ECG in patients with chest pain

7/30/2019 ECG in patients with chest pain

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The ECG in patients with chest pain: diagnosis andmanagement

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Pre-test

1. An 82 year old woman presents with a two day history of chest tightness,

palpitations, and breathlessness. She has a recent history of increasing

angina symptoms. Her electrocardiogram (ECG) shows atrial fibrillation with

a heart rate of 160 beats per minute. Her high sensitivity troponin T level is

elevated at 475 ng/l and 382 ng/l six hours and 12 hours after presentation.

What is the likely diagnosis?

a.

Acute pulmonary oedema

b.

Supraventricular tachycardia

c.

Atrial fibrillation with fast ventricular response and rate related

ischaemia

d.

Fast atrial fibrillation

e.

Non-ST segment elevation myocardial infarction with atrial fibrillation

A 26 year old woman presents with a three day history of sharp chest pain,

which is exacerbated by deep breaths and lying flat. She has been unwell

with flu-like symptoms. An ECG shows widespread saddle shaped ST

segment elevation. Which one of the following statements about her

prognosis is correct?


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.

Her prognosis is good with complete recovery

a.

She is at high risk of cardiac tamponade

b.

She is at high risk of developing pericardial constriction

c.

There is a high likelihood of recurrence

d.

Corticosteroids are given routinely to reduce the likelihood of

recurrence

A 76 year old woman is admitted with a sudden onset of severe chest pain

that radiated through to her back and caused her to collapse. Her blood

pressure is 180/102 mm Hg in her right arm and 138/60 mm Hg in her left arm.

Her heart rate is 112 beats per minute. Her ECG shows non-specific T wave

inversion in leads II, III, and aVF. Her chest x ray shows clear lung fields.

Which one of the following statements describes the most appropriate

course of action?

.

The history suggests acute coronary syndrome. You should treat with

antiplatelets and wait for troponin level results to confirm the diagnosis

a.

The history suggests acute myocardial infarction. You should treat with

fibrinolysis

b.


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The history suggests thoracic aortic dissection. You should treat

conservatively with antihypertensive drugs

c.

The history suggests thoracic aortic dissection. You should request

urgent computed tomography (CT) or magnetic resonance imaging

(MRI), reduce blood pressure with antihypertensive therapy, and

obtain a cardiothoracic surgical opinion when the diagnosis is

confirmed

d.

The history suggests thoracic aortic dissection. You should treat with

antihypertensive drugs and book an echocardiogram to confirm the

diagnosis

A 28 year old woman presents with her first episode of palpitations. She

had been treated for asthma by her GP. Her blood pressure is 110/70 mm Hg

and her oxygen saturation is 95% on room air. Her presenting ECGs are as

follows:


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What is the immediate management?

.

Immediate electrical cardioversion


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a.

Treat as acute coronary syndrome

b.

Give intravenous digoxin and wait for a senior colleague to review

c.

Give intravenous verapamil in the presence of asthma

d.

Give intravenous flecainide or amiodarone

A 72 year old man with a previous history of angina and hypertension is

admitted with a two hour history of chest pain. He describes the chest pain

as similar to his usual angina but more severe. He has a permanent

pacemaker in situ. His blood pressure is 120/70 mm Hg and heart rate is 70

beats per minute. His ECG shows regular ventricular pacing spikes. What

should you do?

.

Treat as ST segment elevation myocardial infarction and give

fibrinolysis

a.

Give aspirin and pain relief

b.

Treat as high risk acute coronary syndrome

c.

Give aspirin and pain relief and wait for the cardiac troponin level

result

d.


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Admit him under a cardiologist

A 54 year old woman presents with a two day history of pleuritic chest pain

and breathlessness. She is tachypnoeic with a respiratory rate of 30 breaths

per minute. Her oxygen saturations are 88% with 28% oxygen. Her blood

pressure is 102/70 mm Hg and her heart rate is between 140 beats per minute

and 160 beats per minute.

What does her ECG show?

.

Lateral ST depression

a.

Left bundle branch block

b.

Right bundle branch block and S1Q3T3 pattern


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c.

Inferior ST segment elevation myocardial infarction

d.

Paced rhythm

An 86 year old man with a longstanding history of angina is brought to the

emergency department after collapsing at home. Although alert, he appears

weak and reports chest pain. His blood pressure is 80/52 mm Hg and his

heart rate is 40 beats per minute. On listening to his chest there are

widespread bilateral crackles. The chest x ray confirms pulmonary oedema.

He was given atropine in the ambulance.

ECG after giving atropine 3.0 mg in cumulative doses

What should be his immediate management?

.

Fibrinolytic therapy


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a.

Intravenous fluid

b.

Intravenous furosemide

c.

Intravenous nitrate

d.

Temporary pacing

A 56 year old man is admitted with severe central chest and epigastric pain.

He has coffee grounds vomiting. He is a smoker who drinks eight pints of

lager each day. He is normally hypertensive but not compliant with his

medications, which include aspirin. His blood pressure is 90/60 mm Hg. His

ECG shows a sinus tachycardia with a rate of 120 beats per minute. His chest

x ray shows clear lung fields. His haemoglobin level is 79 g/l and his high

sensitivity troponin T level is elevated at 50 ng/l and 83 ng/l (at six hours and

12 hours respectively) after the onset of his symptoms. What should you do

next?

.

Treat as acute coronary syndrome. Give antiplatelet treatment with a

proton pump inhibitor

a.

Give a proton pump inhibitor and a blood transfusion, and stop aspirin

b.

Give an intravenous beta blocker as an anti-ischaemic agent

c.

Give intravenous fluids and analgesia


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A 30 year old man consults his GP because of a cold. He is found to have

an aortic systolic murmur, and an ECG shows voltage criteria for left

ventricular hypertrophy (sum of R wave in V6 and S wave in V1 = 42 mm). He

is otherwise healthy and slim, with a BMI of 25 and a blood pressure of 120/80

mm Hg. Because of these findings he is referred to the outpatient clinic.

Which one of the following investigations is most useful?

.

Carotid Doppler measurements

a.

Dobutamine stress echocardiogram

b.

Transthoracic echocardiogram

c.

Chest radiograph

d.

24 hour ambulatory blood pressure

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Section 3 of 6 - Question 1 (of 11)

The ECG in patients with chest pain: diagnosis andmanagement

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1. A 62 year old man presents to the emergency department with central chest

pain that started one hour ago. He looks pale and clammy. He is a smoker

with a history of hypertension. His blood pressure is 100/60 mm Hg. The

paramedic gave the man oxygen and aspirin in the ambulance.

Appearance of the QRS in lead V4R (reverse V4): ST elevation

(V7 to V9 are posterior leads and on this ECG have substituted

the usual V4 to V6 positions to show posterior ST elevation, for
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ease of showing all these changes on one ECG. ST elevation in

lead V4R is shown on the next ECG with three beats)

What is the diagnosis?

a.

Anterior ST segment elevation myocardial infarction

b.

Inferior ST segment elevation myocardial infarction

c.

Lateral ST segment elevation myocardial infarction

d.

Inferoposterior ST segment elevation and right ventricular myocardial

infarction

e.

Posterior ST segment elevation myocardial infarction

1. A 62 year old man presents to the emergency department with central chest

pain that started one hour ago. He looks pale and clammy. He is a smoker

with a history of hypertension. His blood pressure is 100/60 mm Hg. The

paramedic gave the man oxygen and aspirin in the ambulance.


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Appearance of the QRS in lead V4R (reverse V4): ST elevation

(V7 to V9 are posterior leads and on this ECG have substituted

the usual V4 to V6 positions to show posterior ST elevation, for

ease of showing all these changes on one ECG. ST elevation in

lead V4R is shown on the next ECG with three beats)

What is the diagnosis?

Youranswer

Coan

a.Anterior ST segment elevation myocardial infarction


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b.Inferior ST segment elevation myocardial infarction

c.Lateral ST segment elevation myocardial infarction

d.Inferoposterior ST segment elevation and right ventricular myocardial infarction

e.Posterior ST segment elevation myocardial infarction

a : Anterior ST segment elevation myocardial infarction

Anterior refers to leads V1 to V6. This patient has inferoposterior ST segment

elevation and right ventricular myocardial infarction.

b : Inferior ST segment elevation myocardial infarction

Inferior refers to leads II, III, and aVF. This patient has inferoposterior ST segment

elevation and right ventricular myocardial infarction.

c : Lateral ST segment elevation myocardial infarction

Lateral refers to leads V5, V6, I, and aVL. This patient has inferoposterior ST

segment elevation and right ventricular myocardial infarction.

d : Inferoposterior ST segment elevation and right ventricular myocardial

infarction

Inferoposterior refers to leads II, III, aVF, and V7 to V9. Right ventricular infarction

can be diagnosed if there is ST segment elevation in the reverse V4 lead (rV4).

ST segment elevation refers to the presence of J point elevation of 2 mm in two or

more adjacent V1 to V3 leads, and/or 1 mm in two or more adjacent V4 to V6, V7

to V9, and/or standard limb leads.

e : Posterior ST segment elevation myocardial infarction


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Posterior ST segment elevation myocardial infarction is diagnosed by the presence

of ST segment elevation in V7 to V9. To diagnose posterior myocardial infarction if

these posterior leads are not available, look for:

ST segment depression in V1 to V3

R/S ratio 1 in V1 or V2

Upright tented T wave in V1 or V2

2. What is the management?

a.

Pain relief

b.

Pain relief and intravenous fluids

c.

Pain relief and beta blockers

d.

Pain relief, clopidogrel, and primary angioplasty or fibrinolysis

e.

Pain relief, clopidogrel, fibrinolysis, and pacing

management

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2. What is the management?

Youranswer

Coan

a.Pain relief


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b.Pain relief and intravenous fluids

c.Pain relief and beta blockers

d.Pain relief, clopidogrel, and primary angioplasty or fibrinolysis

e.Pain relief, clopidogrel, fibrinolysis, and pacing

3. a : Pain relief

4. Pain relief is important but not the only treatment. You should use intravenous

morphine or diamorphine with an antiemetic, such as metoclopramide. Avoid

cyclizine because it can worsen pulmonary oedema by causing peripheral

vasoconstriction.

5. b : Pain relief and intravenous fluids

6. You should avoid intravenous fluids in most episodes of acute myocardial

infarction, except in right ventricular infarction and where there is evidence of

hypovolaemia, such as in patients with low central venous pressure.

7. c : Pain relief and beta blockers

8. Beta blockers reduce death and reinfarction in patients with acute myocardial

infarction.1 2 You should give beta blockers orally in the first 24 hours in patients

without heart failure, cardiogenic shock, asthma, or other contraindications. You

should consider giving beta blockers intravenously at presentation to patients who

are hypertensive and without contraindications.3

9. d : Pain relief, clopidogrel, and primary angioplasty or fibrinolysis

10. Primary percutaneous coronary intervention is the method of choice for

reperfusion.4 It is indicated in patients who present within 12 hours of symptom

onset and are suitable for invasive coronary management. Primary percutaneous


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coronary intervention is associated with a higher rate of infarct related artery

patency, lower stroke and mortality rates, and shorter hospital stays.5 6

11. Fibrinolytic therapy has, until recently, been widely used for coronary reperfusion in

the United Kingdom. If primary percutaneous coronary intervention is not available,

you should aim to give fibrinolytic therapy as soon as possible, preferably within 20

minutes of the patient arriving in hospital, because the benefit is greatest within the

first two hours of symptom onset.7 8

12. You should consider clopidogrel (with aspirin) as additional antiplatelet therapy in

all patients with ST segment elevation myocardial infarction. Clopidogrel reduces

death, myocardial reinfarction, stroke, and recurrent ischaemia needing urgent

revascularisation.9 10 There are other, newer antiplatelet drugs available such as

prasugrel and ticagrelor. You should follow your local guidelines when using them.

13. e : Pain relief, clopidogrel, fibrinolysis, and pacing

14. Transcutaneous or transvenous temporary pacing is indicated for patients with

symptomatic bradycardia, advanced heart block, and asystole accompanied by

haemodynamic instability and/or cardiogenic shock. This patient does not have any

of these indications.

15. KEY POINTS

ST segment elevation myocardial infarction occurs when there is a

complete obstruction of a coronary artery. In clear cases of ST

segment elevation myocardial infarction, patients should receive

reperfusion therapy without delay

The ECG in patients with chest pain: diagnosis and

management10013552 45

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3. A 52 year old heavy goods vehicle driver presents with a three hour history of

retrosternal chest tightness that radiates to his jaw and left arm. He is a


17/53

heavy smoker of 40 cigarettes per day, and has no previous history of heart

disease. When he attended a well man clinic recently, his blood pressure was

high at 150/90 mm Hg.

His BMI is 34 and he has marked central obesity. On arrival at the medical

admissions unit his blood pressure is 152/90 mm Hg, and his oxygen

saturations are 98% on air. His heart sounds are normal and his lungs are

clear.

What is the most likely initial diagnosis?

a.

Acute coronary syndrome

b.

Non-ST segment elevation myocardial infarction

c.

Pulmonary embolism

d.

Pericarditis


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e.

Hypertensive heart disease

You have changed your answer. Your first answer will count.

10013552 45

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3. A 52 year old heavy goods vehicle driver presents with a three hour history of

retrosternal chest tightness that radiates to his jaw and left arm. He is a

heavy smoker of 40 cigarettes per day, and has no previous history of heart

disease. When he attended a well man clinic recently, his blood pressure was

high at 150/90 mm Hg.

His BMI is 34 and he has marked central obesity. On arrival at the medical

admissions unit his blood pressure is 152/90 mm Hg, and his oxygen

saturations are 98% on air. His heart sounds are normal and his lungs are

clear.

What is the most likely initial diagnosis?

Youranswer

Coan

a.Acute coronary syndrome


19/53

b.Non-ST segment elevation myocardial infarction

c.Pulmonary embolism

d.Pericarditis

e.Hypertensive heart disease

a : Acute coronary syndrome

Acute coronary syndrome is a term used to describe a constellation of clinical

symptoms that are related to acute myocardial ischaemia. It broadly comprises ST

segment elevation myocardial infarction and non-ST segment elevation acute

coronary syndromes. The latter are further subdivided into non-ST segment

elevation myocardial infarction and unstable angina, depending on the presence or

absence of evidence of myocardial necrosis.11 12

Patients with acute coronary syndrome and ST segment depression are at high risk

of developing heart failure or death, and you should actively treat them with

antiplatelet agents (aspirin and clopidogrel) and anticoagulant therapy

(fondaparinux (factor Xa inhibitor) or low molecular weight heparin), unless

contraindicated.

b : Non-ST segment elevation myocardial infarction

Non-ST segment elevation myocardial infarction describes acute myocardial

infarction with an ECG pattern other than ST segment elevation (ST segment

depression, T wave inversion, normal ECG, bundle branch block, or paced rhythm).

Acute myocardial infarction is diagnosed by the presence of a typical rise and fall in

cardiac biomarkers, with characteristic ischaemic symptoms or ECG changes of

acute ischaemia, or both.11

c : Pulmonary embolism


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Pulmonary embolism is a differential diagnosis. Here the chest pain is characteristic

of cardiac ischaemia, and normal oxygen saturation makes pulmonary embolism

less likely.

d : Pericarditis

Symptoms of pericarditis are usually more insidious. Chest pain is characteristically

sharp and stabbing, and is exacerbated by inspiration, movement, and supine or

erect posture. There may be a recent history of viral illness with symptoms such as

running nose, cough, pyrexia, myalgia, or arthralgia.

e : Hypertensive heart disease

Hypertensive heart disease can present with chest pain, and usually occurs inpatients with uncontrolled hypertension. Left ventricular hypertrophy may be

present on the ECG. This diagnosis can coexist with other cardiac diseases, such

as acute coronary syndrome, and should be made only after excluding other

causes of chest pain.

KEY POINTS

Non-ST segment elevation acute coronary syndrome is much more

common than ST segment elevation myocardial infarction

Non-ST segment elevation acute coronary syndrome presents with a

variety of ECG changes. High risk features include ST segment

depression, transient ST elevation, bundle branch block or paced

rhythm on the ECG, and elevated cardiac troponin

CLINICAL TIPS

Start treatment for acute coronary syndrome promptly to stabilise

patients

Consider early invasive coronary revascularisation in suitable

patients

4. A 78 year old man presents with a three day history of breathlessness and a

cough productive of green purulent sputum. His blood pressure is 120/78 mm

Hg and his oxygen saturations are 97% on 28% oxygen. His chest x ray

shows patchy consolidation in the right lower zone. His high sensitivity


21/53

troponin T level is 35 ng/l and 36 ng/l (on admission and six hours later

respectively. The normal level is


22/53

e.

Start treatment for pneumonia and acute coronary syndrome

5. A 70 year old man presents with a four day history of feeling breathless and a

cough productive of green purulent sputum. On examination his pulse is 145

beats per minute and irregularly irregular. His blood pressure is 120/78 mm

Hg and his oxygen saturations are 97% on 28% oxygen. His chest x ray

shows patchy consolidation in the right lower zone. His high sensitivity




23/53




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Sepsis

Bleeding (remember that a patient with upper gastrointestinal

bleeding may present with severe chest pain as well as epigastric

pain)

Renal failure

Pulmonary embolism

Stroke

Multiorgan failure.

The most likely diagnosis in this patient is pneumonia precipitating atrial fibrillation.

b : The troponin level is spuriously elevated so you should ignore it

The newer generation of troponin bioassays are highly sensitive and specific, so

the level is unlikely to be spuriously elevated.

c : The troponin level is elevated because of the tachyarrhythmia and

pneumonia, and is a marker for an adverse prognosis

Given the history and ECG changes it is highly likely that the troponin level is

elevated because of the tachyarrhythmia and pneumonia. A raised troponin level is

a marker for adverse prognosis, in both acute coronary syndrome and other

conditions.16 17

d : A single raised level of cardiac troponins is sufficient to make a diagnosis

of acute myocardial infarction

The new universal definition of acute myocardial infarction requires two or more

measurements of cardiac troponins, showing a rise and/or fall pattern, and also in

the presence of an appropriate clinical setting.18

Learning bite: Universal definition of acute myocardial

infarction18

It is possible to confirm a diagnosis of acute myocardial infarction in an appropriate

clinical setting (for example, where the patient has chest pain lasting 15 minutes or

longer) by the presence of a rise and/or fall pattern of cardiac troponins where at


25/53

least one value is above the normal reference value and there is at least one of the

following clinical features:

Symptoms of cardiac ischaemia (for example, chest pain that is

ischaemic in nature, or pain in the shoulder or arm that has no other

causes such as musculoskeletal pain)

New changes on the electrocardiogram indicating ischaemia (ST-T

changes, left bundle branch block, or development of a Q wave)

New regional wall abnormality on echocardiography, or another

imaging modality showing new loss of viable myocardium.

e : You should always interpret a troponin result in conjunction with other

cardiac enzymes, such as creatine kinase

In the context of acute coronary syndrome, a raised troponin level may or may not

be accompanied by a rise in other cardiac enzymes. A raised troponin level in the

absence of a rise in other cardiac enzymes, for example, creatine kinase, is usually

the result of a small infarct.

KEY POINTS

Atrial fibrillation with a fast ventricular rate is a common acute

medical problem

You should:

Identify and treat precipitating conditions

Maintain haemodynamic stability

Consider anticoagulation.

CLINICAL TIPS

Beta blockers (if not contraindicated) are a useful and reliable way ofcontrolling heart rate

Atrial fibrillation with a fast ventricular rate, of less than 48 hours

onset and without a precipitating cause may be suitable for

antiarrhythmic or synchronised electrical cardioversion


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6. A 72 year old man presents with a two hour history of central chest pain

radiating to his jaw and left arm. He is known to suffer with angina. His pain

came on at rest, feels worse than his usual angina, and is not relieved by his

glyceryl trinitrate spray. He is pale, clammy, and breathless. He has a

previous history of hypertension, myocardial infarction, and coronary artery

bypass grafting, and he has a permanent pacemaker.

What is the most likely diagnosis?

Youranswer

Coan

a.Acute coronary syndrome with left bundle branch block

b.Acute coronary syndrome with right bundle branch block

c.

Acute coronary syndrome with idioventricular rhythm

d.Acute coronary syndrome with paced rhythm


27/53

e.Acute coronary syndrome with biventricular paced rhythm

a : Acute coronary syndrome with left bundle branch block

This patient has a dual chamber permanent pacemaker and acute coronary

syndrome. Left bundle branch block morphology consists of:

Positive R wave in the left ventricular leads (V5, V6, I, and AVL)

Secondary R wave in the left ventricular leads, with an M shaped

QRS complex in these leads

QRS duration 120 ms.

ECG showing left bundle branch block

b : Acute coronary syndrome with right bundle branch block


syndrome. Right bundle branch block morphology consists of:


28/53

Secondary R wave in the right ventricular leads (V1, V2) with an M

shaped complex in these leads

Broad S wave in the left ventricular leads, especially lead I

QRS duration 120 ms.

ECG showing right bundle branch block

The QRS morphology in lead V1 in right bundle branch block,

showing a typical M appearance


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c : Acute coronary syndrome with idioventricular rhythm


syndrome. Idioventricular rhythm consists of a monomorphic broad complex

ventricular rhythm at a rate of less than 100 beats per minute. This is also known

as accelerated idioventricular rhythm, with a faster rate of up to 120 beats per

minute.19

ECG showing an idioventricular rhythm (broad ventricular

complexes at a rate of less than 100 beats per minute)

d : Acute coronary syndrome with paced rhythm

This patient has a dual chamber permanent pacemaker. The ECG shows the

pacemaker is sensing native atrial depolarisation and pacing the ventricle.

Ventricular pacing is commonly right ventricular apical pacing. As ventricular

depolarisation starts in the right ventricle by the pacemaker and spreads to the left

ventricle, this results in left bundle branch block type morphology. Unlike the usual

left bundle branch block, a pacing spike is usually visible at the start of each QRS

complex.

You should regard patients with symptoms of acute coronary syndrome who

present with a paced rhythm as being at high risk. This is because important

ischaemic ECG changes are often masked by the paced QRS complex. Moreover,

patients with pacemakers are usually older and have other comorbidities.

Fibrinolytic therapy is not indicated because ST repolarisation changes are often

present in ventricular paced beats, and are not a reliable guide for fibrinolytic

therapy.

e : Acute coronary syndrome with biventricular paced rhythm


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Biventricular pacing represents cardiac resynchronisation therapy. There are two

ventricular leads: the first is in the right ventricle, while the second is placed through

the coronary sinus into one of the cardiac veins, and onto the epicardial surface of

the left ventricle. The aim is to achieve synchronised depolarisation and contraction

within the left ventricle and between the right and left ventricles. The QRS complex

in biventricular pacing usually shows a fusion of both left and right bundle branch

block type morphology.

ECG showing biventricular pacing with atrial flutter and a right

bundle branch block pattern in V1

KEY POINT

Treat patients presenting with acute coronary syndrome and paced

rhythm with care because ischaemic changes on the ECG are often

masked by pacing

CLINICAL TIP

In patients with acute coronary syndrome and paced rhythm,

ischaemic changes on the ECG are often masked by pacing. You

should use other risk markers, such as cardiac troponin levels and

pulmonary oedema, to further risk stratify a patient for acute

coronary syndrome


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7. A 38 year old woman presents with a three week history of exertional chest

pain and palpitations. She is a non-smoker and has no other medical

problems. You note that her younger sister had a pacemaker fitted recently,

and an older brother died suddenly at age 42.

What is the diagnosis from the ECG?

Youranswer

Coan

a.Ischaemic lateral ST segment depression

b.Within normal limits

c.QT prolongation

d.Left ventricular hypertrophy with a repolarisation abnormality (also referred to as strain)


32/53

e.Right ventricular hypertrophy

a : Ischaemic lateral ST segment depression

Left ventricular hypertrophy with a repolarisation abnormality (also referred to as

strain) refers to the presence of ST segment depression and T wave inversion in

the left ventricular leads (I, aVL, V5, and V6).20

In the presence of left ventricular hypertrophy, ST depression may indicate strain,

ischaemia, or both. You should consider ST depression as possibly ischaemic in

origin in patients presenting with chest pain. Serial ECGs and comparison with an

old ECG may help you to differentiate ischaemia from strain. ST segment

depression is an adverse prognostic feature in acute coronary syndrome.

Because this patient is a young woman with no cardiovascular risk factors, she is

unlikely to have ischaemia. Conversely, she has a highly significant ECG showing

left ventricular hypertrophy with massive voltage.

b : Within normal limits

This is an abnormal ECG.

c : QT prolongation

Long QT syndrome is a group of hereditary genetic mutations involving cardiac cell

membrane ion channel subunits. It is suspected when the QTc interval is 450 ms

if accompanied by symptoms, or 470 ms in asymptomatic people. The QT is

normal in this ECG. QTc is best interpreted with a non-acute ECG. Computer

analysis tends not to be accurate in the presence of tachycardia, beat to beat RR

interval difference, indistinct T wave ending, and motion artefact. For clarity, it

would be better to blank out the QTc measurement on the ECG. Genetic historyand testing confirm the diagnosis. Patients with long QT syndrome are at risk of

ventricular arrhythmias, particularly torsades de pointes and sudden cardiac death.

Familial screening and genetic counselling are indicated. QT prolongation can also

be an acquired condition.


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d : Left ventricular hypertrophy with a repolarisation abnormality (also

referred to as strain)

There are many different ECG criteria for left ventricular hypertrophy. In general

terms, the likelihood of left ventricular hypertrophy is increased when more of the

following criteria are met20:

Sum of R wave in V5 or V6 and S wave in V1 35 mm

Sum of tallest R wave in V4, V5 or V6 and deepest S wave in V1, V2

or V3 40 mm

R wave in lead I or aVL 13 mm

R wave in V4, V5 or V6 27 mm

R wave in aVF 20 mm when the frontal plane QRS axis is vertical

S wave in V1 or V2 25 mm

ST depression and T wave inversion in the left ventricular leads (I,

AVL, V5, and V6)

Slow ventricular activation time 50 ms

Left axis deviation.

Causes of left ventricular hypertrophy on the ECG include:

Systemic hypertension

Aortic stenosis or regurgitation

Hypertrophic cardiomyopathy

Coarctation of the aorta

Athletes heart.

It may also be a normal variant, especially in thin people.

e : Right ventricular hypertrophy

Right ventricular hypertrophy is shown on an ECG by:

A dominant R wave in V1 with an R/S ratio 1


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Right axis deviation

ST or T wave changes in the right ventricular leads (V1 and V2).

ECG showing right ventricular hypertrophy

Causes of right ventricular hypertrophy include:

Pulmonary hypertension (primary or secondary)

Cor pulmonale

Fallots tetralogy

Pulmonary stenosis.

KEY POINT

Left ventricular hypertrophy is commonly seen in clinical practice.

Ensure that the ECG is correctly calibrated, that is 10 mm/millivolt

and 25 mm per second

CLINICAL TIPS

Transthoracic echocardiography is a useful tool for investigating the

cause of left ventricular hypertrophy


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The ECGs of slim people sometimes show apparent voltage criteria

for left ventricular hypertrophy. You should exclude left ventricular

hypertrophy by measuring the thickness of the ventricle wall using

an echocardiogram. If left ventricular hypertrophy is confirmed, you

can consider further investigating its cause

8. A 32 year old woman presents with a three day history of left sided chest pain

that worsens with inspiration, coughing, and lying flat. She has been feeling

unwell and notices she has a mild temperature. She has no significant past

medical history.


Youranswer

Coan

a.Pleurisy

b.Acute coronary syndrome


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c.Acute pericarditis

d.Brugada syndrome

e.Pulmonary embolism

a : Pleurisy

Pleurisy is a differential diagnosis, but pleurisy alone is not associated with these

ECG changes unless accompanied by coexisting pericarditis.

b : Acute coronary syndrome

Acute coronary syndrome can present with atypical symptoms, and ECG changes

can resemble those of acute pericarditis. Varying degrees of ST elevation in more

than one coronary artery territory support the diagnosis of acute pericarditis.

Repeating the ECG at regular intervals can help you to distinguish between

pericarditis and acute coronary syndromes. Progressive loss of R wave,

development of Q wave or T wave inversion in the leads with initial ST segment

elevation, or the presence of reciprocal ST segment depression support the

diagnosis of acute coronary syndrome.

c : Acute pericarditis

These symptoms and ECG changes are characteristic of acute pericarditis. A

pericardial rub would help to confirm the diagnosis, but is usually transient. Beside

saddle shaped ST segment elevation, PR segment deviation occurs early in acute

pericarditis.21 Later, T wave inversion appears and can occasionally persist after

recovery. The presence of pr-depression on the ECG is pathognomonic of acute

pericarditis.

If a patient has uncomplicated pericarditis, you can discharge them from hospital

quickly. A raised cardiac troponin level in a patient with pericarditis should alert you

to the possibility of coexisting myocarditis, and you should arrange a transthoracic


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echocardiography. Cardiomegaly on a posterior-anterior chest radiograph suggests

the presence of pericardial effusion or myocarditis.

d : Brugada syndrome

Brugada syndrome is characterised by the presence of right bundle branch block,

persistent ST segment elevation in leads V1-3, and sudden cardiac death in the

absence of structural heart disease.22 In familial cases, Brugada syndrome is

inherited in an autosomal dominant manner. There are three classic ECG features:

Type I - "coved" - which is diagnostic of the condition

Types II and III - "saddle back" - which are suspicious but not

diagnostic.

Type III can also be found in healthy people.

ECG showing Brugada syndrome (ST elevation changes in lead

V1)

Published with permission from Brugada R, Brugada P, Brugada J.

Electrocardiogram interpretation and class I blocker challenge in Brugada

syndrome. J Electrocardiol2006;39(4 Suppl):S115-18.

e : Pulmonary embolism

From the history pulmonary embolism is a differential diagnosis, and you should

use your clinical judgment to exclude it. However, pericarditis is much more likely.

KEY POINTS


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More benign conditions (such as acute pericarditis) commonly

present in younger people with chest pain

More serious chest pain problems (such as ischaemic heart disease

and pulmonary embolism) are more common in older people

CLINICAL TIP

If you suspect that a patient has pericarditis, ask about a recent

history of viral illness

A 72 year old woman collapses with chest pain while gardening. On waking, she recalls having

severe central chest pain that radiated to her back between her shoulder blades. She has type 2 diabetes

mellitus and a history of hypertension. On examination she is alert, but pale and clammy. Her blood pressure

is 92/60 mm Hg.


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Youranswer

Coan

a.Acute coronary syndrome

b.Bilateral hilar lymphadenopathy

c.Acute thoracic aortic dissection

d.Tension pneumothorax

e.Pulmonary embolism

a : Acute coronary syndrome

Aortic dissection causes an instantaneous shearing chest pain. Acute coronary

syndrome is a differential diagnosis. The onset of cardiac chest pain that is

ischaemic in origin is normally slower, persistent, or crescendo in nature.

b : Bilateral hilar lymphadenopathy

Her chest x ray shows a widened mediastinum and not bilateral hilar

lymphadenopathy. The sudden onset of severe chest pain and the widened

mediastinum should make you suspect aortic dissection in this patient.

c : Acute thoracic aortic dissection

Clinical signs of acute thoracic aortic dissection can be subtle and few. Beside

characteristic symptoms, look for blood pressure or pulse difference in both arms.Examine all pulses. The presence of aortic regurgitation suggests aortic root

dissection. The coronary arteries can be affected.

d : Tension pneumothorax


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Pneumothorax has a specific appearance on the chest x ray: the lung collapses

towards the mediastinum and there is a lack of pulmonary vascular markings

peripherally. Tension pneumothorax is associated with a contralateral shift of the

mediastinum due to high intrapleural pressure on the affected side. You should

treat it urgently.

e : Pulmonary embolism

Pulmonary embolism is a differential diagnosis and can be difficult to differentiate

from aortic dissection clinically. You should arrange urgent investigations to confirm

the diagnosis.

11. A 45 year old bus driver is brought into hospital after developing sudden

onset left sided chest pain and breathlessness while at work. His chest painis worse on inspiration. He is sweaty and clammy. His blood pressure is

70/40 mm Hg and his oxygen saturation is 93% on 10 l of oxygen through a

rebreather bag. His high sensitivity troponin T level is elevated at 285 ng/l at

four hours after onset of chest pain.


Youranswer

Coan


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a.Acute massive pulmonary embolism

b.Acute coronary syndrome

c.Acute pulmonary oedema

d.Acute pericarditis

e.Acute myocarditis

a : Acute massive pulmonary embolism

ECG changes for acute pulmonary embolism are often non-specific and can be

confused with those of acute coronary syndrome. The ECG shows a

supraventricular tachycardia with complete right bundle branch block, most likely

sinus in origin, at 125 beats per minute, with inferior T wave inversion and lateral

ST depression and T wave inversion. The most common ECG change is sinus

tachycardia.

You should also look for:

Right ventricular strain - dominant R wave V1 to V3 with ST

depression, T wave inversion, or both

New partial or complete right bundle branch block

Right axis deviation

P pulmonale - a taller, peaked p wave that reflects right atrial strain

Classic S1Q3T3 changes - this pattern is present in only 20% of

patients with acute pulmonary embolism and comprises an S wave

in lead I, and Q wave and T wave inversion in lead III. It has a

sensitivity of 54% and a specificity of 62%.23

b : Acute coronary syndrome


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Acute coronary syndrome is a differential diagnosis, but the history and ECG in this

man make it less likely than a pulmonary embolism.

c : Acute pulmonary oedema

Acute pulmonary oedema is a differential diagnosis. A chest x ray is an important

part of management in both conditions because it can help you to narrow the

diagnosis. In pulmonary embolism look for pulmonary oligaemia - a reduction or

absence in pulmonary vascular markings, a "pear shaped" hilum due to blockage of

pulmonary arterial branches, and a pulmonary infarct - one or more radio-opaque

densities within the lung parenchyma, and a pleural effusion.

d : Acute pericarditis

Acute pericarditis is usually more gradual in onset, and does not usually cause

hypotension or systemic desaturation.

e : Acute myocarditis

Acute myocarditis causing systemic oxygen desaturation and hypotension suggests

widespread and severe myocardial impairment. Myocarditis is most commonly

preceded by constitutional symptoms such as pyrexia and flu-like symptoms, which

may be followed by symptoms and signs of heart failure.

Learning bite: managing patients with massive or submassive

pulmonary embolism

Emergency pulmonary embolectomy in a highly specialised surgical unit has been

shown to be successful in some patients with massive or submassive pulmonary

embolism.24 However, you should consult with a senior colleague about the

appropriateness of the referral.

Because of anticipated complications and the high mortality associated with shock

and poor oxygenation, admission to the intensive care unit would be advantageous.

Low molecular weight heparin is the mainstay of treatment in pulmonary embolism.


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Although definite evidence of benefit is lacking in pulmonary embolism, you should

consider fibrinolytic therapy in massive pulmonary embolism associated with

haemodynamic instability.25

KEY POINTS

Acute pulmonary embolism can be diagnosed by a lung perfusion

ventilation (V/Q) scan, or by CT of the pulmonary artery

ECG changes and chest x ray findings in acute pulmonary embolism

can be non-specific and easily missed

Right ventricular dysfunction or failure, haemodynamic instability,

and a raised cardiac troponin level are markers for increased

mortality and complications26

CLINICAL TIPS

A normal D dimer level can have a negative predictive value of

>99% for patients with a low or intermediate likelihood of having

pulmonary embolism, depending on the assay used27

A normal jugular venous pressure and oxygen saturation 94% on

air make the diagnosis of acute pulmonary embolism less likely

Learning bite

As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and antithrombin therapy have been

offered, formally assess individual risk of future adverse cardiovascular events using an established risk scoring

system that predicts six month mortality (for example, Global Registry of Acute Cardiac Events (GRACE)).

Include in the formal risk assessment:

A full clinical history (including age, previous myocardial infarction (MI), and

previous percutaneous coronary intervention (PCI) or coronary artery bypass

grafting (CABG))

A physical examination (including measurement of blood pressure and heart rate)

Resting 12-lead electrocardiography (ECG) (looking particularly for dynamic or

unstable patterns that indicate myocardial ischaemia)

Blood tests (such as troponin I or T, creatinine, glucose, and haemoglobin).


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Record the results of the risk assessment in the patient's care record.

Use risk assessment to guide clinical management, and balance the benefit of a treatment against any risk of related

adverse events in the light of this assessment.

Use predicted six month mortality to categorise the risk of future adverse cardiovascular events as follows:

Predicted six month mortality Risk of future adverse cardiovascular events

1.5% or below Lowest

>1.5 to 3.0% Low

>3.0 to 6.0% Intermediate

>6.0 to 9.0% High

over 9.0% Highest

The NICE Guideline Development Group selected six month mortality as the outcome measure for risk stratification

because:

Mortality is a hard endpoint, which is available for most clinical trials

Mortality cannot be misinterpreted (as can an endpoint such as myocardial

infarction, the definition of which has evolved over time, and varies between trials)

A six month time frame captured the majority of clinical events that occur after

presentation with unstable angina or NSTEMI, and which may be influenced by an

in hospital intervention (pharmacological or interventional). Shorter follow up

intervals may miss events related to the index acute coronary syndrome event,

and longer follow up may become increasingly influenced by other factors such as

the effects of post-discharge secondary prevention interventions. Moreover, trials

often do not report findings beyond the six month follow up period.

It is recommended that treatment with clopidogrel in combination with low dose aspirin should be continued

for 12 months after the most recent acute episode of non-ST segment elevation ACS. Thereafter, standard

care, including long term treatment with low dose aspirin alone, is recommended.


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Current NICE guidance for drug eluting stents does not recommend any specific duration of clopidogrel

therapy in addition to aspirin. However, NICE refers to the recommendations from the American College

of Cardiologists/American Heart Association PCI guidelines and the British Cardiovascular Intervention

Society advising a duration of at least 12 months, after which time continuation of clopidogrel should be

reviewed taking into account the risk of further ischaemic events (particularly the risk of subsequent

stent thrombosis) and potential bleeding complications on an individual patient basis.

A 2010 interim analysis of data from two studies (Park S-J, et al. Duration of dual antiplatelet therapy

after implantation of drug-eluting stents. N Engl J Med2010. Published online 15 March (doi:

10.1056/NEJMoa1001266) suggests no benefit for continuing to use clopidogrel in addition to aspirin for

more than 12 months after implantation of drug eluting stents. However, because of limitations, further

studies are required to confirm or refute these findings. The findings of this analysis are insufficient to

recommend a change in practice.

Learning bite

Consider discontinuing clopidogrel treatment five days before CABG in patients who have a low risk of

adverse cardiovascular events. For patients at intermediate or higher risk of adverse cardiovascular

events, discuss the continuation of clopidogrel before CABG with the cardiac surgeon and base the

decision on the balance of ischaemic and bleeding risk.

Offer fondaparinux to patients who do not have a high bleeding risk, unless coronary angiography is planned within

24 hours of admission. Based on the OASIS-5 trial, the NICE guideline advocates fondaparinux as the routine

antithrombin

1. : Eptifibatide or tirofiban

Consider intravenous eptifibatide or tirofiban as part of the early management for patients who have an

intermediate or higher risk of adverse cardiovascular events (predicted six month mortality above 3.0%),

and who are scheduled to undergo angiography within 96 hours of hospital admission. Consider

abciximab, usually in the catheter laboratory, as an adjunct to PCI for patients at intermediate or higher

risk of adverse cardiovascular events who are not already receiving a glycoprotein IIb/IIIa inhibitor.

Balance the potential reduction in a patient's ischaemic risk with any increased risk of bleeding, when

determining whether a GPI should be offered.

Full details, including contraindications, adverse effects, dosage regimens, and modifications are in the

makers Summary of Product Characteristics which can be found athttp://www.medicines.org.uk
http://dx.doi.org/10.1056/NEJMoa1001266http://dx.doi.org/10.1056/NEJMoa1001266http://www.medicines.org.uk/http://www.medicines.org.uk/http://www.medicines.org.uk/http://www.medicines.org.uk/http://dx.doi.org/10.1056/NEJMoa1001266


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Offer unfractionated heparin as an alternative to fondaparinux to patients who are likely to undergo coronary

angiography within 24 hours of admission, and use monitoring of blood clotting (such as the activated clotting time

(ACT)) to determine the appropriate dose.

4. You should give unfractionated heparin.

Learning bite

Carefully consider the choice and dose of antithrombin in patients who have a high

risk of bleeding associated with any of the following:

Advancing age

Known bleeding complications

Renal impairment

Low body weight.

Offer systemic unfractionated heparin (50-100 U/kg) in the cardiac catheter

laboratory to patients receiving fondaparinux who are undergoing PCI.

As an alternative to the combination of a heparin plus a GPI, consider bivalirudin for

patients who:

Are at intermediate or higher risk of adverse cardiovascular events

(predicted six month mortality above 3.0%), and

Are not already receiving a GPI or fondaparinux, and

Are scheduled to undergo angiography (with follow on PCI if

indicated) within 24 hours of admission.

As an alternative to the combination of a heparin plus a GPI, consider bivalirudin for

patients undergoing PCI who:

Are at intermediate or higher risk of adverse cardiovascular events,

and

Are not already receiving a GPI or fondaparinux.

CLINICAL TIP

All anticoagulants are necessarily associated with a risk of bleeding complications

and weighing this risk against the potential benefits of such agents requires an


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understanding of the factors associated with bleeding risk, measures by which the

magnitude of this risk can be estimated, and the potential for benefit from these

agents in reducing the rate of ischaemic events. Close attention to appropriate

dosing of these agents is particularly important

Offer coronary angiography (with follow on PCI if indicated) within 96 hours of first admission to hospital to patients

who have an intermediate or higher risk of adverse cardiovascular events (predicted six month mortality above 3.0%)

if they have no contraindications to angiography (such as active bleeding or comorbidity). Perform angiography as

soon as possible for patients who are clinically unstable or at high ischaemic risk. An early invasive strategy does

have benefit, mainly in reducing recurrent ischaemia/infarction in the short term, but also in reducing longer term

mortality or reinfarction. However, this benefit appears to be greatest in those people at higher absolute risk of such

events (with the most benefit seen in those at the highest risk).

1. Assessment of LV function is recommended in all patients who have had an MI.

Consider assessing LV function in all patients with unstable angina.

Record measures of LV function in the patient's care record and in correspondence

with the primary healthcare team and the patient.

It is logical to assess LV function in all people with unstable angina and NSTEMI so

that specific treatment for LV dysfunction can be offered to improve symptoms and

outcome. Left ventricular function may improve after an acute ischaemic event with

the resolution of myocardial stunning and the onset of healing. It may also

deteriorate because of myocardial remodelling or progression of coronary disease.

It may therefore also be important to monitor LV function during follow up, because

of this potential for change with time.

b : Assessing his LV function is not needed as he is at low risk

Assessment of LV function is recommended in all patients who have had an MI.

Learning bite

To detect and quantify inducible ischaemia, consider ischaemia testing before

discharge for patients whose condition has been managed conservatively and who

have not had coronary angiography.

If untreated, the prognosis of patients with non-ST elevation myocardial infarction is

poor and mortality high, particularly in people who have had myocardial damage


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1. In May 2009 the product information for all clopidogrel containing medicines was amended to discourage the

concomitant use of PPIs and clopidogrel unless absolutely necessary.

Since then, the Committee for Medicinal Products for Human Use (CHMP) has

become aware of the results of a number of new studies, some of which put in

question the clinical relevance of interactions between PPIs as a class and

clopidogrel. However, two studies, completed at the end of August 2009, looked

into the effect of omeprazole on the blood levels of the active form of clopidogrel.

The studies confirmed that omeprazole can reduce the levels of the active form of

clopidogrel in the blood and reduce its antiplatelet effects, therefore supporting the

conclusion that there is an interaction between clopidogrel and omeprazole and

esomeprazole.

Taking all of the currently available data into account, the CHMP and its

Pharmacovigilance Working Party concluded that there are no solid grounds to

extend the warning to other PPIs. The class warning for all PPIs has been replaced

with a warning stating that only the concomitant use of clopidogrel and omeprazole

or esomeprazole should be discouraged

KEY PRINCIPLES

You should adapt your consultation style to the needs of individual patients so

that all patients have the opportunity to be involved in decisions about their

medicines at the level they wish

Establish the most effective way of communicating with each patient and, if

necessary, consider ways of making information accessible and understandable

(for example, using pictures, symbols, large print, different languages, an

interpreter, or a patient advocate)

Offer all patients the opportunity to be involved in making decisions about

prescribed medicines. Establish what level of involvement in decision making the

patient would like

Be aware that increasing patient involvement may mean that the patient decides

not to take or to stop taking a medicine. If in the healthcare professional's view

this could have an adverse effect, then the information provided to the patient on

risks and benefits and the patient's decision should be recorded


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Accept that the patient has the right to decide not to take a medicine, even if you

do not agree with the decision, as long as the patient has the capacity to make an

informed decision and has been provided with the information needed to make

such a decision

Be aware that patients' concerns about medicines, and whether they believe they

need them, affect how and whether they take their prescribed medicines

Offer patients information that is relevant to their condition, possible treatments,

and personal circumstances, and that is easy to understand and free from jargon

Recognise that non-adherence is common and that most patients are non-

adherent sometimes. Routinely assess adherence in a non-judgmental way

whenever you prescribe, dispense, and review medicines

Be aware that although adherence can be improved, no specific intervention can

be recommended for all patients. Tailor any intervention to increase adherence to

the specific difficulties with adherence the patient is experiencing

Review patient knowledge, understanding, and concerns about medicines, and a

patient's view of their need for medicine at intervals agreed with the patient,

because these may change over time. Offer repeat information and review to

patients, especially when treating long term conditions with multiple medicines

KEY POINTS

As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and

antithrombin therapy have been offered, formally assess individual risk of future

adverse cardiovascular events using an established risk scoring system that

predicts six month mortality (for example, Global Registry of Acute Cardiac

Events (GRACE))

Consider intravenous eptifibatide or tirofiban as part of the early management for

patients who have an intermediate or higher risk of adverse cardiovascular events

(predicted six month mortality above 3.0%), and who are scheduled to undergo

angiography within 96 hours of hospital admission

Offer coronary angiography (with follow on PCI if indicated) within 96 hours of first

admission to hospital to patients who have an intermediate or higher risk of

adverse cardiovascular events (predicted six month mortality above 3.0%) if they

have no contraindications to angiography (such as active bleeding or


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comorbidity). Perform angiography as soon as possible for patients who are

clinically unstable or at high ischaemic risk

When advising patients about the choice of revascularisation strategy (PCI or

CABG), take account of coronary angiographic findings, comorbidities, and the

benefits and risks of each intervention. When the role of revascularisation or the

revascularisation strategy is unclear, resolve this by discussion involving an

interventional cardiologist, cardiac surgeon, and other healthcare professionals

relevant to the needs of the patient. Discuss the choice of revascularisation

strategy with the patient

To detect and quantify inducible ischaemia, consider ischaemia testing before

discharge for patients whose condition has been managed conservatively and

who have not had coronary angiography

Before discharge offer patients advice and information about:

Their diagnosis and arrangements for follow up

Cardiac rehabilitation

Management of cardiovascular risk factors and drug therapy for

secondary prevention

Lifestyle changes

CLINICAL TIPS

NICE Technology Appraisal 182 states "Prasugrel in combination with aspirin is recommended as an option for

preventing atherothrombotic events in people with acute coronary syndromes having percutaneous coronary

intervention, only when:

Immediate primary percutaneous coronary intervention for ST-segment-elevation

myocardial infarction is necessary

Stent thrombosis has occurred during clopidogrel treatment

The patient has diabetes mellitus."

The common side effects of clopidrogel include bruising, haematoma (normally seen associated with a procedure,

surgery, or trauma), epistaxis, gastrointestinal haemorrhage, diarrhoea, abdominal pain, dyspepsia, bleeding at

puncture site.

THE ALGORITHM


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To download this algorithm please go to:

4. NICE Technology Appraisal 182 states Prasugrel in combination with aspirin is recommended as an

option for preventing atherothrombotic events in people with acute coronary syndromes having

percutaneous coronary intervention, only when:

Immediate primary percutaneous coronary intervention for ST-segment-elevation

myocardial infarction is necessary

Stent thrombosis has occurred during clopidogrel treatment

The patient has diabetes mellitus."

Prasugrel is currently a black triangle medicine. A black triangle is assigned to a product if the drug is an

active substance which has been newly licensed for use in the UK. The black triangle symbol is not


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removed until the safety of the drug is well established. The MHRA wishes to receive all reports of

suspected adverse reactions associated with black triangle products, in order to:

Confirm risk/benefit profiles established during the premarketing phase

Increase our understanding of the safety profiles of new medicines

Ensure that previously unrecognised side effects are identified as quickly as possible.

Specific contraindications to prasugrel are:

Hypersensitivity to the active substance or to any of the excipients

Active pathological bleeding

History of stroke or transient ischaemic attack (TIA)

Severe hepatic impairment (Child-Pugh class C).

Full details of caution in use and side effects are included in the makers SPC available at

http://www.medicines.org.uk/emc/

Safety in patients with acute coronary syndrome undergoing PCI was evaluated in one clopidogrel

controlled study (TRITON) in which 6741 patients were treated with prasugrel (60 mg loading dose and

10 mg once daily maintenance dose) for a median of 14.5 months (5802 patients were treated for over

six months, 4136 patients were treated for more than one year). The rate of study drug discontinuation

due to adverse events was 7.2% for prasugrel and 6.3% for clopidogrel. Of these, bleeding was the

most common adverse reaction for both drugs leading to study drug discontinuation (2.5% for prasugrel

and 1.4% for clopidogrel).
http://www.medicines.org.uk/emc/http://www.medicines.org.uk/emc/http://www.medicines.org.uk/emc/

ECG in patients with chest pain

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