Plavix

The Algoritm of Diagnose Acute Coronary Syndromeand It’s Spectrum

Azhari Gani

Coronary Artery Disease

Etiology Risk factors Nonmodifiable vs. modifiable risk

factors Clinical manifestations Goals of therapy Medications

ATHEROSCLEROSIS

START

END

Pembuluh darah yang mengalami aterosklerosis & trombosis

STEMI UA/NSTEMI

CORONARY ARTERY

RCA

LM

LCX

LAD

Acute Coronary Syndrome

EKG changes with MI

Initial 12-Lead ECG

ECG changes with time

What If the Look Like This?

AMI

Ischaemia

Injury

Infarction

What If the Look Like This?

Location of MI

Depends on which artery is affectedLV receives most of the CA supply and

so it is the most affectedLeft Anterior Descending (LAD)Left Circumflex artery (LCA)Right Coronary Artery (RCA)

General Types of MI

Transmural-invades full thickness of myocardium

Subenedocardial-invades partial thickness

Collateral Circulation

A network of blood vessels present at birth that can dilate and become functional a/r/o coronary artery occlusion and ischemia. “collateral circulation”

Natural “bypass” mechanism helps decrease the size of the MI

Risk Factors and Etiology

CAD and its risk factors Any situation requiring increased O2

in the presence of decreased O2 supply.

Non atherosclerotic coronary artery occlusions

Effects of MI

Cell death Contractility in the affected areas

reduced or absent Electrical instability

Dysrhythmias occur in 90% of patients PVCs V tach V fib Bradycardia

Complications of MI

CHF Mitral Valve Insufficiency Dysrhythmias Pericarditis Post Infarction MI Thromboembolic Complications Rupture of Ventricular Wall

MI Precipitating Factors

None in most cases Severe exertion and stress 59% occur at rest or while asleep

Clinical Manifestations

Angina-Chest Pain Vital Signs Heart and Lung Associated S&S

Diagnosis of MI

Based on 2 out of 3 criteria1. Chest pain indicative of ischemic

heart disease2. Characteristic EKG changes (ST

elevation)3. Marked rise and eventual decline in

serum markers of cardiac injury

Diagnostic studies

EKG Serum Enzymes/Cardiac Biomarkers Cardiac Catheterization Other lab tests Echocardiogram CXR Pulse Ox

Goals

Limit size of infarct/prevent further damage

Increase O2 supply and decrease O2 demand

Prevent and /or recognize complications early

Reduce pain

Management of Patients with ST Elevation

ST elevation

12 h

AspirinBeta-blocker

Eligible forfibrinolytic therapy

> 12 h

Fibrinolytic therapycontraindicated

Not a candidate forreperfusion therapy

Persistent symptoms ?

Fibrinolytic therapy PrimaryPTCA or CABG

Other medical therapy:ACE inhibitors

? NitratesAnticoagulants

ConsiderReperfusion

Therapy

No Yes

Modified from Antman EM. Atlas of Heart Disease, VIII; 1996

ECG MONITORING

Records and allows early detection of arrhythmias.

Lethal arrhythmias occur most commonly in the first 4 hours of AMI.

INTRAVENOUS ACCESS

IV access must be established for administration of drugs and fluid.

Peripheral venous cannulation should be the first choice.

OXYGEN THERAPY Hypoxia may aggravate myocardial damage

and increase the risks of complications. Supplemental oxygen may be provided

using nasal prongs or a face mask. Advanced airway support may be necessary.

Aim for a SaO2 of > 95 %

RELIEF OF PAIN

Pain increases secretion of catecholamines which leads to arrhythmias.

Therefore it is important to relieve pain. IV morphine may be prescribed Avoid IM injection.

Angina Pectoris Episode of chest pain or pressure due to insufficient artery flow of oxygenated blood. Myocardial 02 demand exceeds 02 supply. CAD is the most common cause. One coronary artery branch becomes completely occluded; therefore, 02 is not perfused to the myocardium, resulting in transient ischemia and subsequent retrosternal pain.

Angina PectorisPrecipitating Factors: Warning Sign for MIClinical Signs & Symptoms: do not occur until

lumen is 75% narrowed. Sternal pain: mild to severe. May be described as heavy, squeezing, pressing, burning, crushing or aching. Onset sudden or gradual. May radiate to L. shoulder and arm. Radiates less commonly to R. shoulder, neck, jaw. Pt may have weakness/numbness of wrist, arm, hands. pain usually short duration and relieved by removal precipitating factors,rest or NTG. Can be gradual (CAD) or sudden(vasospasm)

Associated Symptoms: dyspnea, N & V, tachycardia, palpitations, fatigue, diaphoresis, pallor, weakness, syncope, factors

Types of Angina Stable: There is a stable pattern of onset, duration

andintensity of sx, pain is triggered by a predictabledegree of exertion or emotion.

Variant Angina (Prinzmetal's) Cyclical, may occur at rest.

Ventricular arrhythmia, brady arrhythmia andconduction disturbances occur.

Syncope associated with arrhythmia may occur Nocturnal Angina only at night. Possible

associated with REM sleep. Unstable Angina AKA Pre infarction angina Pain is more intense, lasts longer

Medications for Angina

1. Nitrates decrease myocardial 02 demand via

peripheral vasodilation and reverse coronary artery spasm thus increase 02 supply to myocardial tissue.

2. Understanding how Nitrates Work: peripheral vasodilation results in:-decreased 02 demand-decreased venous return to heart-decreased ventricular filling which results in decreased wall tension and thus

-decreased 02 demand

NTG Forms:• SL (Nitrostat)• Lingual Sprays - similar to SL in use

(Nitrolingual)• Sustained release capsules/tablets

(Nitrobid)• Ointments 2% (Nitrobid)- wear gloves when

applying• Transdermal Patch (Nitro-Dur)• IV (Tridil) For attacks unresponsive to other

tx

Side/Adverse Effects

Vascular HA (may be severe) Hypotension (may be marked) Tachycardia Palpitations

REPERFUSION THERAPY Thrombolytic Agent Anti-Platelet Therapy - GP IIb/IIIa Percutaneous Transluminal Coronary

Angioplasty (PTCA) Coronary Artery Bypass Grafting (CABG) Adjunctive Therapy

ASPIRIN (21% reduction at 24 hrs) BETA BLOCKERS Nitroglycerin to be used with caution in RV

infarct, bradycardia or BP<90mmHg systolic

ACE I

Evidence of successful reperfusion. Despite giving SK within the optimal time

about 30 % of patients will not have successful reperfusion.

This due to the existence of streptococcal Ab in the patients.

Thus evidence of successful reperfusion is when ; a 50 % or > reduction in chest pain within 3- 6hrs of

SK a 50 % or > reduction of the ST segment elevation a rapid reduction of the Cardiac enzymes on serial

measurements reperfusion arrhythmias.

Complications of SK Anaphylatic shock

Common due to SK being derived from streptococcous and higher in those with a h/o allergy.

Presents with sudden drop in BP. Have to r/o extension of AMI

Hypotension May be part of the above or is a known SE of

SK.

Bleeding Usually mild and easily rx with basic

principles May need specific Rx if severe.

ANTICOAGULANTS – LMWH

Rx with LMWH is for 3 - 7 days , depends on the response to Rx.

ANTICOAGULANTS - LMWH

ORAL ANTIPLATELET AGENTS

Cyclo-oxygenase inhibitors- Acetylsalicylic acid (ASA)

Adenosine Diphosphate Receptor Antagonists- Clopidogrel (Plavix)- Ticlopidine

Clopidogrel Indication

PI Clopidogrel : BPOM RI

- Unstable Angina

|

Ischemicstroke- Myocardial

infarction

Peripheral arterialdisease

- PCI / Stenting

Clopidogrel in Unstable angina to prevent Recurrent ischaemic Events (CURE)

12,562 ACS patients treated with aspirin were randomised to clopidogrel 300 mg stat followed by 75 mg dly vs placebo x 9 mths

Primary endpoint (CV deaths, non fatal MI and stroke) reduced from 11.4% to 9.3%

Bleeding more common in clopidogrel group especially in those with aspirin > 100 mg/d

CURE: Early and Long-Term Benefits of Clopidogrel1,2

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0.02

0.04

0.06

0.08

0.10

0.12

0.14

0 3 6 9 12

Months of follow-up

Cum

mul

ativ

e ha

zard

rate

1. The CURE Trial Investigators. N Engl J Med 2001; 345: 494–502.

2. Data on file, 2002, p73 internal CSR-EFC 3307.

Placebo*(n = 6,303)

Clopidogrel* (n = 6,259)

20% relativerisk reduction

p = 0.00009

Cumulative Events(Myocardial Infarction, Stroke, or Cardiovascular Death)

*On top of standard therapy (including ASA)

ESC Guidelines

ACC AHA - PCI

- Loading dose for all P2Y12 inhibitors is recommended (Class I-A)- 600 mg loading dose recomended- Population limitation, prasugrel - Patients compliance issues, ticagrelor

Pharmacology Therapy

ASA Clopidogrel Nitrates Beta blockers Calcium channel blockers ACEs and ARBs Statins

Are You Still Awake??????

Non-Pharmacologic Therapy

Percutaneous transluminal coronary angioplasty (PTCA)

Dilates coronary arteries obstructed by plague. 30% restenosis rate within first 6 months.

Patient Criteria Non-calcified lesions less than 2 cm. The

ideal candidate would have less than a one year history of angina and be able to undergo coronary artery by-pass grafting if necessary. Patients with calcified lesions or lesions in branch vessels are not considered good candidates

Non-Pharmacologic Therapy

Cardiac Catheterization/ Balloon Angioplasty

Performed in the cardiac cath lab. A catheter with a balloon tip is passed into the obstructed artery and is alternately inflated and deflated to increase arterial diameter and perfusion.

Complications Arterial rupture, spasm, emboli, MI Post-procedure care

Other Procedures Coronary Artery Stents Stainless steel mesh stent is placed in

lumen to prevent restenosis after angioplasty. Requires anticoagulation and antiplatelet tx to prevent local-thrombosis.

Coronary Laser Surgery Laser can destroy atherosclerotic plaque.

Research is being conducted in transluminal laser angioplasty to coronary arteries.

Atherectomy - surgical removal of atheroma.

Stent thrombosis of LAD bifurcation

Thrombosuction

Kissing balloon dilatation

Final Result

Coronary Artery By-Pass Grafting (CABG)

Procedure - Surgical revascularization to increase coronary blood flow.

Patients with severe disease may not be candidates. Longevity after surgery still being debated. Surgery does not cure atherosclerosis and patients must still control risk factors

Post-op CABG Post-Operative Nursing Assessments & Care Cardiovascular function Respiratory function - pt may be on

mechanical ventilator for short time. Renal Function Neurologic Function Peripheral Vascular Function Fluid & Electrolyte Balance Pain management Psychological Status Safety - Pt may be restrained to present self

extubation

Cardiac Tamponade of CABG

Etiology - heart is compressed by fluid within the pericardial sac. Ventricular filling is thus impaired resulting in decreased cardiac output and circulatory collapse.

Clinical SignsPulsus Paradoxus Blood PressureNeck Veins Heart SoundsRespirations Mental StatusPain

TreatmentThoracotomyPericardiocentesis

Post MI Cardiac rehab

Begins in acute phase and continues indefinitely as outpatient

Includes: education activity progression counseling medical management

Patient education

Lifestyle modifications for controllable risk factors. Support groups are helpful, Example: Weight watchers,

Smoke-enders, stress workshops, cardiac rehabilitation. Supply patients with information, name of contact

person and phone numbersIdentify precipitating factors for Anginal

painMedication compliance

Issues in Clinical Practice

Unfortunately, for healthcare providers and their patients, most patients prefer the prescription of pills to the proscription of harmful lifestyles.

Double Cheeseburger, Large Fries, Jumbo Coffee.. Oh And An Aspirin -Gotta Take Care Of The Ticker Y’Know.

Aspirin May Reduce Risk Of Heart Attack

New Yorker Magazine. 1988.

French Fries

How to burn* 400 calories: Walk 2 hour 20 minutes

20 years ago Today

210 calories2.4 ounces How many calories are

in these fries?610 calories6.9 ounces

Calorie difference: 400 Calories

*Based on 130-pound person.

Darwinism and Risk of Cardiovascular Disease

Walking the Dog

Established Risk Factors for CHD

Blood cholesterol10% = 20%-30% in CHD

High blood pressure5-6 mm Hg = 42% in Stroke = 16% in CHD

Cigarette smokingCessation = 50%-70% in CHD

Body weight BMI<25 vs BMI>27 = 35%-55% in CHD

Physical activity20-minute brisk walk daily = 35%-55% in CHD

SUMMARY Acute coronary syndrome develops as a

result of an abrupt rupture of the atherosclerotic plaque.

Early diagnosis of AMI is of utmost importance as mortality is highest if treatment is delayed

And treatment is most effective in the early stage.