CASE PRESENTATION
DR. NANCY KUNYIHA
77 year old Asian male
C/o Chest pain for 3 days that had worsened in
the last 4 hours.
Radiating to the left arm
Sweating
Palpitations
PMHX
Not significant for any illnesses. Had never
had a hospital admission
Risk factors were Age & Sex, being Non
smoker, non diabetic with no family H/o
hypertension, hypercholestrolaemia, cardiac
disease or sudden death
Widower. Works in Insurance business in the
UK.
EXAMINATION
Sick looking BP 100/60mmHG Pulse 60/min regular
Diaphhemorrhagicpallor, jaundice or edema. No LN.
No thrush
CVS: S1 & S2 heard with added S4. No murmurs
heard.
ABD: Soft. No organomegaly
CNS: Oriented and alert with no neurological deficit
RESP: Chest clear bilaterally
INVESTIGATIONS
Hgram: Normal
UEC : Normal
Troponin I : 0.4 ng/ml, 1020,
CK 1104, CKMb 67
LFT :Normal
CXR: Normal
Lipids Not available
TSH Not available
DRUG THERAPY
DAY 1
ASA 300mg stat then 75mg OD
Streptokinase 1.5 MU stat over 60 minutes
Clopilet 75 mg
Clexane 60mg sc BD
GTN spray
Aztor 40 mg
Lasix 20mg IV OD
Aldactone 25mg OD
DAY 2
Carvedilol 1.565 mg commenced
GTN was to be stopped as long as patient pain
controlled if BP fell
2D ECHO 23/9/10 Akinetic septum
anterolateral walls. Base to apex. No
intramural thrombus. EF 40 – 45% Trace MR.
Mild LA. Mild AV Sclerosis
DAY 3
Patient developed pain again and enzyme
levels noted to rise. ST segment changes
persisted
Trop 1550 from 1020, CKMB 362 from 67
Transferred on Day4 to Nairobi Hospital for
Coronary angiography and stenting.
DAY 7
Patient re -admitted from Nairobi Hospital to
the ICU with difficulties in breathing
O/E Tachypnoeic RR 36/Min No pedal edema
Bi basal coarse crepitations.
No organomegaly
S3 gallop heard with tachycardia of 90/ min
CXR Mild pulmonary congestion
MANAGEMENT
Lasix 40mg iv stat
Combivent Nebs PRN
Other meds continued. Post stenting had
additional Avelon 400mg OD.
DDx Pulmonary edema rule out chest infection
DRUG THERAPY…….
Addition of ACE Inhibitor of Tritace 1.25mg
on day 8 was reported to have caused a drop in
blood pressure and was withdrawn till day 12
of therapy.
Captopril 3.125mg BD for last 3 days
Aldactone increased to 25mg BD
Patient has shown improvement and
transferred to the ward. BP now 110/70 mmHg
Managing off oxygen
DISCUSSION
Anatomy important .
RCA Posterior Descending and Marginal
Branches. Supplies nodes and part of the
interventricular septum
LCA LAD and Lt Circumflex Artery
Supplies Ant part of Lt and Rt ventricle Ant
septum, Ant LV wall
Sinus node 60% RCA 40% Left Circumflex
AVN RCA 90% LCA 10%
DIAGNOSIS OF AMI
Chest pain Nb: DM and Elderly
ECG changes including new LBBB
Enzyme elevation 1mm limb leads and 2 mm
in 2 consecutive chest leads
?Angina lasting 30minutes to 12 hours
unrelieved by GTN
ECG IN DIAGNOSIS
The early and accurate identification of the
infarct related artery on the ECG can help
predict the amount of myocardium at risk and
guide decisions regarding the urgency of
re vascularization therapy
Also important in identifying new conduction
abnormalities that may infleunce short and
long term outcome.
ECG IN DIAGNOSIS…
ST elevation V1 V2 V3 = Occlusion of LAD
ST elevation V1 V2 V3 AVL and ST dep > 1mm in
AVF = Prox Occlusion of LAD
ST elevation with V2 V3 AVF depression = LAD
occlusion distal to origin of diagonal branch that also
supplies the inferoapical section of the Lt ventricle
New RBBB with Q wave preceeding the R wave in
V1 is a specific but not sensitive marker of LAD
occlusion (1)
RECOMMENDED DRUG MODALITIES
FOR MANAGEMENT OF AMI
Aspirin and Antiplatelet agents
Thrombolytic agents
Heparin/ Clexane
Analgesia
Nitrates
Beta blockers
Ace Inhibitors
Spironolactone
Statins
ANTIPLATELET AGENTS
ASA
CLOPIDOGREL
GLYCOPROTEIN INHIBITORS
ASPIRIN
Prevents formation of thromboxane A2
50% reduction in mortality and re infarction
ISIS 2 trial 17000 pts with 4 arms ASA,
streptokinase , ASA & STREP, Placebo
Benefits persisted in all sub groups even at 4 years
post event
No actual difference has been noted in regards to
timing of the ASA as long as given within the first 24
hours but prudence has it that we should give as soon
as possible even on onset of suspicious chest pain at
home.
CLOPIDOGREL
Action at the ADP receptor.
Prolonged ant platelet action therefore should
only be used where there is low possibility of
surgical intervention
AHA 2002 guidelines suggest its use in ACS
NSTMI and unstable angina
Allergy to ASA or NSAIDS
With ASA in patients with stents
GLYCOPROTEIN 11B 111B
INHIBITORS
Block the binding of fibrinogen to platelet receptors
Poor response to aggressive medical therapy with on
going ischaemia
STEMI patients going for emergent diagnostic
angiography or acute PCI
NSTEMI going for elective Angiography
Studies to date have not shown any superiority to use
of these agents over LMW with thrombolytic agents
NITRATES
Mainly Vasodilatory effect thereby reducing
peripheral vascular resistance and LV pressure at
systole
Cause venous pooling that diminishes venous return
to the heart and reducing LV end diastolic pressure
Only Pre thrombolytic era trials have suggested
benefit but only in Ant wall MI.(2)Suggested a 49%
reduction in [Link] as flawed as did not
have adequate nos.
ISIS 4 Study Mg, Captopril, Isosorbide
mononitrate. Primary end point was mortality
at 5 weeks. 6.98% cf 7.22% among the
placebo group
Hence the role of nitrates not clearly beneficial
in regards to mortality but useful for pain
management.
Contraindicated with BP below 90/50 MMHg
Useful in HTN or CHF
BETA BLOCKERS
Reduce Sympathetic activity
Reduce heart rate therefore oxygen demand
Prevention of arrhythmias
Reduction of infarct size indirectly by he above
mechanisms
14 to 15% risk reductions for vascular mortality
TIMI 11B Trial. Compared the early use of
metoprolol i.e within 12 hours cf with their use at 6
days Primary end point was resting global EF which
was not found to be significantly different in the two
groups
BETA BLOCKERS…
Sub group analysis of secondary end points
showed significant findings . Incidence of
death and re infarction at 6 weeks among the
early introduction was 5.4% cf 13.7% in those
with delayed beta blockade
There was a lower incidence of recurrent chest
pain and of re-infarction in the former group
ACE INHIBITORS
A large no. of trials have looked a t this therapy
SAVE ( Survival and ventricular enlargement)
AIRE ( Acute infarction Reperfusion Efficacy)
TRACE : Trandolapril cardiac Evaluation
All showed benefit of commencing ACE within 3
days of large anterior infarction where there is LV
dysfunction.
CONSENSUS : Cooperative new scandanavian
enalapril survival study. Used iv early ACE then oral
Stopped due to side effects and hypotension
especially the elderly
ISIS 4 Oral Captopril, Mg ,Monotrate No
significant reduction in mortality
CSS Chinese Cardiac Study . Oral captopril
and placebo. 9.05% vs 9.59% risk reduction
Reduce adverse ventricular remodelling
STATINS
Have been shown to reduce cardiovascular
mortality by reduction of artheroma formation
Also long term benefit by modification of the
endothelium
Aim Total Cholestrol of 4.8 to 5.5 mmol .LDL
of 2.6 mmol
Studies PROVE IT TRIAL
REVERSAL TRIAL
MIRACLE TRIAL
SPIRONOLACTONE
Hormone that is involved in regulation of
water, sodium and potassium
Aldosterone is produced in larger amounts
after an MI with activation of the RAS
Definate recommendation in patients in
NYHA 3,4 failure according to the AHA. In
patients with 1 & 2 it is not certain if it reduces
mortality
Can be initiated at any point but usually before beta
blockers have been instituted.
30% risk reduction for death and 35% reduction of
admissions for heart [Link] for potassium.
Few cases of significant hyperkalaemia are reported.
( 4)
RALES : Random Aldactone Evaluation Study Study
there was a 30% reduction in mortality and 2%
incidence of hyperkalaemia in aldosterone group as cf
1% in placebo
LMWT AND UF HEPARIN
STEMI and NSTEMI except when
streptokinase is used
Heparin should be used with tPA rTPA and
TNK
Clexane is recommended where warfarin will
be used usually in anterior MI
Heparin has been shown to be more superior
in NSTEMI than Clexane
DIGOXIN
No proven benefit in pump failure
Used where there is Atrial fibrillation
THROMBOLYTIC AGENTS
Streptokinase Cardiogenic shock and age over 75 years,Cost
Benefit
well Alteplase 15,50 35,
Reteplase 10 units, 10
Tenecteplase
N.B Low weight ha been noted to be asstd with increased risk of
bleed therefore calculate
Alteplase 15mg,50mg ,35mg
Reteplase 10 units, 10units
Tenecteplase
N.B Low weight has been noted to be
associated with increased risk of bleed
therefore calculate doses carefully
CI TO THROMBOLYSIS
AHA GUIDELINES
ABSOLUTE
[Link] internal bleeding
[Link] haemorragic stroke
[Link] neoplasm
[Link] Aortic dissection
RELATIVE
Severe uncontrolled hypertension 180/100mmHg
H/O CVA
Anticoagulant use with INR 2 -3 or Bleeding diasthesis
Recent internal bleeding or significant trauma
Streptokinase within 5 days to 2 years or previous allergy
Pregnancy
Active PUD
Chronic HTN
COMPLICATIONS
Arrhythmias. Tachys, Bradys
Heart failure
Cardiogenic shock
MR
Septal perforation
Vetricular aneurysm
PTE
RV Infarction
Post Infarction Angina
Pericarditis
Dresslers
PCI
Haemodynamically unstable patients
Patients who have been thrombolysed recently
and return with unstable angina
Aim for door to balloon time of 90 minutes
Currently advised to deal with the occluded
vessel first and sort out surgical
revascularization of the others after patient has
been stabilized
PTCA
Balloon dilatation of the stenotic vessel
NICE recommends 70% of dilatations should
be accompanied by stenting as it reduces re
stenosis rates.
Heparinized stents with Ticlopidine reduce
thrombosis
Complications of PCI
Local dissection of blood vessels
Distal embolization
30% re-occlusion in 6 months
Acute occlusion in 2%
Death < 0.5%
PCI or CABG
Left main, 2 vessel or 3 vessel dz with LAD
involvement and evidence of ischaemia,failed
angioplasty
FRISC 11 and TACTIS TIMI 18 trial suggests
benefit of early PCI and CABG within 48
hours, if required, to reduce the incidence of
major cardiac events
REPERFUSION
Patients have majority of functional improvement
occurring within the first two weeks post infarction
therapy.
Peak creatinine kinase level seemed to be the
strongest independent predictor of subsequent
recovery of ventricular function after anterior Q wave
infarction(3)
Early functional assessment on day 1 had limited
ability to predict recovery of ventricular function
Presence of epicardial flow does not always co
relate with microvascular perfusion “No
reflow phenomenon”
Absence of tissue perfusion is the most potent
predictor of impaired ventricular function and
risk of death.
ST resolution is an excellent marker of tissue
reperfusion. Over 70% reduction in elevation
is very favourable
RISK STRATIFICATION
2DECHO LV EF
Pre- Discharge EST with Modified Bruce
protocol. If Negative then home and out
patient full stress test in 6 weeks
If positive then Coronary Angiography
Non modifiable factors eg Sex and Age,
Family history
Modifiable eg Lifestyle, Smoking, Cholestrol
etc
INCREASED RISK
Over 70 years
Ant MI
Hypotension with tachycardia
Previous MI
DM
Continued smoking
A fibrillation
CONCLUSION
AMI is a very wide subject of discussion
ACE, ASA, BETA
BLOCKERS,STATINS,SPIRONOLACTONE IN
NYHA 3 AND 4 have been definitely shown to
reduce cardiac mortality and are recommended for
use in all patients who have had an AMI
ACE has been found to be beneficial especially in
Anterior MI and and where there is LV dysfunction
Holistic but individualized approach must be
considered in each patient.
1. Engelen et al 1999 NEJM Value of ECG in
localizing LAD involvement in Ant wall
infarction Lancet1995
2. Jugdutt and Warnica lancet 1995:345
(8951):669-85
3. HEART Study Healing and Early Afterload
Reducing Therapy Study Annals of Int Med
Mar2001:vol134:6
[Link] 1999 2;341(10)709-17
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