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Canadian Cardiovascular Society Functional Classification of
Angina Pectoris
KelasKeteranganIAktivitas fisik sehari-hari tidak menyebabkan
angina (misal: berjalan atau naik tangga). Angina terjadi pada
aktivitas berat, cepat, atau berlangsung lama. IIHambatan ringan
terhadap aktivitas fisik sehari-hari. Angina terjadi bila berjalan
atau naik tangga dengan cepat, mendaki bukit, berjalan atau naik
tangga sesudah makan, dalam cuaca dingin, sewaktu hujan atau stres
emosional, atau hanya beberapa jam setelah bangun tidur.
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IIIHambatan berat terhadap aktivitas fisik sehari-hari. Angina
terjadi saat berjalan 1-2 blok pada jalan datar dan naik tangga 1
tingkat dengan tempo biasa dan dalam keadaan biasa.IVKetidakmampuan
melakukan aktivitas fisik apapun, gejala dapat terjadi dalam
keadaan istirahat.
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Kelas fungsional menurut New York Heart
AssociationKelasKeteranganITidak terbatas. Aktivitas fisik
sehari-hari tidak menyebabkan lelah, sesak nafas atau
palpitasi.IISedikit pembatasan aktivitas fisik, aktivitas
sehari-hari menyebabkan lelah, palpitasi, sesak nafas atau
angina.IIIAktivitas fisik sangat terbatas, saat istirahat tanpa
keluhan namun aktivitas kurang dari sehari-hari menimbulkan
gejala.IVTidak mampu melakukan aktivitas fisik apapun tanpa
keluhan, gejala gagal jantung timbul bahkan saat istirahat dan
bertambah berat bila melakukan aktivitas.
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Diagnosis
Patient historyComplete physical examination
ElectrocardiogramLaboratory blood tests, stress testing, and
cardiac catheterization may be necessary to obtain further
diagnostic insight.
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Diagnostic and Imaging Studies
Electrocardiography. Electrocardiographic results are normal in
approximately 50% of patients with chronic stable anginaChest
Radiography. Cardiac Computed Tomography Angiography.
Echocardiography. recommended for patients with stable angina and
physical findings suggesting concomitant valvular heart
disease.
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Laboratory Studies
fasting glucose and fasting lipid levels (total cholesterol,
high-density lipoprotein [HDL] cholesterol, triglycerides, and
calculated low-density lipoprotein [LDL] levelsOther markers such
as lipoprotein (a) (Lp[a]) and high-sensitivity C-reactive protein,
may be useful in assessing cardiac risk. High-sensitivity
C-reactive protein is gaining greater prominence in assessing the
inflammatory level of vascular disease and predicting future risk
of vascular events, such as myocardial infarctions and
cerebrovascular accidents.
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Pretest Probability of Coronary Artery Disease (CAD) by Age,
Gender, and Symptom Status
- *High probability, >90%; intermediate, 10%-90%; low,
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Stress Testing
Stress testing is another method for determining the presence of
flow-limiting, functionally significant coronary artery disease.
All stress testing techniques include electrocardiography and blood
pressure monitoring.
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Absolute and Relative Contraindications to Exercise Stress
Testing
Absolute Contraindications Acute MI within 2 daysSymptomatic or
severe aortic stenosisDecompensated heart failureSymptomatic or
hemodynamically significant cardiac arrhythmiasUnstable angina not
previously stabilized by medical therapyAcute aortic
dissectionAcute myocarditis or pericarditisAcute pulmonary embolus
or pulmonary infarction
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Relative ContraindicationsLeft main coronary artery
stenosisElectrolyte imbalance Systolic blood pressure > 200 mm
HgDiastolic blood pressure > 110 mm HgTachyarrhythmias or
bradyarrhythmiasHypertrophic cardiomyopathy, other forms of outflow
tract obstruction High-degree atrioventricular blockModerate
stenotic valvular heart diseaseMental or physical impairment
leading to inability to exercise adequately
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Cardiovascular stress testing takes two forms, exercise and
pharmacologic administration. The preferred method of
cardiovascular stress testing is exercise, using a treadmill or
bicycle.The most common pharmacologic agents used for nonexercise
stress testing are dobutamine, dipyridamole, and adenosine.
Dobutamine echocardiography is useful for determining the presence
of functionally significant obstructive coronary artery disease and
assessing a postmyocardial infarction patient.
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Nuclear stress testing concept of coronary flow reserve and
differential myocardial blood flow. In the presence of exercise or
the administration of a pharmacologic coronary vasodilator, the
normal response is hyperemia, with a significant increase in
myocardial blood flow.severe coronary artery stenosis,
radiopharmaceuticals (Tc 99m sestamibi or Tc 99m tetrofosmin)
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Indications for Cardiac Stress Imaging
Resting ST-segment depression >1 mmComplete left bundle
branch blockVentricular paced rhythmVentricular pre-excitation
syndromePrevious revascularization with PCI or CABGInability to
exerciseAdapted from Gibbons RJ, Balady GJ, Beasley JW, et al:
ACC/AHA guidelines for exercise testing: Executive summary. A
report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee on
Exercise Testing). Circulation 1997;96:345-354.
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Prognostic markersDuke treadmill score, heart rate recovery
(HRR) score, and the chronotropic response index (CRI).Duke
treadmill scoring system
Risk GroupAnnual Mortality RateLow (>4)0.25%Intermediate (10
to 4)1.25%High (
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The Duke treadmill score is calculated according to the
following formula:Exercise time (min) 5(max ST-segment deviation
[in mm, during or after exercise]) angina scorewhere the score is 0
if there is no angina, 4 if angina occurs, and 8 if angina is the
reason for stopping the test.
Adapted from Mark DB, Shaw L, Harrell FE Jr, et al: Prognostic
value of a treadmill exercise score in outpatients with suspected
coronary artery disease. N Engl J Med 1991;325:849-853.
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HRR scoreHRR score = HR (at peak exercise) - HR (1 min
postexercise)
HR is in beats/min. Normal HRR score (more than 12 beats/min) is
associated with a low risk of deathlow HRR score (less than 8
beats/min) is associated with a high risk. HRR scores from 8 to 12
beats/min indicate an intermediate risk.
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CRI The CRI is calculated according to the following
formula:
(Peak HR - resting HR)/([220 - patient's age] - resting HR) HR
is in beats/min.
A normal CRI (more than 0.8) is associated with a decreased
probability of coronary artery disease and a lower risk of death. A
low CRI (less than 0.8) in a patient who is not on beta blocker
therapy is associated with an increased likelihood of coronary
artery disease and a higher risk of death.
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Risk Stratification Based on Noninvasive Testing
High Risk (>3% Annual Mortality Rate) 1. Severe resting left
ventricular dysfunction (LVEF < 0.35) 2. High-risk treadmill
score (score -11) 3. Severe exercise left ventricular dysfunction
(exercise LVEF < 0.35) 4. Stress-induced large perfusion defect
(particularly if anterior) 5. Stress-induced multiple perfusion
defects of moderate size 6. Large, fixed perfusion defect with LV
dilation or increased lung uptake (thallium-201) 7. Stress-induced
moderate perfusion defect with LV dilation or increased lung uptake
(thallium-201) 8. Echocardiographic wall motion abnormality
(involving more than two segments) developing at low dose of
dobutamine (10 g/kg/min) or at a low heart rate (
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Intermediate Risk (1-3% Annual Mortality Rate) 1. Mild/moderate
resting left ventricular dysfunction (LVEF = 0.35-0.49) 2.
Intermediate-risk treadmill score (-11 < score < 5) 3.
Stress-induced moderate perfusion defect without LV dilation or
increased lung intake (thalium-201) 4. Limited stress
echocardiographic ischemia with a wall motion abnormality only at
higher doses of dobutamine involving two segments or less
Low Risk (
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Coronary ArteriographyCardiac catheterization is currently the
gold standard for determining the presence of obstructive coronary
artery disease.
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Treatment
Once a cardiac catheterization has been performed, the three
most common therapeutic options are medical therapy, percutaneous
coronary intervention (PCI), coronary artery bypass grafting
(CABG).
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Lifestyle ModificationSmoking. Exercise. at least 30 minutes of
exercise 3 or 4 days/week; Weight Control
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Pharmacologic Therapy
Antiplatelet Agents Aspirin is the mainstay of antiplatelet
therapy Aspirin inhibits both cyclooxygenase and the synthesis of
thromboxane A2.
Clopidogrel (Plavix), a thienopyridine derivative, blocks
adenosine diphosphateinduced platelet activation. Clopidogrel is
indicated as an alternative for patients who cannot take
aspirin.
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Antianginal Agents
Beta blockers, calcium channel blockers, and nitrates are the
mainstays of antianginal therapy.
Beta blockers are recommended as first-line therapy for the
management of stable angina
Beta blockade reduces myocardial O2 requirements, primarily by
slowing the heart rate; the slower heart rate in turn increases the
fraction of the cardiac cycle occupied by diastole, with a
corresponding increase in the time available for coronary
perfusion.
Two major subtypes of beta receptors, designated beta1 and
beta2. Beta1 receptors predominate in the heart, and stimulation of
these receptors leads to an increase in heart rate,
atrioventricular (AV) conduction, and contractility, release of
renin from juxtaglomerular cells in the kidneys, and lipolysis in
adipocytes. Beta2 stimulation causes bronchodilation, vasodilation,
and glycogenolysis. Nonselective beta-blocking drugs (e.g.,
propranolol, nadolol, penbutolol, pindolol, sotalol, timolol,
carteolol) block both beta1 and beta2 receptors.cardioselective
beta blockers (e.g., acebutolol, atenolol, betaxolol, bisoprolol,
esmolol, metoprolol) block beta1 receptors while having less effect
on beta2 receptors. Thus, cardioselective beta blockers reduce
myocardial O2 requirements while tending not to block
bronchodilation, vasodilation, or glycogenolysis
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Calcium Antagonists
Inhibit calcium ion movement through slow channels in cardiac
and smooth muscle membranes by noncompetitive blockade of
voltage-sensitive L-type calcium channels.Three major classes of
calcium antagonists are the dihydropyridines (nifedipine is the
prototype), the phenylalkylamines (verapamil is the prototype), and
the modified benzothiazepines (diltiazem is the prototype)
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Nitratesrelax vascular smooth muscle. The vasodilator effects of
nitrates are evident in systemic (including coronary) arteries and
veins, predominant in the venous circulationANTITHROMBOTIC
EFFECTS.
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Mechanism of action of nitratesEvidence exists that
biotransformation of mononitrates occurs through the action of
mitochondrial aldehyde reductase, producing nitric oxide (NO). NO
activates soluble guanylyl cyclase, resulting in increased
production of cyclic guanosine monophosphate (cGMP). The second
messenger cGMP reduces cytoplasmic calcium (Ca2+) by inhibiting
inflow and stimulating mitochondrial uptake of calcium, thus
mediating the relaxation of smooth muscle cells and causing
vasodilation. Isosorbide dinitrate is metabolized by the liver,
whereas the liver is bypassed by mononitrates. GTP = guanosine
triphosphate. R-ONO2 = mononitrate.
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Risk Factor ManagementHypertension Hyperlipidemia Diabetes
Mellitus
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Surgical ManagementRevascularizationPercutaneous coronary
intervention and coronary artery bypass grafting surgery.The most
common PCI techniques are percutaneous transluminal coronary
angioplasty and coronary stenting. A major limitation of PCI is
restenosis at the intervention site.The most common conduits for
CABG are the saphenous vein and the internal thoracic (mammary)
artery.
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