Transcript Acute chest pain

Acute Coronary
(Confusional) Syndrome
Dr.A.M.Thirugnanam
MD.,MSICP.,Ph.D.,FSCAI.(USA)
Interventional Cardiologist
IPCARD Heart Institute
Global Hospitals- Hyderabad.
Date: 09-02-2008
ACS- the confusion kills
the Patients
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1. One in six patients with ACS treated as atypical
chest pain.
2. one in three acute MI goes into complications.
3. 25% of the acute MI did not get proper
reperfusion.
4. At least one half die within 1 hr of symptoms
onset or before reaching the hospital.
5. 24% men and 42% women die within one year.
6. 66% fail to achieve full recovery.
7. 21% men and 30 women develops CHF within 6
years.
ACS the confusion kills the
patients-Global registry of
acute coronary events
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Median time from symptoms onset to
presentation was 2-3 hrs for age <45,
and 3 hrs for >85 years age.
Atypical presentation, a worse
prognosis with 3 fold higher risk of
mortality due to delay in diagnosis and
treatment.
Atypical presentation of
ACS-Worcestor Heart Attack
Study report
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63% experience chest pain.
Above 75 years women only 50%
22% experience only dyspnea
32% experience dizziness, arm numbness,
head ache, syncope, sweating, palpitation,
weakness and confusion, due to diminished
autonomic response, age related diastolic
dysfunction, lung diseases, and associated
pulmonary diseases.
Acute chest pain-Vascular
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Aortic dissection-Excruciating, ripping
pain on sudden onset in anterior
chest.
Causes: HTN, connective tissue
disorders
ECG- no significant
Cardiac Enzyme: no elevation except
CRP.
Acute chest pain-Vascular
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Pulmonary Embolism: Sudden onset of
dyspnea and pain, pleuritic with
pulmonary infarction.
Causes: DVT,CTD,CAD,etc
ECG: RBBB, ST,ST-T changes, Q in III
and S1
Enzyme: no elevation
Acute chest pain-Vascular
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Pulmonary HTN: Substernal chest
pressure and exacerbated by excertion
Pain associated with dyspnea and
evidence of PHT
ECG-no significant ST elevation or
depression
Enzyme: d-dimer in case of PTE
Acute chest painPulmonary cause
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Pleuritis/Pneumonia: brief over
involved area, lateral to mid line pain
with dyspnea.
Tracheobronchitis / Spontaneous
Pneumothorax: burning in midline
associated with cough and pain
ECG: no significant
Enzyme: no
Acute chest painGastrointestinal cause
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Esophageal reflux: burning epigastric,1060min, aggravated by large meal, relieved
by antacid.
Peptic ulcer: Prolonged epigastric or
Substernal burning, relieved by antacid of
food.
Gallbladder disease: prolonged epigastric,
right upper quadrant pain, unprovoked
Pancreatitis: Prolonged, intense epigastric
and Substernal pain, RF include alcohol,
medications and hypertryglyceridemia.
Acute chest painMusculoskeletal Cause
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Costochondritis: Sudden onset of
intense fleeting type pain, by affected
joints, occasional swelling and
inflammation.
Cervical disc Diseases: Sudden onset
of Fleeing pain, may be reproduced
with movement of neck.
Acute chest pain- other
causes
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Infections: herpes zoster, prolonged
burning pain in dermatomal
distribution. Vesicular rash.
Psychological: Panic pain, chest
tightness or aching often accompanied
by dyspnea and lasting 30 min, may
have with emotional disorders.
What is mean ACS?
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Chest pain: Precipitation by stress, emotion, cold,
2-20 min, MI->30 min.
ECG Classification: ST-T changes, Q waves, LBBB,
and RBBB with ST elevation
ECG: 75% STEMI develops into QWMI. 25%
persists STEMI with absence of R wave.
Pathology- cell death
Imaging studies: loss of perfusion and RWMA
Biomarkers: C-Troponin-necrosis, CRP-inflammation,
BNP- LV overload.
Atypical Presentation of
ACS
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Patient older than 75 years,
ECG in evolution, non specific ST-T
changes.
Diabetic patients.
Previous MI
Stuttering chest pain
IL1,TNF,IL6,I
L18,MCP1
MMPS,IL18
ICAM,VCAM,
,MPO.MRP,
S selectin
CD40L,tPA,PAI1,Ddimer,VWF,
MPO,MRP
Evolution of ECG in Acute
Diagnostic markers ACS
Non–ST-segment
elevation ACSe
Stable
angina
ST-segment
elevation AMI
Unstable
angina
Non–Q-wave
AMI
Q-wave
AMI
CK-MB
Troponin T or I
C-Reactive Protein
Antman EM. In: Braunwald E, ed. Heart Disease: A Textbook in Cardiovascular Medicine, 5th ed. Philadelphia, Pa: WB
Saunders; 1997.
ECG-Enzyme changes in
ACS
Stable
angina
Creatine kinase
evidence of necrosis
ECG early
ECG late
Unstable Non–Q-wave Q-wave
angina
AMI
AMI
None
Positive
Positive
ST-segment
ST-segment ST-segment
depression
depression
elevation
and/or
and/or
T-wave inversionT-wave inversion
No Q
No Q
Q develops
Antman EM. In: Braunwald E, ed. Heart Disease: A Textbook in Cardiovascular Medicine, 5th ed. Philadelphia, Pa: WB
Saunders; 1997.
Biomarkers and mortality
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CRP and cardiac Troponin -T and I
have direct proportion to mortality.
CD40L had 5 times higher mortality in
ACS.
Management of ACSSTEMI
Dose
STK 1.5m
Altep100mg
Retep20mg
TNK-tPA50mg
TIMI-3
32%
54%
60%
63%
90min patency
50%
75%
75%
75%
1 month mortality in
STEMI
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14.7% in who did not receive
reperfusion
9% In hospital
7-9% in Primary PCI
2-3% in Pre hospital fibrinolysis
ECG changes and 1 year
mortality in ACS
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No ST elevation 5%
T wave inversion 13%
ST elevation
17%
ST depression
19%
ST dep and ST ele 26%
Improvement in 30 days
mortality
Pre ICCU era
30%
ICCU era
15%
PTCA
5%
Identifying Patients for
Reperfusion
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ECG indications: ST elevation, LBBB,
RBBB with ST elevation
Biomarker Indication: elevated CK-MB,
cTnT and I, CD40L,
The best way to treat ACS
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Thrombolysis with in 30 min.
If possible shift the patient
immediately to PCI within 90 min.
Measure all biomarkers to assess the
prognosis and outcome, include BNP,
CRP, Troponin I or T, CD40L, MPO
Ensure the administration of all
important drugs.
Medical management
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Anti Platelets: Aspirin, Clopidogrel
Anticoagulants: UFH, LMWH, DTI
Fibrinolytics: STK, UK, ALTE,RETE,
TNK.
Statins, ACEIS, BBS, Flavinoids,
Adenosine, and antioxidants.
Glycoprotein Receptor Blockers:
Abciximab, Eptifibatide, Tirofiben.
Invasive management
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Primary PTCA and Stenting.
Administration of GP2b3aRBs, which
reduces CRP-32%, IL6-76%, TNF
alpha-100%.
Intra coronary infusion of adenosine
for no flow or sluggish flow after
PTCA.
Primary PTCA in AMI
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55 yrs male H/O smoker, No DM, no
HTN, No lipid abnormalities.
ECG- ST elevation in V2-V6
Elevated CK-MB, Troponin Positive,
CRP positive
Echo- severe LV dysfunction
CAG- mid LAD total occlusion.
Normal coronary arteries
Left coronary
artery
Right coronary
artery
Acute AWMI- LAD mid
100% occlusion
Echocardiogram of AWMI-LAD region
After Primary Stenting to
LAD mid
Time dependence in
occlusion
Cross-sections of left ventricle after experimental
coronary artery occlusion
xx
x xx
xx
x x
x
x xxx x
x x xx
x
Duration of
occlusion
Necrosis
40
min
XXX
X
Ischemic but viable
Reimer KA, et al. Circulation. 1977;56:786-794.
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x
x
x x xx
x
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x
3h
Nonischemic
24 h
Area supplied by
occluded artery
ACS-RCA ostial tight
lesion
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58 male. Smoker, alcoholic, no DM, no
HT, no CVA, no BA, No APD, no H/O
previous surgical history.
complaints: DOE Class-2, EA-class 2
ECG: ST depression in inferolateral
leads, more than 3mm.
Echo-Severe LV dysfunction. EF-30%.
CAG: ostial RCA 99% tight lesion.
RCA ostial tight lesion
99%
Dilating the lesion with
Balloon 3mm/12mm
After stent deployment
Asymptomatic Male
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50 years male. Known DM, HTN, no smoker,
no alcoholic, no CVA, no BA, no APD. No
chest pain, only SOB
Underwent routine cardiac check up. TMT
positive.
ECG: NSR, No ST-T changes
Echo: normal LV fxn, no RWMA.
CAG: LAD severe disease, RCA-distal 90%,
LCX-mid 60% lesion.
LAD in DM asymptomatic
LAD
65 years old female.
Cardiogenic shock
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Known HTN, DM, DNP, smoker.
Admitted with cardiogenic shock. BP50/60mmhg, HR-120/min, O2-92% ra,
ECG- Wide QRS in all leads, ST
elevation in all leads
Echo- global hypokinesia, EF-25%
CAG- LM-100%, RCA-normal non
dominant.
Left main -100%
occlusion
Emergency management
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Dopamin, Dobutamin, noradrenalin,
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IV integrillin, Enclex, Clopivas-AP.
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IABP support
Post PTCA and Stenting of
LM
Home taking Points
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Multi biomarkers approach will reduce the
mortality.
New Biomarkers: PDGF, PF-4, CD152,
CD40L, PMN chemokines, Thrombospondin,
TGF-B and Nitric oxide.
Door to needle time less than 30 min, Door
to Balloon time less than 90 min.
Ensure all the essential drugs before
discharge.