Professional Documents
Culture Documents
Content.
• Brief overview.
• Risk factors
• Enzymes
• Cases
• Trial
Acute Coronary Syndromes
Noncardiac
Unstable angina
Variant
Progressive
NQWMI angina
Rest New onset angina
Post MI Prior CABG/PTCA
Prior MI
What time of day is it?
Non-ST Segment Elevation - Acute
Coronary Syndromes
A Spectrum
CPK/ troponin
rise
Clinical Trials HowA big
do we
pilemake
of
sensespaghetti
of this mess ?
FRISC ESSENCE FRIC TIMI 11
EPIC HIT III
PARADIGM RAPPORT
TIMI 12
PROLOG PRISM
EPILOG
ERASER HERO
GUSTO II TIMI 14
PURSUIT PARAGON IMPACT AMI
HELVETICA
EPI-STENT CAPTURE TIMI 9
MINT
RESTORE SPEED TAMI 8 PRISM-PLUS
REDUCE AMI IMPACT II
ORBIT IMPACT SOAR
How do you keep up with the
stats/subset argument?
• Should the first question be
Endothelial Dysfunction
From
From 1st
1st Decade
Decade From
From 3rd
3rd Decade
Decade From
From 4th
4th Decade
Decade
Growth
Growth Mainly
Mainly by
by Lipid
Lipid Accumulation
Accumulation Smooth
Smooth Muscle
Muscle Throm
Thrombosis,
bosis,
&& Collagen
Collagen Hematoma
Hematoma
Adapted From Stary HC et al. Circulation
Circulation.. 1995;92:1355-1374
A paradigm issue
• Is it innocent till proven guilty
• OR
• Guilty till proven innocent.
Acute chest pain ::::inputs
C h e s t p a i n
1 0 % S T c h a n2 g0 e% s A M 3I 0 % U n s t a b l 4e 0 a % n g Ni no a A
p r o b n o n c
Acute chest pain ::::outcomes
Traumatic
Nontraumatic.
Not Traumatic Chest Pain
• Most Challenging
• Somatic fibres
Numerous
Enter @ single level(spinal cord)
Results in sharp localized pain.
• Visceral Afferents
Internal organs
Less numerous
Enter (SC) @ multiple levels
Visceral Pain
Dull
Aching
Poorly localized
Differential Dx of Non traumatic CP.
• Cardiac Cause
Stable angina
Unstable angina
Variant angina
AMI
Pericarditis
Valvular Diseases AS
MVP
• Vascular Causes
Aortic Dissection
PE
PH’Tension
• Pulmonary Causes
Pleural irritations
Infections
Inflammation
Infiltrations.
• Pulmonary Causes(cont…)
Barotrauma
Pneumothorax/Mediastinum.
Tracheobronchitis.
Musculoskeletal.
Costochordritis
Muscle strain
Cervial Thoracic spine problem
• Gastrointestinal Causes
Reflux
Mallory Weiss tear
Biliary Colic
Pancreatitis
Dyspepsia
Miscellaneous Causes
Herpes Zoster
Chest Wall Tumors.
What is the safest initial approach to pts
presenting with CP?.
• Approach with assumption of a life-
threatening aetiology.
• Before any Diagnostic studies
Suplemental O2
IV access
ECG
How do I begin to assess the Pt with CP?
• An accurate + targeted Hx (Most important
component)
@ triage
RMO
patter n of radiation
Duration of pain
Associated symptoms.
Precipitating factors
Exertion
Movement
Inspiration
Relieving Factors.
Rest
GTN
Antacids
Body position
Major Risk Factors with IHD?.
• Family Hx,
• Cigarette smoking,
• HBP,
• Hypercholesterolemia ,
• Diabetes Mellitus.
• Age >40.
Major Risk Factors(cont……)
• Male Sex,
Anxiety
Diaphoresis
Elevated Temperature
Inflammatory(Pericarditis)
Infectious process(Pneumonia).
Are there any physical examination finding which
may help differentiate among the causes of acute
CP?.
Myoglobin
• Elevation within 1hr post AMI
• Peaks within 4-12hrs
• Elevated in ~ 60% pts with AMI @ 1hr post
presentation.
• Does not detect UAP+
• Elevated in ~ 100% within 3hrs of AMI.
ECG findings of
New St-segment deviation of 0.5mm or> in
limb and or precordial leads.
New pathological Q waves.
Sustained VT.
Markers
• Significant elevation.
If all of the above are Negative
• Low risk
• Treat the suspected aetiology
• Consider Stress Testing to provoke
ischemia (prior to discharge or as an OPD)
• Follow up as needed.
If Positive for high risk
• Enoxaparin (preferred) or unfractionated
heparin.
• Why Enoxaparin??
Why Use Low Molecular Wt Heparin (LMWH)?.
• Unlike UFH, enoxaparin has
1.More predictable kinetics,
2.Is less protein-bound,
3.Has less potential for platelet activation,
4.Requires no monitoring;
• 30mins.
• If NO.
• Consider cardiac catheterization.
Fibrinolytic Therapy: The Current
Landscape
• Rapid lysis
• Enhances tissue-level perfusion
• Reduces intracranial and systemic hemorrhage
• Has a long half-life enabling single-bolus
administration
• Has no antigenicity
• Has a low reocclusion rate.
• Enhanced fibrin specificity also is desirable
because it permits preferential activation of
fibrin-bound plasminogen at the clot surface
• This has the potential to increase
patency and produce higher initial
patency rates, and may be
associated with fewer bleeding
complications.
• Greater fibrin specificity also decreases
activation of circulating plasminogen
and degradation of fibrinogen, resulting
in less bleeding and reducing the need
for transfusion.
Candidacy for Fibrinolysis—patient
Screening, Identification, and
Stratification
following UA by 31-50%.
Some more antiplatelet agent
apart from aspirin
• GPIIb/IIIa inhibitors
Abciximab(Reopro)
Tirofiban (aggrastat).
• ADP inhibitors
Ticlopidine
Clopidogril(Plavix)
platelet aggregation.
Fibrinogen
Fibronectin
Vitronectin
vWF
• Beta Blockers.
– ISIS 1 (Lancet 1986)
• 16,027 patients
• 15% reduction in mortality
– Most trials pre thrombolysis
– TIMI 2b(TPA and iv BB)
• Decrease angina and reinfarction
• No change in mortality
THE FORGOTTEN THERAPIES.
• GUSTO 1.
– Early iv use, limited value. Use oral when
stable.
• Beta Blockers.
– Long term therapy reduces mortality and reinfarction
by 25%.
– Early use of oral beta blockers in the first 24 hours is
recommended.
– Early iv use in selected patients.
THE FORGOTTEN THERAPIES.
• ACE Inhibitors.
– ISIS 4 (Lancet 1995)
– 58,050 patients
– 7% reduction in mortality at 5/52
– 1/3 in first day and 1/2 in the first week
– Early therapy is indicated, within 24 hours
– Greatest benefit in LV dysfunction
THE FORGOTTEN THERAPIES.
• Ca Channel Blockers.
– None of the trials has shown a reduction in
acute or long term mortality benefit in AMI.
• Nitrates
– ISIS 4.
– No significant reduction in 5/52 mortality.
– Routine long term use not supported.
THE FORGOTTEN THERAPIES.
• Magnesium.
– Early studies including LIMIT ?benefit.
– ISIS 4 No benefit
– ? Time of administration
– ? Prior to reperfusion
– Further trials unlikely
ST elevation “ on arrival”::PTCA
• If it is available AND fast (1hr) then it is the
absolutely best Rx!Mortality moves from
1% @< 60 min
• to 6% @>90 min.
• I.e.approx lysis results.
• Average US data is 110 mins
ST elevation “ on arrival”::PTCA
• Some data from HERO shows if patient
present very early 1-3 hrs then lysis is equal
or better than PTCA.
• PTCA is better in delayed presenters.
ST elevation “ on arrival”::PTCA
admission of ACS is 9%
ST elevation “ on arrival
• FUTURE PREDICTION
• 1 Everyone gets lysed!
• 2 THEN everyone gets
“cathed”
• 3 then stent or CABAG.
Current practice.
• If you do not think they can be inside the
lab within the hour Perth figures 63 mins