Overview In Managements Of Acute Coronary Syndrome

(American Heart Association Guidelines)

Dr. Ayman Selim Ibrahim AbougalambouMB,CHB(UOG),M.MED(USM) ,Malaysian Board Of Medicine, Clinical and

Interventional Cardiology Fellowship(IJN)

Associate Consultant Interventional Cardiologist,, Senior Physician

King Abdullah Cardiac CenterKing Abdullah Medical City- Mecca

(18thsep 2013)

Objectives

Cases

Pathology, Pathophysiology, and Epidemiology

ACUTE CORONARY SYNDROMESETIOLOGY

The Vulnerable Plaque

Reproduced with permission from Falk E, et al. Circulation. 1998;92:657-671.

Large Lipid Core

Thin, Vulnerable, Fibrous Cap

Ruptured Plaque with Occlusive Thrombus Formation

Reproduced with permission from Falk E, et al. Circulation. 1998;92:657-671.

ThrombusFormation

Atherothrombosis: Thrombus Superimposed on Atherosclerotic Plaque

Adapted with permission from Falk E, et al. Circulation. 1998;92:657-671. Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.

ACUTE CORONARY SYNDROMESDEFINITION

Diagnosis of Acute MI (STEMI / NSTE-ACS)

At least 2 of the above

Diagnosis of ACS

Diagnosis of Angina Pectoris

Management

Chest pain suggestive of ischemia

ECG assessment

ECG assessmentINFARCT LOCATION

INTERPRETATION OF TROPONINS

Risk Stratification

UA or NSTE-ACS

- Evaluate for Invasive vs.

conservative treatment

- Directed medical therapy

Based on initialBased on initialEvaluation, ECG, andEvaluation, ECG, and

Cardiac markersCardiac markers

- - Assess for reperfusion

- Select & implement

reperfusion therapy

- Directed medical therapy

STEMI Patient?

YESYES NONO

STEMI Cardiac Care STEP 1: Assessment

STEMI Cardiac CareSTEP 2: Determine preferred reperfusion strategy

Primary PCI

Absolute contraindications for fibrinolysis

Relative contraindications for fibrinolysis therapy in patients with acute STEMI

• History of chronic, severe, poorly controlled hypertension.• Severe uncontrolled hypertension on presentation (SBP greater than 180

mm Hg or DBP greater than 110 mmHg).

• History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications

• Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks).

• Recent (within 2-4 weeks) internal bleeding.• Noncompressible vascular punctures.• For streptokinase/anistreplase: prior exposure (more than 5 days ago) or

prior allergic reaction to these agents.• Pregnancy.• Active peptic ulcer.• Current use of anticoagulants: the higher the INR, the higher the risk of

bleeding.

Relative contraindications for fibrinolysis

Unstable Angina /NSTE-ACS Cardiac care• Evaluate for conservative vs. invasive therapy based upon:

• Risk of actual ACS• TIMI risk score• ACS risk categories per AHA guidelines

LowLowIntermediateIntermediate

HighHigh

TIMI RISK SCORE FOR UA/NSTEMI

• HISTORICAL POINTS• age >/= 65 y 1• >/= 3 CAD risk factors 1• known CAD (stenosis >/= 50%) 1• ASA use in past 7 days 1• PRESENTATION• severe angina </= 24 hours 1• elevated cardiac markers 1• ST deviation >/= 0.5 mm 1 RISK

SCORE: /7

TIMI RISK SCORE FOR UA/NSTEMI

RISK OF CARDIAC EVENT IN 14 DAYS

Low risk

High risk

Conservative Conservative therapytherapy

Invasive Invasive therapytherapy

Chest Pain Chest Pain centercenter

Intermediate risk

Medical Therapy

• Morphine (class I, level C)• Analgesia• Reduce pain/anxiety—decrease sympathetic tone, systemic

vascular resistance and oxygen demand.• Careful with hypotension, hypovolemia, respiratory

depression.

• Oxygen (2-4 liters/minute) (class I, level C)• Up to 70% of ACS patient demonstrate hypoxemia• May limit ischemic myocardial damage by increasing

oxygen delivery/reduce ST elevation.

• Nitroglycerin (class I, level B)• Analgesia—titrate infusion to keep patient pain free.• Dilates coronary vessels—increase blood flow.• Reduces systemic vascular resistance and preload.• Careful with recent ED meds, hypotension, bradycardia,

tachycardia, RV infarction.

• Aspirin (160-325mg chewed & swallowed) (class I, level A)• Irreversible inhibition of platelet aggregation.• Stabilize plaque and arrest thrombus.• Reduce mortality in patients with STEMI.• Careful with active PUD, hypersensitivity, bleeding

disorders.

• Beta-Blockers (class I, level A)• 14% reduction in mortality risk at 7 days at 23% long term

mortality reduction in STEMI• Approximate 13% reduction in risk of progression to MI in

patients with threatening or evolving MI symptoms• Be aware of contraindications (CHF, Heart block,

Hypotension).• Reassess for therapy as contraindications resolve.

• ACE-Inhibitors / ARB (class I, level A)• Start in patients with anterior MI, pulmonary congestion,

LVEF < 40% in absence of contraindication/hypotension• Start in first 24 hours• ARB as substitute for patients unable to use ACE-I.

• Heparin (class I, level C to class IIa, level C)– LMWH or UFH (max 4000u bolus, 1000u/hr)

• Indirect inhibitor of thrombin• less supporting evidence of benefit in era of reperfusion• Adjunct to surgical revascularization and thrombolytic /

PCI reperfusion.• 24-48 hours of treatment• Coordinate with PCI team (UFH preferred).• Used in combo with aspirin and/or other platelet inhibitors• Changing from one to the other not recommended.

Additional medication therapy• Clopidodrel (class I, level B)

• Irreversible inhibition of platelet aggregation• Used in support of cath / PCI intervention or if unable to

take aspirin• 3 to 12 month duration depending on scenario

• Glycoprotein IIb/IIIa inhibitors (class IIa, level B)• Inhibition of platelet aggregation at final common pathway• In support of PCI intervention as early as possible prior to

PCI.

Additional medication therapy

• Aldosterone blockers (class I, level A)– Post-STEMI patients

• No significant renal failure (Cr < 2.5 men or 2.0 for women)

• No hyperkalemis > 5.0• LVEF < 40%• Symptomatic CHF or DM

Secondary Prevention• Disease

– HTN, DM, HLP.

• Behavioral– smoking, diet, physical activity, weight.

• Cognitive – Education, cardiac rehab program.

Secondary Prevention disease management• Blood Pressure

– Goals < 140/90 or <130/80 in DM /CKD– Maximize use of cardio-selective beta-blockers & ACE-I

• Lipids– LDL < 100 (70) ; TG < 200– Maximize use of statins; consider fibrates/niacin first line

for TG>500; consider omega-3 fatty acids.

• Diabetes– HBA1c < 7%

Secondary prevention behavioral intervention• Smoking cessation

– Cessation-class, meds, counseling.

• Physical Activity– Goal 30 - 60 minutes daily– Risk assessment prior to initiation.

• Diet– DASH diet, fiber, omega-3 fatty acids.– <7% total calories from saturated fats.

Medication Checklist after ACS

• Antiplatelet agent– Aspirin* and/or Clopidorgrel

• Lipid lowering agent– Statin*– Fibrate / Niacin / Omega-3

• Antihypertensive agent– Beta blocker*– ACE-I*/ARB– Aldactone (as appropriate)

CASE ONE

• Frail 67 year old hypertensive male• 8/10 substernal chest pain • Radiation down left arm, into jaw• Diaphoresis, tachypnea, nausea• Onset within past four hours• No relief with nitro• T 37.1 C HR 112/min BP 150/100 RR 22/min

CASE ONE

Immediate Assessment: • IV access – Oxygen – Monitors• EKG• Targeted history and exam• CXR• Eligibility for thrombolysis/PCI• Labs

CASE ONEELECTROCARDIOGRAM

CASE ONE

• Risk stratify:– STEMI, TIMI score >8 (VERY HIGH RISK)

• Immediate Treatment:– ASA 160 mg po– Oxygen– +/- nitro sl– Metoprolol– Heparin– Emergent revascularization strategy

CASE ONE

• Adjunctive Treatment:

– Clopidogrel po– Nitroglycerine iv– Morphine iv

– Consider IIb/IIIa agents if primary PCI

CASE TWO

• 65 year old diabetic female• Retrosternal/epigastric pressure with no radiation • Occurs at rest, duration </= 15minutes• Associated with nausea and diaphoresis• Pain free currently• Onset 1/12 ago but increasing 4/7

CASE TWO

Immediate Assessment: • IV access – Oxygen – Monitors• EKG• Targeted history and exam

– smoker, dyslipidemic, hypertension, proteinuria– on ASA, HCTZ, metformin, glyburide, celexa– normal cardiac exam

• CXR• Labs

CASE TWO ELECTROCARDIOGRAM

CASE TWO

• Risk stratify:– UA/NSTEMI, TIMI score >4 (INTERMEDIATE RISK)

• Immediate Treatment:– ASA 160 mg po– Heparin (LMWH > UFH)– +/- Clopidogrel– Coronary angiogram

CASE TWO

• Adjunctive Treatment:

– Beta Blockers– ACE Inhibitors– +/- Nitrates

CASE THREE

• 37 year old male complains of a retrosternal dull ache for 3 hours

• No radiation of pain• No associated symptoms• Smoker, significant family history

CASE THREE

Immediate Assessment: • IV access – Oxygen – Monitors• EKG• Targeted history and exam• CXR• Labs

CASE THREE ELECTROCARDIOGRAM

CASE THREE

• Risk stratify:– UA/NSTEMI, TIMI score 1 (LOW RISK)

• Immediate Treatment:– ASA 160 mg po– Monitor– Serial EKG and enzymes (X2)– Exercise Stress Test

SUMMARY• • Acute coronary syndrome is a spectrum of UA/NSTE-ACS and

STEMI. The clinical presentation will depend on the acuteness and severity of coronary occlusion.

• • The diagnosis of UA/NSTE-ACS is based on history + dynamic ECG changes (without persistent ST elevation), + raised cardiac biomarkers.

• • In UA cardiac biomarkers are normal while in NSTE-ACS it is elevated.

• • Risk stratification is important for prognosis and to guide management

• • Initial management of intermediate/high risk patients includes optimal medical therapy with ASA, clopidogrel (or ticagelor) and UFH or LMWH or fondaparinux. Prasugrel may be considered as an alternative to clopidogrel after coronary angiography if PCI is planned.

• • Patients with refractory angina and/or hemodynamically unstable should be considered for urgent coronary angiography and revascularization.

• • Intermediate/high risk patients should be considered for early invasive strategy (<72 hours). If admitted to a non-PCI centre, they should be considered for transfer to a PCI centre.

• • Low risk patients should be assessed non-invasively for ischemia.

• • All patients should receive optimal medical therapy at discharge. This includes ASA, clopidogrel (ticagrelor or prasugrel if given during PCI), β -blockers +CCBs, ACE-I or ARB and statins.

• • These drugs should be uptitrated as outpatient to the recommended tolerated doses.

• • Cardiac rehabilitation and secondary prevention programs which includes lifestyle modification is an integral component of management.

Thank you so much for your Auscultations….

Diagnosis of Acute MI (STEMI / NSTE-ACS)

• At least 2 of the following

• Ischemic symptoms.

• Diagnostic ECG changes.

• Serum cardiac marker

elevations.

Diagnosis of Unstable Angina• Patients with typical angina - An episode of angina

• Increased in severity or duration• Has onset at rest or at a low level of exertion• Unrelieved by the amount of nitroglycerin or rest that had

previously relieved the pain

• Patients not known to have typical angina• First episode with usual activity or at rest within the

previous two weeks• Prolonged pain at rest

Focused History

• Aid in diagnosis and rule out other causes:– Palliative/Provocative factors– Quality of discomfort– Radiation– Symptoms associated with

discomfort– Cardiac risk factors– Past medical history -

especially cardiac

• Reperfusion questions:

– Timing of presentation– ECG c/w STEMI – Contraindication to

fibrinolysis– Degree of STEMI risk

Targeted Physical

• Recognize factors that increase risk• Hypotension• Tachycardia• Pulmonary rales, JVP,

pulmonary edema,• New murmurs/heart sounds• Diminished peripheral pulses• Signs of stroke

• Examination– Vitals– Cardiovascular system– Respiratory system– Abdomen– Neurological status

Cardiac markers• Troponin ( T, I)

– Very specific and more sensitive than CK.

– Rises 4-8 hours after injury

– May remain elevated for up to two weeks.

– Can provide prognostic information.

– Troponin T may be elevated with renal dz, poly/dermatomyositis.

• CK-MB isoenzyme

– Rises 4-6 hours after injury and peaks at 24 hours

– Remains elevated 36-48 hours

– Positive if CK/MB > 5% of total CK and 2 times normal

– Elevation can be predictive of mortality.

– False positives with exercise, trauma, muscle dz, DM, PE

Assessment Findings indicating HIGH likelihood of ACS

Findings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findings

Findings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findings

History Chest or left arm pain or discomfort as chief symptomReproduction of previous documented anginaKnown history of coronary artery disease, including myocardial infarction

Chest or left arm pain or discomfort as chief symptomAge > 50 years

Probable ischemic symptomsRecent cocaine use

Physical examination

New transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or rales

Extracardiac vascular disease

Chest discomfort reproduced by palpation

ECG New or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptoms

Fixed Q wavesAbnormal ST segments or T waves not documented to be new

T-wave flattening or inversion of T waves in leads with dominant R wavesNormal ECG

Serum cardiac markers

Elevated cardiac troponin T or I, or elevated CK-MB

Normal Normal

Risk Stratification to Determine the Likelihood of Acute Coronary Syndrome

ACS risk criteria

Low Risk ACSNo intermediate or high

risk factors

<10 minutes rest pain

Non-diagnositic ECG

Non-elevated cardiac markers

Age < 70 years

Intermediate Risk ACSModerate to high likelihood

of CAD

>10 minutes rest pain, now resolved

T-wave inversion > 2mm

Slightly elevated cardiac markers

High Risk ACS

*Elevated cardiac markers.

*New or presumed new ST depression.

*Recurrent ischemia despite therapy.

*Recurrent ischemia with heart failure.

*High risk findings on non-invasive stress test.

*Depressed systolic left ventricular function.

*Hemodynamic instability.

*Sustained Ventricular tachycardia.

*PCI with 6 months.

*Prior Bypass(CABG)surgery.