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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.

  • 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.

  • 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.

  • Diagnosis

    Patient historyComplete physical examination ElectrocardiogramLaboratory blood tests, stress testing, and cardiac catheterization may be necessary to obtain further diagnostic insight.

  • 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.

  • 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.

  • Pretest Probability of Coronary Artery Disease (CAD) by Age, Gender, and Symptom Status

  • *High probability, >90%; intermediate, 10%-90%; low,
  • 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.

  • 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

  • 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

  • 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.

  • 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)

  • 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.

  • 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 (

  • 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.

  • 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.

  • 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.

  • 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 (

  • 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 (

  • Coronary ArteriographyCardiac catheterization is currently the gold standard for determining the presence of obstructive coronary artery disease.

  • 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).

  • Lifestyle ModificationSmoking. Exercise. at least 30 minutes of exercise 3 or 4 days/week; Weight Control

  • 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.

  • 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

  • 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)

  • Nitratesrelax vascular smooth muscle. The vasodilator effects of nitrates are evident in systemic (including coronary) arteries and veins, predominant in the venous circulationANTITHROMBOTIC EFFECTS.

  • 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.

  • Risk Factor ManagementHypertension Hyperlipidemia Diabetes Mellitus

  • 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.

  • Terimakasih..


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