VAISHNAVI SURESH NAIRGROUP:7

NON -ST ELEVATION MYOCARDIAL INFARCTION

Case:

An 81-year-old African American female (AAF) with

a past medical history (PMH) of hypertension (HTN),

diabetes type 2 (DM2), coronary artery disease

status post myocardial infarction (CAD S/P MI) 5

years ago, and chronic abdominal pain for 2 years

without a clear reason, was admitted to the hospital

with a worsening of the same abdominal pain for 2-3 days.

No chest pain (CP) or shortness of breath (SOB).

She complains of nausea and vomiting.

Physical examination

38.8 C HR-78 bpm-210/100 mm/Hg

Abdomen: RLQ tenderness, no rebound, soft, +BS.

The rest of the examination was not remarkable.

What laboratory workup would you suggest?

CBC, Comprehensive Metabolic Panel, Amylase, Lipase, Urinalysis were all normal.

KUB (Kidney Ureter Bladder) was nonspecific.

CT of abdomen showed a dilated stomach,

stable 3.6 cm AAA (the same size as 2 years ago) and old renal cysts.

Patient was started on IVF,

Pain meds and Zosyn for T* 38.3. Blood cx were taken.

What is the most likely diagnosis?

Diverticulitis?

Appendicitis? (no, appendectomy was

done years ago).

DM Gastro paresis?

Gastroenteritis?

What happened?

ECG on admission showed deep Qs

waves in the inferior leads - probably an

old MI.

Cardiac enzymes x 1 were ordered.

EKG BEFORE MI

EKG AFTER MI

showing acute

changes ofNSTEMI

Cardiac enzymes were positive, showing troponin elevation

Final diagnosis

Non-ST elevation myocardial infarction (Non-STEMI).

The catheterization showed a 99%

occlusion of one of the branches of the

circumflex artery (Cx). Two stents were

placed. The right coronary artery (RCA)

had a 90% proximal stenosis but both

stent placement and PTCA

(percutaneous transluminal coronary angioplasty) were unsuccessful. The

patient was scheduled for a repeated

catheterization for stent placement in RCA within 2-3 weeks.

A diagram of the stent placement in the Cx artery

TREATMENT IN THIS CASE:

SO???!!!

Always keep the possibility of an acute myocardial infarction (AMI) in

patients with risk factors, even with atypical symptoms. MI can be

completely painless in diabetics and women. We do not need the symptoms of chest pain (CP) to diagnose an MI.

In this case, the RLQ pain was not related to the MIbut with the previously diagnosed renal cyst.

It may be defined as a development of heart muscle necrosis (a form of cell death) without the ECG

(electrocardiography) change of ST-segment elevation, resulting from an acute interruption of blood

supply to a part of the heart and can be demonstrated by an elevation of cardiac markers (CK-MB or

troponin) in the blood.

ST-segment elevation indicates full thickness injury of heart muscle. Absence of ST-segment elevation

in NSTEMI involve (partial thickness) damage of heart muscle. Therefore, NSTEMI is less severe typeof heart attack compared to STEMI in which full thickness damage of heart muscle develops.

The most common mechanism of NSTEMI is rupture or erosion of an atherosclerotic plaque that triggers

platelet aggregation, which lead to formation of a thrombus (blood clot) in a coronary artery. This arterial

thrombus causes interruption of blood supply to part of the heart muscle; profound changes take place in

the heart muscle that lead to irreversible changes and death of myocardial cells. Usually, partial thickness damage of heart muscle occurs.

NSTEMI usually occurs by developing a partial occlusion of a major coronary artery or a complete

occlusion of a minor coronary artery previously affected by atherosclerosis. Atherosclerosis is a disease

of artery in which mainly cholesterol deposition occur within the wall of the artery. This deposited

cholesterol ultimately forms a plaque called atherosclerotic plaque. Many years are required to establish an atherosclerotic plaque.

NSTEMI:

Major risk factors:

1.High serum cholesterol level

2.Hypertension

3.Diabetes mellitus

4.Cigarette smoking

Minor risk factors:

1.Increasing age

2.Male gender

3.Family history

4.Physical inactivity

5.Obesity

6.Excess alcohol consumption

7.Excess carbohydrates intake

8.Social deprivation

9.Competitive and stressful lifestyle with type A personality

10.Diets deficient in fresh vegetables, fruit and polyunsaturated

fatty acids.

Symptoms:

(1)Chest pain: Chest pain is the main symptom. It is constricting, tightening, choking or heavy in character,

usually located in the centre of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most

commonly left arms). Occasionally, pain may be felt only at the sites of radiation. In older patients or those with

diabetes mellitus, painless attack may occur (pain conducting autonomic nerve of the heart are degenerated in

old age and in diabetes).

(2) Difficulty in breathing: Breathing difficulty occur when the damage to the heart muscle limits the pumping

action of the left ventricle, causing acute left heart failure and consequent lung congestion.

(3) Nausea, vomiting, and sweating: These are due to autonomic nervous system upset.

(4) Palpitation: It is due to sympathetic nervous system activation.

(5) Cardiogenic shock: If NSTEMI involve a large territory of heart, patients may present with shock due to

impaired myocardial function.

Diagnosis:

Initially, patients with suspected NSTEMI, ECG and cardiac markers estimation are mandatory

Electrocardiography (ECG): The usual ECG findings of NSTEMI are ST-segment depression

or T-wave inversion.

Cardiac markers:

Cardio-specific isoenzyme CK-MB (creatine kinase myocardial band), and cardiospecific proteins

troponin T and troponin I are rises in blood in NSTEMI. These are released from damaged heart muscle

cells during and after attack. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours.

Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two weeks.

Full blood count:

WBC (white blood cell) count is usually elevated. ESR (Erythrocyte sedimentation rate) and CRP (C-

reactive protein) may also elevate.

Chest X-ray:

Assess for signs of lung edema.

Echocardiography:

It is done for assessing the function of heart chamber and for detecting important complications.

Complications:

NSTEMI can lead to several complications immediately following an attack or later in recovery. Usually,

complications depend on what part of the heart is damaged and the extent of damage.

Immediate complications

(A) Heart arrhythmia – Heart arrhythmia is a disturbance of the electrical rhythm of the heart. In

NSTEMI, damaged heart muscle disrupts electrical signals and produces arrhythmia in which

heartbeat may be too fast, too slow or irregular. It is the most common complication following an

attack. The following types of arrhythmia may develop:

1.Ventricular fibrillation

2.Ventricular tachycardia

3.Ventricular ectopics

4.Accelerated idioventricular rhythm

5.Atrial fibrillation

6.Atrial tachycardia

7.Atrioventricular block

8.Sinus bradycardia

In majority of cases arrhythmia is mild and transient. It is controlled by rest, pain relief and medication.

But, life threatening arrhythmia may develop that is the major cause of death during the first 24 hours

after an attack.

In majority of cases arrhythmia is mild and transient. It is controlled by rest, pain relief and medication.

But, life threatening arrhythmia may develop that is the major cause of death during the first 24 hours

after an attack.

(B) Acute heart failure – It may develop when the damage area of the heart muscle is large. Suddenly,

this damaged heart cannot pump enough blood to meet the body’s demand and developed acute heart

failure.

(C) Cardiogenic shock – It may develop after the large territory heart muscle damage. It leads to failure

of the pumping action of the heart. The end results are very low blood pressure with an inadequate supply

of oxygen rich blood to the tissues of the body.

(D) Mitral regurgitation – Papillary muscle damage sometimes causes mitral regurgitation.

Late complications

(A)Dressler’s syndrome – This syndrome is characterized by fever, pleuritis and percarditis. It is caused

by an autoimmune reaction to damage heart muscle. It occurs a few weeks or even months after an

NSTEMI.

(B) Chronic heart failure – It occurs slowly over time after an attack in which the heart cannot pump

enough blood to meet the body’s demand.

Treatment:

Patients should be admitted immediately to hospital, preferably to a cardiac care unit because there

is a significant risk of death.

(1) Bed rest with continuous monitoring by ECG.

(2) Inhaled oxygen therapy.

(3) Relief of pain by opiate analgesic:

Intravenous morphine 10 mg or diamorphine 5 mg is usually used and may have to be repeated to

relieve severe pain.

(4) Antiplatelet therapy:

Antiplatelet drugs prevent platelet aggregation within coronary artery. A 300 mg tablet of aspirin should

be given orally as early as possible then 75 mg daily should be continued indefinitely if there are no

side effects occur. Aspirin reduces the mortality rate of NSTEMI by approximately 25%. In combination

of aspirin, clopidogrel 600 mg should be given orally as early as possible, followed by 150 mg daily for 7

days and 75 mg daily thereafter, gives a further reduction in mortality. Ticagrelor 150 mg followed by 90

mg two times daily is more effective than clopidegrol. High risk patients, especially patients with

diabetes mellitus or patients who undergo percutaneous coronary intervention (PCI), should also be

considered for intake of glycoprotein IIb/IIIa receptor blocker (block the final common pathway of

platelet aggregation), such as tirofiban, abciximab, or eptifibatide.

(5) Anticoagulant therapy:Anticoagulant drugs prevent reinfarction, and reduces the risk of thromboembolic complications.

Anticoagulation can be achieved by using unfractionated heparin, low molecular weight heparin (also

called fractionated heparin and includes enoxaparin, dalteparin) or a pentasaccharide (fondaparinux).

Comparatively low molecular weight heparin is more safety and efficacious than unfractionated heparin,

and pentasaccharide is more safety and efficacious than low molecular weight heparin. The dose

regimens are:

1.Enoxaparin: 1 mg/kg body weight two times daily usually for 8 days by subcutaneous injection.

2.Dalteparin: 120 units/kg body weight two times daily usually for 8 days by subcutaneous injection.

3.Fondaparinux: 2.5 mg daily usually for 8 days by subcutaneous injection.

(6) Beta-blockers:Beta-blockers reduce arrhythmias, heart rate, blood pressure and myocardial oxygen demand, and relive

pain. Oral beta-blocker atenolol 25-50 mg twice daily, metoprolol 25-50 mg twice daily, or bisoprolol 5 mg

once daily are usually adequate. Patients with heart rate more than 90 beats/minute or patients with

hypertension (systolic blood pressure more than 150 mmHg or diastolic more than 90 mmHg),

intravenous beta-blockers (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be given. Beta-

blockers should be avoided if there is heart failure, heart block, hypotension, or bradycardia.

(7) Nitrates:

Nitrates act as a vasodilator and relief pain. Nitrates should first be given buccally or by sublingual (under

tongue) spray. If the patient experiencing persistent ischemic chest pain after 3 doses given 5 minutes

apart, then intravenous glyceryl trinitrate 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour can be given

until pain relieved or systolic blood pressure falls to less than 100 mgHg. Oral or sublingual nitrates can be

used once the pain has resolved.

(8) Statins:

Irrespective of serum cholesterol level, all patients should receive statin such as atorvastatin, simvastatin,

or rosuvastatin after NSTEMI.

(9) ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor blockers):

An ACE inhibitor such as ramipril, enalapril, captopril, or lisinopril is started 1 or 2 days after NSTEMI.

ACE inhibitor therapy reduces ventricular remodeling, prevent the onset of heart failure, and reduce

recurrent infarction. An ARB (valsartan, candesartan, losartan or olmesartan) is suitable alternatives in

patients who are intolerant of ACE inhibitors (ACE inhibitors can cause dry cough).

(10) Coronary angiography and revascularization:

Before giving revascularization treatment, risk analysis in patients with NSTEMI should be done

immediately after hospital admission. Several systems are available for risk stratification, but TIMI

score and GRACE score are the best. These systems categorized the patients into low, medium

and high risk groups.

Medium to high risk patients should be considered for early coronary angiography and

revascularization, either by PCI (percutaneous coronary intervention) or by CABG (coronary artery

bypass grafting). Early medical treatment is appropriate in low risk patients, and coronary

angiography and revascularization are reserved for those who fail to settle with medical treatment.

Prognosis:

Early death in NSTEMI is usually due to an arrhythmia. Long term mortality is high in those who have

extensive damage of heart muscle, poor left ventricular function and persistent ventricular arrhythmia.

Depression, social isolation and old age are also associated with a higher mortality. According to GRACE

score, in-hospital death is less than 1% in low risk, 1-9% in medium risk and more than 9% in high risk

patients with non-ST segment elevation myocardial infarction. After hospital discharge, more than 80%

patients survive for a further year, approximately 75% for 5 years, 50% for 10 years and 25% for 20 years.

Lifestyle after NSTEMI:

► Restrict physical activities for four to six weeks after attack – death tissue in damage heart muscle

takes 4-6 weeks to be healed with fibrous tissue.

► Cessation of cigarette smoking.

► Maintaining an ideal body weight.

► Eating a Mediterranean style diet (diet rich in monounsaturated fatty acids and omega-3 fatty acids,

but low in saturated fatty acids).

► Achieving well control of high pressure and diabetes mellitus if present.

► Taking regular exercise up to, but not beyond, the point of chest discomfort.

► Continue secondary prevention drugs therapy including aspirin, clopidogrel, beta-blocker, ACE inhibitor, and statin.

GRACE SCORE:

GRACE (Global Registry of Acute Coronary Events) score is used for risk assessment in ACS

(acute coronary syndrome) which includes NSTEMI, STEMI and unstable angina. This score

is more accurate because it is derived from a multinational registry of unselected patients and

includes hospitals in Europe, Asia, North America, South America, Australia and New Zealand.

Risk assessment should be performed at the time of hospital admission and is important

because it gives an idea about probability of in-hospital death and also guides the appropriate treatment plan in NSTEMI and unstable angina.

Calculation of GRACE score:

Eight parameters are used for calculating GRACE score that include patient’s age,

heart rate, systolic blood pressure, Killip class, serum creatinine level, cardiac

arrest at hospital admission, ST-segment deviation in ECG and elevated

cardiac marker.

Treatment plan according to GRACE risk stratification:

In low risk patients with NSTEMI or unstable angina, medical treatment is appropriate and surgical

intervention is reserved for those who fail to settle with medical treatment. By contrast, medium and

high risk patients with NSTEMI or unstable angina should be treated with multiple drugs and

considered for early coronary angiography and revascularization. Revascularization can be done

either by percutaneous coronary intervention (PCI) or by coronary artery bypass grafting (CABG).

Treatment plan in STEMI is not depend on risk stratification. All patients with STEMI should be

treated immediately with reperfusion therapy by primary percutaneous coronary intervention (PCI)

along with multiple drugs. Where PCI cannot be achieved within 120 minutes of diagnosis or PCI is

not available, thrombolytic therapy (streptokinase, alteplase, tenecteplase, or reteplase) may be

given.

Age (years) Score

≤ 30 0

30-39 8

40-49 25

50-59 41

60-69 58

70-79 75

80-89 91

≥ 90 100

1. Age: 2. Heart rate:

Heart rate (beats/minute)

Score

≤ 50 0

50-69 3

70-89 9

90-109 15

110-149 24

150-199 38

≥ 200 46

Systolic blood pressure (mm Hg)

Score

≤ 80 58

80-99 53

100-119 43

120-139 34

140-159 24

160-199 10

≥ 200 0

3. Systolic blood

pressure:

Killip class Score

I (No heart failure) 0

II (Crackles audible in lower half of lung field) 20

III (Crackles audible in whole lung field) 39

IV (Cardiogenic shock) 59

4. Killip class:

Serum creatinine (μmol/L)

Serum creatinine (mg/dl)

Score

0-34 0-0.38 1

35-70 0.39-0.79 4

71-105 0.80-1.19 7

106-140 1.20-1.58 10

141-176 1.59-1.90 13

177-353 2.0-3.99 21

≥ 354 ≥ 4 28

5. Serum creatinine level:

Cardiac arrest at hospital admission Score

Absent 0

Present 39

6. Cardiac arrest at hospital admission:

ST-segment deviation in ECG Score

Absent 0

Present 28

7. ST-segment deviation in ECG:

Elevated cardiac marker

Score

Absent 0

Present 14

8. Elevated serum cardiac marker (Troponin or

CK-MB):

Total score Risk assessment

≤ 100Low risk patients– In-hospital death rate less than 1%

101-170Medium risk patients – In-hospital death rate 1-9%

≥ 171High risk patients – In-hospital death rate more than 9%

Risk assessment by GRACE score:

We can assess risk by summation of score for all eight parameters.

Total score In-hospital death (%)

≤ 60 ≤ 0.2

70 0.3

80 0.4

90 0.6

100 0.8

110 1.1

120 1.6

130 2.1

140 2.9

150 3.9

160 5.4

170 7.3

180 9.8

190 13

200 18

210 23

220 29

230 36

240 44

≤ 250 ≤ 52

Probability of in-hospital death by GRACE score:

TIMI score

TIMI (Thrombolysis In Myocardial Infarction) score is used in patients with NSTEMI (Non ST-segment

elevation myocardial infarction), STEMI (ST-segment elevation myocardial infarction) and unstable

angina to define risk. TIMI Study Group established this risk score. TIMI Study Group is an Academic

Research Organization affiliated with Harvard Medical School, and Brigham and Women’s Hospital in

Boston. This score was derived from patients enlisted to randomized controlled trials of low molecular weight heparins. The main advantages of TIMI score are its simplicity and ease of use.

TIMI risk score for patients with NSTEMI or unstable angina:

Seven variables are used to assess risk in NSTEMI or unstable angina including age of patient, risk

factors for coronary artery disease, prior coronary artery stenosis, ST-segment deviation on ECG, prior

aspirin intake, severe anginal chest pain within 24 hours and elevated cardiac markers. It is done immediately after an attack.

Age of patient Score

Less than 65 years

0

65 years or more 1

1. Age of patient:

2. Risk factors for coronary artery disease:

Five risk factors are included. These are:

•Hypertension (high blood pressure)

•Hypercholesterolemia (high blood cholesterol level)

•Family history of coronary artery disease

•Diabetes

•Smoking

Number of risk factors for coronary artery disease

Score

Presence of less than three 0

Presence of three or more 1

3. Prior coronary artery stenosis:

Coronary angiography is done to see the stenosis.

Prior coronary artery stenosis

Score

Less than 50% 0

50% or more 1

4. ST-segment deviation on ECG:

It includes horizontal ST-segment depression or transient

ST-segment elevation more than 1 mm.

ST-segment deviation on ECG

Score

Absent 0

Present 1

Prior aspirin intake Score

No aspirin intake in the last 7 days

0

Aspirin intake in the last 7 days

1

5. Prior aspirin intake:

Severe anginal chest pain Score

No or one episode in last 24 hours

0

Two or more episodes in last 24 hours

1

6. Severe anginal chest pain:

Elevated cardiac markers Score

Absent 0

Present 1

7. Elevated cardiac markers (CK–MB or troponin):

Risk stratification by TIMI score in patients

with NSTEMI or unstable angina:

Risk stratification Score

Low risk patients 0 – 2

Medium risk patients 3 – 4

High risk patients 5 – 7

Plan of treatment according to TIMI score:

In low risk patients with NSTEMI or unstable angina, drug therapy is appropriate and surgical

intervention is reserved for those who fail to settle with drug therapy. By contrast, medium to high risk

patients with NSTEMI or unstable angina should be treated with multiple drugs and considered for early coronary angiography and revascularization.

Interpretation of TIMI score in NSTEMI or unstable angina:

Total score

Rate of death, or new or recurrent myocardial infarction, or severe recurrent anginal chest pain requiring urgent revascularization in 14 days

0 – 1 4.7%

2 8.3%

3 13.2%

4 19.9%

5 26.2%

6 – 7 40.9%

TIMI risk score for patients with STEMI:

Eleven variables are used to assess risk in STEMI that are age of patient, history of anginal chest pain,

history of hypertension, history of diabetes, systolic blood pressure, heart rate, Killip class, weight of

patient, anterior myocardial infarction in ECG, left bundle branch block (LBBB) in ECG and delay to treatment after an attack.

Total score Risk of death at 30 days

0 0.8%

1 1.6%

2 2.2%

3 4.4%

4 7.3%

5 12.4%

6 16.1%

7 23.4%

8 26.8%

9 – 16 35.9%

Interpretation of TIMI score in STEMI:

PAHOPHYSIOLOGY OF NSTEMI:

NSTEMI occurs by developing a complete occlusion

of a minor coronary artery or a partial occlusion of a

major coronary artery previously affected by

atherosclerosis. This causes a partial thickness damage of heart muscle.

PATHOPHYSIOLOGY OF STEMI:

STEMI occurs by developing a complete occlusion

of a major coronary artery previously affected by

atherosclerosis. This causes a full thickness damage of heart muscle.

NSTEMI VS STEMI

ECG FINDINGS OF NSTEMI:

The usual ECG findings of NSTEMI are ST-segment

depression or T-wave inversion. NSTEMI does not

show ST segment elevation in ECG (due to partial

thickness injury of heart muscle) and later does not

progress to a Q-wave. For this reason, it is also called a non–Q-wave myocardial infarction (NQMI).

ECG FINDINGS OF STEMI:

STEMI shows ST segment elevation in ECG (due to

full thickness injury of heart muscle) and later

progress to a Q-wave. For this reason, it is also

called a Q-wave myocardial infarction (QWMI). The

ultimate ECG findings of STEMI are ST-segment

elevation, pathological Q-wave formation and T-wave inversion.

DDX OF NSTEMI & STEMI:

1) BY ECG:

The diagnosis of a NSTEMI is based on a

typical history of chest pain, no ST segment

elevation in ECG plus elevation of cardiac

markers in serum.

The diagnosis of a STEMI is based on a typical

history of chest pain, ST segment elevation in

ECG plus elevation of cardiac markers in

serum.

2) CARDIAC MARKERS:

Cardiac markers including CK-MB (creatine

kinase myocardial band), troponin I and

troponin T, all elevate both in cases. But the

elevation of these markers is often mild in NSTEMI compared with STEMI

COMPLICATIONS:

Complications like cardiogenic shock, left ventricular

failure, severe mitral regurgitation due to papillary

muscle rupture, cardiac tamponade due to

ventricular wall rupture are more in STEMI (due to full thickness heart muscle damage) than NSTEMI.

PROGNOSIS:

Long-term mortality is similar or higher in NSTEMI

compared to STEMI (two year mortality is approximately 30% in both cases).

Antiplatelets (Aspirin, Clopidogrel, Ticagrelor), Anticoagulants (Enoxaparin, Dalteparin, Fondaparinux),

Beta-blockers (atenolol, metoprolol, bisoprolol), Nitrates (isosorbide dinitrate, glyceryl trinitrate), Statins

(atorvastatin, rosuvastatin, simvastatin, pitavastatin), ACE inhibitors (Ramipril, enalapril, captopril,

Lisinopril) or ARBs (valsartan, candesartan, losartan, olmesartan) are given both in NSTEMI and STEMI.

In case of reperfusion therapy, primary PCI (percutaneous coronary intervention) is the treatment of choice

for STEMI. Where primary PCI cannot be achieved within 120 minutes of diagnosis or PCI is not available,

thrombolytic therapy such as streptokinase, tenecteplase, alteplase or reteplase should be given.

On the other hand, early coronary angiography and revascularization, either by PCI or by CABG (coronary

artery bypass grafting) is the treatment of choice for medium to high risk patients with NSTEMI.

Drug treatment is appropriate in low risk patients with NSTEMI, and coronary angiography and

revascularization reserved for those who fail to settle with drug treatment (low, medium and high risk

patients are categorized in NSTEMI by GRACE score) . Thrombolytic therapy is harmful in NSTEMI. The

aggregate data suggest that patients with NSTEMI may be put at risk of re infarction if thrombolytic therapy

is used.

TREATMENT:

http://emedicine.medscape.com/article/1910735-overviewhttp://nstemi.org/grace-score/http://nstemi.org/http://nstemi.org/timi-score/

REFERENCE: