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Coronary Artery Disease Partial Total 1 coronary artery and
branchesBlood flow Occluded of the coronary artery1
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Left Coronary Artery
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Right Coronary Artery
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Global Burden of Cardiovascular DiseaseIn 2002 : CVD contributed
to approximately a third of all global deaths (17 million). 80% of
burden is in low and middle income countries.By 2020 : CHD and
Stroke will become the leading cause of death and disability
worldwide. Mortality for CVD will increase to 20 million.
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Worldwide StatisticsEach year:> 4 million patients are
admitted with unstable angina and acute MI > 900,000 patients
undergo PTCA with or without stent
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Risk Factors for cardiovascular diseaseModifiable : - Smoking -
Dyslipidemia (Raised LDL-C, Low HDL-C, Raised triglycerides) -
Raised Blood pressure - Diabetes melitus - Obesity
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Risk factors for cardiovascular diseaseNon-Modifiable : -
Personal History of CVD - Family History of CVD - Age - Gender
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Family History Premature CHD
Men (first degree) < 55 years. Women (first degree)
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Serum lipids and lipoproteins: risk factors for coronary heart
disease Lipid/LipoproteinEffect on coronary heart disease risk if
level is:DecreasedIncreased
Total cholesterol LDL-cholesterol HDL-cholesterol Triglycerides
LDL= low-density lipoprotein; HDL=high-density lipoproteinShaper et
al (1985)
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CORONARY ARTERY DISEASE1. Stable angina pectoris2. Acute
Coronary Syndrome A. Unstable angina pectoris B. Q wave acute
myocardial infarction : -NSTEMI -STEMI C. Non Q wave AMI : -NSTEMI
-STEMI
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STABLE ANGINA PECTORISStable angina is a clinical syndrome
characterized by discomfort in the chest, jaw, shoulder, back or
arms, typically elicited by exertion or emotional stress and
relieved by rest or nitroglycerin. Less typically, discomfort may
occur in the epigastric area.
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Diagnosis of stable anginaClinical assesmentLaboratory
testSpecific cardiac investigations
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HistoryFeatures of the history important in risk stratification
include current smoking, increasing age, prior MI, symptoms of
heart failure, and the pattern of occurance(recent onset or
progressive), and severity of angina, particularly if unresponsive
to therapy.
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Physical examinationPatient with (suspected) angina pectoris
should be focused on identification or exclusion of causal or
associated conditions or precipitating factors and on risk
stratification.
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LABORATORY TESTFasting plasma glucose and lipid profile
(TC,HDL,LDL,TG) should be evaluated in all patients with stable
angina, to establish the patients risk profile and ascertain the
need for treatment. A full blood count and serum creatinine are
also indicated in all patients.
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LABORATORY TESTFuther laboratory testing, including OGTT,
cholesterol subfractions (ApoA, ApoB), hemocysteine, Lpa, NT-BNP,
haemostatic abnormalities and markers of inflammation such as
hsCRP, may a role in selected patients.
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LABORATORY TESTMeasurement of markers of myocardial damage such
as troponin, should be measured if evaluation suggests clinical
instability or acute coronary syndrome. Thyroid function should be
tested if dysfunction suspected clinically.
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Chest X-rayShould be requesed only in patients with suspected
heart failure, valvular disease or pulmonary disease.The presence
of cardiomegaly, pulmonary congestion, atrial enlargement and
cardiac calcifications have been related to prognosis.
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ECGAll patient with suspected angina pectoris based upon
symptoms should have a resting 12 lead ECGResting ECG
abnormalities, ST depression, Q waves, left anterior hemiblock and
left bundle-branch block, are associated with an adverse prognosis
in stable angina.
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Normal conduction wave from an electrocardiogramTime
(ms)ST200400600-0.500.5QP1.0Voltage (mV)R
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Ischemia & Infarction Types of ST-segment depression
UPSLOPING very nonspecific for the diagnosis of ischemia.
Associated with a lot of false positive exercise tests.HORIZONTAL
likely associated with ischemia. DOWNSLOPING almost certainly
associated with an ischemic myocardium
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ECG STRESS TESTINGIn the majority of patients the exercise ECG
is the initial test of choice to diagnosis coronary disease and
risk stratify.
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ECG STRESS TESTINGDIAGNOSIS OF CAD. ST segment depression during
exercise is used to define a positive test.Sensitivity and
spesificity are 68% and 77% respectively.Exercise ECG testing is
not of diagnosis value in presence of LBBB, paced rhythm and WPW
syndrome.
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ECG STRESS TESTINGResult are less reliable in patients with an
abnormal resting ECG in the presence of LVH, electrolyte imbalance,
intraventricular conduction abnormalities and during use of
digitalis.Exercise ECG testing is also less sensitive and specific
in women.
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STRESS TESTING IN COMBINATION WITH IMAGINGExercise testing with
echocardiograpySingle Photon Emission Computed Tomography
(SPECT)Stress Cardiac magnetic Resonance (CMR)
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OTHER INVESTIGATIONSECHOCARDIOGRAPHY AT RESTELECTRON BEAM CT and
MULTI-SLICE CT.MAGNETIC RESONANCE (MR) ARTERIOGRAPHYCORONARY
ANGIOGRAPHY.
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CORONARY ARTERIOGRAPHYProviding reliable anatomical information
to identify the presence or absence of coronary lumen stenosis,
define therapeutic options (suitability of medical treatment or
myocardial revascularization) and determine prognosis.
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TREATMENTAims of treatment. A. Improve prognosis by preventing
myocardial infarction and death B. Minimize or abolish
symptoms.
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Non-pharmacological Advice should be given for the management of
an acute attack, i.e. to rest, at least briefly, from the activity
that provoked the angina and the use of sublingual nitrate for
acute relief of symptoms.Need to seek medical advice if angina
persist >10-20 minutes after rest and/or is not relieved by
sublingual nitrates.
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Non-PharmalogicalStop cigarette smokingMediterranean diet, with
vegetables, fruit, fish and poultry being the mainstays.Weight
reduction diet --- OverweightAlcohol in moderation may be
beneficial, but excessive consumption is harmful
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Non-PharmacologicalFish oil rich in omega-3 fatty acids (n-3
polyunsaturated fatty acids) are recommended at least once
weeklyPhysical activity within the patients limitation should be
encouraged.Concomitant disorders such as diabetes and hypertension
should be managed appropriately.Sexual intercouse may trigger
angina. Nitroglycerine prior to intercourse may be helpful.
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Pharmacological therapyAntitrombotic drugs. Antiplatelet therapy
to prevent coronary trombosis is indicated. Low dose aspirin
(75-100 mg) is the drug of choise in most cases.Aspirin allergic
--- clopidogrelAspirin + clopidogrel --- post stenting or after
ACSHistory of GI bleeding --- aspirin + proton pum inhibitor
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Pharmacological therapyAnticoagulant drugs (warfarin or thrombin
inhibitors), which are combined with aspirin in certain high risk
patients, such as post MI, are not indicated in the general stable
angina pectoris without a separate indication such as atrial
fibrillation for example.
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Pharmacological therapyLipid lowering drugsACE
inhibitorsBeta-blockersAntianginal drugs : beta-blockers, calcium
antagonist and organic nitrates
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Coronary artery bypass surgeryTwo main indications ---
prognostic and symptomaticPrognostic benefit : reduction in cardiac
mortalityCABG has also been shown to effectively reduce symptoms of
angina and ischemia in patients with coronary disease.
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Better Prognosis with Coronary artery bypass surgerySignificant
stenosis of the left main Significant proximal stenosis of the
three major coronary arteriesSignificant stenosis of two major
coronary arteries, including high grade stenosis of the proximal
left anterior descending coronary arteryThree vessel disease with
impaired ventricular function.
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Percutaneous coronary intervention (PCI)PCI may be considered an
alternative to CABG for relief of symptoms in almost all casesOn
available evidence, PCI compared to medical therapy does not
provide survival benefit in stable angina, but PCI is more often
effective than medical treatment in reducing events that impair
quality of life
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Acute Coronary Syndrome
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Unstable PlaqueOcclusive ThrombusFixed Coronary
Obstruction(Chronic Ischemic Heart Disease)PATOGENESIS Kuliah PJK,
20047
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Acute Coronary SyndromeIschemic Discomfort Unstable SymptomsNo
ST-segment elevation ST-segment elevationUnstable Non-QQ-Wave
angina AMI AMIECGAcute ReperfusionHistory Physical Exam
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Unstable Angina - Definitionangina at rest (> 20
minutes)new-onset (< 2 months) exertional angina (at least CCSC
III in severity)recent (< 2 months) acceleration of angina
(increase in severity of at least one CCSC class to at least CCSC
class III)Agency for Health Care Policy Research - 1994Canadian
Cardiovascular Society Classification
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CANADIAN CARDIOVASCULAR SOCIETY FUNCTIONAL CLASSIFICATIONCLASS I
No angina with ordinary activity. Angina with strenuous, rapid or
prolonged exertion.CLASS II Slight limitation of ordinary activity
; angina when walking up stairs briskly, or walking on a cold or
windy day.CLASS III Marked limitation ; angina when walking at
normal pace up flight of stairs, or walking 1-2 blocks
distance.CLASS IV Angina on minimal exertion or at rest.
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Unstable Anginaprecipitating factorsInappropriate
tachycardiaanemia, fever, hypoxia, tachyarrhythmias,
thyrotoxicosisHigh afterloadaortic valve stenosis, LVHHigh
preloadhigh cardiac output, chamber dilatationInotropic
statesympathomimetic drugs, cocaine intoxication
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Unstable Anginaprognostic indicatorsPresence of ST-T-wave
changes with painHemodynamic deteriorationpulmonary edema, new
mitral regurgitation,3rd heart sound, hypotensionOther
predictorsleft ventricular dysfunction, extensive CAD, age,
comorbid conditions (diabetes mellitus, obstructive pulmonary
disease, renal failure, malignancy)
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Unstable Anginapathogenesis
Plaque disruptionAcute thrombosisVasoconstriction
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Unstable AnginaRisk StratificationLow Risknew-onset exertional
anginaminor chest pain during exercisepain relieved promptly by
nitroglycerineManagementcan be managed safely as an outpatient
(assuming close follow-up and rapid investigation)
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Unstable AnginaRisk StratificationIntermediate Riskprolonged
chest paindiagnosis of rule-out MIManagementobserve in the ER or
Chest Pain Unitmonitor clinical status and ECGobtain cardiac
enzymes (troponin T or I) every 8 to 12 hours
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Unstable AnginaRisk StratificationHigh Riskrecurrent chest pain
ST-segment changehemodynamic compromiseelevation in cardiac
enzymesManagementmonitor in the Coronary Care Unit
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Unstable AnginaTherapeutic GoalsTherapeutic GoalsReduce
myocardial ischemia Control of symptoms Prevention of MI and
deathMedical ManagementAnti-ischemic therapyAnti-thrombotic
therapy
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Unstable AnginaMedical TherapyAnti-ischemic therapynitrates,
beta blockers, calcium antagonistsAnti-thrombotic
therapyAnti-platelet therapyaspirin, ticlopidine, clopidogrel, GP
IIb/IIIa inhibitorsAnti-coagulant therapy heparin, low molecular
weight heparin (LMWH), warfarin, hirudin, hirulog
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Unstable AnginaAnti-ischemic Therapyrestrict
activitiesmorphineoxygennitroglycerinepain relief, prevent silent
ischemia, control hypertension, improve ventricular
dysfunctionnitrate free period recommended after the first 24-48
hours
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Unstable AnginaAnti-ischemic Therapybeta-blockerslowering angina
thresholdprevent ischemia and death after MIparticularly useful
during high sympathetic tonecalcium antagonistsparticularly the
rate-limiting agentsnifedipine is not recommended without
concomitant -blockade
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Unstable AnginaAnti-thrombotic Therapy
Thrombolytics are not indicatedlytic agents may stimulate the
thrombogenic process and result in paradoxical aggravation of
ischemia and myocardial infarctionTIMI IIIB Investigators
Circulation 1994; 89:1545-1556
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Unstable AnginaAnti-platelet Therapyaspirin is the gold
standardirreversible inhibition of the cyclooxygenase pathway in
platelets, blocking formation of thromboxane A2, and platelet
aggregationin AMI, ASA reduced the risk of death by 20-25%in UA,
ASA reduced the risk of fatal or nonfatal MI by 71% during the
acute phase, 60% at 3 months, and 52% at 2 yearsbolus dose of
160-325 mg, followed by maintenance dose of 80-160 mg/d
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Unstable AnginaAnti-platelet TherapyThienopyridinesticlopidine
clopidogrel block platelet aggregation induced by ADP and the
transformation of GP IIb/IIIa into its high affinity state
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Unstable AnginaAnti-platelet TherapyGP IIb/IIIa
inhibitorsabciximab (monoclonal antibody)eptifibatide (peptidic
inhibitor)lamifiban and tirofiban (non-peptides) direct occupancy
of the GP IIb/IIIa receptor by a monoclonal antibody or by
synthetic compounds mimicking the RGD sequence for fibrinogen
binding prevents platelet aggregation
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Unstable AnginaAnti-coagulant TherapyHeparinrecommendation is
based on documented efficacy in many trials of moderate
sizemeta-analyses (1,2) of six trials showed a 33% risk reduction
in MI and death, but with a two fold increase in major
bleedingtitrate PTT to 2x the upper limits of normal1. Circulation
1994;89:81-882. JAMA 1996;276:811-815
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Unstable AnginaAnti-coagulant TherapyLow-molecular-weight
heparin advantages over heparin:better bio-availabilityhigher ratio
(3:1) of anti-Xa to anti-IIa activitylonger anti-Xa activity, avoid
reboundinduces less platelet activationease of use (subcutaneous -
qd or bid)no need for monitoring
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Unstable Angina Coronary InterventionsTIMI 3B early intervention
vs conservative strategy (coronary angiography within 24-48 hrs,
followed by angioplasty or bypass surgery)1473 patients with UA or
non-Q-wave MI were randomized, there were no difference between the
groups in the rates of death or MI at 1 yearCirculation
1994;89:1545-1556
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Acute Myocardial Infarction
Myocardial Infarction if the rapid development of myocardial
necrosis by a critical imbalance between oxygen supply and demand
to the myocardium
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HistoryChest Pain- anterior precordium tightnessPain may radiate
to jaw, neck and epigastriumDyspnea- angina equivalent, poor LV
functionNausea/abdominal pain with posterior MIAnxiety
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HistoryNausea with and without vomitingDiaphoresis or
sweatingSyncope or near syncopeElderly present - fatigue, syncope
or weaknessAs many as half of MI are clinically silent
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Physical
- Hypertension - Hypotension - Acute valvular dysfunction may be
present - Rales - Neck vein distention
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Physical
Third heart sound may be presentA fourth heart sound poor LV
complianceDysrhythmiasLow grade fever
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CausesMost frequent cause is rupture of an atherosclerotic
lesion within coronary wall with subsequent spasm and thrombus
formationCoronary artery vasospasmVentricular
hypertrophyHypoxiaCoronary artery emboli
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CausesCocaineCoronary anomaliesAortic dissectionPediatrics
Kawasaki disease, Takayasu arteritisIncreased afterload which
increases myocardial demand
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DifferentialsAcute coronary syndromeAnxietyAortic
stenosisAsthmaCholecystitis and biliary colicCholethiasisCOPD
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DifferentialsAortic
DissectionEndocarditisEsophagitisShockMyocarditisPericarditisPulmonary
embolism
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Mechanisms of Myocardial damageThe severity of an MI is
dependent of three factorsThe level of the occlusion in the
coronaryThe length of time of the occlusionThe presence or absence
of collateral circulation
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ElectrocardiogramA normal ECG does not exclude ACSHigh
probability include ST segment elevation in two contiguous leads or
presence of q waves Intermediate probability ST depressionT wave
inversions are less specific
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Ischemia & InfarctionAcute anterior MI
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Cardiac BiomarkersCardiac biomarkers are protein molecules
released into the blood stream from damaged heart muscle Since ECG
can be inconclusive , biomarkers are frequently used to evaluate
for myocardial injuryThese biomarkers have a characteristic rise
and fall pattern
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Troponin T and IThese isoforms are very specific for cardiac
injuryPreferred markers for detecting myocardial cell injuryRise
2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14
days
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Creatinine Kinase ( CK-MB)Creatinine Kinase is found in heart
muscle (MB), skeletal muscle (MM), and brain (BB)Increased in over
90% of myocardial infractionHowever, it can be increased in muscle
trauma, physical exertion, post-op, convulsions, and other
conditions
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Creatine Kinase (MB)Time sequence after myocardial infarction
Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2
daysMB2 released from heart muscle and converted to MB1.A level of
MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates
myocardial injury
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MyoglobinDamage to skeletal or cardiac muscle release myoglobin
into circulationTime sequence after infarction Rises fast 2hours
Peaks at 6-8 hours Returns to normal in 20-36 hoursHave false
positives with skeletal muscle injury and renal failure
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Ischemia & Infarction Biomarkers in an MI:Days after MI
OnsetMultiples of the AMI cutoff Limit012345678MyoglobinCardiac
TroponinCK-MBCardiac Troponin after unstable angina0125102050AMI
decision limitUpper normal limit
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CBC
CBC is indicated if anemia is suspected as precipitant
Leukocytosis may be observed within several hours after
myocardial injury and returns returns to levels within the
reference range within one week
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Chemistry Profile
Potassium and magnesium levels should be monitored and
corrected
Creatinine levels must be considered before using contrast dye
for coronary angiography and percutanous revascularization
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C-reactive Protein (CRP)
C- reactive protein is a marker of acute inflammation
Patients without evidence of myocardial necrosis but with
elevated CRP are at increased risk of an event
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Chest X-Ray
Chest radiography may provide clues to an alternative diagnosis
( aortic dissection or pneumothorax)
Chest radiography also reveals complications of myocardial
infarction such as heart failure
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EchocardiographyUse 2-dimentional and M mode echocardiography
when evaluating overall ventricular function and wall motion
abnormalities Echocardiography can also identify complications of
MI ( eg. Valvular or pericardial effusion, VSD)
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Therapy The goals of therapy in AMI are the expedient
restoration of normal coronary flow and the maximum salvage of
functional myocardium
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Antiplatelet AgentsAspirin at lease 160mg immediately Interferes
with function of cyclooxygenase and inhibits the formation of
thromboxaneASA alone has one of the greatest impact on the
reduction of MI mortality.Clopidogrel, ticlopidine, have not been
shown in any large scal trail to be superior to Aspirin in acute
MI
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Supplemental OxygenBecause MI impairs the circulatory function
of the heart, oxygen extraction by the heart and other tissues may
be diminished Supplemental oxygen should be administered to patient
with symptoms and or signs of pulmonary edema or pulse oximetry
readings less than 90%.
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NitratesIV nitrates to all patients with MI and congestive heart
failure, persistent ischemia, hypertension, or large anterior wall
MIPrimary benefit vasodilator effectMetabolized to nitric oxide in
the vascular endothelium, relaxes endotheliumVasodilatation reduces
myocardial oxygen demand and preload and afterload
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Beta-blockersRecommended within 12 hours of MI symptoms and
continued indefinitelyReduces Myocardial mortality by decreasing
arrythmogenic deathDecrease the rate and force of myocardial
contraction and decreases overall oxygen demand
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Unfractionated heparinForms a chemical complex with antithrombin
III inactivates both free thrombin and factor XaRecommended in
patients with MI who undergo PTCA or fibrinolytic therapy with
alteplase
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Low-molecular weight heparinDirect activity against factors Xa
and IIaProven to be effective in treating ACS that are
characterized by unstable angina or non ST- elevation MITheir fixed
doses are easy to administer and laboratory testing to measure
their therapeutic effect is not necessary makes them attractive
alternative of un-fractionated heparin
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ThrombolyticsIndicated with MI and ST segment elevation greater
than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who
present less than 12 hours but not more than 24 hours after symptom
onsetThe most critical variable in achieving successful
fibrinolysis is time form symptom onset to drug administration
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ThrombolyticsAs a class the plasminogen activators have been
shown to restore coronary blood flow in 50-80% of
patientsContraindication active intracranial bleeding, CVA 2months,
CNS neoplasm, HTN, coagulopathyRetaplase slightly higher
angiographic patency but did not translate into survival
benefitIntracranial bleed risk major drawback
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Glycoprotein IIb/IIIa AntagonistsPotent inhibitors of platelet
aggregationUse during PCI and in patients with high risk features
ACS have been shown to reduce the composite end points of death,
reinfraction and the need for target lesion
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Surgical RevascularizationEmergent or surgical revascularization
in setting of failed PTCA in patients with hemodynamic instability
and coronary anatomy amendable to surgical graftingAlso indicated
of mechanical complications of MI including VSD, free wall rupture,
or acute MRCarries a higher risk of perioperative mortality than
elective CABG
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- Lipid ManagementAll post MI patients should be on AMA step II
diet ( < 7% of calories from saturated fats)Post MI patients
with LDL > 100 mg/dl are recommended to be on drug therapy to
try to lower levels to
- Long term MedicationsMost oral medications instituted in the
hospital at the time of MI are continued long termAspirin, beta
blockers and statin are continued indefinitelyACEI indefinitely in
patients with CHF, ejection fraction
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T H A N K Y O U
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