Acute Coronary Syndrome.ppt

Acute Coronary Syndromes
Prof. Bernard C. Nkum
MD FRCP FWACP
School of Medical Sciences
Hon. Consultant Cardiologist KATH

Objectives
• To understand the role of inflammation in the
pathogenesis of atherosclerosis
• To distinguish between stable and vulnerable plaque
• To become acquainted with the pathophysiology of
coronary thrombus
• To become familiar with the systemic and diffuse nature
of atherosclerosis
• To diagnose and manage ACS
• To appreciate that therapy must address stabilization of
vulnerable plaques in addition to revascularizing fixed
stenosis

Coronary Circulation
• Right coronary Artery (RCA)
– Posterior Descending Coronary Artery (PDA)
• Left Main Coronary Artery (LM )
– Left Anterior Descending Coronary Artery
(LAD)
– Left Circumflex Coronary Artery (LCx)
Delineation (4 epicardial aa-base. septum)

External Heart: Anterior View
Figure 18.4b

External Heart: Posterior View
Figure 18.4d

Coronary Tree Anatomy-Additional
Branches
•As you can see by the diagram on
the right, there are multiple
branches that we have not
discussed in detail.
•Most of these derive from the left
coronaries.
•Two important ones to mention
are:
•Diagonal Arteries (Diag)
•Derive off the LAD
•Obtuse Marginal (OM1, OM2)
•Derive off the Circumflex

Circulation cont’d
Collateral Circulation
• In obstruction dilate providing an avenue for
significant blood flow beyond the stenoses
• Most numerous
– Vent septum (between septal perforators of the LAD
and PDA)
– Vent apex (between LAD septal perforators)
– Ant R vent free wall (between LAD and RCA(
• The most common sites for plaques are
the proximal one-half of the LAD and the LCx
and the origin and entire length of the RCA

Physiology of the Coronary
Circulation
• Heart requires continuous O2 supply
• Never stops beating
• Myocardial O2 consumption (MVO2) is 8-15
ml/min/100g. Skeletal muscle resting MVO2 is
0.3ml/min/100g
• Major determinants are related to contraction:
heart rate, wall stress (chamber pressure x
chamber vol / myocardial wall thickness), and
contractility

Coronary Blood Flow Regulation:
Unique Features
• Energy is supplied by aerobic metabolism-
continuous source of O2 required
• O2 extraction cannot be increased appreciably.
Extra need supplied by augmenting blood flow
• Autoregulation in resistance arterioles less
effective in subendocardium than subepicardium
• NO pathway for vasodilatation impaired in CAD
• Sympathetic activation leads to vasoconstriction
and parasympathetic to vasodilatation

Normal Arterial Wall
Lumen
Media:
Smooth muscle cell
Matrix proteins
Internal elastic membrane
Endothelium
Intima:
External elastic membrane

Pathogenesis of Atherosclerotic
Plaques
Protective response results in production of
cellular adhesion molecules
Monocytes and T lymphocytes attach to
‘sticky’ surface of endothelial cells
Migrate through arterial wall to subendothelial space
Lipid-rich foam cells
Endothelial damage
Macrophages take up oxidised LDL-C
Fatty streak and plaque

Endothelium
• Normal endothelium regulates many processes that are key for the
maintenance of vascular structure and function, including vascular
tone, growth, haemostasis, inflammation, and redox state.
Endothelial dysfunction is involved in the vasomotor dysfuction of
coronary arteries.
• Excessive production of oxygen free radicals and subsequent
metabolism of NO results in oxidative stress.
• Overproduction of oxygen free radicals counteracts the effects of
NO and stimulates the expression of adhesion molecules, which
facilitates the attachment of leukocytes to the vascular endothelium.
This process results in acute inflammation, proliferation of smooth
muscle cells, and synthesis of extracellular matrix molecules, all of
which contribute to the development of CVD

‘activated’
endothelium
CELLULAR
ADHESION
MOLECULES
induces cell
proliferation and
a prothrombic
state
attracts monocytes and T
lymphocytes
which adhere to
endothelial cells
cytokines (eg. IL-1, TNF-)
chemokines (eg.MCP-1, IL-8)
growth factors (eg. PDGF, FGF)
Koenig W. Eur Heart J Suppl 1999;1(Suppl T);T19-26.
The ‘Activated’ Endothelium

Upregulation of endothelial
adhesion molecules
Increased endothelial
permeability
Migration of leucocytes into
the artery wall
Leucocyte adhesion
Lipoprotein infiltration
Endothelial Dysfunction in
Atherosclerosis

Types of Atherosclerotic Plaque
• Fatty streak
• Fibrous plaque
• Complex (Complicated) plaque
• Ulcerative lesions
• Intraplaque haemorrhage

Formation of foam cells
Adherence and entry of
leucocytes
Activation of T cells
Migration of smooth
muscle cells
Adherence and aggregation
of platelets
Fatty Streak Formation in
Atherosclerosis

Formation of
the fibrous cap
Accumulation of
macrophages
Formation of
necrotic core
Formation of the Complicated
Atherosclerotic Plaque

Libby P. Circulation 1995;91:2844-2850.
The Synthesis and
Breakdown of Atheromatous
Plaques

The Pathophysiology Of
Atherosclerosis
• Arterial wall structure
– Elastic vs. muscular arteries
– Histologic layers: Endothelium/ Intima /Media
/Adventitia
Cells: Platelets (adhesion, activation, aggregation
/Macrophages /SMCs
Regulatory substances of mitogenic and other
functions: CRP induces expression of adhesion
molecules (VCAM-1); monocyte chemoattractant
protein-1, macrophage colony stimulating factor (M-
CSF)
Atherosclerotic plaque: Fatty streak /Fibrous plaque
/Fibrous cap or layered

Risk Factors Associated with
Impaired Endothelium Dependent
Vasodilatation
• Dyslipidaemia
• Hypertension
• Diabetes Mellitus
• Cigarette Smoking
• Aging
• Menopause
• Family History of premature CAD/1st degree rel
• Risk factors cause endothelial damage and do
so rapidly

Less Reliable but Probable Risk
Factors
• Physical inactivity
• Excess alcohol ingestion
• Insufficient fruits and vegetables in the diet
• Emotional stress
• Elevated cardiac CT scan calcium scores
• Positron emission tomography (PET)
scanning

Atherogenic Influence of Risk
Factors
Biology Dyslipi HBP Smoke FHx DM
End inj + + + - +
Monoc ++ - - ++ ++
Platelet + - ++ - ++
SMC + + - ++ ++
Plaque ++ + - ++ -
Throm + - ++ + ++
Micova + ++ + - ++

The Progression from CV Risk
Factors to Endothelial Injury and
Clinical Events
Risk factors
Oxidative stress
Endothelial dysfunction
NO Local mediators Tissue ACE-Ang II
PAI-1 VCAM
ICAM cytokines
Endothelium Growth factors
matrix
Proteolysis
LDL-C BP Heart failure
Smoking
Diabetes
Vasoconstriction
Vascular lesion
and remodelling
Plaque rupture
Inflammation
Thrombosis
Clinical endpoints
NO Nitric oxide
Gibbons GH, Dzau VJ. N Engl J Med 1994;330;1431-1438.

Unified Hypothesis for the
Pathogenesis of Atherosclerosis
• Plaques occur in the intima
• Acceleration by dyslipideamia. Lipid
lowering improve by anti-inflammation
• Mediation through macrophages and
smooth muscle cells
• The functional state of the atheroma, not
merely its size or the luminal degree of
encroachment, determines ACS
development

• An inflammatory component in the
subendothelial area further weakens and
predisposes the plaque to rupture. Speed
of blood flow, turbulence and vessel
anatomy may be contributory factors.

Vulnerable Patient
Unstable coronary atheromata are often not
the “tight” stenoses
• Lipid profile
• Active inflammation in coronary arteries
• LVEF
• LV hypertrophy
• Long QT, wide QRS, NSVT
• Serologic markers of vulnerability

Libby P. Circulation 1995;91:2844-2850.
The Vulnerable Atherosclerotic
Plaque
SMC – smooth muscle cell
HDL-DR – transplantation antigen indicating ‘activation’ of SMCs

Vulnerable plaque
• Warm plaque
• Thin cap surface
• Acidic plaque
• Soft plaque
• Adventitious inflammation
• Adjacent lipid pool

Pathophysiology cont’d
• Mechanism
-plaque fissuring or rupture/thrombus formation
Presentation depends on:
-rapidity of vessel occlusion
-extent of occlusion
-recruitment of distal collaterals by infarct-related
artery
-transient occlusion with recurrent cycles of
thromboses and spontaneous lyses that may
allow time for conditioning and the dpt of
collaterals

Imaging Techniques Used to
Assess Atherosclerosis
• Invasive techniques
– Intravascular ultrasound (IVUS)
– Coronary angiography
• Non-invasive techniques
– Magnetic resonance imaging (MRI)
– Computed tomography (CT)
– Ultrasound (B-mode)

Intravascular Ultrasound (IVUS)
Showing Atheromatous Plaque
Reproduced from Circulation 2001;103:604–616, with permission from Lippincott Williams & Wilkins.
Angiogram IVUS
atheroma
normal
vessel

Computed Tomography (CT)
Showing Atherosclerotic Artery

Spectrum of ACS
• UA
• NSTEMI
• STEMI
• Non-Q wave MI
• Q wave MI
• Sudden cardiac death

WHO Criteria for Acute MI
• STEMI
– Chest pain or classic symptoms ≥30min
– ST ↑of .1mV in 2 contiguous leads or new
LBBB
– ↑Cardiac enzyme levels
• NSTEMI
– Chest pain or classic symptoms ≥30min
– ST ↓ or T inv
– ↑Cardiac enzyme levels

Angina
• Angina is likely to occur under the ff
circumstances:
– Brisk walking outdoors on a cold windy day
– Exertion after a heavy meal
– Working under the pressure of a deadline
– Speaking in public
– During sexual activity
– During worry, tension or anger

Triggers of ACS
• Physical exertion
• Anger
• Sexual activity
• Cocaine use
• Bereavement

Definitions
• Angina: Discomfort in the chest with or
without radiation to the arms, neck or back
which is caused by myocardial ischemia
and can se associated with a disturbance
of myocardial function but not with
necrosis
• Ischemia: Recurrent chest discomfort
considered to be probable or definite
angina that is at least 10min in duration

Unstable Angina
• Sudden acceleration in the severity of
previously stable angina, rest angina or
post-MI angina
• Pathologically characterized by incomplete
or transient coronary artery occlusion
• Initial thrombus platelet-derived with vaso-
constrictive response

UA Definition
• Angina pectoris or equivalent ischaemic
discomfort with at least one of 3 features
– It occurs at rest or with minimal exertion
usually lasting >10 min
– It is severe and of new onset (i.e. within the
prior 4-6wk)
– It occurs with a crescendo pattern ( i.e.
distinctly more severe, prolonged, or frequent
than previously

STEMI vs. NSTEMI
• Myocardial damage /in-hospital prognosis
• Fibrin- (red) vs. platelet (grey) -rich
thrombus
• Benefit from thrombolysis
• Angiographic occlusion by thrombus
• Single vessel CAD and plaque < 50% vs.
more extensive CAD and more developed
collaterals

Diagnosis of UA/NSTEMI
• Spectrum of ACS
• ECG changes (12 lead ECG every 8h X3)
• Cardiac Biomarkers (CK, CK-MB,
Troponin I)

Protein
Molecular
mass (kD)
First
detection
Duration of
detection
Sensiti
vity
Specifi
city
Myoglobin 16 1.5–2 h 8–12 h +++ +
CK-MB 83 2–3 h 1–2 d +++ +++
Troponin I 33 3–4 h 7–10 d ++++ ++++
Troponin T 38 3–4 h 7–14 d ++++ ++++
CK 96 4–6 h 2–3 d ++ ++
Biochemical Markers

Gheorghiade, Am J Cardiol 2005;96(suppl):18G-25G

Cardiac Biomarkers
• Positive Cardiac Markers
– cTnI>0.1, CK-MB>5, CK> 266
– CK, CK-MB every 8h x3d
– cTnI X1 (at least 3h after the onset of chest
discomfort)
• CTnI
– cTnI begins to increase 3h after ischaemia, peaks at
14-18h and remains elevated for 5-7days
– cTnI levels 1.0-1.6: About 1/3 of patients previously
diagnosed as unstable angina because of normal CK-
MB levels actually have elevated cTnI levels and
therefore are experiencing a micro MI

Immediate Assessment < 30min
• Measure vitals/BP
• Measure O2 saturation
• Obtain IV access
• Obtain 12 lead ECG
• Perform brief targeted history and PE
• Obtain initial serum cardiac marker levels
• Evaluate initial electrolyte and coagulation
studies
• Request, review portable CXR

Immediate General Treatment
• O2
• Aspirin 300mg
• Nitroglycerin (0.4mg SL or spray)
• Morphine (if pain not relieved by NTG)
(Memory MONA)
Bed rest

Nursing
• Telemetry Monitoring
– HR every 2h and rhythm every 4h or as patient condition warrants
• O2
– O2 sat every 4h. Delivery via nasal prongs for 2-3h. Continue if low
arterial sat (<90%)
• Activity level
– Bedrest with commode privileges for 12 h
– If haemodynamically stable progress activity as tolerated with
ambulation to the bathroom, bathing, and light ambulation
– A patient with an uncomplicated Mi is likely to return to prior activities
within 2 weeks
• Exercise test
– Before discharge from hospital or shortly thereafter
– Submaximal at 4-7days
– Symptom limited at 10-14days
• X

Assess Initial ECG
• ST segment elevation or new LBBB
1mm in 2 or more anatomically contiguous
leads (0.04s after the J point, TP baseline)
• ST depression or T wave inversion
• Non-diagnostic or normal ECG

Risk Stratification in UA/NSTEMI
• ECG Troponin /TIMI Risk Score /
Multimarker approach (CRP, BNP)
• High risk
– Persistent symptoms
– Recurrent ischemia
– Depressed LV function
– Widespread ECG changes
– Prior AMI, PCI, CABG

UA/NSTEMI Adjunctive Rx Anti-
Ischemic Rx
• Nitrates
• Beta blockers
• ACEI
• Calcium channel blockers 2nd line
• Angiography
– High risk
– Low EF, prior PCI or CABG

UA/NSTEMI Adjunctive Rx
(Antiplatelet/Anticoagulant)
• Aspirin 300mg daily
• LMWH > UFH
• GP IIb/IIIa inhibitors (Check package insertion)
– Inhibit the integrin glcoprotien receptor in the
membrane of the platelets inhibiting platelet
aggregation
– Epitifibitide: 180µ/kg IV bolus then 2µ/kg/min IV
infusion
– Tirofiban: 0.4µ/kg/min IV for 30min, then 0.1µ/kg/min
IV infusion
• Clopidogrel

UA/NSTEMI Long-term Rx
• ASA
• Beta blockers
• Clopidogrel < 1 year
• Lipid lowering (LDL <70)
• ACEI (if low EF, DM, HBP)
– No benefit if CAD alone
NTG prn

Structure of Lipoproteins
Free cholesterol
Phospholipid
Triglyceride
Cholesteryl ester
Apolipoprotein

Types of Lipoprotein
Particles
• Triglyceride-rich lipoproteins
– Chylomicrons
– Very low-density lipoprotein (VLDL)
• Cholesterol-rich lipoproteins
– Low-density lipoprotein (LDL)
– High-density lipoprotein (HDL)

Lipid Abnormalities Associated with
Endothelial Dysfunction
• Ox-LDL
• Small dense LDL
• HDL
• Remnant Particles
• Lp(a)
• LDL

Additional Emerging Lipid
Parameters
• Apolipoprotein (Apo) B
• Apo C-III
• Nonfasting triglyceridews
• Remnants of triglyceride-rich lipoproteins
containing Apo-III
• X

LDL cholesterol
• Strongly associated with atherosclerosis and
CVD events
• 10% increase results in an approximate 20%
increase in CHD risk
• Most of the cholesterol in plasma is found in
LDL particles
• Smaller denser LDL are more atherogenic
than larger, less dense particles
• Risk associated with LDL-C is increased by
other risk factors:
– low HDL-C
– smoking
– hypertension
– diabetes and the metabolic syndrome

HDL cholesterol
• HDL-C has a protective effect for risk of
atherosclerosis and CHD
• Epidemiological studies show the lower the
HDL-C level, the higher the risk for
atherosclerosis and CHD
– low level (<40 mg/dL, 1 mmol/L) increases risk
• HDL-C tends to be low when triglycerides are
high
• HDL-C is lowered by smoking, obesity and
physical inactivity

Triglycerides
• May be associated with increased risk of
CHD events
• Link with increased CHD risk is complex
– may be direct effect of smaller TG-rich
lipoproteins and/or
– may be related to:
• low HDL levels
• highly atherogenic forms of LDL-C
• hyperinsulinaemia/insulin resistance
• procoagulation state
• hypertension
• abdominal obesity

0
1
2
3
4
5
1 2 3 4 5
LDL-C
CRP
CRP (mg/L) (0.49) (>0.049-1.08) (>1.08-2.09) (>2.09-4.19 ) (>4.19)
LDL-C (mg/dL) (97.6) (>97.6-115.4) (>115.4 –132.2) (>132.2 –153.9) (>153.9)
Quintiles
Ridker PM. New Engl J Med 2002;347:1557-1565.
CRP is a Strong Predictor for
Future CV Events: Women’s
Health Study

Lipid Lowering Medications
Range of Lipid Effects (% Change)
TG HDL-C LDL-C
Fibric 35-50 10-25 10-15
Bile acid - - 15-30
Nicotinic
acid
25-30 10-30 10-25
Statins 20-30 5-10 20-45

Effect of Lipid-modifying Therapies
on Lipids
Therapy
Bile acid
sequestrants
Nicotinic acid
Fibrates
Probucol
Statins*
Ezetimibe
TC–total cholesterol, LDL–low density lipoprotein, HDL–high density lipoprotein, TG–triglyceride.
*Daily dose of 40 mg of atorvastatin, simvastatin, pravastatin and fluvastatin.
TC
Down
20%
Down
25%
Down
15%
Down
25%
Down
19–37%
-
LDL
Down
15–30%
Down
25%
Down
5–15%
Down
10–15%
Down
25–50%
Down
18%
HDL
Up
3–5%
Up
15–30%
Up
20%
Down
20–30%
Up
4–12%
Up
1%
TG
Neutral or up
Down
20–50%
Down
20–50%
Neutral
Down
14-29%
Down
8%
Patient
tolerability
Poor
Poor to
reasonable
Good
Reasonable
Good
Good
Yeshurun D, Gotto AM. Southern Med J 1995;88(4):379–391. Knopp RH. N Engl J Med 1999;341:498–
511. Product Prescribing Information. Gupta EK, Ito MK. Heart Dis 2002;4:399-409.

Dyslipidaemia Update
• Linear relationship between chol levels and CV events. Inverse for
HDL
• Lowering LDL with statins decreased CV events
• Exetimibe (chol absorption inhibitor can be used with statins
• Statins: Most potent for reducing LDL and most tolerated. Night
• Fibric acid derivatives: Stimulate lipoprotein lipase which results in
enhanced TG clearance
– Gemfibrozil (mixed: TG, LDL)
– Fenofibrate: (TG)
• Atorvastatin 80mg (LDL not effective for HDL or TG); Pravastatin,
Rosuvastatin, Simvastatin
• Nicotinic acid: cheap; most potent for HDL; Aspirin for flushing, IGT,
myopathy in combo with statin
• Bile acid sequestrants: Cholestyramine: Reduce total chol and LDL.
by binding positively charged bile acids in the gut to interrupt
enterohepatic circulation

NCEP ATP III Guidelines
* TLC: therapeutic lifestyle changes
Adapted from NCEP, Adult Treatment Panel III. JAMA 2001;285:2486-2497.
Patients with
Drug therapy
considered if LDL-C
Initiate TLC*
if LDL-C
LDL-C
treatment
goal
0-1 risk factors 160 mg/dL† 190 mg/dL
(160-189
mg/dL: drug
optional)
<160 mg/dL†
2 risk factors
(10-year risk 20%)
130 mg/dL† 10-yr risk 10-20%:
130 mg/dL
10-yr risk <10%:
 160 mg/dL
<130 mg/dL†
CHD and CHD risk
equivalents
(10-year risk >20%)
100 mg/dL† 130 mg/dL
(100-129
mg/dL: drug
optional)
<100 mg/dL†
† 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L; 190 mg/dL = 5 mmol/L

NCEP ATP III: LDL-C Goals
Adapted from NCEP, Adult Treatment Panel III, 2001. JAMA 2001:285;2486-2497.
CHD or
CHD risk
equivalents
< 2 risk
factors
≥ 2 risk
factors
LDL-C
level
100 -
160 -
130 -
190 -
goal
100
mg/dL
goal
130
mg/dL
goal
160
mg/dL
100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

NCEP ATP III: LDL-C Goals
(2004 proposed modifications)
*Therapeutic option
70 mg/dL =1.8 mmol/L; 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160
mg/dL = 4.1 mmol/L
High Risk
CHD or CHD risk
equivalents
(10-yr risk
>20%)
LDL-C
level
100 -
160 -
130 -
190 -
Lower
Risk
< 2 risk
factors
Moderately
High Risk
≥ 2 risk
factors
(10-yr risk
10-20%)
goal
160
mg/dL
goal
130
mg/dL
70 -
goal
100
mg/dL
or
optional
70
mg/dL*
Moderate
Risk
≥ 2 risk
factors
(10-yr risk
<10%)
goal
130
mg/dL
or
optional
100
mg/dL*
Grundy SM et al. Circulation 2004;110:227-239.
Existing LDL-C goals
Proposed LDL-C goals

Effects of Statins on Lipids
Statin
rosuvastatin (10 mg)
atorvastatin (10 mg)
simvastatin (20 mg)
pravastatin (20 mg)
fluvastatin (20 mg)
LDL-C
% change
-52
-39
-33
-32
-22
HDL-C
% change
TG
% change
+14
+6
+8
+2
+3
-10
-19
-19
-11
-12
US Product Data Sheets.

2013 ACC/AHA Guidelines
• Shift from focusing on LDL-c as primary
target for cholesterol lowering therapy to
the appropriate intensity of statin therapy
to reduce ASCVD risk in those most likely
to benefit
• 4 statin benefit groups identified
• High/Moderate/Low Intensity6 statin
therapy

Groups
• Clinical ASCVD
– Age < 75yr - high intensity
– Age >75yr - moderate
• Primary prevention
– >21yr LDL-c <190mg/dl – high
– Ages 40-75 with DM, LDL-c 70-189mg/dl,
without clinical ASCVD
• Estimated 10yr ASCVD risk <7.5% - Moderate
• Estimated 10yr ASCVD risk >7.5% - High

Groups cont,d
• Primary prevention
– Ages 40-75 without clinical diabetes or clinical
ASCVD. Estimated 10yr ASCVD risk greater
than or equal to 7.5% LDL-c 70-189 – mod to
high intensity

Intensity of Statin Rx
• High
– Atorvastatin (40) – 80mg
– Rosuvastatin 20 – (40)mg
• Moderate
– Atorvastatin 10- (20)
– Rosuvastatin 5-(10)
– Simvastatin 20 - 40
– Fluvastatin 40mg bd (XL 80mg)
• Low –Simv, Fluva and Prava

STEMI Adjunctive Rx
• IV Beta blocker
• IV NTG
• IV Heparin (start immediately and continue
for 48h if tPA is used)
• ACEI (after 6h or when stable)

Indications for Fibrinolysis
• ST elevation (≥1mm in ≥2 contiguous
leads) or new or presumably new LBBB
strongly suspicious of injury (BBB
obscuring ST analysis).
• In context of signs and symptoms of MI
• Time from onset of symptoms <12 hours

Specific Exclusion Criteria
• Acute internal bleeding (except menses) within 21 days
• Hx of CV, intracranial or intraspinal event within 3/12 (CVA, AV mal,
neoplasm, aneurysm,recent trauma, recent surgery)
• Major surgery or serious trauma within 14 days
• Aortic dissection
• Severe uncontrolled HTN
• Known bleeding disorders
• Prolonged CPR with evidence of thoracic trauma
• Lumbar puncture within 7 days
• Recent arterial puncture at non-compressible site
• During the first 24 h of fibrinolytic therapy for acute ischaemic CVA
do not administer aspirin or heparin

STEMI Fibrinolytic Rx
• tPA (3-hour infusion)
– Give 10mg IV bolus
– Then 50mg in the first hour
– Then 20mg/h for 2 additional hours
• For AMI the total dose should not exceed
100mg; for acute CVA not exceed .90mg

STEMI Fibrinolytic Rx
• tPA (Accelerated infusion 1.5hours(
– 15mg IV bolus
– Then 0.75mg/kg over the next 30min (not to
exceed 50mg)
– Then 0.5mg/kg over the next 60 min (not to
exceed 35mg)
• Streptokinase
– 1.5 million IU in a 1h infusion

STEMI Reperfusion
• Angiography
• PCI (Angioplasty + stent)
• Rates of restenosis within 6/12 of PCI
– No stenting 30-40%
– Bare met5al stent 15-30%
– Drug-eluting stent <10%
• CABG

Arrhythmias During Acute STEMI
Electrical Instability
• VPCs: K+, Mg2+, Beta blocker
• VT: Antiarrhythmics, DC shock
• AIVR: Observe unless heamodynamic
compromise
• NJPT: Search for cause (e.g. Dig toxicity)
• It is sound clinical practice to maintain
serum K+ > 4mmol/l and Mg2+ > 2mmol/l

Arrhythmias During Acute STEMI:
AV Conduction Disturbances
Proximal Distal
Site of Block Intranodal Infranodal
Site of
Infarction
Inferoposterior Anteroseptal
Infarct Artery RCA (90%) LAD (septals)
ECG Pattern 1O AV block
Mobitz 1
IVCD
Mobitz 2

Arrhythmias During Acute
AV Conduction Disturbance
Proximal Distal
Escape rhythm His bundle
<120 ms
45-60
Distal to His
>120 ms
Often < 30
Duration of AVB 2-3 days Transient
Mortality Low High (HF, VT)
Rx Observe PM / ICD

Mechanical Complications In
STEMI
• Ventricular septal rupture
• Ventricular free wall rupture
• Mitral regurgitation
– Chordal /papillary muscle rupture

• Thank You For Your Attention

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