ticagrelor vs clopidogrel, but with a cost of slightly increased minor bleeding risk
- Patients with UA/NSTEMI that are high risk, or those with persistent chest pain despite maximum medical therapy, should be managed with intravenous glycoprotein IIb/IIIa inhibitors. Percutaneous coronary intervention should be considered at this stage if the patient is for invasive management
- Routine early use of GP IIb/IIIa inhibitors has been linked to an increased risk of non-life-threatening bleeding
- Abciximab is the preferred glycoprotein IIb/IIIa inhibitor in patients scheduled for immediate angiography and PCI; IV eptifibatide or tirofiban may be considered for other cases
ANALGESIA
- Although morphine has been traditionally used in pain management for ACS, the CRUSADE study demonstrated that use of morphine either alone or in combination with nitrates in NSTEMI patients could lead to higher mortality
- Current guidelines continue to recommend use of morphine in patients with pain refractory to nitrates
- Fentanyl, which has minimal vasoactivity can be used as an alternative to morphine and is particularly useful if hypotension is a concern
- The primary goal is to maximize use of nitrates and add non-vasoactive narcotics as needed
ANTI-ISCHAEMIC THERAPY
- Nitroglycerin (NTG) is the cornerstone of anti-ischemic therapy. NTG acts on collateral vessels and causes venous and arterial dilation, which reduces both preload and afterload and ultimately decreases myocardial oxygen demand. Key aspects relating to use of NTG include:
- Taken sublingually every 3-5 minutes until the pain is resolved
- Contraindicated in hypotension or when sildenafil or similar agents have been taken within the previous 24-72hrs
- Caution in patients with evidence hypertrophic cardiomyopathy
- Extreme caution if right sided infarction present (these patients are often extremely dependent on preload, and NTG can often result in severe hypotension in these patients)
- Serial blood pressure measurements should be taken when administering NTG
- beta blockers reduce pain and area of infarct by decreasing contractility, heart rate, blood pressure, and oxygen requirement, and by increasing perfusion time.
- B-blockers should be commenced within 24 hours of admission and continued at time of discharge
- Intravenous B-blockers may be used in patients with hypertension or persistent tachycardia or SVT
- B-blockers should not be administered acutely in patients with cardiogenic shock or evidence of heart failure. Contraindications for use include heart block, asthma or hypotension
- Calcium channel blockers, dihydropiridones (i.e. verapamil or diltiazem) should be used as they slow conduction through AV node as well as causing arteriolar vasodilatation. They are recommended for use in 3 specific groups of patients:
- Patients with persistent angina despite maximum therapy with NTG and B-blockers
- Patients with contra-indications to beta-blockers
- Patients with Prinzmetal variant angina
ANTICOAGULATION THERAPY
- Current guidelines recommend use of any one of the following four agents for use as early as possible following presentation of patients with UA/NSTEMI:
- Unfractionated heparin (UFH)
- Enoxaparin (LMWH)
- Fondaparinux (Indirect Factor Xa inhibitor)
- Bivalirudin (Direct Factor Xa inhibitor)
- 2007 ACC/AHA guidelines give a class IIa recommendation for use of enoxaparin or fondaparinux over UFH in patients who will be treated conservatively. Fondaparinux has a class I recommendation for use in patients who are selected for conservative management and are at increased risk of bleeding. Fondaparinux has ~ 50% less anti-coagulant effect than LMWH subsequently, if used inpatient undergoing PCI, an addition dose of heparin should be given to reduce the increased thrombogenic risk at time of catherization
- Bilvalirudin is currently only approved for use when patient is undergoing elective or urgent PCI. It has been shown to have a significantly reduced bleeding risk when compared with Heparin in the REPLACE-2 trial
OPTIMISATION OF CARDIAC FUNCTION
- Statins should be prescribed in all patients with ACS regardless of their LDL cholesterol levels. If LDL level is > 100 mg/dL (2.6 mmol/L), therapy should be intensified to reduce levels below this. Several large scale studies have shown a significant improvement in long-term mortality in patients managed with statins
- Inhibitors of RAS (renin-angiotensin system) are currently recommended for use within the first 24hrs of presentation. According to 2007 ACC/AHA guidelines, this recommendation has level I evidence for all patients with pulmonary congestion or LVEF 40% and level IIa evidence for all other patients. ACE inhibitors are first line, but angiotensin II receptor blockers can be used in patients who do not tolerate ACE inhibitors
REPERFUSION THERAPY
- Reperfusion therapy
- Reperfusion therapy: Reperfusion aims at early reinstatement of myocardial blood flow in patients with acute STEMI, through fibrinolytic therapy or PCI
- Per ACCF/AHA guidelines, PCI is the preferred reperfusion method (class IA recommendation), to be performed within 90 minutes of first medical contact
- Fibrinolysis is an alternative to primary PCI (class 1B recommendation), if the probability of initiating PCI within 90 minutes is unlikely, the emergency physician should initiate fibrinolysis within 30 minutes of presentation to hospital, and transfer the patient to a PCI capable facility as soon as possible. The most commonly used fibrinolytic agents include alteplase, reteplase, and tenecteplase
- Delayed PCI may be considered in patients with contraindications to fibrinolytic therapy, such as high risk for heart failure, or unconfirmed STEMI diagnosis
- Coronary artery bypass grafting (CABG) is a surgical alternative for ACS, which bypasses the stenosed artery by grafting a healthy artery or vein retrieved from another part of the body
- CABG is recommended as preferred strategy for patients with significant left main disease (>50%) OR with 2 or 3 vessel disease associated with proximal left anterior descending artery disease and abnormal LV function (LVEF 50%)
- The majority of studies have demonstrated reduced risk for MI and mortality with CABG vs PCI. Consideration of co-morbidities and suitability for extensive surgery is taken into account when determining appropriate intervention
Medications indicated with specific doses
Ace Inhibitors
- Benazepril
- Captopril
- Enalapril
- Enalapril [IV]
- Fosinopril
- Lisinopril
- Moexipril
- Perindopril
- Quinapril
- Ramipril
- Trandolapril
Angiotensin Receptor Blockers
- Azilsartan
- Candesartan
- Eprosartan
- Irbesartan
- Losartan
- Olmesartan
- Telmisartan
- Valsartan
Anticoagulants
- Bivalirudin
- Enoxaparin [SC]
- Heparin [IV/SC]
Antiplatelet agents
- Abciximab|
- Clopidogrel
- Eptifibatide
- Prasugrel
- Ticagrelor
- Tirofiban
beta blockers
- Atenolol
- Bisoprolol
- Metoprolol [IV]
- Metoprolol [Oral]
Calcium Channel Blockers
- Diltiazem [Oral]
- Verapamil [Oral]
Nitrates
- Nitroglycerin [IV]
- Nitroglycerin [Sublingual]
Non-steroidal anti-inflammatory (NSAID)
Opioid analgesics
- Fentanyl [IM/IV]
- Morphine [Injectable]
Fibrinolytics
- Alteplase [IV]
- Reteplase [IV]
- Tenecteplase [IV]
Disposition
Admission Criteria
- Patients presenting to hospital for evaluation of possible ACS are risk stratified into low, high and intermediate risk categories
- Low risk patients can be discharged safely followed up with their community Physician within 72hrs. Intermediate risk patients are usually admitted to a short stay unit for serial troponin measurements and further non-invasive testing to exclude or confirm the diagnosis. High risk patients are admitted for further management and investigation
- Intensive care unit monitoring may be indicated in those patients with Unstable angina/NSTEMI, STEMI, or signs of cardiogenic failure/shock
Discharge Criteria- Varies between hospitals, but generally if the patient is categorized as low risk and is unlikely to have ACS on clinical presentation, they can be safely discharged from the emergency department
[Outline]
Prognosis
- Patients with ACS are at significant risk of morbidity and mortality (unstable angina carries a worse outcome than stable angina). In hospital mortality for patient with myocardial infarction were 14.6% for women and 10.3% in men in a 2012 review of over 1 million admissions for MI in the U.S.
- Both the magnitude and number of leads showing ST depression correlates with a greater extent of ischemia and overall a poorer prognosis
- The higher the troponin level, the greater the risk for poor outcome
- 36% of admitted patients with presumed ACS may subsequently be diagnosed with MI. The 30-day and 6-month mortality in patients with ACS with unstable angina is 4.5% and 8.6% respectively
- Poor prognostic indicators for mortality associated with NSTEMI-ACS include
- Dementia
- Diabetes - patients with diabetes and ACS are at ~ 50% higher risk of adverse outcome
- History of heart failure
- History of MI
- Peripheral artery disease
- Renal impairment
Synonyms/Abbreviations
Abbreviations
Acute Coronary Syndrome=ACS
ICD-9-CM
- 410.0 ST-elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI)
- 411.1 Intermediate coronary syndrome
ICD-10-CM
- I20.0 Unstable angina
- I21.11 ST-elevation (STEMI) myocardial infarction involving right coronary artery
- I21.19 ST-elevation (STEMI) myocardial infarction involving other coronary artery of inferior wall
- I21.21 ST-elevation (STEMI) myocardial infarction involving left circumflex coronary artery
- I21.29 ST-elevation (STEMI) myocardial infarction involving other sites
- I21.3 ST-elevation (STEMI) myocardial infarction of unspecified site
- I21.4 Non-ST elevation (NSTEMI) myocardial infarction
[Outline]
