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Stable Angina Pectoris (SAP)

dan
Acute Coronary Syndrome (ACS)
“UAP, Acute Non-STEMI, STEMI”
Dr. Ilham Uddin, Sp JP (K), FIHA, FAsCC
Kariadi Hospital / RSND Hospital /
Diponegoro University
Semarang 02-2017
Coronary Heart Disease
• Anatomy Coroner
• Atherosclerosis
• Basic Physiology / Determinants of MVO2
• Autoregulatory Mechanisms / Coronary Flow
Reserve
• Pathophysiology of Coronary Ischemia
• Clinical Syndromes
– Stable Angina
– Acute Coronary Syndromes
• Unstable Angina
• Acute MI (UA, AMI)
Coronary Arteries Anatomy
Coronary arteries--anatomy
Coronary Heart Disease (CHD)

atherosclerosis

Coronary stenosis coronary spasm

Myocardial ischemia, anoxaemia

Coronary heart disease, CHD


Ischemic heart disease
Atherosclerosis
Events During Atherogenesis

3
Atherosclerosis Time-line
Complicated
Foam Fatty Intermediate Fibrous Lesion/
Cells Streak Lesion Atheroma Plaque Rupture

Endothelial Dysfunction
From First From Third From Fourth
Decade Decade Decade

Adapted from Pepine CJ. Am J Cardiol. 1998;82(suppl 104).


Risk Factors for Atherosclerotic
Disease
Non-modifiable Modifiable
 Age  Cigarette smoking
 Family history  Diabetes mellitus
 Sex  Hyperlipidemia
 Hypertension
 Obesity
 Physical inactivity

Dr.Sarma@works Hoeg JM. JAMA. 1997;277:1387–1390.


Atherosclerosis
Major Risk Factors
• Smoking
• Hypertension (>=140/90 or on
antihypertensive treatment)
• HDL < 40*
• Family History premature CAD (<55
males, <65 females)
• Age (men >=45; women >=55)
• Diabetes Mellitus (DM)
* HDL >60 is a negative risk factor, its presence removes one risk factor from total count
• Basic Physiology / Determinants of MVO2
• Autoregulatory Mechanisms
(Coronary Flow Reserve)
• Pathophysiology of Coronary Ischemia
Ischemic Heart Disease - Overview
Parameters
Pathophysiology
Anatomy: Atheroma / Atherothrombosis
Subjective: Angina
Atherosclerosis
Objective: EKG T wave ST seg
Epicardial &
changes
Microvascular Spam
Chemistry: Cardiac serum
Atherothrombosis biomarkers:
CPK, CK-MB,
Troponins

Silent ischemia

Stable angina Acute Coronary Prevalence & severity of


Syndromes
stenosis

Clinical Presentations 2
Effect of Fixed Stenosis on Myocardial Blood Flow

6
Progression of coronary plaque over time Clinical Findings

Acute Coronary Syndromes


Sudden Cardiac Death

Acute silent
Angina occlusive
pectoris process
Endothelial dysfunction
Atherogenic Thrombogenic
risk factors risk factors
Age
20 years 60 years 7
IHD – Clinical Spectrum
Chronic
Stable Angina
Silent Ischemia
Mixed Angina
Microvascular Angina
(Syndrome X)
Stunned & Hibernating
Acute
Unstable Angina
Acute Myocardial
Infarction (NSTEMI,
STEMI)
Sudden Cardiac Death
Prinzmetal Angina
8
Stable Angina Pectoris
(SAP)
Clinical Classification of Chest Pain
Typical angina (define) Canadian Cardiovascular Society
1.Substernal chest discomfort with a characteristic Classification ( CCSC)
quality and duration that is Class Activity Limits to
2.Provoked by exertion or emotional stress and evoking normal
3.Relieved by rest or nitroglycerin angina activity

Atypical angina ( probable) I Prolonge None


Meets 2 of the above characteristics d
exertion
Noncardiac chest pain II Walking > Slight
Meets one or none of the typical angina 2 blocks
characteristics
III Walking < Marked
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN 2 blocks
Cardiovascular: Pericarditis, Aortic Valve Disease,
Aortic Dissection, Pulmonary Embolism, Mitral Valve
Prolapse IV Minimal Severe
Gastrointestinal: Esophageal, Biliary, Peptic ulcer, or rest
Pancreatitis
Pulmonary: Pneumothorax, Pneumonia, Pleuritis
Chest Wall: Costochondritis, Rib fracture, Herpes zoster
Psychological: Anxiety disorders
9
(SAP)
Myocardial Ischemia:
Occurs when myocardial oxygen demand
exceeds myocardial oxygen supply
(SAP)

Pxr
Wall Stress =
2h

4
Stable angina pectoris
(SAP)

definition:
acute and transient myocardial ischemia
and anoxaemia
usually caused by coronary insufficiency
during exertion
(SAP)
SAP Symptoms
• mid-substernal chest pain
• squeezing, pressure-like in quality (closed fist =
Levine’s sign)
• builds to a peak and lasts 2-20 minutes
• radiation to left arm, neck, jaw or back
• associated with shortness of breath, sweating, or
nausea
• exacerbated by exertion, cold, meals or stress
• relieved by rest, NTG
Stable angina pectoris
(SAP)

Pathology

in angiography
Significant coronary lesion with
diameter stenosis > 70% in 75% pts

No significant stenosis in about 5-


10% pts, Ischemia may be related to
coronary spasm or microvascular
dysfunction.
What about non-invasive test?
(SAP)

• Metabolic abnormalities
- Lipids
• LDL< 100 mg/dl is optimal
- Esp for patients with multiple risk factors,
DM and established CAD
• HDL<40 mg/dl is an independent risk factor
• TG’s > 200 mg/dl should be treated (lifestyle)
- Glucose
• Impaired fasting glucose= 110-126 mg/dl
• DM = FBS > 126 mg/dl
- Others
– presence increase the risk of future CV events
– no consensus on routine measurement
-C-reactive protein; homocysteine; lipoprotein Lp(a)
What about non-invasive test?
(SAP)

• ECG
- Resting ECG is normal in 50% patients
with stable angina
- Most common abnormality with chronic
CAD is non-specific ST-T wave changes
- Non specific changes also seen in
electrolyte abnormalities, LVH,
antiarrhythmic drugs
CHD----Diagnosis
(SAP)

ECG Cardiac Echo Chest X ray

Treadmill ECT Angiograph


(SAP)

Myocardial Coronary
ischemia stenosis

ST segment depression

Normal coronary
Normal
flow

Normal ST segment

Myocardial
infarction Coronary
occlusions
ST segment elevation
Stable Angina - Diagnosis (SAP)

Exercise Treadmill Test


(SAP)
Stable CHD: Non invasive tests
• Exercise ECG ( treadmill test )
- Looking for ST segment depression and
symptoms
• 1mm (+) typical symptoms = 90% positive predictive
value
• 2mm (+) typical symptoms= diagnostic
• 1mm (-) typical symptoms= 70% predictive value
• 2mm (-) typical symptoms = 90% predictive value
• Overall sensitivity = 70%; Specificity = 80%
- Patients need to get to >85% predicted maximal
• Predicted max HR = (220 – age)
(SAP)

Cardiac Echo
(SAP)
Soft or
‘Vulnerable’
Plaque
Imaging by
64 slice MSCT
(SAP)

Stable CHD invasive tests


Coronary angiography
- golden standard
(SAP)
Coronary angiography
Left Coronary Angiogram ( LCA)
(SAP)

Arterial Anatomy & Projections


Left Coronary Artery
Right Anterior Oblique RAO 30
(SAP)
Coronary Angiography
(SAP)
Stable angina pectoris

Prevention and treatment

1. General consideration:
 rest,avoid provocative factors , risk factors
control
2. Drug therapy:
 prevent MI and death
 symptom relief and quality of life improvment
3. Coronary revascularization:
 percutaneous coronary intervention (PCI)
 Coronary artery bypass surgery (CABG)
SVG, LIMA
(SAP)
Stable angina pectoris
Drug therapy
antianginal and anti-ischemic therapy

Oxygen Oxygen
supply demand

a.nitrates
b.beta-adrenergic blockers
c.Calcium antagonists
d.Drugs improving metabolism
Drug therapy (SAP)

a.nitrates
•Nitroglycerin
•Isosorbide dinitrate 5 mg, 10 mg
•isosorbide 5-mononitrate (long-acting nitrates)
b. ß-blockers:
ß1-selective:metoprolol 50 mg, atenolol 50 mg,
bisoprolol 5 mg
c.Calcium antagonists:
Mis: Diltiazem, Verapamil
d. Drugs improving metabolism:
trimethazidine,selectively inhibit 3-KAT(),partly
inhibit FA oxidation,
Drug therapy (SAP)

prevent MI and death therapy

a.antiplatelet angents:
ASA,75-325mg/d
clopidogrel; ticlopidine: ADP receptor- antagonists:
Cilostazol: phosphodiesterase inhititor,50-100mg bid

b. Lipid-lowering angents: statins (Atorvastatin 20 mg,


Rosuvastatin 10 mg)

c. Angiotesin-converting enzyme inhibitor (ACEI):


Captopril, Ramipril, Lisinopril etc
(SAP)
Mechanical Dilation: Angioplasty / PCI dgn Stent

Stent
(ring?)
(SAP)
Acute Coronary Syndromes
(ACS)
Atherothrombosis: A Generalized and
Progressive Process
Thrombosis

Unstable
angina ACS
MI
Ischemic
stroke/TIA
Critical leg
Atherosclerosis ischemia
Intermitent
claudication
CV death

Stable angina/
Intermittent claudication
Adapted from Libby P. Circulation. 2001;104:365-372.
Spectrum of Chronic Coronary Syndrome
Risk Factors + Hypertension
Endothelial Dysfunction
Atherosclerosis
IHD/Angina Pectoris

Chronic Myocardial Ischemia Acute


Coronary Coronary Thrombosis Coronary
Syndrome Syndrome
Myocardial Infarction
Arrhythmia & Loss of Muscle

Remodeling
Ventricular Dilation
Congestive Heart Failure

Endstage Heart Disease


Baroldi G, The Etiopathogenesis of Coronary Heart Disease. 2nd ed. 2004.
PATHOGENESIS OF ACS

Dr.Sarma@works
Pathophysiology of ACS
Characteristics of Unstable and
Stable Plaque
Much
Less smooth inflammatory Much smooth Less
muscle cells cells muscle cells inflammatory
Thin fibrous Thick cells
cap fibrous cap

Eroded Integrated
endothelium endothelium
Active Foam cells
macrophage

Unstable plaque Stable plaque


Adapted from Libby. Circulation. 1995;91:2844-2850
Risk Factors for Plaque Rupture

Local Factors Systemic Factors


Cap Smoking
Fatigue
Cholesterol
Atheromatous Core
(size/consistency)
Diabetes
Mellitus Fibrinogen
Cap
Thickness/
Consistency
Cap Homocysteine
Impaired
Inflammation
Fibrinolysis

Plaque
Rupture
Fuster V, et al. N Engl J Med. 1992;326:310-318.
Falk E, et al. Circulation. 1995:92:657-671.
Atherothrombosis: Thrombus Superimposed
on Atherosclerotic Plaque

Adapted from Falk E, et al. Circulation. 1995;92:657-671.


Hemostatic Plug Formation

PRIMARY
AGGREGATION

Platelet Aggregation Clotting


Hemostatic
Clot

Fibrin
SECONDARY
COAGULATION Thrombin

0 min 5 min 10 min

Adapted from Ferguson JJ, et al. Antiplatelet Therapy in Clinical Practice. 2000:15-35.
Platelets Role in Thrombosis
1. Platelet Adhesion
Platelet

GP Ib 2. Platelet Activation

Plaque rupture Activated Platelet


GP IIb/IIIa
3. Platelet Aggregation
TxA2
ASA,
Clopidogrel/Ticlopidine

GP IIb/IIIa Inhibitors

ASA, acetylsalicyclic acid. Fibrinogen


Cannon and Braunwald, Heart Disease. 2001.
Platelets: Role in Thrombosis

High Flow Slow Flow

Fibrin RBCs Platelets Fibrin RBCs Platelets

White Thrombus Coagulation Thrombus


RBCs, red blood cells.
Stable Unstable Non-Q Q wave
Angina Angina wave MI MI

CAD UA/NSTEMI STEMI


Days- Mins-
weeks hours

Antithrombotic Thrombolysis
Therapy Primary PCI

Cannon CP J Thromb Thrombolysis. 1995;2:205-218.


Acute Evaluation of ACS
Presentation Chest pain or Short of Breath

ST-segment ST-segment
ECG Normal Depression Elevation

Markers – + – + +

Diagnosis Unstable
Rule-Out Acute MI
Angina
Anderson JL. J Am Coll Cardiol 2007;50:e1-157
Stable Unstable Non ST ST Elevation
Angina Angina Elevation MI MI

ECG – ST ↑
ECG - ST ↓
CK-MB
Troponin

CRP/BNP

<- + Markers Identify MI patients,


who are High-Risk Patients ->
Unstanle Angina (UAP)
/ Acute Non STEMI
CAUSES OF UA/NSTEMI
Thrombosis Mechanical
Obstruction

.
Dynamic  MVO2
Obstruction
Inflammation/
Infection
Mechanical
Thrombosis
Obstruction

.
Dynamic  MVO2
Obstruction
Braunwald, Circulation Inflammation/
98:2219, 1998 Infection
Dr.Sarma@works
Unstable Angina Pectoris (UAP)

• angina at rest (> 20 minutes)


• new-onset (< 2 months) exertional angina (at
least CCSC III in severity)
• recent (< 2 months) acceleration of angina
(increase in severity of at least one CCSC
class to at least CCSC class III)
• decrease in exertion required to provoke
• any prolonged episode (>10-15min)
• failure to abate with >2-3 S.L. NTG
• onset at rest or awakening from sleep
Distinguishing Features of Acute Coronary Syndromes

Unstable Angina Myocardial Infarction

NSTEMI STEMI
Anginal •Rest angina - Rest or nocturnal Prolonged ( > 30 min )
Presentatio Angina ≥ 20 minutes occurring
ns within a week of presentation. crushing, strangling
•New onset angina - ( < 2 months chest pain more severe
) exertional angina progressing to and wider radiation
CCSA III
•Crescendo angina - < 2 moths
than usual angina
acceleration of previously stable
angina to at least CCSA III.
•Within 30 day post MI, PCI or
CABG
EKC initial Dynamic, transiet < 24 hours ST depression ST elevation (
findings T-wave inversion and/or ST seg and/pr T Wave and Q waves
depression inversion later)

Cardiac Negative (-) Positive (+) Positive (+)


Serum
Biomarkers
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Unstable Angina Pectoris -
High Risk Features
• prolonged rest pain
• dynamic EKG changes (ST depression)
• age > 65
• Diabetes Mellitus (DM)
• Left Ventricular systolic dysfunction
• angina associated with congestive heart
failure (CHF), new murmur, arrhythmias or
hypotension
• elevated Troponin I or T
ED MANAGEMENT OF
UA/NSTEMI ST ?

NO YES

Nondiagnostic ECG ST and/or T wave changes


Normal serum cardiac markers Ongoing pain
+ cardiac markers
Hemodynamic abnormalities
Observe
Follow-up at 4-8 hours: ECG, cardiac markers
Evaluate
for
No recurrent pain; Recurrent ischemic pain or Reperfusion
Neg follow-up studies + UA/NSTEMI follow-up studies
Diagnosis of UA/NSTEMI
Stress study to provoke confirmed
ischemia prior to discharge
or as outpatient

Neg: nonischemic
discomfort;low-risk UA/NSTEMI + UA/NSTEMI confirmed ADMIT

Outpatient follow-up
Dr.Sarma@works
Early Treatment: Class I Indications
 Bedrest/chair with continuous ECG Monitoring
 O2 therapy with saturation <90%, respiratory distress, or
other high-risk features for hypoxemia
 SL NTG 0.4 mg q5min x3 then assessment of need for IV NTG
 IV NTG indicated first 48 hours for treatment of persistent
ischemia, CHF or HTN; should not preclude tx with beta-
blockers or ACE
 Oral Beta-Blocker in first 24 hours for pt who do not have
 Signs of CHF
 Low out-put state
 Increased risk of cardiogenic shock
 Contraindication to Beta blockers/heart block/COPD
 If Beta-Blockers are contraindicated a nondihydropyridine
calcium channel blocker may be used if no LV dysfunction
Wright RS et al. Circ 2011;123;2022-2060.
ACC/AHA Guidelines
ACS Treatment Overview: UA/NSTEMI

Diagnosis of UA or NSTEMI is likely or definite

Aspirin or clopidogrel (if patient is aspirin


intolerant)
Initial
conservative
management Initial invasive
management
Medical Diagnostic
PCI or CABGa
therapy angiography

Evaluation of LV
Function in pt Long-term medical management:
Clopidogrel, aspirin, β-blocker, ACEI,
with ischemia
statin

aIf possible, clopidogrel should be withheld for 5-7 days prior to the procedure.
Anderson JL, et al. Circulation. 2007;116:803-877.
Selection of Initial Treatment

Wright RS et al. Circ 2011;123;2022-2060.


Unstable Angina
Anti-coagulant Therapy
• Heparin
– recommendation is based on documented
efficacy in many trials of moderate size
– meta-analyses (1,2) of six trials showed a 33%
risk reduction in MI and death, but with a two
fold increase in major bleeding
– titrate PTT to 2x the upper limits of normal

1. Circulation 1994;89:81-88
Dr.Sarma@works 2. JAMA 1996;276:811-815
Unstable Angina
Anti-coagulant Therapy
• Low-molecular-weight heparin: Enoxaparine,
Fondaparinux
advantages over heparin:
– better bio-availability
– higher ratio (3:1) of anti-Xa to anti-IIa
activity
– longer anti-Xa activity, avoid rebound
– induces less platelet activation
– ease of use (subcutaneous - qd or bid)
– no need for monitoring
Dr.Sarma@works
STEMI (Myocardial Infarction)
Chest Pain Assessment
• ECG most important single source of
data .
• ECG findings in patients with acute
chest pain
- New ST-segment elevation of >=1 mm
• Probability of MI = 80%
- ST-segment depression or T-wave inversion no
know to be old
• Sensitivity = 90%; Specificity = 80%
Diagnosis of STEMI
History

• Classic symptoms: intense, oppressive


chest pressure radiating to left arm
• Other symptoms:
 chest heaviness, burning
 radiation to jaw, neck, shoulder, back,
arms
 nausea, vomiting
 diaphoresis
 dyspnea
 lightheadedness
• Symptoms may be mild or subtle
Diagnosis of STEMI
Physical Examination

• Tachycardia or bradycardia
• Extrasystoles
• S3 or S4, mitral regurgitation
murmur
• Lung rales
• Hypertension or hypotension
• Pallor, distress
Acute MI
Typical rise and gradual
fall (troponin) or more
rapid rise and fall of CK-
MB, markers of
myocardial necrosis,
with at least one of the
following:
•Ischemic symptoms
•EKG changes indicative
of ischemia (ST-seg
elevation or depression)

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Cardiac Biomarkers “enzymes”
• Enzymes (cardiac biomarkers) diffuse into
the cardiac interstitium after MI and
become detectable in the blood within
hours.
• CK-MB detectable 4 hours after MI and up
to about 2 days
- Some CK-MB detectable in healthy patients

• Troponin I detectable 4 hours after an MI


and up to a week afterwards
- Therefore, difficult to use to diagnose re-infarction
- Troponin I not detectable in healthy patients
- “Microinfarctions” can increase troponin I and not increase CK-MB (30%
of patients with UA)
Time Course of Cardiac Biomarkers after
MI
Causes of Troponin elevation
 Any cause of prolonged (>15 – 20
minutes) subendocardial ischemia
 Prolonged angina pectoris
 Prolonged tachycardia in setting of CAD
 Congestive heart failure (elevated LVEDP
causing decreased subendocardial
perfusion)
 Hypoxia, coupled with CAD
 “aborted” MI (lytic therapy or spontaneous
clot lysis)
 CKD
T Wave – ST seg. changes
T-wave ∆

ST-seg ∆

Zone of ischemia
Path. Q waves
Zone of injury

Zone of necrosis
>0.03 seconds
Lateral
Septal Anterior >1/3 the total of
QRS

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Inferior
Diagnosis of Acute MI : ECG
Defines location, extent, and prognosis of
infarction
• ST elevation diagnostic of coronary
occlusion
• Q-waves do NOT signify completed infarction
• ST depression or T inversion: unlikely total
coronary occlusion
• ST elevation in RV4 for RV infarction
• Observe up to 24 hrs for non-diagnostic ECG
• Differentiate from early repolarization in V1-2
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If the clinical picture is consistent with acute STEMI
(including True Posterior MI) or new left bundle branch block
(LBBB) is present in EKG,
 select and implement reperfusion therapy, Fibrinolysis or
PCI as quickly as possible within 12 hours of symptoms
onset to obtain and sustain optimal flow in the infarct-
related artery (IRA).
 Do not wait for serum cardiac biomarkers result before
implementing reperfusion strategy !

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“ Time is muscle”

Myocardial Infarction is a true


emergency in cardiac care.
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STEMI
ischemia
ischemic necrosis

Reopen the vessels


Reduce the area of
infarction Best time
Mild impairment
Rescue the dying Slightly injury

myocardium
Mild injured

Time = Myocardium! Moderate


impairment
Time = Life ! Severe injured

severe
impairment
Management: onset of STEMI
CHD –Sudden death (arrhythmia)

Ventriclar Tachycardia

Ventricular flutter

Ventricular fibrillation
Initial Management in ED
• Initial evaluation with 12-lead ECG in < 10 minutes
– targeted history (for AMI inclusion, thrombolysis
exclusion)
– vital signs, focused examination
• Continual ECG, automated BP, HR monitoring
• IV access
• Draw blood for serum cardiac markers, electrolytes,
magnesium, hematology, lipid profile panel

Dr.Sarma@works
Initial Management in ED
• Aspirin165-325 mg (chew and swallow)
• Sublingual NTG unless SBP <90 or HR <50 or >100:
test for prinzmetal’s angina, reversible spasm, anti-
ischemic, antihypertensive effects
• O2 by nasal prolongs, first 2-3 h in all; continue if PaO2
<90%
• Analgesia: small doses of morphine (2-4 mg) as needed
• Fibrinolysis or PCI if ST elevation > 1mV or LBBB
(Goal: door-needle < 30 min or door-dilatation < 60-90
min)
Dr.Sarma@works
Management of Patients with ST
Elevation
ST elevation

Aspirin
Beta-blocker

 12 h > 12 h

Eligible for Fibrinolytic therapy Not a candidate for Persistent


fibrinolytic therapy contraindicated reperfusion therapy symptoms ?

No Yes
Primary
Fibrinolytic therapy
PTCA or CABG
Other medical therapy: Consider
ACE inhibitors Reperfusion
? Nitrates Therapy
Anticoagulants

Dr.Sarma@works Modified from Antman EM. Atlas of Heart Disease, VIII; 1996
Comparison of Fibrinolytic Agents
Streptokinase Anistreplase Alteplase
Reteplase

Dose 1.5 MU 30 mg 100 mg


10U x 2
in 30-60 min in 5 min in 90 min
over 30 min
Bolus administration NO Yes No Yes
Antigenic Yes Yes No No
Allergic reactions Yes Yes No No
(mostly hypotension)
Systemic fibrinogen Marked Marked Mild Moderate
depletion
90-min patency rate ~50% ~65% ~75% ~75%
TIMI-3 flow 32% 43% 54% 60%
Mortality rate 7.3% 10.5% 7.2% 7.5%
Dr.Sarma@works
Cost /dose (US) $294 $2116 $2196 $2196
ContraindicatIons and Cautions for
Fibrinolytic Used in STEMI

Absolute Contraindications:
• Previous hemorrhagic stroke at any time: other strokes or
cerebrovascular events within one year
• Known intracranial neoplasm
• Active internal bleeding (does not include menses)
• Suspect aortic dissection

Dr.Sarma@works
ContraindicatIons and Cautions for
Fibrinolytic Used in STEMI
Cautions / Relative Contraindications
• Severe uncontrolled HTN on • Noncompressible vascular
presentation (BP >180/110 punctures
mmHg) • Recent (within 2-4 weeks)
• History of prior CVA or known internal bleeding
intra-cerebral pathology not • For streptokinase/anistreplase:
covered in contraindications prior exposure (especially
• Current use of anticoagulants in within 5d-2 yrs) or prior allergic
therapeutic doses (INR  2-3); reaction
no bleeding diathesis • Pregnancy
• Recent trauma (within 2-4 • Active peptic ulcer
weeks) including head trauma • History of chronic hypertension
Dr.Sarma@works
Primary Percutaneous
Coronary Intervention (PCI) Recommendations
Class I Recommendations
1. As an alternative to fibrinolytic therapy if:
– ST segment elevation or new or presumed new LBBB
– Within 12 hrs of symptoms or > 12 hrs of persistent pain
– In a timely fashion (90  30 min)
– By experienced operators
– In appropriate environment
2. In cardiogenic shock patients < 75 yrs or within 36 hrs of AMI and
revascularization can be performed within 18 hrs of onset of shock
Class IIa Recommendations
1. As reperfusion strategy in candidates for reperfusion who have
contraindications to fibrinolytic therapy

Dr.Sarma@works
Primary Percutaneous
Coronary Intervention (PCI) Recommendations
Class IIb Recommendations
1. In patients with AMI who do not present with ST elevation but who
have reduced (< TIMI grade 2) flow of the infarct-related artery and
when angioplasty can be performed within 12 hrs of onset of
symptoms
Class III Recommendations
1. This classification applies to patients with AMI who:
• undergo elective angioplasty in the non-infarct-related artery at the time of
AMI
• are beyound 12 hrs after the onset of symptoms and have no evidence of
myocardial ischemia
• have received fibrinolytic therapy and have no symptoms of myocardial
ischemia
• are fibrinolytic-eligible and are undergoing primary angioplasty by and
Dr.Sarma@works
unskilled operator in a laboratory that does not have surgical capability
Advantages of Fibrinolytic Therapy
• More universal access
• Shorter time to treatment
• Greater clinical trial evidence of:
– reduction in infarct size
– improvement of LV function
• Results less dependent on physician experience
• Lower system costs

Dr.Sarma@works
Primary PCI of STEMI
Primary PCI of STEMI
Advantages of Primary PTCA
• Higher initial reperfusion rates
• Lower recurrence rates of ischemia / infarction
• Less residual stenosis
• Less intracranial bleeding
• Defines coronary anatomy and LV function
• Utility when fibrinolysis contraindicated

Dr.Sarma@works
Pharmacologic Management of Patients with
MI
Heparin Recommendations
Class I Recommendations
1. In patients undergoing percutaneous or surgical revascularization
Class IIa Recommendations
1. Intravenously in patients undergoing reperfusion therapy with
alteplase/reteplase (note change in recommendations)
1999 1996
Bolus Dose 60 U/kg 70 U/kg
Maintenance ~12 U/kg/hr ~15 U/kg/hr
Maximum 4000 U bolus None
1000 U/h if >70kg
aPTT 1.5-2.0 x control 1.5-2.0 x control
(50-70 sec) for 48 hrs (50-70 sec) for 48
hrs
Dr.Sarma@works
Pharmacologic Management of Patients with
MI
Heparin Recommendations
Class IIa Recommendations (continued)
2. Intravenous unfractionated heparin (UFH) or low molecular weight
heparin (LMWH) subcutaneously for patients with non-ST elevation
MI
3. Subcutaneous UFH (eg, 7,500 U b.I.d.) or low molecular weight
heparin (eg, enoxaparin 1 mg/kg b.I.d.) in all patients not treated with
fibrinolytic therapy who do not have a contraindication to heparin. In
patients who are at high risk for systemic emboli (large or anterior MI,
AF, previous embolus, or known LV thrombus), intravenous heparin is
prefered
4. Intravenously in patients treated with nonselective fibrinolytic agents
(streptokinase, anistrplase, urokinase) who are at high risk for systemic
emboli (large or anterior MI, AF, previous embolus, or known LV
thrombus)
Dr.Sarma@works
MI Management in 1st 24 Hours
• Limited activity for 12 hours, monitor  24 hours
• No prophylactic antiarrhythmics
• IV heparin if: a) large anterior MI; b) PTCA; c) LV
thrombus; or d) alteplase/reteplase use (for ~48 hours)
• SQ heparin for all other MI (7,500 u b.I.d.)
• Aspirin indefinitely
• IV NTG for 24-48 hrs if no / HR or BP
• IV beta-blocker if no contraindications
• ACE inhibitor in all MI if no hypotension

Dr.Sarma@works
Therapeutics--patients with ACS
Anti-ischemic therapy
• Nitrates
- relieve pain and ischemia, given sublingually or IV acutely
• Morphine sulfate
- Relieve pain, decreases agitation and decreases preload
(decreased venous congestion)
• B- Blockers
- Decreases myocardial oxygen demand, decreases heart
rate, stabilizes membranes thereby decreasing
arrhythmia risk
Do not use short acting Calcium channel
blockers (nifedipine)
Therapeutics--patients with ACS
Antiplatelet and anticoagulant therapy
• Antiplatelets
- ASA
• Give promptly
- Clopridogel
• Give promptly
• Anticoagulants
- Heparin – LMWH or unfractionated
RE-vascularization (thrombolytics or PTCA
with stent) in patients with STEMI
Treatment Strategy for
Right Ventricular Ischemia/Infarction
• Maintain right ventricular preload
– Volume loading (IV normal saline)
– Avoid use of nitrates and diuretics
– Maintain AV synchrony (AV sequential pacing for
symptomatic high-degree heart block unresponsive to
atropine)
– Prompt cardioversion for hemodynamically significant SVT
• Inotropic support
– Dobutamine (if cardiac output fails to increase after volume
loading)

Dr.Sarma@works
Treatment Strategy for
Right Ventricular Ischemia/Infarction
• Reduced right ventricular afterload with LV dysfunction
– Intra-aortic balloon pump
– Arterial vasodilators (sodium nitroprusside, hydralazine)
– ACE inhibitors
• Reperfusion
– Fibrinolytic agents
– Primary PTCA
– CABG (in selected patients with multivessel disease)

Dr.Sarma@works
Complications of Ml

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COMPLICATIONS OF INFARCTION

Papillary Muscle Rupture Left Ventricular Thrombus Ventricular Septal Rupture

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Ventricular Free Wall Rupture
ACS Treatment
 Revascularization
 Mechanical: PCI, CABG
 Pharmacologic: Thrombolytics
 Stabilization of Vulnerable Plaque Aspirin
 Antithrombotics
 Beta-Blockers
 ACE-Inhibitors
 Lipid-Lowering Agents (+stantins)
 Antioxidants
 Aggressive Risk Factors Modifications

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Take Home Messages
Atherosclerosis is the leading cause of death and
disability, also the main cause of CHD
Risk factors and prevention of atherosclerosis
CHD is due to the imbalance between myocardial oxygen
supply and demand
Two large groups of CHD: chronic(stable angina pectoris)
and ACS
ACS composed of UAP/NSTEMI and STEMI, resulting
from the plaque rupture or erosion, with differing degree
of thrombosis and distal embolization, with different
obstruction of the coronary artery.
 reperfusion either by fibrinolysis or primary PCI is the
mainstay of therapy of STEMI
Thanks!