The usual cause of an acute coronary syndrome is the rupture of an atherosclerotic plaque

(Phalen and Aehlert, 2006, p. 61)

Acute Coronary Syndrome

Plaque Rupture

Classifications

1.ST-Segment Elevation Myocardial Infarction2. Unstable Angina and Non–ST Elevation Myocardial Infarction3. Stable Ischemic Heart Disease

Acute Coronary Syndrome

Unstable Angina

Cause: Thrombus partially or intermittently

occludes the coronary artery

Diagnostic Findings:ST-segment depression or T-wave

inversionNormal Cardiac Markers

(Overbaugh, 2009, p. 46)

NSTEMI

Cause: Thrombus partially or intermittently

the occludes coronary artery

Diagnostic Findings:ST-segment depression or T-wave

inversionElevated Cardiac biomarkers

(Overbaugh, 2009, p. 46)

Clinical Indicators of Increased Risk in UA/NSTEMI

• CAUSES OF ACUTE CHEST PAIN

• DIAGNOSTIC CONSIDERATIONS

• IMMEDIATE MANAGEMENT

Approach to the Patient with Chest Pain

• Acute chest pain is one of the most common reasons for presentation to the emergency department

• 15% to 25% of patients with acute chest pain actually have ACS

• The diagnosis of ACS is missed in approximately 2% of patients

• Mortality for patients with acute myocardial infarction (MI) who are mistakenly discharged from the ED increases twofold

ACUTE CHEST PAIN

• Myocardial Ischemia or Infarction,

• Pericardial Disease,

• Vascular Disease,

•  Pulmonary Conditions,

•  Gastrointestinal Conditions,

•  Musculoskeletal and Other Causes,

CAUSES OF ACUTE CHEST PAIN

IschemiaMay occur as a result of either or both of the

following:

Demand Ischemia: Increased myocardial O2 demand

(Anemia, hypoxemia, coronary artery narrowing due to a thrombus, vasospasm, or rapid progression of

atherosclerosis)

Supply Ischemia: Reduced myocardial O2 supply(Exercise, smoking, heavy meals, fever, HF,

tachydysrhythmias, OCM, cocaine, amphetamines, emotional stress, hypertension, cold weather, aortic

stenosis, pheochromocytoma, thyrotoxicosis)

Injury

Ischemia prolonged more than just a few minutes results in myocardial injury.

Injured myocardial cells are still alive but will infarct if the ischemia is not quickly corrected

ECG Changes: ST-segment elevation(Injured myocardial cells do not depolarize

completely, remaining electrically more positive than the uninjured areas

surrounding them)

Infarction

A myocardial infarction occurs when blood flow to the heart muscle stops or is suddenly decreased long

enough to cause cell death

Infarcted cells are without function and cannot respond to electrical stimulus or provide any mechanical

function

(Thalen and Aehlert, 2006, p, 67)

ECG Changes: ST-segment elevation, T-wave inversion, abnormal Q waves

• Evaluation of the patient with acute chest pain

• Hemodynamic instability

• A 12-lead electrocardiogram (ECG)

Initial Assessment

• History

• Physical Examination

• Electrocardiography

• Chest Radiography

• Biomarkers

Initial Assessment

• Vital signs,

• Examination of the peripheral vessels

– Bruits or absent pulses

• Identify potential precipitating causes

– Uncontrolled hypertension, anemia, hyperthriodism

• Important comorbid conditions

– Chronic obstructive pulmonary disease

• Evidence of hemodynamic complications

– Congestive heart failure,

– New mitral regurgitation, hypotension

Physical Examination

• 10 minutes after presentation

• New persistent or transient ST-segment abnormalities (≥0.1 mV) and T inversion (≥0.2 mV)

• During a symptomatic episode at rest and resolve

Electrocardiography

• Usually non-diagnostic

• Pulmonary edema (ischemia-induced diastolic or systolic dysfunction)

• Pneumothorax, Pneumonia

Chest Radiography

• A cardiac troponins (T or I; cTnT or cTnI)

• Creatine kinase MB isoenzyme (CK-MB, less sensitive)

Biomarkers

Biomarkers for Evaluation of Patients with STEMI

• Myocarditis,

• Myocardial contusion,

• Cardioversion or defibrillation,

• Left ventricular strain from congestive heart failure

• Hypertensive crisis,

• Extreme exercise,

• Right ventricular strain from pulmonary embolus,

• Other causes of acute pulmonary hypertension

Troponins_True myocardial damage

• Patients with renal disease

• Severe sepsis

Troponins_mechanism remains unclear

• Blood should be obtained for testing at hospital presentation, and at 6 to 9 hours

• A normal reference values 0.01 to 0.07 ng/ml

• Ultrasensitive assays <0.001 ng/ml or <1 pg/ml

• Serial sampling up to 12 hours after presentation %90 to %95

• 3 hours of the onset of chest pain 80% to 85%

Troponins

• Found in – Skeletal muscle,– Tongue, – Diaphragm, – Small intestine, uterus, and prostate

• Eleveted– Muscular dystrophy– High-performance athletics– Rhabdomyolysis– Alcohol abuse or trauma vs

• Shorter half-life – Useful for gauging the timing of an MI– Diagnosing reinfarction

Creatine Kinase MB Isoenzymelack of specificity

• Serum myoglobin• heart-type fatty acid binding protein• C-reactive protein• serum amyloid A, • myeloperoxidase • interleukin-6• D-dimer • B-type natriuretic peptides

Other Markers

Acute Coronary SyndromeLikelihood That Signs and Symptoms

ST Elevation Myocardial Infarction

Step 1: Assess time and risk.

• Time since onset of symptoms  

• Risk of STEMI

• Risk of fibrinolysis

• Time required for transport to a skilled PCI laboratory

Assessment of Reperfusion Options for STEMI Patients

A B

C D

• Skilled PCI laboratory is available with surgical backup

– Skilled PCI laboratory is available, defined by

– Medical contact-to-balloon or door-to-balloon less than 90 min

• High risk from STEMI  – Cardiogenic shock  

– Killip class ≥ 3

•  Contraindications to fibrinolysis,

•  Late presentation – Symptom onset was more than 3 hr ago

An invasive strategy is generally preferred if

• Based on Clinical Examination

I. Rales and S3 absent

II. Crackles, S3 gallop, elevated jugular venous pressure

III. Frank pulmonary edema

IV. Shock

Hemodynamic Classifications of Patients with Acute Myocardial Infarction

Modified from Killip T, Kimball J: Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 20:457, 1967

• Based on Invasive Monitoring

I. Normal hemodynamics; PCWP < 18 mm Hg, CI > 2.2

II. Pulmonary congestion; PCWP > 18 mm Hg, CI > 2.2

III. Peripheral hypoperfusion; PCWP < 18 mm Hg, CI < 2.2

IV. Pulmonary congestion and peripheral hypoperfusion; PCWP > 18 mm Hg, CI < 2.2

Hemodynamic Classifications of Patients with Acute Myocardial Infarction

Modified from Forrester J, Diamond G, Chatterjee K, et al: Medical therapy of acute myocardial infarction by the application of hemodynamic subsets. N Engl J Med 295:1356, 1976.

• Delay to invasive strategy:– Prolonged transport

– Medical contact-to-balloon or door-to-balloon more than 90 min

• Early presentation (≤3 hr from symptom onset and delay to invasive strategy; see below)

•  Invasive strategy is not an option: – Catheterization laboratory occupied or not available 

– Vascular access difficulties 

–  Lack of access to a skilled PCI laboratory

Fibrinolysis is generally preferred if

Approved Fibrinolytic Agents

Reperfusion Options for STEMI Patients

Post Myocardial Infarction

Complications

Post MI Complications

Arrhythmias

Cardiac Arrest

Cardiac Muscle Dysfunction

Cardiogenic Shock

(Haworth and Pratowski, 2000 p. 90)

Heart FailureMitral InsufficienciesPericarditisThromboembolismGI Complaints

Post MI: Common ArrhythmiasAtrial Fibrillation

Premature Ventricular Contractions

Ventricular Tachycardia

Accelerated Idioventricular Rhythm

Ventricular Fibrillation

Atrioventricular Block

(Haworth and Pratowski, 2000 p. 91)

Unstable Angina and Non–ST Elevation Myocardial Infarction

Unstable Angina

Cause: Thrombus partially or intermittently

occludes the coronary artery

Diagnostic Findings:ST-segment depression or T-wave

inversionNormal Cardiac Markers

(Overbaugh, 2009, p. 46)

NSTEMI

Cause: Thrombus partially or intermittently

the occludes coronary artery

Diagnostic Findings:ST-segment depression or T-wave

inversionElevated Cardiac biomarkers

(Overbaugh, 2009, p. 46)

Clinical Indicators of Increased Risk in UA/NSTEMI

TreatmentUA

• Oxygen to maintain O2 sat > 90%

• NTG or MSO4 to control

pain• BB’s, CCB’s,

ACEI’s, statins,

clopidogrel, unfractionated heparin or

LMWH, glycoprotein

IIb/IIIa inhibitors

NSTEMISame as UA plus: Cardiac cath &

possible PCI for patients with ongoing CP, hemodynamic instability, or increased risk of worsening clinical condition

• Antiplatelet Therapy

• Anticoagulant Therapy

• Control of Cardiac Pain– Analgesics

– Nitrates

– Beta Blockers

– Oxygen

• Limitation of Infarct Size– Early reperfusion

– Reduction of myocardial energy demand

General Treatment Measures

• Aspirin

–  162-325 mg, nonenteric-coated ASA to be chew

–  maintenance of 75-162 mg daily

Antiplatelet Therapy

• Clopidogrel 300-600 mg loading 75 mg/day

• Prasugrel oral loading dose of 60 mg and 10 mg orally daily

• Ticagrelor a loading dose of 180 mg and 90 mg twice daily

Antiplatelet Therapy

• Heparin activated partial thromboplastin time (aPTT) target of 1.5 to 2 times that of control

• Low-Molecular-Weight Heparins

• Bivalirudin (STMI)

Anticoagulant Therapy

– Analgesics

• meperidine, pentazocine, and morphine

• Morphine 2 to 8 mg/ 5 to 15 minutes --until the pain is relieved or there is evident toxicity

– Nitrates

• sublingual nitrates, intravenous nitroglycerin

• systolic pressure <90 mm Hg

• right ventricular infarction

Control of Cardiac Pain

– Beta Blockers

• Killip class II or higher (precipitating cardiogenic shock)

• Patients with heart failure (rales > 10 cm up from diaphragm),

• hypotension (blood pressure < 90 mm Hg),

• bradycardia (heart rate < 60 beats/min),

Control of Cardiac Pain

• Oxygen

– pulse oximetry

– Sao2 < 90%

– 2 to 4 liters/min of 100% oxygen

– 6 to 12 hours

Control of Cardiac Pain

• Early reperfusion

• Routine Measures for Infarct Size Limitation

– Beta blocker (HR 50-70)

– Inhibitors of the renin-angiotensin-aldosterone system (RAAS)

– Arterial oxygenation

Limitation of Infarct Size

•  Angiotensin-converting enzyme (ACE) inhibitor  

– Start ACE inhibitor orally in patients with pulmonary congestion or LVEF <40%

– if the following are absent: hypotension (SBP <100 mm Hg or <30 mm Hg below baseline) or known contraindications to this class of medications.

•  Angiotensin receptor blocker (ARB) 

– Start ARB orally in patients who are intolerant of ACE inhibitors and with either clinical or radiologic signs of heart failure or LVEF <40%

Limitation of Infarct Size

• Risk factor control, particularly smoking, must be stringent. • Antiplatelet therapy is indicated indefinitely. • Dual antiplatelet therapy is indicated up to 12 months. • Oral treatment with beta-blockers is indicated in patients with

heart failure or left ventricular dysfunction. • A fasting lipid profile must be obtained in all patients. • A high-dose statin should be initiated or continued early after

admission in all patients without contraindication or history of intolerance.

• ACE inhibitors are indicated in patients with heart failure, LV systolic dysfunction diabetes or an anterior infarct.

• An ARB is an alternative to ACE inhibitors. • Aldosterone antagonists are indicated if EF ≤40% or heart

failure or diabetes, provided there is no renal failure or hyperkalaemia.

Long term therapies