Date post: | 07-May-2015 |
Category: |
Health & Medicine |
Upload: | uday-prashant |
View: | 722 times |
Download: | 1 times |
ACS – INITIAL DIAGNOSIS &
MANAGEMENT
Dr Uday Prashant M.D D.M
Very Alarming Scene
• India is the Diabetic capital of the world:- Highest no of diabetics in world at present
• Indians have one of highest rates of CAD
• Obesity in India is in rapid rise
Coronary Artery Disease in Indians = CADI
• How is it different from western world
• CADI strikes early !
• CADI strikes almost any one !!!
• CADI strikes unexpectedly !!!!
• Conventional RF can’t explain it away
• CADI is malignant in its onslaught.
The CADI Volcano• We are in the middle of the wave of CAD We are in the middle of the wave of CAD
epidemicepidemic
• This CADI epidemic will peak by 2015This CADI epidemic will peak by 2015
• 50% deaths in India are CVD deaths. 50% deaths in India are CVD deaths.
• CADI will overtake Infectious diseases in CADI will overtake Infectious diseases in morbidity toomorbidity too
• By 2015 CADI will be By 2015 CADI will be six timessix times more than the more than the WestWest
• CADI will be CADI will be 20 times20 times more than the Chinese, more than the Chinese,
ACS
• Spectrum of presentation– Myocardial infarction ( 25% – 30%)– Non Q wave MI ( 30% - 35% )– unstable angina (30% - 35%)– Sudden Cardiac Death (5% - 10%)
Non Q wave MI / USA compromises 2/3 rd of ACS cases
15% - 20% of USA are high risk cases.
Sudden Cardiac Death
Immediately next ECG
New Terminology in ACS
ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention.Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
AntithromboticTherapy
Stable Angina
UnstableAngina
Non–Q-wave MI
ThrombolysisPrimary PCI
Q-wave MI
Minutes-hours
Days-weeks
STEMIUA/NSTEMIAtherothrombosisNew term
Old term
PlaqueRupture
Acute Coronary Syndrome
Ischemic DiscomfortUnstable Symptoms
No ST-segmentelevation
ST-segmentelevation
Unstable Non-Q Q-Waveangina AMI AMI
ECG
AcuteReperfusion
HistoryPhysical Exam
Pathogenesis of ACS
Non-Vulnerable Atherosclerotic
Plaque
Non-Vulnerable Atherosclerotic
Plaque
Vulnerable Atherosclerotic
Plaque
Vulnerable Atherosclerotic
Plaque
Davies MJ. Circulation. 1996;94:2013-2020.
Fissures inthe fibrous cap
The Matrix Skeleton of UnstableCoronary Artery Plaque
Vulnerable plaques
• Vulnerable plaques cause ACS• Depends upon inner free lipid content, thin
fibrous cap, active inflammation, hemodynamic stresses.
• More than one vulnerable plaques can be present which are not Rx by PCI.
• Vulnerable plaques cannot be detected by routine CAG.
• Can be inferred indirectly by hsCRP – Rx high dose statins
Chest pain with ACS
• 15 -25 % of chest pain cases in ED have ACS
• 2 % of ACS are missed• These are current US data• In India the percentages are far
higher• For Pt mortality / for us medicolegal
implications
Clinical Classification of Chest Pain
Diamond . J Am Coll Cardiol 1983
Typical Angna
• Cardiac symptoms: Presence of acute chest, epigastric, neck, jaw, or arm pain or discomfort or pressure without apparent noncardiac source.
• Levine`s sign may be +ve.• More general, atypical symptoms, such as
fatigue, nausea, vomiting, diaphoresis, faintness, and back pain, should not be used as a diagnosis of Angina
1. Diabetes Mellitus2. Peripheral Vascular Disease (PVD)3. Framingham risk score of > 20%
4. Carotid artery disease – • Stroke, TIA• > 50% Narrowing, Carotid Bruit
5. Abdominal Aortic Aneurysm (AAA)
CHD Risk Equivalents
Adult Treatment Panel III. NIH publication 01-3095.
Epidemiological definition of MI
• Typical chest pain lasting for > 30 min not relieved by nitrates
• ECG showing characteristic changes of MI
• Positive cardiac biomarkers of injury
WHO states any of two from above three should be present.
Definition of Acute/Evolving/Recent MI
1) Typical rise and fall of biochemical markers of MI with atleast 1 of them
• Ischaemic symptoms• ECG changes indicative of ischaemia (ST
elevation or depression or LBBB)• Development of pathological Q waves in
ECG
• New RWMA or imaging e/o loss of viable myocardium
ACC/AHA/EU/WHO Task force for redefinition of MI 2007 guidelines
ST elevation
R
P
Q
ST
• Occurs in the early stages
• Occurs in the leads facing the infarction
• Slight ST elevation may be normal in V1 or V2
Deep Q wave
R
P
Q
T
ST
• Only diagnostic change of myocardial infarction
• At least 0.04 seconds in duration
• Depth of more than 25% of ensuing R wave
T wave changes
R
P
Q
T
ST
• Late change
• Occurs as ST elevation is returning to normal
• Apparent in many leads
Bundle branch block
I II IIIaVR aVL aVF
V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Anterior wall MI Left bundle branch block
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
QT
STR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
QT
ST
R
P
Q
T
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary artery
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
Location of infarct combinations
aVR V1 V4I
II
III
LATERAL
INFERIOR
ANTPOST ANT
SEPTAL
ANT
LAT
aVL
aVF
V2
V3
V5
V6
Right Ventricular InfarctionRight Ventricular Infarction
Clinical findings:Shock with clear lungs, elevated JVPKussmaul sign
Hemodynamics: Increased RA pressure (y descent)Square root sign in RV tracing
ECG:ST elevation in R sided leads
Echo:Depressed RV function
Rx:Maintain RV preloadLower RV afterload (PA---PCW)Inotropic supportReperfusion
V4R
Modified from Wellens. N Engl J Med 1999;340:381.
Diagnostic criteria for AMI
• Q wave duration of more than 0.04 seconds
• Q wave depth of more than 25% of ensuing r wave
• ST elevation in leads facing infarct (or depression in opposite leads)
• Deep T wave inversion overlying and adjacent to infarct
• Cardiac arrhythmias
Cor pulmonale
MI presenting as Syncope
• 60 yrs sudden onset chest pain f/b syncope
• H/o associated sweating +
• Afterwards no chest pain
• No risk factors other than age
• Dilemma whether it is arrythmogenic syncope.
Trop T -Ve
Non ischaemic causes of ST elevation
• Early repolarization changes.
• Prinzmetal angina
• Ventricular aneurysm
• Pericarditis myocarditis
• Hyperkalemia, Hypercalcemia
• LVH, LBBB
• IC bleed mistaken as MI
Mistaken MI
• Lingam diagnosed as AWMI
• CAG revealed critical lesion LAD
• Underwent successful stenting to LAD
• But patient still symptomatic
• Presented with Grade IV dyspneoa
• ECHO showed COR PULMONALE
Non MI causes of pathalogical Q waves
• Norma septal Q waves V1-V2, III & AVF (narrow)
• Cardiomyopathies.
• Severe LVH, LBBB
• Dextrocardia/version.
• COPD
Young MI
• Devender 27 yrs male
• Non smoker
• Non diabetic
• H/O travel to dubai, elctrician
• Middle class family
• Chest pain 3 hrs duration
Homocysti(e)ne• Normal value is up to 10 μ mols/L
• Excess of homocystine generates oxidative stress on the cell membranes.
• Folic acid 5 mg/ day + Vit. B6 and B12 are to be given on regular basis
Hyper-homocyst(e)inemia
Blood Homocyst(e)ine Levels
Classification Values mmol/L
Normal
Moderate
Intermediate
Severe
05 – 10
11 – 30
31 – 100
> 100
Lipid Profile in Young Indian Patients with Angiographically Proven CHD
Parameter % Patients
Total cholesterol >200 mg/dl 54.3
Triglyceride >200 mg/dl 56.1
HDL <35 mg/dl 59.6
Lp(a) >30 mg/dl 61.4
n=57; age <40 yrsMishra et al (Cuttack)
Indian Heart J 2001; 53: Abst 60
CHD Risk Factors - Makers
• Modifiable – The New Six– hs-CRP
– Lp(a)
– sLDL
– Endothelial Dysfunction
– Apo B / Apo A1 ratio
– Homocysteine
Risk Factors for Future Cardiovascular Events: WHS
Relative Risk of Future Cardiovascular Events0
Ridker PM et al. N Engl J Med 2000;342:836-843.
Lipoprotein(a)
Homocysteine
IL-6
TC
LDL-C
sICAM-1
SAA
Apo B
TC:HDL-C
hs-CRP
hs-CRP + TC:HDL-C1.0 2.0 4.0 6.0
Post stent MI
• Mr Rathod 60 yrs male.
• 1999 had ACS, uderwent stenting and not on reqular follow up
• Asymptomatic since then
• Presented with typical h/o of MI
Clinical indicators of successful reperfusion
• Resolution of chest pain by > 50%
• Resolution of ST elevations by > 50%
• AIVR
• Rapid rise and fall of cardiac enzymes
• Clinically stable course
For Managment
• ST elevation MI :- Rapid thrombolysis vs immediate revascularization
(Complete occlusion of lumen by red thrombus)
• Non ST elevation MI:- Antithrombotics and plaque stabilization or cooling off. Early invasive strategy is controversial
(Partial occlusion of lumen by white thrombus)
Management of MI
• All management strategies focus on faster reperfusion of culprit artery.
• Spontaneous recanalization rates after MI is
40 %• But it is after 12 – 24 hrs• Permanent damage has already set
in
Management of MI
• Within 30 minutes if reperfused no damage to myocardium.
• Within 2- 4 hrs of reperfusion the damages are minimal.
• After 6 hrs what we save is much less than what myocardium we loose
Management of MI
• After 12 hrs no use of repurfusion • permanent damage sets in though
surrounding hibernating myocardium can be saved.
• To assess for hibernating myocardium we have
Presence of chest pain TMT Nuclear Scans Dobutamine Stress Echo MRI etc
• ITS NOT GIVING RIGHT TREATMENT THAT IS IMPORTANT IN MI MANAGEMENT BUT HOW FAST WE ADMINISTER THAT IS IMPORTANT
• For every 30 min delay in reperfusion the one year risk of relative mortality increases by 8%
y
? MI
• Laksmi presented with 2 hrs duration of severe chest pain
• She 35 years female• ECG not fulfilling criteria of MI• Enzymes useless• Later ECHO except mild apical
hypokinesia normal• CAG Prox LAD 90% stenosis.
Fibrinolysis generally preferred Early presentation ( ≤ 3 hours from symptom onset and delay to invasive strategy)
Invasive strategy not an option Cath lab occupied or not available Vascular access difficulties
No access to skilled PCI lab
Delay to invasive strategy Prolonged transport
Door-to-balloon more than 90 minutes > 1 hour vs fibrinolysis (fibrin-specific agent) now
Reperfusion Options for STEMI PatientsReperfusion Options for STEMI Patients Step 2:Step 2: Select Reperfusion Treatment. Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy.
Invasive strategy generally preferred Skilled PCI lab available with surgical backup
Door-to-balloon < 90 minutes
• High Risk from STEMI Cardiogenic shock, Killip class ≥ 3
Contraindications to fibrinolysis, including increased risk of bleeding and ICH
Late presentation > 3 hours from symptom onset
Diagnosis of STEMI is in doubt
Reperfusion Options for STEMI PatientsReperfusion Options for STEMI Patients Step 2:Step 2: Select Reperfusion Treatment. Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy.
FibrinolysisFibrinolysis
Fibrinolytic therapy should not be administered to
asymptomatic patients whose initial symptoms of
STEMI began more than 24 hours earlier.
Fibrinolytic therapy should not be administered to
patients whose 12-lead ECG shows only ST-
segment depression, except if a true posterior MI
is suspected.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Contraindications and CautionsContraindications and Cautionsfor Fibrinolysis in STEMIfor Fibrinolysis in STEMI
Absolute Contraindications
• Any prior intracranial hemorrhage
• Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
• Known malignant intracranial neoplasm (primary or metastatic)
• Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours
NOTE: Age restriction for fibrinolysis has been removed compared with prior guidelines.
Contraindications and CautionsContraindications and Cautionsfor Fibrinolysis in STEMIfor Fibrinolysis in STEMI
Absolute Contraindications
• Suspected aortic dissection
• Active bleeding or bleeding diathesis (excluding menses)
• Significant closed-head or facial trauma within 3 months
Contraindications and CautionsContraindications and Cautionsfor Fibrinolysis in STEMIfor Fibrinolysis in STEMI
• History of chronic, severe, poorly controlled hypertension
• Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg)
• History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications
• Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks)
RelativeContraindications
Contraindications and CautionsContraindications and Cautionsfor Fibrinolysis in STEMIfor Fibrinolysis in STEMI
RelativeContraindications
• Recent (< 2 to 4 weeks) internal bleeding • Noncompressible vascular punctures • For streptokinase/anistreplase: prior
exposure (> 5 days ago) or prior allergic reaction to these agents
• Pregnancy• Active peptic ulcer • Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding
Choice of Thrombolytic
• Underuse:- 50 – 70% of cases only given thrombolytics.
• tPA:• • Less allergic reactions• • Less fibrinogen depletion (“clot selective”)• • Faster thrombolysis• • Slightly lower overall mortality
• 2) Streptokinase (SK):• • Less expensive ($300 vs $2500)• • Lower stroke rate (0.3% vs 0.8%)• • Can’t use again secondary to antibody formation
Thrombolysis
• 90 minute patency better with rt-PA than SK (70% vs 55% in Euro CoopStudy and 70% vs 43% in TIMI-1)
• Patency at 24 hours roughly equal between tPA and SK• ISIS-3 – mortality identical in head to head comparison of tPA and SK• Many studies favor tPA over SK
Primary PTCA
• Gangasagar 52 yrs male
• H/O Diabetes
• Chest pain for 4 hrs
Adapted from Braunwald E. Circulation 1989;80:410-4
Classification of USA
Class I:- New onset angina or 7.1% accelerated angina.Class II:- Angina at rest but not within 48 hrs. 10.3%Class III:- Angina at rest within 48 hrs. 10.9%
A:- Secondary angina(14%), B:- Primary angina ( 8.5%), C:- Post infarct angina (18.5%)
Medical Management of Unstable Angina
• Nitrates:- ISIS 4• Beta Blockers:- HINT• Aspirin:- Cohen, RISC, Theroux et al• Clopidogrel:- CURE, CREDO, CAPRIE• Heparin • Or LMWH:- ESSENCE, TIMI 11B, FRIC,• GP2b3a inhibitors:- PRISM, EPIC PURSUIT,
CAPTURE, PARAGON• Statin:- LIPID, PROVE IT TIMI 18, TNT, A to Z• ACE:- SAVE, SOLVD
Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
Death, myocardial infarction, and major bleeds at 30 days in randomized trials of glycoprotein IIb/IIIa inhibitors (filled bars) vs. control (open bars) in a conservative strategy
SHOCK Trial
• Early invasive strategy was first proved beneficial in high risk MI patients by SHOCK trail than
No role for Wait & Watch & Intervene
Primary PCI is better than thrombolysisPAMI, DINAMI, etc – 24 RCT`s
Does same apply for USA management?
Answer is:- NO
1) Plaque volume (constant) & vulnerability.
2) Type of Thrombus differs (white vs red)
3) Patent lumen
New Terminology in ACS
ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention.Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
AntithromboticTherapy
Stable Angina
UnstableAngina
Non–Q-wave MI
ThrombolysisPrimary PCI
Q-wave MI
Minutes-hours
Days-weeks
STEMIUA/NSTEMIAtherothrombosisNew term
Old term
PlaqueRupture
Risk Stratification Tools• Clinical Assessment• Standard ECG and Non-standard ECG
leads• Markers
– Other: IMA, BNP, CRP
• Non-Invasive Studies– Echocardiogram– Exercise testing– Technetium-99m-sestamibi– MR angio, CT angio
Ischaemia
Inflammation
Myocyte Necrosis
Accelerated Atherosclerosis
Hemodynamic Stress
HbA1cBlood
glucose
IMA
Troponin
BNP, NT-proBNPhs-CRP, CD40L
Morrow DA, et al. Circulation. 2003;108:250-252.
Multimarker Strategy in ACS
Short-Term Risk of Death or Nonfatal Myocardial Infarction in Patients With Unstable Angina
Braunwald E et al.: Unstable angina: diagnosis and management. AHCPR Publication No 94-0602
Risk of Death or Myocardial Infarction According to Treatment Strategy and cTnI: TACTICS TIMI 18
Morrow DA et al. JAMA 2001;286:2405-12
TIMI, thrombosis in myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; CAD, coronary artery disease.Antman EM, et al. JAMA. 2000;284:835-842.
TIMI Risk Score for UA/NSTEMI: 7 Independent Predictors
– ≥3 CAD risk factors
– Aged ≥65 years
– Prior CAD (stenosis >50%)
– Aspirin in last 7 days
– >2 anginal events in ≤24 hours
– ST deviation
– Elevated cardiac markers (CK-MB or troponin)
Global Registry of Acute Coronary Events (GRACE) risk score
• The GRACE risk score (on a scale of 1 to 372, with higher scores indicating greater risk) is derived from readily available hospital admission variables,
- including age, - heart rate, - systolic blood pressure, - creatinine level, - Killip class, - cardiac arrest at admission, - presence of ST-segment deviation, and - elevated cardiac biomarkers.
Values for these variables can be entered into the GRACE risk calculator
Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
GRACE Prediction Score Card and Nomogram for All-Cause Mortality From Discharge to 6 Months
Indications for early invasive strategy
• Recurrent rest angina
• Elevated troponin• New ST changes• LVF• Positive stress test
• EF<40%• Haemodynamic
instability• Malignant
arrhythmias• PCI<6 months• CABG
Timing of Invasive strategy in Non ST Elevation MI
What is early and late
• Early intervention is < 24 - 48 hours of presentation.
• Late intervention is >36 - 48 hours of presentation
ISAR COOL
• Early treatment reduces long term MI, mortality.
• However procedure complications increase.
• To offset it “cool off” or plaque pacifying strategy using prolonged antithrombotic & GP2b3a inhibitors.
ISAR COOL
SYNERGY Trial
(Circulation. 2007;116:2669-2677.)
Conclusions SYNERGY Trial
• High-risk patients with NSTE ACS who received earlier coronary angiography had a decreased risk of death/MI through 30 days.
Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
Decision-making algorithm for the management of patients with non-ST-elevation acute coronary syndrome
Case of USA
• Mr Sheik Ahhmed 45 yrs male• Chronic smoker• Labourer• For past 2 months not able to work due to
chest pain• Somebody has to hit him in back for relief
of pain• Increasing frequency & duration of pain
y
Wallen`s Warning
Care of IHD patients
• Primary prevention
• Secondary prevention
The Progressive Development of Cardiovascular Disease
End stage Heart DiseaseEnd stage Heart Disease
Congestive Heart FailureCongestive Heart Failure
Ventricular DilationVentricular Dilation
RemodelingRemodeling
Arrhythmia & Muscle LossArrhythmia & Muscle Loss
Myocardial InfarctionMyocardial Infarction
Myocardial IschemiaMyocardial Ischemia
CADCAD
AtherosclerosisAtherosclerosis
Endothelial DysfunctionEndothelial Dysfunction
Risk FactorsRisk Factors
Coronary ThrombosisCoronary Thrombosis
Intervene here}
Public Awareness
A survey of people with Diabetes• Findings
– 68% do not consider cardiovascular disease to be complication of diabetes
– 50%+ don’t feel risk for heart condition or stroke
– 60% don’t feel at risk for high blood pressure or cholesterol
– Awareness lowest among elderly, minorities
2
Why is CAD becoming so rampant
• Is it people are living longer?
• Is it increasing habits like smoking cocaine?
• Is it raise in Diabetes?
• Is it food we eat?
• Or is it all in the genes?
With in no time !!
Where are we heading ? ?
Journal of internal medicine 2003:254(2):114-25
20000 B.C. 2004
Hunting-gatheringsubsistence
High level ofphysical activity
Processedfoods
Animal fatsand glucidesDietary fibre¯
Sedentary life
Paleolithic sup. age Neolithic age 19th century 21st century
Thrifty genotype Susceptibility genotype
This is how we take our dog to walk!
Secondary Prevention of CAD
Secondary prevention
• The above drugs are minimum for post MI/USA patients
• If diabetic then OHA`S 1 + 2 drugs• If severe LV dysfunction diuretics, digoxin• If PVD or BPH or OA or ED – extra drugs• Post stent tripple antiplatelets common• Antacids, vitamins, calcium etc
Hippocrates said ….
Let your FOOD be your Medicine – Lest,
Your Medicines will replace your Food !!
MedSlides.comMedSlides.com 1461465/985/98
THANK THANK YOUYOU