1. Acute Myocardial Infarction in the Young
Presented by
Glenn Michael L . Gayos M.D.
MAKATI MEDICAL CENTER
MEDICAL GRAND ROUNDS

2. 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

3. GENERAL DATA:
W.V.
35 YEAR OLD
MALE
FILIPINO
MARRIED

4. CHIEF COMPLAINT
CHEST PAIN

5. 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

6. PAST MEDICAL HISTORY:
CVD May 2008 (2 weeks PTA )with right sided residuals, medications prescribed but not taken
(-) DM
(-) HTN
(-) allergies
(-) CA

7. Personal Social History
Family History
Hypertension both sides
(-) DM, (-) Cancer, (-) Thrombosis, (-) early stroke or MI
Personal Social History
25 pack year smoking history
Occasional alcoholic beverage drinker
Denies history of drug intake or stimulants

8. REVIEW OF SYSTEMS (-) headache, (-) loss of consciousness
(-)easy bruisability (-) rashes
(-) easy fatigability, (-) palpitations,
(-) abdominal pain (-) diarrhea no constipation
(-) edema (-) rashes (-) caudication
(-) arthralgia, (-) limitation of motion

9. Physical Examination on Admission
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

10. Physical Examination on Admission
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

11. SALIENT FEATURES 35 year old male
chest tightness of more than 30 minutes duration
Diaphoresis
CVD 2 weeks PTA
Smoker 25 pack years
Bp 130/80 HR 106 RR 24
Equal chest expansion
Tachycardic
Equal Pulses
Shallow nasolabial fold R

12. AT THE EMERGENCY ROOM 12 Lead ECG, Chest x ray, serum electrolytes
cardiac enzymes,
CBC
Urinalysis
Nitroglycerine
ISDN drip
Enoxaparin
Morphine
ASA/ Clopidogrel
02 via nasal cannula
Diazepam

13. WORKING DIAGNOSIS
S-T elevation Myocardial Infarction Anterolateral Wall
S/P Cerbrovascular Disease
To consider Hypercoagulable State

14. Admitted under Cardiology Service
Immediately Referred Patient to interventional cardiology for Primary PTCA
Neuro Referral
Recommendations: CT Scan
CVD Infarct noted

15. REPERFUSION
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

16. CATH LAB REPORT OF CORONARY ANGIO AND PCI
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

17. Coronary Angiography: Totally occluded Left Main Segment

18. 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

19. 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 atm for 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.

20. CARDIAC CATHETERIZATION REPORT
BALLOON INFLATION
Lesion dilated: Left main-proximal LAD
SITE
Balloon/ Stent
Size
Duration
(sec)
Pressure
(atm)
Left Main LAD
Ryujin balloon
2.0 x 15 mm 23 12
Sprinter balloon
3.0 x 15 mm 11 33 14
Taxus stent
3.5 x 20 mm 36 8
Delivery balloon 13

21. PTCA CONCLUSION
Successful Primary PCI/stent deployment of the Left Main - LAD

22. Total Occlusion of Left Main Coronary Artery
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

23. POST PTCA 30 minutes Post PTCA Patient had episodes of desaturation
O2 inhalation increased to fio2 100 % (02 sat 80-90%)
Patient intubated
Pulmo referral done
CXR post intubation revealed pulmonary congestion/ pulmonary edema
ABG done

24. CHEST X-RAY (POST INTUBATION)
BASELINE CXRAY
CXRAY AFTER
< 6 HOURS

25. AT THE TELEMETRY Episodes of non-sustained ventricular tachycardia
Patient started on AMIODARONE for Post PTCA arrythmia
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 ng/ ml (<500 ng/ ml)

26. 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)

27. CT ANGIOGRAPHY
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

28. ECG POST PTCA
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

29. 2020H non-sustained v-tach
Magnesium Sulfate 4 gram in 50ml D5w x 30min
Dopamine inotropic support

30. First Hospital Day Coffee ground/per NGT Enoxaparine discontinued
Repeat Cardiac Enzymes
Diagnostic Test
Hypercoagulable Work-up
Medications
Dopamine / Dobutamine
Furosemide 40mg
Piperacillin Tazobactam
Metoprolol
Nicorandil

31. ECG on 1st HD

32. 2nd HD Episodes of hypotension Bilateral Rales (base-mid)
CXR increased congestion
Episodes of Chest Pain
Treatment
Dopamine /Dobutamine
Furosemide Increased
NTG patch
transfer of patient to ICU was done.

33. Continuous titration of Dopamine/ Dobutamine
3rd HD
Episodes of Hypotension
Persistence of pulmonary congestion
Electrolyte abnormalities
Continuous titration of Dopamine/ Dobutamine
Increased Furosemide
Correction with KCL

34. 4th 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)

35. 6th HD Weaning Started via SIMV IV amiodarone shifted to Oral
Tapering of Pressors Started
CXR showed clearing of pulmonary congestion

36. 7th HD Patient extubated NGT removed Clear liquid diet with 1.2L/day
Tapering of Dobutamine Started

37. On the 10th HD Normal CXR Dobutamine tapered off
Anti-Cardiolipin Results
Warfarin 5mg initially
Warfarin 2.5mg OD

38. On the 24th HD Discharged Stable and Improved 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

39. DISCHARGE DIAGNOSIS:
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
Anti-phospholipid Antibody Syndrome Suspect

40. DISCUSSION

41. DEFINITION
Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia.
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

42. Epidemiology
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

43. 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

44. Causes of MI the Young

45. Causes of MI in the Young
Cocaine Abuse
Atheromatous Coronary Artery Disease
Coronary Artery Dissection/ Aneurysm
Kawasaki’s, Takayasus
Hypercoagulable State
Anti-phospolipid Antibody Syndrome (primary/secondary)
Factor V Leiden

46. Atheromatous Coronary Artery Disease
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

47. Non-Atheromatous Coronary Artery Disease
Aortic Dissection
Aneurysms, ectasia, and anomalous origin of coronary arteries
Coronary artery aneurysms
congenital or acquired secondary to Kawasaki’s disease in childhood

48. MI with Normal Coronary Arteries
1-12% occurence based on Coronary Angiography
Typical patient is young, without any previous history of chest pain
Mean age at largest series of MI in patients with normal coronary arteries patients, was 43 years and 43% were women.
significantly less frequent angina prior to myocardial infarction.
cardiovascular risk profile is lower than that of patients with CAD,
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

49. MI related to substance Abuse
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 after cocaine use.
Cardiovascular Complications of Cocaine Use Richard A. Lange, M.D., and L. David Hillis, M.D.

50. 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

51. Clotting Cascade

52. 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

53. Anti-phospholipid Antibody Syndrome
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: ) Seijas M ; Martínez Vázquez C ; Rivera A ; Rayo N ; Ordi-Ros J ; Nodar A ; Picón J

54. 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)
• Recurrent pregnancy loss.
• Anticardiolipin antibody of IgG and/or IgM isotype on two
occasions at least 12 weeks apart.
• Lupus anticoagulant in plasma on two occasions at least 12 weeks apart.
* Anti b2 glycoprotein I Antibody of IgG or IgM isotype in serum or plasma present on two occasions at least 12 weeks apart

55. ANTIPHOSPHOLIPID ANTIBODY SYNDROME

57. ALGORITHMIC APPROACH TO APAS

58. Management of Acute Myocardial Infarction
Reperfusion (minimize total ischemic time)
Restoration of balance between O2 supply and demand
Pain Relief
Prevention of Compilations

59. GOLDEN PERIOD

60. MEDICAL MANAGEMENT ANALGESIA- MORPHINE ASPIRIN BETA BLOCKERS
ACE INHIBITORS/ ARB
THIENOPYRIDINES

61. REPERFUSION Primary Invasive Strategy Fibrinolytic Therapy
Goal Door To balloon time 90 minutes
May give >12 hours
Patients with caridogenic shock
Primary PTCA
Facilitated PTCA
Rescue PTCA
Fibrinolytic Therapy
Door to needle time 30minutes
May give within 12 hours of onset of symptoms
Contraindications
Hemorrhage
Intracranial mass/stroke
AVM
Active bleeding
2007 Focused Update of the ACC/AHA

62. SECONDARY PREVENTION CONTROL OF MODIFIABLE RISK FACTORS
SMOKING CESSATION
WEIGHT LOSS
EXERCISE
Lipid and Sugar Management
Anti-coagulation for Hypercoagulable States

63. PROGNOSIS IN THE YOUNG
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

64. MODIFIABLE RISK FACTORS
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

65. APAS TREATMENT 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

66. RECOMMENDATIONS
REPEAT ANTI-Cardiolipin Anti-body testing after 12 weeks
Continue Clopidogrel and ASA for at least 14 days
Rheumatology Follow-up
Ant-coagulation

67. Thank You

68. ECG on admission

69. CXR On admission

70. Admission 17.0 47.9 17.17 3.3 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: % activity, 0.9 INR
PTT: Patient 28.2 (25.1 – 33.9 sec)
Control 29.1 seconds

71. 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

72. 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

73. URINALYSIS COLOR YELLOW TRANSPARENCY HAZY PH 7.5 GRAVITY 1.01 PROTIEN
NEGATIVE
KETONES
NITRITES
ESTERASE
BLOOD 3
RBC
255
EPITHELIAL 1
WBC 2
BACTERIA

74. HYPERCOAGULABLE Work up
ANTI-CARDIOLIPIN IgG
ANTI-CARDIOLIPIN IgM
HOMOCYSTIENE
12.5
(5-15)
Protein c
4.59
( )
Protein s 17
( )

75. Hypercoagulable Work-Up
Functional assay for antihrombin III, C , S
Lupus anticoagulant
Plasma homocysteine
Antiphospholipid antibodies
Clotting assay activated protein C resistance
Factor V Leiden
Prothrombin gene mutation

76. WORK-UP Anti-Cardiolipin Ig G 3 mpl(<15) Anti-Cardiolipin Ig M
6/16/08
ESR 43
ANA
Negative
CRP
negative

77. Chest X-ray
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

78. Diagnostics 6/3/2008 6/3/2008 6/4/2008 1250H 1646H D-dimer 642.6
6/3/2008 6/3/2008 6/4/2008
1250H 1646H
D-dimer
CPK
cpkmb
trop I 0

79. ALGORITHMIC APPROACH TO APAS

80. ECG
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

81. Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee consensus report. Lupus.  2003; 12(7):518-23 (ISSN: ) 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.
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 cholesterol-lowering 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:

82. 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.

83. Ct scan
6/3/08
Suggestive lacunar infarct in the left temporo-parietal subcortical area
Unremarkable Ct scan examination of the rest of the brain

84. 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

85. 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

86. 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

87. 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

88. 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

89. 6/3/08
1125.9
6/4/08
1073.5
6/5/08
-253
6/6/08
-350
6/7/08
-390
6/8/09
-150
40mg q12
40mg q 12
40mg q 6
40mg/od

91. 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, tissue-
type plasminogen activator (t-PA) and urokinase-type plasminogen
activator (u-PA) convert plasminogen to plasmin. Once
generated, plasmin proteolytically degrades fibrin (