NSTEMI DrHafiz

NON-ST ELEVATION MIBBH, Bangalore

Ahmad Hafiz

Nov 2011

ACUTE CORONARY SYNDROME SPECTRUM

Ischemic Heart Disease

Acute Coronary Syndrome

STEMI

NSTEMI

Minimal Myocardial

Necrosis

Unstable Angina

Coronary Artery Disease

Stable Angina

ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency >

Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention

WHAT IS NSTEMI?

Unstable angina = angina pectoris with at least one of three features:

1. it occurs at rest (or with minimal exertion) usually lasting more than 20 minutes (if not interrupted by nitroglycerin)

2. it is severe and described as frank pain and of new onset (i.e., within 1 month); and

3. it occurs with a crescendo pattern (i.e., more severe, prolonged, or frequent than previously). With or without ischemic ECG changes

NSTEMI = UA with evidence of myocardial necrosis on the basis of the release of cardiac markers



Davidson pg. 589

PATHOPHYSIOLOGY

UA/NSTEMI is caused by

reduction in oxygen supply

and/or increased myocardial

oxygen demand

superimposed on an

atherosclerotic coronary

plaque with varying

degrees of obstruction



1. Plaque rupture or erosion with superimposed non-occlusive thrombus

2. Dynamic obstruction

3. Progressive mechanical obstruction

4. Secondary unstable angina related to increased myocardial oxygen demand and/or decreased supply

RISK FACTORS

Increasing age

Male gender

Family history

Smoking

Hypertension

Hyper-cholesterol-

emia

Diabetes mellitus

Physical activity

Obesity

Alcohol

Personality

CLINICAL PRESENTATION

SYMPTOMS:

chest discomfort

epigastric discomfort

shortness of breath

nausea and vomiting

excessive sweating

palpitation, anxiety, sense of

impending doom, and feeling of

being acutely ill



PHYSICAL EXAMINATION

Resembling that of stable angina

Large NSTEMI may resemble that of large STEMI e.g. diaphoresis, pale cool skin, sinus tachycardia, S3 or S4, basilar rales and sometimes hypotension

Signs of co-morbidities e.g. peripheral or cerebrovasculardiseases

Autonomic disturbances e.g. pallor, sweating

Complications e.g. arrhythmia or heart failure



ECG CHANGES

1. ST depression (70-80%)

2. T wave inversion (10-20%)

3. Both ST depression and T

wave inversion

4. Post MI NSTEMI - ECG

changes variable (Ironically,

even a residual ST elevation

may be present)

5. Normal ECG



CARDIAC MARKERS



TROPONIN-T

Peak – 12 hours

Troponin is released during MI from the cytosolic

pool of the myocytes

Its subsequent release is prolonged with

degradation of actin and myosin filaments

Differential diagnosis of troponin elevation

includes acute infarction, severe pulmonary

embolism causing acute right heart overload,

heart failure, myocarditis

Troponins can also calculate infarct size but the

peak must be measured in the 3rd day. released

in 2–4 hours and persists for up to 7 days.

BNP

B-type natriuretic peptide is a cardiac

neurohormone released upon ventricular myocyte

stretch as proBNP, which is

enzymatically cleaved to the N-terminal proBNP

(NT-proBNP) and, subsequently, to BNP. The

usefulness of assessing this neurohormone was

first shown for the diagnosis and evaluation of

HF.

GLYCOGEN PHOSPHORYLASE

ISOENZYME BB

Peak – 7 hours

Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase

Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue

Because of the blood-brain barrier GP-BB can be seen as heart muscle specific. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the "new cardiac markers" which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1–3 hours after process of ischemia.

MYOGLOBIN (MB)

Myoglobin is used less than the other markers

Myoglobin is the primary oxygen-carrying

pigment of muscle tissue

It is high when muscle tissue is damaged but it

lacks specificity. It has the advantage of

responding very rapidly, rising and falling earlier

than CK-MB or troponin. It also has been used in

assessing reperfusion after thrombolysis

CK-MB

Peak – 10-24 hours

CK-MB resides in the cytosol and facilitates high

energy phosphates into and out of mitochondria

It is distributed in a large number of tissues even

in the skeletal muscle

Since it has a short duration, it cannot be used

for late diagnosis of acute MI but can be used to

suggest infarct extension if levels rise again

This is usually back to normal within 2–3 days.

MANAGEMENT GUIDELINE

Suspicion

Early management

-Emergency management

-Hospital phase management

-Pharmacotherapy

Late Management

-Risk stratification

-Life style modification

-Secondary prevention drug therapy

ALGORITHM FOR EVALUATION AND

MANAGEMENT OF PATIENTS SUSPECTED OF

HAVING ACS

EMERGENCY MANAGEMENT

ABC, Pulse Oximeter, Attach ECG monitor and record 12-lead ECG,

High flow O2 by face mask

IV access [bloods for CBC, U&E, glucose, lipids, cardiac enzymes]

Brief assessment

History of CVS disease, risk factors for IHD

Examination: pulse, BP, JVP, cardiac murmurs, scar from previous cardiac surgery

Aspirin 300 mg or Clopidogrel 75mg

Morphine 5-10 mg IV + metoclopramide 1 mg IV

GTN sublingually

Thrombolysis management

Beta blockers + ACEI



ACUTE REPERFUSION THERAPY

1. Thrombolysis

2. PCI

3. CABG

Aim :•Restore coronary patency•Preserves left ventricular function•Improves survival rate and reduced mortality rate.

THROMBOLYSIS

Indication:

Ischaemic chest pain > 30 minutes

duration

Less than 12 hours from the onset of pain

ECG changes:

new ST elevation of at least 2 mm in two

consecutive chest leads;

or ST elevation of at least 1 mm in two

consecutive limb leads;

or a new left bundle branch block.



FibrinolysisStreptokinase Dosage : 1.5 million units in 100 ml saline

Route of administration : IV infusion over 1 hour

Mode of action : Catalyze the conversion of plasminogen to active plasmin which further lysethe clots.

Side effects :-Allergic manifestations-Hypotension-Systemic bleeding

Note: production of circulating neutralizing antibodies following therapy may cause subsequent infusion with streptokinase ineffective

AlteplaseTissue plasminogen activators

MOA : specifically bound to fibrin-bound plasminogen

Route of administration:

IV infusion over 90 minutes duration

Side effects :

less compared to streptokinase

- risk of intracranial bleeding

Other drugs:

Tenecteplase –longer plasma half life

Reteplase - given as double bolus instead of infusion

First 30 mins Bolus dose 15mg

Followed by 0.75mg/kg

Next 60 mins 0.5mg/kg

(not > 35mg)

FULL THERAPEUTIC ANTICOAGULATION

Use either an infusion of unfractionated

heparin or low molecular weight heparin(e.g.,

enoxaparin sodium).

In the context where pathology is not readily

available, low molecular weight heparin is often

easier to use

enoxaparinsodium 1 mg/kg subcutaneously

twice daily

http://vitualis.wordpress.com/2006/06/20/how-to-use-unfractionated-heparin/



http://vitualis.wordpress.com/2006/06/21/how-to-use-low-molecular-weight-heparin/

ADJUNCTIVE THERAPY

Consider intravenous beta-blocker (metoprolol 5

mg IV slow bolus at 0 min, 5 min and 10 min to

give a total dose of 15 mg) then oral therapy (2).

IV beta-blockers decreases mortality when given

early in acute myocardial infarction though the

evidence is less clear in the reperfusion therapy

setting;

it is more commonly used in the United States and

parts of Europe and is routine therapy in

Scandinavia.

ACE-inhibitors: when started within 24 hours

reduce morbidity and mortality.

CONTRAINDICATIONS TO THROMBOLYTIC

THERAPY

Active internal bleeding

Previous history of subarachnoid or

intracerebral bleeding

Uncontrolled hypertension

Recent surgery (less than 1 month)

Recent trauma

High probability of active peptic ulcer

Pregnancy

PRIMARY PERCUTANEOUS CORONARY

INTERVENTION

Primary percutaneous intervention is more effective

than thrombolysis for treatment of AMI.

Death, non fatal reinfarction and stroke reduced

from 14% with thrombolytic therapy to 8% with

primary PCI

Keeley EC, et al. Lancet 2003;361:13-20



Treatment of choice to prevent reinfarction

Avoid hemostatic problems encounter with thrombolytic therapy

Preferred in case of presence of cardiogenic shock, bleeding risk, symptoms of more than 2-3h

Disadvantage

Expensive in terms of facilities and personnel, limited availability.

CORONARY ARTERY BYPASS GRAFTING

(CABG) surgical procedure performed

to relieve angina and reduce the risk of death from coronary artery disease.

Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic

narrowing and improve the blood supply to the coronary circulation supplying the myocardium.



HOSPITAL PHASE MANAGEMENT

Coronary care units- provide intensive care. Duration of stay

depends on the condition of patient.

Activity – advise bed rest for first 12 hours, as increase workload

to the heart may cause increase size of the infarct.

Diet – clear liquids for first 4-12 hours due to risk of emesis and

aspiration. Diet should contain 50% complex carbohydrate and low

fat contents.

Bowels – prevention of constipation by giving high fiber diet,

laxative can be prescribed.

Sedation – Diazepam, oxazepam or lorazepam is given for sedation

to enforced inactivity with tranquility.



LATE MANAGEMENT

Risk stratification and investigation

1. Left ventricular functions

Assess by physical findings i.e tachycardia,3rd heart

sounds, crackles at lung bases

Echocardiography and radionuclide imaging to assess LV

ejection fraction.

2. Arrhythmias

Presence of ventricular arrhythmias during convalescence

phase may benefit from specific anti arrhythmic therapy

such as implantable cardiac defibrillator.



3. Early post MI ischemia is managed like unstable angina

If no spontaneous ischemia, assess by exercise testing to look for residual ischemia

-Good exercise tolerance – 1-4% chance of adverse event in 12 months

-Low exercise tolerance – consider revascularization by CABG

4. Other risk factors include age >75,diabetic patient, prolonged sinus tachycardia, hypotension and silent ischemia

SECONDARY PREVENTION

Long term drug therapy with low dose aspirin, clopidogrel, beta blockers and ACEI

Cessation of smoking

Control of hypertension and hyperlipidemia

Regular exercise

Diet – diet high in fibers, fruit, oily fish, low in saturated fat, weight control

Returning to work after 4-6 weeks



REFERENCE

2011 ACC/AHA Guidelines for the Management

of Patients With Unstable Angina/Non–ST-

Elevation Myocardial Infarction

http://content.onlinejacc.org/cgi/content/short/57/19/

e215

Harrison's Principles of

Internal Medicine, 17e

Davidson’s Principles & Practice of Medicine, 20e

wikipedia

Medscape

http://emedicine.medscape.com/article/811905-

overview#aw2aab6b3

http://content.onlinejacc.org/cgi/content/short/57/19/e215

http://content.onlinejacc.org/cgi/content/short/57/19/e215

http://emedicine.medscape.com/article/811905-overview



The End

Health & Medicine

NSTEMI DrHafiz