The document discusses a case of a 63-year-old male patient who presented with chest pain, diaphoresis, and collapse and was found to have ST elevation on electrocardiogram consistent with acute myocardial infarction. The patient's medical history included diabetes, hypertension, and previous percutaneous coronary intervention. He was taken for cardiac catheterization which showed a tight mid right coronary artery lesion and received treatment including aspirin, Plavix, statins, and ACE inhibitors upon discharge.

1. ACUTE CORONARY SYNDROME
(A CASE DISCUSSION)
BY
Dr Ijaz Hussain
MBBS , MCPS, MRCGP, Dip Avn Med
Prince Sultan Military Medical City
Riyadh

2. Case Presentation
• Patient’s Name: Mohammad Al Shahrani
• Age: 63 Yrs
• Sex: ♂
• Nationality: Saudi
• Resident of al Oainah

3. Chief Complaints
• Mohammad al Shahrani was brought in the AnE with
Brief History of :
– Chest Pain
– Diaphoresis
– Collapse
• History of Present Illness:
– Patient had an out door BBQ party
– While coming back he exerted to pack-up and kept lifting
heavy luggage etc.
– Since last abt 15 minutes he had been c/o chest “discomfort”.
Family rushed to the hospital as he collapsed.
• Past History: Known Case if IHD: had undergone
cardiac cath one year and a half.

4. Initial Work-up
• Although the patient was in distress but his
vital parameters were stable and as following:
– B.P: 153/ 86 mm Hg
– Pulse: 66 per min
– Temp 36.2 ̊C
– SPO2 99 %
– Reflo: 7.6 mmol/dl
• ECG:
– St Elevation in II, III, aVf
– Reciprocal Changes in aVL, V1 and V2

5. ECG TRACING

6. Initial Work-up in PSMMC
• Cardiac Enzymes
Enzyme 18.11.2012 19.11.2012 Ref Range
– Ck 144 651 {50-190 u/L}
– Ck MB - 93 {0- 24 u/L }
– AST 32 82 {2.0- 37 u/L}
– LDH 530 495 {135-255 u/L}
• Troponine T Level
– 18.11.2012 0.007 1.1 {0.1 ng/ml }
– 19.11.2012 1.540
• FBC NAD
• Renal Functions NAD
• CxR NAD

7. DISCHARGE SUMMARY
• Final Diagnosis:
– Diabetes ; Hypertension ; IHD e Hx of PCI in Asir 4 Yrs
ago
• History:
– Pt is 63 yrs old saudi male with Dx as above.
Presented in A’nE with C/O acute onset chest pain of
few hrs duration with no SOB, Orthopnoea,
Paraxysmol Nocturnal dyspnoea or Palpitaion.
• Physical Examination:
– Chest clear, CVA Ex S1+S2+0 ; Abdomen soft lax ;
CNS intact ; B.P was normal
• Investigation Results :
– Showed ST elevation in Inf leads with still having pain

8. DISCHARGE SUMMARY
• Hosp Course & Mngmnt: Pt was taken directly from
A’nE to cath Lab. Shown tight mid RCA lesion ,with aspiration
of thrombosis. Echo was done which shown slight irregularity.
Pt was kept under observation for 24 hrs. Was discharged in a
good condition, with no complaints and was doing fine.
• Drugs on Discharge:
– Aspirin 81 mg 1xTab PO OD
– Plavix 75 mg 1xTab PO OD
– Prindopril 2.5 mg 1xTab PO OD
– Isordil 20 mg 1xTab PO OD
– Lipitor 40 mg 1xTab PO OD
– Lasix20 mg 1xTab PO OD
– Pantoperazole 40 mg 1xTab PO OD
• Future Plan : Pt was given an appt 24/52 to be seen in OPD

9. Case Discussion

10. • Heart is capable of pumping blood
to every cell in the body in under
one minute
• During the course of the day, your
heart will beat approx 100,000
times driving 2,000 gallons of
oxygen-rich blood through 60,000
miles of blood vessels.

11. DEFINITION
Myocardial infarction, commonly known as a
heart attack, is the irreversible necrosis of
heart muscle secondary to prolonged
ischemia. This usually results from an
imbalance in oxygen supply and demand,
which is most often caused by plaque
rupture with thrombus formation in a
coronary vessel, resulting in an acute
reduction of blood supply to a portion of the
myocardium.

12. DEFINITION
Myocardial infarction is considered part of a
spectrum referred to as acute coronary syndrome (
ACS). The ACS continuum representing ongoing
myocardial ischemia or injury consists of
unstable angina, non–ST-segment elevation
myocardial infarction (NSTEMI), and ST-segment
elevation myocardial infarction (STEMI). Patients
with ischemic discomfort may or may not have ST-
segment or T-wave changes denoted on the
electrocardiogram (ECG). ST elevations seen on the
ECG reflect active and ongoing transmural
myocardial injury

13. Types
• STEMI : OR New Onset LBBB ACUTE MI
• NSTEMI : ECG MAY SHOW ST-
DEPRESSION,T-WAVE INVERSION, NON-
SPECIFIC CHANGES OR NORMAL (NON-Q
WAVE MI OR SUBENDOCARDIAL MI)
• UA : ANGINA OF INCREASING FREQUENCY
OR SEVERITY, OCCURS ON MIN; EXERTION OR
AT REST. ASSOCIATED WITH INCREASED
RISK OF MI

14. Clinical Spectrum of Acute
Coronary Syndromes
Stable angina Unstable Non-STE MI STE MI
angina
None Positive Positive
Evidence of necrosis
ST-segment ST-segment ST-segment
ECG early depression depression
elevation
and/or and/or
T-wave inversion T-wave inversion
ECG late No Q No Q Q develops

15. Unstable
Angina N-STEMI STEMI
Non Occluding
occlusive thrombus Complete thrombus
sufficient to cause occlusion
thrombus
tissue damage &
mild ST elevations on
Non myocardial necrosis ECG or new LBBB
specific
ECG ST depression +/- Elevated cardiac
T wave inversion on enzymes
ECG
Normal More severe
cardiac Elevated cardiac symptoms
enzymes enzymes

16. EPIDEMIOLOGY OF
ACS

17.  Single largest cause of death
 515,204 US deaths in 2000
 1 in every 5 US deaths
 Incidence
 1,100,000 Americans will have a new or recurrent
coronary attack each year and about 45% will die*
 550,000 new cases of angina per year
 Prevalence
 12,900,000 with a history of MI, angina, or both
 INCIDENCE IN UK=5/1000/ANNUM FOR STEMI

18. PATHOPHYSIOLOGY

19. Understanding Myocardial
Ischemia
Imbalance

20. Understanding Myocardial Ischemia
Dec O2 supply Inc. Demand
INCREASED
CARDIAC
OUTPUT…..
(THYROTOXICOSIS)
MYOCARDIAL
HYPERTROPHY
(AS,HTN)

21. PATHOPHYSIOLOGY
• RUPTURE OR EROSION OF THE FIBROUS CAP
OF A CORONARY ARTERY PLAQUE.
• PLATELETS AGGREGATION AND ADHESION.
• LOCALIZED
THROMBOSIS.VASOCONSTRICTION.
• DISTAL THROMBUS EMBOLIZATION.
• THROMBUS FORMATION AND
VASOCONSTRICTION PRODUCED BY PLT
RELEASE OF SEROTONIN & THROMBOXANE
A2, RESULT IN MYOCARDIAL ISCHEMIA DUE TO
REDUCTION OF CORONARY BLOOD FLOW.

22. Plaque Rupture, Thrombosis, and Microembolization
Quiescent plaque
Process Marker
Lipid core Plaque formation Cholesterol
LDL
Vulnerable plaque C-Reactive Protein
Inflammation Adhesion Molecules
TF → Clotting Multiple factors Interleukin 6, TNFα,
Inflammation Cascade ? Infection sCD-40 ligand
Collagen →
platelet Plaque Rupture MDA Modified LDL
activation
Foam Cells ? Macrophages
Macrophages
Metalloproteinases Metalloproteinases
Platelet-thrombin micro-emboli
Plaque rupture
Thrombosis D-dimer,
Platelet Activation Complement,
Thrombin Fibrinogen,
Troponin, CRP,
CD40L

24. Pathogenesis of Acute
Coronary Syndromes:
The integral role of
Plaque platelets
Fissure
or
Platelet
Rupture
Adhesion
Platelet
Activation
Platelet
Aggregation
Thrombotic
Occlusion

25. Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Old
Terminology: UA NQMI STE-MI
New Non-ST-Segment Elevation Acute ST-Segment
Terminology: Coronary Syndrome (ACS) Elevation
Acute
Coronary
Syndrome
(ACS)

27. RISK FACTORS
 MODIFIABLE
 NON-MODIFIABLE

28. RISK FACTORS
• AGE.
• INCIDENCE INCREASES
WITH AGE.
• RARE IN CHILDHOOD
EXCEPT IN FAMILIAL
HYPERLIPIDEMIA.
• MALE GENDER.
• MEN > PREMENUPAUSAL
WOMEN.
• AFTER MENUPAUSE
INCIDENCE IS ALMOST
SAME.
• REASON ??? LOSS OF
PROTECTIVE EFFECT OF
OESTROGEN~~~~
• FAMILY Hx OF IHD.

29. MODIFIABLE RISK
FACTORS
•SMOKING
•HYPERLIPIDEMIA
•HTN
•DM
•LACK OF EXERCISE
•BLOOD COAGULATION FACTORS
•CRP
•HOMOCYSTEINAEMIA
•PERSONALITY
•OBESITY
•GOUT
•SOFT WATER
•DRUGS……OCP,COX-2 INHIBITORS
•HEAVY ALCOHOL CONSUMPTION

30. DIAGNOSIS OF ACS
INC CARDIAC
TYPICAL HISTORY ECG CHANGES
ENZYMES

31. Focused History
• Aid in diagnosis and • Reperfusion
rule out other causes questions
– Palliative/Provocative – Timing of
factors presentation
– Quality of discomfort – ECG c/w STEMI
– Radiation – Contraindication to
– Symptoms associated fibrinolysis
with discomfort – Degree of STEMI
– Cardiac risk factors risk
– Past medical history
-especially cardiac

32. SYMPTOMS
• ACUTE CENTRAL CHEST PAIN.
• NAUSEA.
• SWEATING.
• DYSPNOEA.
• PALPITATION.
• SYNCOPE.
• PULM;EDEMA.
• EPIGASTRIC PAIN.
• VOMITING.
• POST-OP HYPOTENSION.
• OLIGURIA.
• ACUTE CONFUSIONAL STATE.
• STROKE.
• DIABETIC HYPERGLYCEMIC STATES.
BE-AWARE OF SILENT

33. SIGNS
• DISTRESS.
• ANXIETY.
• PALLOR.
• SWEATINESS.
• TACHYCARDIA/BRADICARDIA
• HYPO/HYPERTENSION
• S4
• SIGNS OF HEART FAILURE
• PANSYSTOLIC MURMUR
• LOW GRADE PYREXIA
• PERICARDIAL FRICTION RUB
• EDEMA

34. Clinical Presentation
Substernal chest pain or pressure
(>20-30 min)
• Localization or radiation to arms,
back, throat, jaw
• Accompanying features
– Dyspnea
– Nausea/vomiting
– Diaphoresis
– Weakness
• Atypical: syncope ,

35. Targeted Physical
Examination
Recognize factors that
– Vitals increase risk
– Cardiovascul • Hypotension
ar system • Tachycardia
– Respiratory • Pulmonary rhales,
system JVD, pulmonary
– Abdomen edema
• New murmurs/heart
– Neurological
sounds
status
• Diminished
peripheral pulses
• Signs of stroke

36. DIFFERENTIAL
DIAGNOSIS
ANGINA
PERICARDITIS
MYOCARDITIS
AORTIC DISSECTION
PULMONARY
EMBOLISM
ESOPHAGEAL
REFLUX/SPASM

37. Differential Diagnosis
• CHEST PAIN
HEAVY,GRIPPING,TIGHTNESS
• CENTRAL
• RETROSTENAL
ANGINA • MAY RADIATE TO JAW/ARM
• MAY PROVOKE SWEATING AND
PERICARDITIS FEAR
MYOCARDITIS • ASSOCIATED SOB
AORTIC DISSECTION • PROVOKED BY PHYSICAL
PULMONARY EMBOLISM EXERTION,AFTER MEALS, IN
ESOPHAGEAL COLD AND WINDY WEATHER
REFLUX/SPASM • AGGRAVATED BY ANGER AND
EXCITEMENT
• FADES QUICKLY WITH REST OR
NITROGLYCERINE.

38. Differential
Diagnosis
• SHARP CENTRAL CHEST PAIN
• EXACERBATED BY
MOVEMENT,RESPIRATION,AND
LYING DOWN.
ANGINA
• RELIEVED BY SITTING FORWARD
PERICARDITIS • MAY BE REFERRED TO NECK OR
SHOULDER
MYOCARDITIS
• PERICARDIAL FRICTION RUB IN
AORTIC DISSECTION
THREE PHASES OF CARDIAC
PULMONARY EMBOLISM CYCLE
ESOPHAGEAL – Atrial systole
REFLUX/SPASM – Ventricular systole
– Ventricular diastole
• BIPHASIC ‘TO AND FRO’ RUB
• FEVER
• LEUCOCYTOSIS
• LYMPHOCYTOSIS
• FEATURES OF PERICARDIAL
EFFUSION

39. Differential
Diagnosis
• ASYMPTOMATIC
• FATIGUE
ANGINA
• PALPITATIONS
PERICARDITIS • CHEST PAIN
MYOCARDITIS • DYSPNOEA
AORTIC DISSECTION • CCF
PULMONARY EMBOLISM • SOFT HEART SOUNDS
ESOPHAGEAL
REFLUX/SPASM • S3
• TACHYCARDIA
• PERICARDIAL FRICTION
RUB

40. Differential
Diagnosis
• SEVERE CENTRAL
CHEST PAIN.
ANGINA • RADIATES TO BACK.
PERICARDITIS
MYOCARDITIS
• SIGNS OF SHOCK
AORTIC • NEUROLOGICAL
DISSECTION SYMPTOMS
PULMONARY EMBOLISM • RENAL FAILURE
ESOPHAGEAL
• LOWER LIMB ISCHEMIA
REFLUX/SPASM
• VISCERAL ISCHEMIA

41. PULMONARY EMBOLISM
Differential
Diagnosis SYMPTOMS •COUGH
•UNEXPLAINED DYSPNOEA
•PLEURITIC CHEST PAIN
•HAEMOPTYSIS
•DVT ~~~~~******
•FEVER
SIGN •TACHYPNEA
•TACHYCARDIA
ANGINA •SHOCKED
•PALE
PERICARDITIS •SWEATY
•LOCALISED PLEURAL RUB
MYOCARDITIS •CREPTS
•FEBRILE
AORTIC DISSECTION •HYPOTENSION
•PERIPHERAL SHUTDOWN
•RAISED JVP
PULMONARY •RV HEAVE
•GALLOP RHYTHM
•WIDELY SPLIT S2
EMBOLISM INVESTIGATIONS CXR------NORMAL,,,LINEAR ATELECTASIS,,BLUNTING
ESOPHAGEAL OF CP ANGLE,,RAISED HEMIDIAPHRAGM,,,WEDGE-
SHAPED PULM INFARCT,,
REFLUX/SPASM ECG-------NORMAL,,SINUS TACHY,,AF,,,,RV STRAIN,,,
CBC-------PMN LEUCOCYTOSIS
ESR-----RAISED
LDH-----RAISED
PL D-DIMERS
V/Q SCAN
US SCAN
ECHOCARDIOGRAPHY
SPIRAL CT SCAN
MRI

42. Differential
Diagnosis
ANGINA
PERICARDITIS
MYOCARDITIS
AORTIC DISSECTION
PULMONARY EMBOLISM
ESOPHAGEAL
REFLUX/ SPASM
20% OF THE PTS;
ADMITTED INTO CCU
HAVE GORD

43. ECG CHANGES

44. 12-Lead ECG Variations
in AMI and Angina
Baseline
Ischemia—tall or inverted T wave (infarct),
ST segment may be depressed (angina)
Injury—elevated ST segment, T wave may invert
Infarction (Acute)—abnormal Q wave,
ST segment may be elevated and T wave
may be inverted
Infarction (Age Unknown)—abnormal Q wave,
ST segment and T wave returned to normal

45. ECG FINDINGS IN ACS
• NORMAL • REPEAT ECG WHEN
PATIENT IS IN PAIN
• ST-DEPRESSION
• CONTINUOUS ST –
• T-WAVE SEGMENT
INVERSION MONITORING
• PERSISTANT ST-
ELEVATION OR
• LBBB PATTERN

46. ECG Assessment
ST Elevation or new LBBB
STEMI
ST Depression or dynamic
T wave inversions
NSTEMI
Non-specific ECG
Unstable Angina

47. TYPICAL ECG
CHANGES IN
STEMI

48. Normal or non-diagnostic EKG

49. ST-Segment Elevation MI

50. New LBBB
Prominent R wave V1-V3
QRS > 0.12 sec Prominent S wave 1, aVL, V5-V6
L Axis deviation
with t-wave inversion

51. Case 13. A 53 year old man with 3 hours of "crushing" chest pain.
Interpretation
Acute inferior myocardial infarction
ST elevation in the inferior leads II, III and aVF
reciprocal ST depression in the anterior leads

52. Case 16. 51 yr old male with no prior cardiac
history presents with mid-sternal chest
discomfort
Questions
1. Is there ECG evidence of injury or ischemia?
2. Is this patient having an MI? If so, in what anatomic distribution?
Interpretation
1. YES
2. YES, ANTEROSEPTAL

53. post thrombolysis ECG

54. BIOCHEMICAL
MARKERS

55. BIOCHEMICAL MARKERS
• TROP. I CARDIAC TROPONONS
I T C
• TROP T
• CK-MB
• MYOBLOBIN
• FBC
OTHER • S ELECTROLYTES
BLOOD • BGL
INVESTIG
ATIONS
• LIPID PROFILE
• TRANSTHORACIC ECHO CARDIOGRAPHY (TTE)

56. Cardiac Markers
• Troponin ( T, I) • CK-MB isoenzyme
– Very specific and – Rises 4-6 hours after
more sensitive than injury and peaks at 24
CK hours
– Rises 4-8 hours after – Remains elevated 36-48
injury hours
– May remain elevated – Positive if CK/MB > 5%
for up to two weeks of total CK and 2 times
– Can provide normal
prognostic – Elevation can be
information predictive of mortality
– Troponin T may be – False positives with
elevated with renal exercise, trauma,
dz, muscle dz,
poly/dermatomyositis MYOGLOBIN
RAPID DIAGNOSIS BUT
POOR SPECIFICITY

57. Troponins for Evaluation and
Management of ACS
Advantages Disadvantages
• Risk Stratificaton • Low sens. early (< 6h)
• Sens/Spec > CKMB • Repeat at 8-12 h if neg.
• Detect Recent MI • Limited ability to
detect late minor reinfarction
• Selection of Rx
• Detect Reperfusion
Recommendation
• Useful as single test to efficiently Dx NSTEMI
• Clinicians should familiarize themselves with Dx “cutoffs” in local lab

58. Cardiac Markers
Initial Peak Normal
Myoglobin 1-4hr 6-7hr 24hr Nonspecific
CK-MB 3-12hr 24hr 48-72hr Also elevated with Sk muscle
TroponinI 3-12hr 24hr 5-10d Highly sensitive/ specific

59. MANAGEMENT

60. Cardiac Care Goals
• Decrease amount of myocardial
necrosis
• Preserve LV function
• Prevent major adverse cardiac
events
• Treat life threatening complications

61. MANAGEMENT OF ACS
1 2 KEY
QUESTIONS 2
IS THERE IS THERE A
ST- RISE IN
SEGMENT TROPONINS?
ELEVATION? RIGHT ANSWER LEADS
TO SUCCESSFUL
MANAGEMENT

62. Acute Management
• Initial evaluation &
stabilization
• Efficient risk
stratification
• Focused cardiac
care

63. ACS RISK CRITERIA
Low Risk ACS
No intermediate or high
risk factors
<10 minutes rest pain • ASA
• CLOPIDOGRAL
• BETA-BLOCKER
Non-diagnostic ECG
• NITRATES
Non-elevated cardiac
markers
Age < 70 years

64. ACS RISK CRITERIA
• LOW RISK
ACS
• ELEVATED TROPS.
• DYNAMIC ST OR T WAVE
CHANGES.
• DM EARLY <72 HOURS>
CORONARY
• RENAL DYSFUNCTION ANGIOGRAPHY.
• REDUCED LVF + INTERVENTION
• EARLY POST-
INFARCTION ANGINA.
• PCI WITHIN 6 M
• PREVIOUS CABG

65. ACS RISK CRITERIA
HIGH RISK ACS
• PTS WITH PERSISTENT
OR RECURRENT
ANGINA.
• ST CHANGES > 2MM
• OR DEEP NEGATIVE T URGENT CORONARY
WAVE CHANGES. ANGIOGRAPHY
• CLINICAL SIGNS OF
HEAR FAILURE.
• HAEMODYNAMIC
INSTABILITY.
• LIFE THREATENING
ARRHYTHMIAS (VT,VF)

66. Chest pain suggestive of ischemia
Immediate assessment within 10 Minutes
Initial labs Emergent History &
and tests care Physical
– 12 lead ECG  IV access  Establish
– Obtain initial  Cardiac diagnosis
cardiac monitoring  Read ECG
enzymes  Oxygen  Identify
– electrolytes,  Aspirin complication
cbc lipids, s
 Nitrates
bun/cr, glucose,
 Assess for
coags
reperfusion
– CXR

68. REPERFUSION GOALS
EMS-TO-
<30 MIN
DRUGS
EMS-TO-
BALLOON <90 MIN
SYMPTOM ONSET –TO- <120
REPERFUSION MIN REPERFUSION
HOSP
EMS ARRIVAL
PRE-HOSP
ONSET OF ARRIVAL
ECG
SYMPYOMS
INCREASING LOSS OF MYOCYTES

69. STEMI
EARLY MEDICAL MANAGEMENT
• ARRANGE EMERGENCY AMBULANCE
• ASPIRIN 300MG.
• GTN S/L. 0.3-1 MG.----REPEAT
• OXYGEN 2-4 L/M
• ANALGESIA IV DIAMORPHINE 2.5-5MG+
METOCLOPRAMIDE 10 MG.(NOT IM ~~~RISK OF
BLEEDING WITH THROMBOLYSIS.
• BETA-BLOCKER (IF NO C/I ) FOR ONGOING
CHEST PAIN,HTN,TACHYCARDIA
• IF PRIMARY PCI AVAILABLE GIVE GP11b/111a
INHIBITOR.
• ALTERNATIVELY GIVE THROMBOLYSIS.
PRE-HOSPITAL TREATMENT INCLUDING THROMBOLYSIS CAN BE GIVEN BY
TRAINED HEALTHCARE PROFESSIONAL UNDER GUIDELINES

70. IN-HOSPITAL MANAGEMENT OF ACS
IN STEMI
• THROMBOLYSIS OR PRIMARY
ANGIOPLASTY.
• BETA-BLOCKER (ATENOLOL 5MG IV).
– CONTRAINDICATION IN ASTHMATICS
• ACE-INHIBITORS.
– CONSIDER (LISINOPRIL 2.5 MG) IN ALL
NORMOTENSIVE PATIENTS WITHIN 24 HRS OF
ACUTE MI ESPECIALLY IF THERE IS EVIDENCE
OF HEART FAILURE OR ECHO EVIDENCE OF LV
DYSFUNCTION.

71. MANAGEMENT OF AMI
THRMBOLYSIS
INDICATIONS(PRESENTATION WITHIN 12 H)
• ST Elevation>2mm IN 2
OR MORE CHEST
LEADS. OR
• ST elevation>1mm IN 2
OR MORE LIMB LEADS.
OR
• EFFECTIVE IN REDUCING • POSTERIOR
MORTALITY.
INFARCTION (DOMINANT R
• GREATEST BENEFIT IF WAVES & ST DEPRESSION IN V1-
GIVEN <12 H OF ONSET OF V3)
PAIN. • NEW ONSET OF LBBB
• BEST TIME <60MIN (BHF)

72. THRMBOLYSIS
CONTRAINDICATIONS
• HAEMORRHAGIC STROKE OR STROKE
OF UNKNOWN ORIGIN AT ANY TIME
• ISCHEMIC STROKE IN PRECEDING 6
MONTHS
• CNS DAMAGE OR NEOPLASM
• RECENT MAJOR
TRAUMA/SURGERY/HEAD INJURY/
WITHIN PRECEDING 3 WEEKS
• GI BLEEDING WITHIN LAST MONTH
• KNOWN BLEEDING DISORDER
• AORTIC DISSECTION

73. THRMBOLYSIS
RELATIVE CONTRAINDICATIONS
• H/O SEVERE HTN (SBP >180 mmHg.)
• PREGNANCY OR <1 WEEK POSTPARTUM
• ORAL ANTICOAGULANT THERAPY.
• NON-COMPRESSIBLE PUNCTURES.
• TRAUMATIC RESUSSITATION
• ADVANCED LIVER DISEASE
• TRANSIENT ISCHEMIC ATTACK IN
PRECEDING 6 MONTHS.

74. SIDE-EFFECTS OF
THROMBOLYTICS
• NAUSEA
• VOMITING
• BLEEDING
• REPERFUSION ARRHYTHMIA
• RECURRENT ISCHEMIA
• ANGINA
• CEREBRAL EDEMA
• PULM EDEMA
• HYPOTENSION
• FEVER
• CONVULSIONS
• ALLERGIC REACTIONS----RASH, FLUSHING,UVEITIS
• ANAPHYLAXIS
• GB SYNDROME

75. ACUTE MANAGENT OF N-
STEMI )
• ADMIT TO CCU
• MONITOR CLOSELY
• O2:
• ANALGESIA: MORPHINE 2.5-5mg +METOCLOPRAMIDE 10 mg. IV
• NITRATES:GTN SPRAY OR S/L TABS
• ASPIRIN: 300mgPO
• BETA-BLOCKER: METOPROLOL 50-100mg/8H OR ATENOLOL 50-100mg/24H
• IF B-BLOCKER IS CI THEN GIVE RATE LIMITING Ca;
Channel ANTAGONIST.
• VERAPAMIL 80-120 mg/8H PO DON’T USE VERAPAMIL
» OR AND
• DILTIAZEM 60-120 mg/8H PO B-BLOCKER TOGATHER
CAN CAUSE ASYSTOLE

76. ACUTE MANAGENT OF N-
STEMI )
Cont…..
• LMW HEPARIN
• ENOXAPARIN 1mg/kg SC/12h
• Or
• Dalteparin 120u/kg/12h sc
• Alternatively :unfractionated heparin 5000u iv
bolus then IVI infusion @0.25 UNITS/KG/H.
• Check APTT 6-hourly.
• Alter IVI rate to maintain APTT @ 1.5-2.5 times control.
• Nitrates IV if pain continues
• GTN 50mg in 50 ml 0.9%saline @2-10ml/h titrate to pain
and maintain SBP >100mmHg.
• Record ECG while in pain.

77. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT
ELEVATION
(NSTEMI) CONTD: •No further pain
•Flat or inverted T-
waves or normal ECG
LOW Risk Pts. •Negative Troponins
• May be discharged if a repeat troponin
(>12h) is negative.
• Treat medically.
• Arrange further investigations:
• Stress test
• angiography

78. POST-MI DRUG THERAPY
• ASA 75-100MG./D
• A BETA-BLOCKER TO MAINTAIN HR <60/MIN.
(METOPROLOL 50MG BID)
• ACE-INHIBITORS (RAMIPRIL 2.5MG BID TITRATED TO
MAX TOLERATED OR TARGET DOSE)
• IF INTOLERANT OF ACE-INH USE ARB (VALSARTAN
20MG BID)
• STATINS(SIMVASTATIN 20-80MG/D)
• CLOPIDOGREL 75MG/D FOR 9-12 MONTHS.(FOR
MODERATE – HIGH RISK Pts. WITH NST- ACS
• GTN SPRAY FOR SYMPTOMATIC RELIEF OF ANGINA
• ALDOSTERONE ANTAGONIST(EPLERENONE 25MG/D
FOR REDUCED EF AND HF PTS

79. SUBSEQUENT MANAGEMENT IN
ACS
CONTD;
• ADDRESS MODIFIABLE RISK FACTORS.
– DISCOURAGE SMOKING
– ENCOURAGE EXERCISE 20-30MIN/DAY
– DIAGNOSE AND TREAT DM,HTN &
HYPERLIPIDEMIA
– ENCOURAGE TO CONSUME >7 GRAMS OF
OMEGA 3 FATTY ACIDS/WEEK FROM OILY FISH
OR >1 GRAM/D OF OMEGA -3-ACID ETHYL
ESTERS.
– WEIGHT REDUCTION

80. SUBSEQUENT MANAGEMENT IN ACS
CONTD;
GENERAL ADVICE
• DISCHARGE FROM HOSPITAL AFTER 5-7 DAYS
IF UNCOMPLICATED.
• MAY RETURN TO WORK AFTER 2 MONTHS.
• FOLLOWING OCCUPATIONS SHOULD NOT BE
RESTARTED POST-MI.
– AIRLINE PILOTS
– AIR-TRAFFIC CONTROLLERS
– DIVERS

81. SUBSEQUENT MANAGEMENT IN ACS
GENERAL ADVICE CONTD;
• DRIVERS OF HEAVY GOODS VEHICLES AND PUBLIC
SERVICE MAY BE PERMITTED TO RETURN TO WORK IF
MEET CERTAIN CRITERIA.
• LIGHTER JOB PREFERRED AGAINST HEAVY MANUAL
LABOUR.
• DIET:
– HIGH IN OILY FISH LOW IN SATURATED FATS
– FRUITS
– VEGETABLES
– FIBRE
• EXERCISE:REGULAR DAILY EXERCISE.
• SEX: AVOID INTERCOURSE FOR 1 MONTH.
• TRAVEL: AVOID AIR TRAVEL FOR 2 MONTHS.
• F/U REVIEW AT 5 WKS POST-MI: IF ANGINA RECURS
CONSIDER FOR ANGIOGRAPHY.
• REVIEW AT 3 MONTHS : CHECK LIPIDS

82. MANAGEMENT ECG
OF O2
AMI IV ACCESS
TAKE LABS
BRIEF ASSESSMENT
ASPIRIN 300 MG
MORPHINE 2.5-5mg IV
+METOCLOPRAMIDE
10mG
GTN S/L 2 PUFFS OR 1
TAB.
THROMBOLYSIS
BETA-BLOCKER
CXR
CONSIDER GLUCOSE,INSULIN,& POTASSIUM
INFUSION FOR DM PTs.
CONSIDER DVT PROPHYLAXIS
CONT;MEDICATION EXCEPT Ca;CHANNEL ANTAGONIST (UNLESS SPECIFIC
INDICATIONS)

83. SUMMARY
• ACS includes UA, NSTEMI, and STEMI
• Management guideline focus
– Immediate assessment/intervention (MONA+BAH)
– Risk stratification (UA/NSTEMI vs. STEMI)
– RAPID reperfusion for STEMI (PCI vs.
Thrombolytics)
– Conservative vs Invasive therapy for UA/NSTEMI
• Aggressive attention to secondary prevention
initiatives for ACS patients
• Beta blocker, ASA, ACE-I, Statin

84. THANK YOU

87. ACUTE MANAGENT OF ACS WITHOUT
ST-SEGMENT ELEVATION (NSTEMI)
CONTD:
Indications for consideration of
invasive intervention:
• Poor prognosis, e.g pulmonary edema.
• Refractory symptoms.
• Positive ETT. At low workload.
• Non-Q wave MI.

89. Timing of Release of Various Biomarkers After Acute Myocardial
Infarction
Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.

90. THRMBOLYTIC AGENTS
• STREPTOKINASE
– INITIATED WITHIN 12H.
– 1.5 MILLION UNITS IN 100 ML N/S IVI OVER
1 HR
– S/E:
NAUSEA,VOMITING,HAEMORRHAGE,STR
OKE, DYSRHYTHMIA,WATCH FOR
ALLERGIC REACTIONS, ANAPHYLAXIS
– DON’T REPEAT UNLESS IT IS WITHIN 4D
OF THE 1st. ADMINISTRATION.

91. THRMBOLYTIC AGENTS
• ALTEPLASE (rt-PA, TISSUE-TYPE PLASMINOGEN
ACTIVATOR)
– ACCELERATED REGIMEN
• INITIATED WITHIN 6 H. OF SYMPTOMS ONSET.
• 15 MG IV INJECTION FOLLOWED BY IVI OF 50
MG OVER 30 MIN. THEN 35 MG OVER 60MIN.=
TOTAL DOSE= 100MG OVER 90 MIN.
• IN PTS <65KG WT==15MG BY IV
INJ.FOLLOWED BY IVI OF 0.75MG/KG OVER
30 MIN.==THEN 0.5MG/KG OVER 60 MIN.=MAX
TOTAL DOSE 100MG OVER 90 MIN.

92. THRMBOLYTIC AGENTS
• ALTEPLASE
– NON-ACCELERATED REGIMEN
• INITIATED WITHIN 6-12 H. OF SYMPTOMS
ONSET.
• 10 MG IV INJECTION FOLLOWED BY IVI
OF 50 MG OVER 60 MIN. THEN 4
INFUSIONS EACH OF 10 MG OVER
30MIN.= TOTAL DOSE= 100MG OVER 3
HRS.
• IN PTS <65KG WT=MAX TOTAL DOSE
1.5MG/KG.

93. Risk Stratification to Determine the Likelihood
Assessment of Acute Coronary Syndrome
Findings Findings indicating Findings indicating
indicating INTERMEDIAT LOW likelihood of
E likelihood of ACS in ACS in absence of high-
HIGH absence of high- or intermediate-
likelihood of likelihood findings likelihood findings
ACS
History Chest or left arm pain Chest or left arm pain Probable ischemic
or discomfort as chief or discomfort as chief symptoms
symptom symptom Recent cocaine use
Reproduction of Age > 50 years
previous documented
angina
Known history of
coronary artery
disease, including
myocardial infarction
P New transient mitral Extracardiac vascular Chest discomfort
regurgitation, disease reproduced by
hypotension, palpation
diaphoresis,
pulmonary edema or
rales

94. RISK STRATIFICATION
INITIAL RISK LONG-TERM RISK
• DEFINED BY CLINICAL RISK
• DETERMINED BY FACTORS
COMPLICATIONS • AGE
• PRIOR MI
OF ACUTE • CABG
THROMBOSIS. • DM
• HF
• MAY PRODUCE • CRP
RECURRENT MI • FIBRINOGEN
• BNP
• MARKED ST-DEP • MODIFIED ALBUMIN
• S.CREATININE
• DYNAMIC ST • LVD
CHANGE • LT.MAIN OR 3VD
• RAISED TROPS

95. SCORES USED FOR LONG
TERM RISK STRATIFICATION IN
ACS
GRACE
TIMI SCORE PREDICTION SCORE
• THROMBOLYSIS • GLOBAL
IN MYOCARDIAL REGISTRY OF
INFARCTION ACUTE
CORONARY
EVENTS
• BASED ON
AGE,HR,
SBP,S.CREATINI
NE,KILLIP

96. TIMI RISK SCORE IN ACS
NSTEMI/UA
RISK FACTOR SCORE
AGE >65 1
>3 ARTERY DIS RISK FACTORS 1
HTN
HLPD
FMLY HX
DM
SMOKING
CORONARY ART STENOSIS >50% 1
ASA USE IN LAST 7 DAYS 1
SEV ANGINA >2 EPISODES/D @REST 1
ST DEVIATION ON ECG(HORIZONTAL 1
ST DEPRESSION OR TRANSIENT ST
ELEVATION
ELEVATED CARDIAC MARKERS 1
CK-MB OR TROPONIN

97. TIMI RISK SCORE IN ACS
NSTEMI/UA
TOTAL RATE OF RATE OF DEATH /
DEATH /MI MI/ URGENT
SCORE REVASCULARIZATION
IN 14 DAYS %
%
0-1 3 4.75
2 3 8.3
3 5 13.2
4 7 19.9
5 12 26.2
6-7 19 40.9

98. TIMI RISK SCORE IN ACS
STEMI
RISK FACTOR SCORE
AGE >65 2
AGE >75 3
HO ANGINA 1
HO HTN 1
HO DM 1
SBP<100 3
HR>100 2
KILLIP II-IV 2
WEIGHT>67KG 1
ANT MI OR LBBB 1
DELAY TO TREATMENT >4 HRS 1

99. TOTAL SCORE RISK OF DEATH @30
DAYS
%
0 0.8
1 1.6
2 2.2
3 4.4
4 7.3
5 12.4
6 16.1
7 23.4
8 26.8

100. LOW INTERMEDIATE HIGH
RISK RISK RISK
Chest Pain CONSERVATIVE INVASIVE
CORONAR
Y
center THERAPY STENTING
THERAPY CABG
•ANTIPLATELET •GLYCOPROTEINS II
AGENTS B/IIIA INHIBITORS •MYOCARDIAL ENERGY
CONSUMPTION
•ASA •ABCIXIMAB
•ATENOLOL
•CLOPIDOGREL •EPTIFIBATIDE
•METOPROLOL •PLAQUE
•TICLOPIDINE •TIROFIBAN
STIBILIZING/REMO
DELLING OF VENT
•HMG-CoA
•ANTITHROMBINS •CORONARY
•ANALGESIA REDUCTASE
•HEPARIN VASODILATORS
•MORPHINE INHIBITORS
•LMWH •GTN •ACE-
INHIBITORS

101. ACUTE MANAGENT OF ACS WITHOUT ST-
SEGMENT ELEVATION (NSTEMI) ischemia
•Persistent
•Recurrent ischemia
contd:
High Risk Pts. •ST-Depression
•DM
•Increased Troponins
• Infusion of a GP11b/111a antagonist. PREVENT PLT
AGGRGN BY
– Abciximab (250microgram/kg IV OVER 1 Min. THEN 125 BLOCKING
nanogram/kg/min
IVI) BINDING OF
FIBRINOGEN TO
– Aptifibatide RECEPTOR ON
PLT.
– Tirofiban
• Urgent angiography.
• Add clopidogrel
300mg po stat
•Beta-blocker then 75mg/d
•Ca2+; ch antagonist With ASA
OPTIMIZE •ACE-I
DRUGS •Nitrates
•Intensive statin regimens

102. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT
ELEVATION
CONTD: (NSTEMI)
High Risk Pts.
IF SYMPTOMS FAIL TO IMPROVE
• URGENT ANGIOGRAPHY
• URGENT ANGIOPLASTY OR
• CABG

103. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT
ELEVATION
(NSTEMI) CONTD:
Further measures:
• Wean off GTN infusion when stabilized on oral drugs.
• Stop heparin when pain-free for 24h.(give atleast 3-5
days therapy).
• Check serial ECGs. For 2-3 days.
• Check serial cardiac enzymes for 2-3 days.
• Address modifiable risk factors
• Smoking
• HTN
• Hyperlipidemia
• DM
• Gentle mobilization.

104. ACUTE MANAGENT OF ACS WITHOUT ST-
SEGMENT ELEVATION (NSTEMI) CONTD:
Prognosis
• Overall risk of death ~1-2%
• 15% for refractory angina.
Followings are associated with increased
risk
•Haemodynamic instability:
• Hypotension,
•Pulmonary edema RISK
•T-wave inversion or ST segment
depression on restingECG. STRATIFICATION
•Previous MI
•Prolonged rest pain.
•Older age.
•DM