Transcript ACUTE MYOCARDIAL INFARCTION IN YOUNG

Acute Myocardial
Infarction in the Young
Presented by
Glenn Michael L . Gayos M.D.
MAKATI MEDICAL CENTER
MEDICAL GRAND ROUNDS
OBJECTIVES:


To present a case of acute myocardial infarction
in the young.
To discuss the etiology, approach, management
to the young patient with myocardial infarction
GENERAL DATA:
W.V.
35 YEAR OLD
MALE
FILIPINO
MARRIED
CHIEF COMPLAINT
CHEST PAIN
HISTORY OF PRESENT ILLNESS:
One week PTA
(+) CHEST PAIN on the anterior chest
well described as heaviness
with no radiation
(+) Self medicated with Aspirin with
relief of sxs
Few Hours PTA
(+) While watching television,
Recurrence of CHEST PAIN on the left
anterior chest wall described
as heaviness with radiation to the
back. Persisting for more than thirty minutes
Severity of pain 10/10
(+) Difficulty in breathing
PAST MEDICAL HISTORY:
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CVD May 2008 (2 weeks PTA )with right sided
residuals, medications prescribed but not taken
(-) DM
(-) HTN
(-) allergies
(-) CA

Family History
Hypertension both sides
 (-) DM, (-) Cancer, (-) Thrombosis, (-) early stroke or
MI
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Personal Social History
25 pack year smoking history
 Occasional alcoholic beverage drinker
 Denies history of drug intake or stimulants
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REVIEW OF SYSTEMS
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(-) headache, (-) loss of consciousness
(-)easy bruisability (-) rashes
(-) easy fatigability, (-) palpitations,
(-) abdominal pain (-) diarrhea no constipation
(-) edema (-) rashes (-) caudication
(-) arthralgia, (-) limitation of motion
Physical Examination on Admission
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Bp 130/80 HR 106 RR 24 Temp 37.5
W.T. 55 kg H.T. 163cm BMI 20 JVP 8-9
Conscious coherent in cardio-pulmonary
distress
Anicteric sclerae, pink palpebral conjunctivae no
carotid bruits no neck vein distention no CLAD
Equal chest expansion, No retractions, Equal
fremitus clear breath sounds
Physical Examination on Admission
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Adynamic precordium tachycardic regular
rhythm no murmurs distinct S1& S2 no S3
noted
Flat soft non-tender abdomen
Full and equal pulses no edema no cyanosis
Neuro-examination =shallow nasolabial fold ®,
5/5 motor function on all extremities no
sensory deficit
SALIENT FEATURES
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35 year old male
chest tightness of
more than 30 minutes
duration
Diaphoresis
CVD 2 weeks PTA
Smoker 25 pack years
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Bp 130/80 HR 106
RR 24
Equal chest
expansion
Tachycardic
Equal Pulses
Shallow nasolabial
fold R
AT THE EMERGENCY ROOM
 12
Lead ECG,
 Chest x ray,
 serum
electrolytes
 cardiac enzymes,
 CBC
 Urinalysis
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Nitroglycerine
ISDN drip
Enoxaparin
Morphine
ASA/ Clopidogrel
02 via nasal cannula
Diazepam
WORKING DIAGNOSIS
 S-T
elevation Myocardial Infarction
Anterolateral Wall
 S/P Cerbrovascular Disease
 To consider Hypercoagulable State
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Admitted under Cardiology Service
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Immediately Referred Patient to interventional
cardiology for Primary PTCA
Neuro Referral
Recommendations: CT Scan
 CVD Infarct noted
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REPERFUSION
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STEMI px presenting to hospital with PCI
capability should treat with primary PCI
within 90 mins of medical contact
Intervention AHA 2007 STEMI ( MODIFIED
RECOMMENDATION)CLASS, ASSENT-4 PCI
CATH LAB REPORT OF
CORONARY ANGIO AND PCI
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Emergency left heart catherization with
coronary angiography and percutaneous
coronary intervention/stenting of left main
coronary artery were done by percutaneous
seldinger technique using 6f Judkins catheters
via the right femoral artery with no difficulty or
complications
Coronary Angiography:
Totally occluded Left Main Segment
CARDIAC CATHETERIZATION REPORT
CORONARY ANGIOGRAPHY:
Selective cannulation of the LCA with a 6F JL4 catheter shows a TOTALLY
OCCLUDED LEFT MAIN SEGMENT.
Selective cannulation of the RCA with a 6F JR4 cathter shows a very large and dominant
vessel with two large patent posterior descending branches.
PROCEDURE:
Emergency left heart catheterization with coronary angiography and percutaneous
coronary intervention/ stenting of left main coronary artery were done by percutaneous
Seldinger technique using 6F Judkins catheter via the right femoral artery with no
difficulty or complications. The patient tolerated the procedure well (IABP was on
standby).
CATHETERS USED:
6 F JL4 AND JR4 Cordis diagnostic catheters
6F XB 3.5 Cordis Vistabrite tip guide catheter
CONTRAST USED:
130 ML Ultravist 370
PCI
A 6F XB 3.5 Cordis Vistabrite tip guiding catheter was used to engage the left
main. A 0.014” x 180 cm Cordis Supersoft Stabilitzer wire was used to
cross the lesion and positioned into the distal LAD. A 2.0 (15 mm length)
Terumo Ryujin rapid exchange balloon was then advanced across the lesion
and then inflated at 12 atm for 23 seconds. A second balloon 3.0 x 15 mm
Sprinter was used to further dilate the lesion at 12-14 atm for 11-33
seconds. Post balloon angiogram showed a residual stenosis of 40 – 50%.
A Taxus 3.5 x 20 mm stent was then advanced across the lesion and deployed
at 8 atm for 36 seconds. The delivery balloon was re-inflated at 14 atm for
13 seconds. Post-stent angiogram of the left main LAD showed no
significant residual stenosis at the lesion site with TIMI-2 antegrade distal
flow, no contrast staining and no loss of side branches. No significant
change in the post-stenting angiographic results occurred after an
observation period of 5 – 7 minutes. The procedure was terminated with
the patient in stable condition.
CARDIAC CATHETERIZATION REPORT
BALLOON INFLATION
Lesion dilated: Left main-proximal LAD
SITE
Balloon/
Stent
Size
Left Main
LAD
Ryujin
balloon
2.0 x 15 mm
Sprinter
balloon
Taxus stent
Delivery
balloon
Duration
(sec)
23
Pressure
(atm)
12
3.0 x 15 mm
11
33
12
14
3.5 x 20 mm
36
8
13
14
PTCA CONCLUSION
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Successful Primary PCI/stent deployment of
the Left Main - LAD
Total Occlusion of Left Main
Coronary Artery
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Rare occurrence with 2.6% frequency in one
study
Generally presents as pulmonary edema,
cardiogenic shock, or sudden death
PTCA feasible and effective procedure
Effect of Primary Angioplasty on Total or Subtotal Left Main Occlusion
Analysis of Incidence, Clinical Features, Outcomes, and Prognostic Determinants
Hon-Kan Yip, MD; Chiung-Jen Wu, MD; Mien-Cheng Chen, MD; Hsueh-Wen Chang, PhD; Kelvin
Yuan-Kai Hsieh, MD; Chi-Ling Hang, MD and Morgan Fu, MD
POST PTCA
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30 minutes Post PTCA
Patient had episodes of desaturation
 O2 inhalation increased to fio2 100 % (02 sat 8090%)
 Patient intubated
 Pulmo referral done
 CXR post intubation revealed pulmonary
congestion/ pulmonary edema
 ABG done
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CHEST X-RAY
(POST INTUBATION)
BASELINE CXRAY
CXRAY AFTER
< 6 HOURS
AT THE TELEMETRY
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Episodes of non-sustained ventricular tachycardia
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Patient started on AMIODARONE for Post PTCA arrythmia
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INITIAL LOADING DOSE (150 mg)
MAINTENANCE DRIP (900 mg x 24 hours)
Patient admitted to Telemetry Unit
Referral to Nephrology Service for renal prophylaxsis
and decreased urine output
CT angiography with renal prophylaxis done
D-dimer 642.60 ng/ ml (<500 ng/ ml)
2D ECHOCARDIOGRAM (06/03/08)
Concentric left ventricular hypertrophy with hypokinetic anterior
interventricular septum, anterior and lateral left ventricle from mid to
apex. Left ventricular ejection fraction is reduced, 56% (Teicholz) /
52 % (Simpson’s). Normal left atrial dimension. Normal right atrial
and ventricular dimensions. Normal main pulmonary artery diameter.
Normal diameter of aortic root and proximal ascending aorta (2.5
cm). Thickened margins of right and non-coronary cusps of aortic
valve leaflets with normal mobility pattern. Normal mitral, tricuspid
and pulmonic valves.
Color Flow and Doppler study: Mitral regurgitation, mild. Tricuspid
regurgitation, mild. Normal pulmonary artery pressure (by pulmonary
acceleration time >110 msec). Normal left ventricular diastolic
function indices (E/A ratio = 1.3; IVRT = 80 msec)
CT ANGIOGRAPHY
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6/3/08
Bilateral marked pneumonic consolidation in
both lower lobes as well as in the upper lung
regions
Normal Ct angiography of the pulmonary
vessels including the thoracic aorta
No evident pulmonary embolism
ECG POST PTCA
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2020H non-sustained v-tach
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Magnesium Sulfate 4 gram in 50ml D5w x 30min
Dopamine inotropic support
First Hospital Day
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Coffee ground/per NGT
Enoxaparine
discontinued
Repeat Cardiac Enzymes
Diagnostic Test
Hypercoagulable Workup
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Medications
Dopamine /
Dobutamine
Furosemide 40mg
Piperacillin Tazobactam
Metoprolol
Nicorandil
ECG on
st
1
HD
nd
2
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Episodes of hypotension
HD
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Bilateral Rales (base-mid)
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CXR increased
congestion
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Episodes of Chest Pain
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Treatment
Dopamine /Dobutamine
Furosemide Increased
NTG patch
transfer of patient to
ICU was done.
rd
3
HD
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Episodes of
Hypotension
Continuous titration of
Dopamine/ Dobutamine
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Persistence of
pulmonary
congestion
Increased Furosemide
Electrolyte
abnormalities
Correction with KCL
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th
4
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HD
Repeat 2d Echo (6/7/08)
Concentric left ventricular hypertrophy with
segmental wall motion abnormality over left anterior
descending artery distribution with preserved global
systolic function, EF 59%
 Dilated aortic root aortic sclerosis, MR moderate,
TR mild
 Improvement of thickening of anterior and lateral
wall compared to (6/3/08)
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th
6
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HD
Weaning Started via SIMV
IV amiodarone shifted to Oral
Tapering of Pressors Started
CXR showed clearing of pulmonary congestion
th
7
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HD
Patient extubated
NGT removed
Clear liquid diet with 1.2L/day
Tapering of Dobutamine Started
On the
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Normal CXR
Dobutamine tapered off
Anti-Cardiolipin Results
th
10
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HD
Warfarin 5mg initially
Warfarin 2.5mg OD
On the
th
24
HD
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Discharged Stable and Improved
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Home Medications
ASA 80 mg tablet 1 tablet daily
Clopidogrel 75 mg tablet 1 tablet daily
Nicorandil 10 mg tablet ½ tablet 2x a day
Amiodarone 200 mg tablet 1 tablet 2x a day
Cilostazol 100 mg tablet 1 tablet 2x a day
Metoprolol 50 mg tablet ½ tablet 2x a day
Atorvastatin 40 mg tablet 1 tablet once a day
Warfarin (Coumadin) 5 mg tablet T – Th
2.5 mg tablet M W F ST SU
DISCHARGE DIAGNOSIS:
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Myocardial Infarction Left Main Segment
KILLIP III
Pulmonary Congestion
S/P CVD Lacunar Infarct LMCA (May 2008)
S/P PTCA (6/3/08)
T/Connective Tissue Disease
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Anti-phospholipid Antibody Syndrome Suspect
DISCUSSION
DEFINITION
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Myocardial infarction (MI) is the irreversible necrosis
of heart muscle secondary to prolonged ischemia.
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Detection of rise/fall of cardiac biomarkers
together with evidence of myocardial ischemia
with at least one
Symptoms of ischemia
ECG changes
Pathologic Q waves in ECG
Evidence of loss of viable myocardium or wall motion
Epidemiology
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Myocardial infarction (MI) under the age of 40
years accounts for around 3%-10% of cases of
coronary artery disease.
Incidence of MI is approximately 8 times lower
in patients 18 to 45 years than in older patients
Clinical Presentation
-Angina progressing rapidly to fully evolved
myocardial infarction
-Symptoms present less than 1 week duration
-Rarely presents with classic presentation of
worsening angina culminating in MI
Causes of MI the Young
Causes of MI in the Young
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Cocaine Abuse
Atheromatous Coronary Artery Disease
Coronary Artery Dissection/ Aneurysm
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Kawasaki’s, Takayasus
Hypercoagulable State
Anti-phospolipid Antibody Syndrome
(primary/secondary)
 Factor V Leiden
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Atheromatous Coronary Artery
Disease
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80% of acute myocardial infarction in the young
The atheromatous process starts early
CHD was found in 20% of men and 8% of
women between the ages of 30 and 34 years of
age
Rom J Intern Med, January 2006 Ginghin et al
Non-Atheromatous Coronary Artery
Disease
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Aortic Dissection
Aneurysms, ectasia, and anomalous origin of
coronary arteries
Coronary artery aneurysms
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congenital or acquired secondary to Kawasaki’s
disease in childhood
MI with Normal Coronary Arteries
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1-12% occurence based on Coronary
Angiography
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Typical patient is young, without any
previous history of chest pain
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Mean age at largest series of MI in
patients with normal coronary arteries
patients, was 43 years and 43% were
women.
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significantly less frequent angina prior
to myocardial infarction.
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cardiovascular risk profile is lower than
that of patients with CAD,
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Coronary Artery Spasm
Hypercoagulable States
Embolic Phenomena
 Embolic phenomena
 Paroxidical
Phenomena
Characteristics and Prognosis of Myocardial Infarction in Patients With Normal Coronary
Arteries
from CHESTPeter Ammann, MD; Sabine Marschall, MD; Martin Kraus, MD; Lucius
Schmid, MD; Walter Angehrn, MD; Reto Krapf, MD and Hans Rickli, MD
MI related to substance Abuse
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Cocaine use is associated
with various cardiac
complications including
MI.
48% of non-traumatic
chest pain in the young
associated with cocaine
use
6% MI at ER. after
various complications
Cardiovascular Complications of Cocaine
after cocaine use.
Use
Richard A. Lange, M.D., and L. David Hillis, M.D.
Hypercoagulable States
PRIMARY
SECONDARY
Antithrombin deficiency
Antiphospholipid syndrome
Protein C deficiency
Factor V Leiden
Disorders of the fibrinolytic system
Hypoplasminogenemia
Abnormal plasminogen
Plasminogen activator
deficiency
Factor XII deficiency
Dysfibrinogenemia
Others: elevation of factor VIII
Abnormalities of coagulation and fibrinolysis
Trosseau syndrome
Nephrotic syndrome
Abnormalities of the blood vessels and flow
Venous stasis
Homocystinuria
Thrombotic thrombocytopenic purpura
Abnormalities of the platelets
Myeloproliferative disorders
Paroxysmal hemoglobinuria
Diabetes mellitus
Clotting Cascade
Factor V Leiden (resistance to APC)
Site
Venous, occasional arterial,
Dx
-APC resistance assay
aPTT with exogenous APC
/ aPTT without APC
Normal > 2.2
-modified APC-resistance
assay.
-FV leiden DNA-based
analysis by PCR :
Loss of principal aPC cleavage
site on factor V protein→
Resistance to inactivation of
Factor Va by APC
Anti-phospholipid Antibody
Syndrome
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Autoimmune thrombotic disease.
It is characterized by recurrent arterial or venous
thrombosis, recurrent fetal loss or in-utero death
and/or thrombocytopenia
CVD most frequent thromboembolic
manifestations
MI with normal coronary arteries
presence of AAS among young patients with
AMI ranges from 14% to 21%,
Rev Clin Esp. 2001; 201(3):118-21 (ISSN: 0014-2565)
Seijas M ; Martínez Vázquez C ; Rivera A ; Rayo N ; Ordi-Ros J ; Nodar A ; Picón J
DIAGNOSTIC CRITERIA FOR APAS
International Consensus Statement on an update of
the classification criteria for definite Antiphospholipid Syndrome 2006.
Clinical Criteria
Laboratory Criteria
• Vascular thrombosis – one or more
episodes of arterial, venous or small
vessel thrombosis in any tissue or
organ.
(confirmed by imaging, Doppler
studies or histopathology)
• Anticardiolipin antibody of IgG
and/or IgM isotype on two
occasions at least 12 weeks apart.
• Recurrent pregnancy loss.
* Anti b2 glycoprotein I Antibody of
IgG or IgM isotype in serum or plasma
present on two occasions at least 12
weeks apart
• Lupus anticoagulant in plasma on
two occasions at least 12 weeks apart.
ANTIPHOSPHOLIPID
ANTIBODY SYNDROME
ALGORITHMIC APPROACH TO APAS
Management of Acute Myocardial
Infarction
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Reperfusion (minimize total ischemic time)
Restoration of balance between O2 supply and
demand
Pain Relief
Prevention of Compilations
GOLDEN PERIOD
MEDICAL MANAGEMENT
ANALGESIA- MORPHINE
ASPIRIN
BETA BLOCKERS
ACE INHIBITORS/ ARB
THIENOPYRIDINES
REPERFUSION
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Primary Invasive Strategy
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Goal Door To balloon
time 90 minutes
May give >12 hours
Patients with caridogenic
shock
Primary PTCA
Facilitated PTCA
Rescue PTCA
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Fibrinolytic Therapy
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Door to needle time
30minutes
May give within 12 hours
of onset of symptoms
Contraindications
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Hemorrhage
Intracranial mass/stroke
AVM
Active bleeding
2007 Focused Update of the ACC/AHA
SECONDARY PREVENTION
CONTROL OF MODIFIABLE RISK FACTORS
SMOKING CESSATION
 WEIGHT LOSS
 EXERCISE
 Lipid and Sugar Management

Anti-coagulation for Hypercoagulable States
PROGNOSIS IN THE YOUNG
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Better outcomes during medium and short term
follow-up due to better baseline characteristics
but may have higher long term morbidity and
mortality
Greater influence of Modifiable Risk factors
towards prognosis
Increased prevalence of smoking, hypertension
and obesity in the young
Acute Myocardial Infarction in Young Adults from American Heart JournalElvis Brscic, MD, et al
MODIFIABLE RISK FACTORS
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Observed that smoking, obesity, and hypertension
more prevalent in young, high-risk, post-MI
patients
dyslipidemia and diabetes were less prevalent.
Smoking and hypertension were associated with a
differentially increased relative risk of adverse
outcomes in younger patients.
need for aggressive efforts at minimizing
modifiable risk factors in young patients at risk for
and after MI.
High-risk Myocardial Infarction in the Young: The VALsartan In Acute myocardial
iNfarcTion (VALIANT) Trial
APAS TREATMENT
1.
2.
-
PROPHYLAXIS
PREVENTION OF FURTHER THROMBOSES OF
LARGE VESSELS
Low dose Aspirin 80 mg tablet 1 tablet once a day
Hydroxychoroquine (reported to decrease the titers of
APLAS)
According to American College of Chest Physicians 
Low Molecular Weight Heparin followed by Oral
anticoagulants (Warfarin) to maintain INR of at least 2.5
for 12 months or longer
RECOMMENDATIONS
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REPEAT ANTI-Cardiolipin Anti-body testing
after 12 weeks
Continue Clopidogrel and ASA for at least 14
days
Rheumatology Follow-up
Ant-coagulation
Thank You
ECG on admission
CXR On admission
Admission
COMPLETE BLOOD COUNT
HB
HCT
RBC
WBC
LYMPH
SEG
PLT
17.0
47.9
6.0
17.17
70
20
286,000
Na
K
CREAT
TROP I
TCPK
CPKMB
CBG
140.0
3.3
1.0
0.0
64.0
0.6
162.0
PROTIME: 109.9% activity, 0.9 INR
PTT: Patient 28.2 (25.1 – 33.9 sec)
Control 29.1 seconds
ABG POST INTUBATION
PO2
60.3
HCO3
21.6
PH
7.46
02 SAT
92
PCO2
26.4
BE
-3.6
FIO2
100
PEEP
MODE
AC
DAY 2
Na
K
BUN
CREAT
CPKMB
Mg
138.0
3.5
21.0
1.2
1123.2
1.9
HB
HCT
RBC
WBC
SEG
LYMPH
MONO
PLTS
15.10
43.10
5.42
22.27
78
10
12
221,000
COLOR
TRANSPARENCY
PH
GRAVITY
URINALYSIS
YELLOW
HAZY
7.5
1.01
PROTIEN
NEGATIVE
KETONES
NEGATIVE
NITRITES
NEGATIVE
ESTERASE
NEGATIVE
BLOOD
RBC
EPITHELIAL
3
255
1
RBC
255
WBC
2
BACTERIA
1
HYPERCOAGULABLE Work up
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ANTI-CARDIOLIPIN IgG
ANTI-CARDIOLIPIN IgM
(5-15)
HOMOCYSTIENE
12.5
Protein c
4.59 (4.62-4.94)
Protein s
17 (13.5-24.1)
Hypercoagulable Work-Up
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Functional assay for
antihrombin III, C , S
Lupus anticoagulant
Plasma homocysteine
Antiphospholipid
antibodies

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
Clotting assay activated
protein C resistance
Factor V Leiden
Prothrombin gene
mutation
WORK-UP
Anti-Cardiolipin Ig G
3 mpl(<15)
Anti-Cardiolipin Ig M
13mpl (<12.5)
6/16/08
ESR
43
ANA
Negative
CRP
negative
Chest X-ray
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6/3/08 normal
6/3/08 (post intubation) prominent pulmonary
vasculature with pulmonary congestion E.T. 2
cm above the carina
6/5/08 progression of pulmonary congestion,
still with pulmonary edema
6/9/08 complete clearing of pulmonary
congestion
Diagnostics
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6/3/2008
1250H
6/3/2008
1646H
642.6
6/4/2008
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D-dimer

CPK
0.6
1100
1123.2

cpkmb
64
18620
9810

trop I
0
ALGORITHMIC APPROACH TO APAS
ECG
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6/3/08 (1030H) ST Elevation Myocardial
Infarction anterolateral wall elevation
6/3/08( 1330H) Acute St Elevation Myocardial
Infarction MI
6/4/08 antero-septal wall myocardial infarction
with reciprocal changes in the inferior leads
Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee
consensus report.
Lupus. 2003; 12(7):518-23 (ISSN: 0961-2033)
Lockshin M ; Tenedios F ; Petri M ; McCarty G ; Forastiero R ; Krilis S ; Tincani A ; Erkan D
; Khamashta MA ; Shoenfeld Y
Hospital for Special Surgery, Barbara Volcker Center for Women and Rheumatic Diseases,
New York, NY 10021, USA. [email protected]
RECOMMENDATIONS:
Valve abnormalities: anticoagulation is recommended for symptomatic patients with valvulopathy.
Prophylactic antiplatelet therapy may be appropriate for asymptomatic patients
(recommended by 13/17 experts in an independent review).
Committee members disagreed whether corticosteroid therapy is helpful, but agree that
distinguishing among presumptive valvulitis (valve thickening on echocardiogram), valve
deformity and vegetations is important, as treatment implications may differ.
Occlusive arterial disease (angina, myocardial infarction): the Committee recommends
aggressive treatment of all risk factors for atherosclerosis (hypertension,
hypercholesterolaemia, smoking) and liberal use of folic acid, B vitamins and cholesterollowering drugs (preferably statins).
Hydroxychloroquine for cardiac protection in APS patients may be considered.
The Committee also recommends warfarin anticoagulation for those who have suffered
thrombosis in the absence of atherosclerosis, but recognizes that developing data may
support the use of antiplatelet agents instead. Intracardiac thrombi:
the Committee recommends intensive warfarin anticoagulation, and consultation with cardiac
surgeons when appropriate. Ventricular dysfunction:


Summary
The objective of this study was to highlight the need for investigation of
antiphospholipid (aPL) antibodies in patients presenting with myocardial
infarction (MI) and normal coronary arteries at angiography. We present five
patients who were found to have had an MI without evidence of
atherosclerosis. All had aPL antibodies and thus fulfilled the diagnosis of
antiphospholipid syndrome (APS). Who did not have recurrent events on
long-term anticoagulation maintaining an international normalised ratio of
3–4. This study suggests that APS is probably a major cause of MI in those
with normal coronary arteries at angiography. It is an important diagnosis to
make as they do not require anti-atherosclerotic treatment but appear, from
this case series, to do well on high-dose warfarin. Further clinical studies are
necessary to look at prevalence and best management in these patients.
Ct scan
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6/3/08
Suggestive lacunar infarct
in the left temporoparietal subcortical area
Unremarkable Ct scan
examination of the rest
of the brain
BETA-BLOCKER
Oral B-blockers should be given in the first 24 hours
IV B-blockers may be given at time of presentation
Contraindications

1) signs of heart failure,

2) evidence of

a low output state,

3) increased risk* for cardiogenic shock,

4) relative contraindications to beta blockade
(Level of Evidence: B)
2007 AHA STEMI (MODIFIED RECOMMENDATION)
CLASS I
Clopidogrel
recommended to administer loading dosse of
Clopidogrel 300mg
Clopidogrel 75 mg daily + ASA in STEMI px regardless
of whether they undergo reperfusion with fibrinolytic
therapy (at least 14 day

Long term maintenance therapy with clopidogrel 75mg
daily is reasonable for STEMI patient
Lipid Control





HDL >50 in females > 40 in males
LDL 100> in non diabetics, 70>in diabetics and high risk
patients
Increase Omega 3 intake
Promotion of daily physical activity
High Serum Cholesteryl Ester Transfer Rates and Small High-Density Lipoproteins Are Associated
With Young Age in Patients With Acute Myocardial Infarction
Kawasaki





generalized vasculitis of unknown etiology
vasculitis is most severe in medium-sized arteries but can also
occur in veins, capillaries, small arterioles, and larger arteries.
In severely affected vessels, the media develops inflammation
with necrosis of smooth muscle cells. leading to aneurysms.
Vessel wall becomes narrowed or occluded due to stenosis or a
thrombus.
Cardiovascular death usually occurs from a MI secondary to
thrombosis of a coronary aneurysm or from rupture of a large
coronary aneurysm
Takayasu’s Disease



chronic, progressive, inflammatory,
occlusive disease of the aorta and
its branches
Takayasu arteritis is heterogeneous.
Most patients present with
systemic and vascular symptoms;
erythrocyte sedimentation rate is
elevated in most







Classification criteria (3 of 6
criteria are necessary), a
Age of 40 years or younger at
disease onset
Claudication of the extremities
Decreased pulsation of one or
both brachial arteries
Difference of at least 10 mm Hg in
systolic blood pressure between
arms
Bruit over one or both subclavian
arteries or the abdominal aorta
Arteriographic narrowing or
occlusion of the entire aorta, its
primary branches, or large arteries
in the upper or lower extremities
6/3/08 6/4/08 6/5/08 6/6/08 6/7/08 6/8/09
1125.9 1073.5 -253
-350
-390
-150
40mg
q12
40mg q 40mg q 40mg q 40mg q 40mg/o
12
6
6
6
d



















Figure 1.
The Clotting Cascade.
Coagulation is initiated by the exposure of blood to tissue factor
bound to cell membranes. Tissue factor interacts with factor
VIIa to convert factor IX to factor IXa and factor X to factor Xa
(only the activated forms are shown). Factor IXa converts factor
X to factor Xa. Factor Xa generates factor IIa (thrombin) from
factor II (prothrombin). Each of these reactions takes place on
an activated cell surface. Once factor IIa is generated, it cleaves
plasma fibrinogen to generate fibrin. The tissue-factor-pathway
inhibitor forms a quaternary structure with tissue factor, factor
VIIa, and factor Xa (shown in blue). The thrombomodulin–protein
C–protein S pathway (shown in yellow) inactivates factors
Va and VIIIa. Antithrombin III inactivates factors XIa, IXa, Xa,
and IIa (shown in orange) in a reaction that is accelerated by
the presence of heparan sulfate. In the fibrinolytic pathway, tissuetype plasminogen activator (t-PA) and urokinase-type plasminogen
activator (u-PA) convert plasminogen to plasmin. Once
generated, plasmin proteolytically degrades fibrin (