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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.