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Differences between Stable angina & Acute coronary syndrome (Unstable angina, NSTEMI, STEMI) Features Stable Angina Unstable angina Myocardial infarction Site Same Same Retrosternal area, Epigastrium (inferior MI) Onset & Precipitating factor Physical exertion Cold temperatures. Emotions like anger or fear or excitement. Smoking Eating a heavy meal. Using cocaine (promote vasospasm & thrombosis) or amphetamines. At rest or minimal exertion 3-5mins Severe and New onset of chest pain At rest Character Heavy, tight, griping, squeezing, crushing Same More severe than angina Radiation Lower jaw, neck, left arm Alleviating factor unchanged exertional pain lasting 5-15 minutes and relieved by rest or nitroglycerin Sublingual Glyceryl Trinitrate relieve for a few mins Not relieved by rest or nitrate. Only relieved by opiates Timing Short Short, usually a few mins > 30 minutes Associated symptoms No sweating No sweating Mild or No - Sweating, nausea, vomiting,

Differences Btw ACS, Stable Angina

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Summarized table with combination of information from different books.

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Page 1: Differences Btw ACS, Stable Angina

Differences between Stable angina & Acute coronary syndrome (Unstable angina, NSTEMI, STEMI)

Features Stable Angina Unstable angina Myocardial infarction

Site Same Same Retrosternal area,Epigastrium (inferior MI)

Onset&

Precipitating factor

Physical exertionCold temperatures.Emotions like anger or fear or excitement.SmokingEating a heavy meal.Using cocaine (promote vasospasm & thrombosis) or amphetamines.

At rest or minimal exertion 3-5minsSevere and New onset of chest pain

At rest

Character Heavy, tight, griping, squeezing, crushing

Same More severe than angina

Radiation Lower jaw, neck, left arm

Alleviating factor unchanged exertional pain lasting 5-15 minutes and relieved by rest or nitroglycerin

Sublingual Glyceryl Trinitrate relieve for a few mins

Not relieved by rest or nitrate.Only relieved by opiates

Timing Short Short, usually a few mins > 30 minutes

Associated symptoms No sweating No sweatingMild or No anxiety

- Sweating, nausea, vomiting, palpitation

- Anxiety, sense of impending doom

- Collapse/syncope- SOB due to pulmonary

edemaUnderlying pathology

Vessel architecture and

Blood flow

Critical coronary artery stenosis >70% caused by atherosclerotic plaque

Blood flow limited during exertion

Ischemia during

Unstable plaque rupture

Platelet thrombus begins to form and spasm limits blood flow at rest

NSTEMI- Unstable platelet thrombus on ruptured plaque- Transient or incomplete vessel occlusion (lysis occurs)-difference from

STEMI-Platelet thrombus on ruptured atheromatous plaque-Complete vessel occlusion (no

Page 2: Differences Btw ACS, Stable Angina

exercise without acute thrombosis but transient platelet aggregation

UA is that there is myocardial necrosisNon-Q wave/Subendocardial MI

lysis) Q wave/ Transmural MI

Physical findings - Diaphoresis - Tachycardia or

bradycardia - Transient

myocardial dysfunction (eg, systolic blood pressure < 100 mm Hg or overt hypotension,

- elevated jugular venous pressure, dyskinetic apex, reverse splitting of S2, presence of S3 or S4, new or worsening apical systolic murmur, or rales or crackles)

Peripheral arterial occlusive disease (eg, carotid bruit, supraclavicular or femoral bruits, or diminished peripheral pulses or blood pressure)

Anxious, diaphoreticS4 Gallop : myocardial non-compliance due to ischemiaS3 Gallop : severe systolic dysfunctionNew apical systolic murmur of MR : Ischemic papillary muscle dysfunction

Cardiac Enzymes No raised in CE

Mild rise in troponin Rise in serum troponin or CKMB

Typically shows a rise in CE following the sequence ofCKMB (every 6-8 hours during the first

Page 3: Differences Btw ACS, Stable Angina

24 hours)CKMB:CK (2.5/3)Troponin I, TASTLDH

Management Lifestyle modification

LMWH double

antiplatelet

NSTEMI LMWH douple

antiplatelet GPIIb/IIIa

antagonist

STEMI

thrombolysis (streptokinase, alteplase)

primary/percutaneous coronary intervention,

double antiplatelet

Notes: In patient >70 years/ who is diabetic, transplanted heart, female acute MI maybe painless and a/w only vague discomfort, but maybe heralded by sudden onset of dyspnea, pulmonary edema, or ventricular arrhythmias.

Early death in AMI are due to ventricular fibrillation

Process of infarction takes more than 8 hours and most patient present when it is still possible to salvage myocardium and improve outcome

Diagnosis

Diagnosis of acute MI is made by finding at least 2 of the following features:

Typical chest pain > 30 mins Typical ECG findings Elevated cardiac enzyme levels

ST-elevations of 1 mm or more in two contiguous limb leads (high lateral: I, aVL; inferior: II, III, aVF) or 2 mm elevations in the precordial leads (anterior: V1, V2, V3; lateral: V4, V5, V6).

Localizing MI

Location ST Elevations Reciprocal Affected Example

Page 4: Differences Btw ACS, Stable Angina

ST-depressions Artery ECG

Anterior MI V1-V6 none LAD need

Septal MI V1-V3 none LAD need

Inferior MI II, III, aVF I, aVL RCA (80%) orR Cx (20%)

need

Lateral MI I, aVL, V5, V6 II, II, aVF R Cx, LCX need

Posterior MI V7, V8, V9 V1-V3 R Cx need

Right Ventricular MI

V1, V4R I, aVL RCA need

The following laboratory studies are recommended within the first 24 hours in the evaluation of a patient with unstable angina:

Serial cardiac biomarker assays (eg, creatine kinase MB isoenzyme [CK-MB], troponins, C-reactive protein [CRP], and brain natriuretic peptide [BNP])

Complete blood count (CBC) with hemoglobin level Serum chemistry panel (including magnesium and potassium) Lipid panel electrolyes, BUN and creatinine (may effect treatment regimens)

Cardiac markers

Marker Initial Elevation Peak Elevation Return to Baseline

Myoglobin 1-4 h 6-7 h 18-24 h

CK-MB 4-12 h 10-24 h 48-72 h

Cardiac Trop I 3-12 h 10-24 h 3-10 d

Cardiac Trop T

3-12 h 12-48 h 5-14 d

The troponin I is the most sensitive cardiac marker, detectable in serum 3-6 hours after an MI, and its level remains elevated for 14 days.

Other tests that may be used to assess patients include the following:

Creatinine level Exercise testing when patients are stable(either exercise or chemically-induced

exertion to look for EKG changes and/or decreased radionuclide uptake in the ischemic region)

Page 5: Differences Btw ACS, Stable Angina

The following imaging studies may be used to assess patients with suspected unstable angina:

Chest radiography (may show pulmonary edema or other causes of chest pain) Echocardiography (usually after admission to look for regional wall motion

abnormality) Computed tomography angiography Magnetic resonance angiography Single-photon emission computed tomography Magnetic resonance imaging Myocardial perfusion imaging

Management

Obtain intravenous (IV) access, and provide supplemental oxygen. The course of unstable angina is highly variable and potentially life-threatening ; therefore, quickly determine whether the initial treatment approach should use an invasive (surgical management) or a conservative (medical management) strategy.

The following medications are used in the management of unstable angina:

Antiplatelet agents (eg, aspirin and clopidogrel) Lipid-lowering statin agents (eg, simvastatin, atorvastatin, pitavastatin, and

pravastatin) Cardiovascular antiplatelet agents (eg, tirofiban, eptifibatide, and abciximab) Beta blockers (eg, atenolol, metoprolol, esmolol, nadolol, and propranolol) Anticoagulants (eg, heparin) Low-molecular-weight heparins (eg, enoxaparin, dalteparin, and tinzaparin) Thrombin inhibitors (eg, bivalirudin, lepirudin, desirudin, and argatroban) Angina nitrates (eg, nitroglycerin IV) Angiotensin-converting enzyme inhibitors (eg, captopril, lisinopril, enalapril, and

ramipril)

Surgical intervention in unstable angina may include the following:

Cardiac catheterization Revascularization

Those with persistent ST-elevations will need some sort of revascularization procedure - either pharmacological (thrombolytic) or an angioplasty in the cardiac catheterization lab.

Those without ST-elevations should get an angiogram when appropriately as determined by the interventional cardiologist.