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Acute Coronary Syndrome PowerPoint Presentation

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Slide 1 - Acute Coronary Syndrome Howard To MD. Taipei Medical University-Municipal Wan-Fang Hospital
Slide 2 - Worldwide Statistics > 4 million patients are admited with unstable angina and actue MI > 900,000 patients undergo PTCA with or without stent Each year:
Slide 3 - Myocardial Ischemia Spectrum of presentation Silent ischemia Exertion-induced angina Unstable angina Acute myocardial infarction
Slide 4 - Cumulative 6-month mortality from ischemic heart disease
Slide 5 - Ischemic Heart Disease evaluation Based on the patient’s History / physical exam electrocardiogram Patients are categorized into 3 groups Non- cardiac chest pain Unstable angina Myocardial infarction
Slide 6 - Acute Coronary Syndrome
Slide 7 - Acute Coronary Syndrome The spectrum of clinical conditions ranging from: Unstable angina Non-Q wave MI Q-wave MI Characterized by the common pathophysiology of a disrupted atheroslerotic plaque
Slide 8 - Angina 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)
Slide 9 - Unstable Angina Likelihood of CAD Previous history of CAD Presence of risk factors Older age ST-T wave ischemic ECG changes
Slide 10 - Unstable Angina precipitating factors Inappropriate tachycardia Anemia,fever,hypoxia,tachyarrhythmias,thyrotoxicosis High afterload Aortic valve stenosis,LVH High preload High cardiac output, chamber dilatation Inotropic state Sympathomimetic drugs,cocaine intoxication
Slide 11 - Unstable Angina prognostic indicators Presence of ST-Twave changes with pain Hemodynamic deterioration Pulmonary edema, new mitral regurgitation 3rd heart sound, hypotension Other predictors Left ventricular dysfunstion extensive CAD, age, comorbid conditions(diabetes mellitus, obstructive pulmonary disease, renal failure, malignancy)
Slide 12 - Unstable Angina Pathogenesis Plaque disruption Acute thrombosis vasoconstriction
Slide 13 - Unstable Angina Pathogenesis Plaque disruption Passive plaque disruption soft plaque with high concentration of cholesteryl esters and a thin fibrous cap Active plaque disruption Macrophage-rich area with enzymes that may degrade and weaken the fibrous cap; predisposing it to rupture
Slide 14 - Unstable Angina Pathogenesis Acute thrombosis Vulnerable plaque Disrupted plaque with ulceration Occurring in 2/3 of unstable patients The exposed lipid-rich core abunant in cholesteryl ester is highly thrombogenic Systemic Hyperconagulables State Distrupted plaque with erosion Occurring in 1/3 of unstable patients
Slide 15 - Unstable Angina Pathogenesis Vasoconstriction The culprit lesion in response to deep arterial damage or plaque disruption Area of dysfuncitonal endothelium near the culprit lesion Platelet-dependent and thrombin-dependent vasoconstriction, mediated by serotonin and thromboxane A2
Slide 16 - Acute Coronary Syndrome Process of resolution Spontaneous thrombolysis Vasoconstricion resolution Presence of collateral circulation Delayed or absence or resolution may lead to non-Q-wave or Q-wave myocardial infarction
Slide 17 - Non-Q-Wave MI clues to diagnosis Prolonged chest pain Associated symptoms from the autonomic nervous system Nausea, vomiting, diaphoresis Persistent ST-segment depression after resolution of chest pain
Slide 18 - Prinzmetal’s Angina clues to diagnosis Transient ST-segment elevation during chest pain Intermittent chest pain Often repetitive Usually at rest Typically in the early morning hours Rapidly relieved by nitroglycerine Syncope (rare), Raynaud’s, migraine
Slide 19 - Unstable Angina Risk Stratification Low risk New-onset exertional angina Minor chest pain during exercise Pain relieved promptly by nitroglycerine Management Can be managed safety as an outpatient (assuming close follow-up and rapid investigation)
Slide 20 - Unstable Angina Risk Stratification intermediate risk Prolonged chest pain Diagnosis of rule-out MI Management Observe in the ER or Chest Pain Unit Monitor clinical status and ECG Obtain cardiac enzyme (troponin T or I) every 8 to 12 hours
Slide 21 - Unstable Angina Risk Stratification High risk Recurrent chest pain ST-segment change Hemodynamic compromise Elevation in cardiac enzyme Management Monitor in the coronary Care Unit
Slide 22 - Risk Stratification by ECG The risk of death or MI at 30 days is stongly related to the ECG at the time of chest pain ST depression 10 % T-wave inversion 5 % No ECG changes 1~2 %
Slide 23 - Unstable Angina Therapeutic Goals Therapeutic Goals Reduce myocardial ischemia Control of symptoms Prevention of MI and death Medical Management Anti-ischemic therapy Anti-thrombotic therapy
Slide 24 - Unstable Angina Medical Therapy Anti-ischemic therapy Nitrates, beta blockers, calcium antagonists Anti-thrombotic therapy Anti-platelet therapy Aspirin, ticlopidine, clopidolgrel, GP IIb/IIIa inhibitors Anti-coagulant therapy Heparin, low molecular weight heparin (LMWH), warfarin, hirudin, hirulog
Slide 25 - Unstable Angina Anti-ischemic Therapy Restrict activities Morphine oxygen nitroglycerine Pain relief, prevent silent ischemia, control hypertension, improve ventricular dysfunction Nitrate free period recommended after the first 24-48 hours
Slide 26 - Unstable Angina Anti-ischemic Therapy Beta-blockers Lowering angina threshold Prevent ischemia and death after MI Particularly useful during high sympathetic tone Calcium antagonists Particularly the rate-limiting agents Nifedipine is not recommended without concomitant ß-blockade
Slide 27 - Unstable Angina Anti-ischemic Therapy Thrombolytics are not indicated “lytic agents may stimulate the thrombogenic process and result in paradoxical aggravation of ischemia and myocardial infarction”
Slide 28 - Platelets in Acute coronary Syndromes Platelets play a key role in ACS Sources of platelet activation(triggers) Thromboxane A² (TXA²) ADP Epinephrine Collagen thrombin
Slide 29 - Unstable Angina Anti-ischemic Therapy Aspirin is the “gold standard” Irreversible inhibition of cyclooxygenase pathway in platelets, blocking formation of thromboxane A², and platelet aggregation In 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 years Bolus dose of 160~325 mg, followed by maintenance dose of 80~160 mg/d
Slide 30 - GP IIb/IIIa Receptor Final Pathway to Platelet Aggregation Platelet activation and aggregation are early events in the development of coronary thrombosis GP IIb/IIIa receptors on activated platelets undergo a conformational change allowing recognition and binding of fibrinogen Fibrinogen”acts like glue”,bridging GP IIb/IIIa recptors on adjacent platelets, leading to platelet aggregation
Slide 31 - GP IIb/IIIa Receptor KVGFFGR There are approcimately 50,000 GP IIb/IIIa receptors on each platelet KVGFFGR is a specific region within GP IIb/IIIa receptor that is thought to be involved in platelet activation
Slide 32 - Incidence of Ischemic Events
Slide 33 - Unstable Angina Anti-Platelet Therapy Thienopyridines Ticlopidine (Ticlid; Roche) Clopidogrel (Plavix; BMS) block platelet aggregation induced by ADP and the transformation of GP IIb/IIIa into its high affinity state
Slide 34 - Unstable Angina Anti-Platelet Therapy Ticlopidine In a open-label, randomized study in patients with unstable angina Ticlopidine 250 mg bid vs. placebo reduced the risk of fatal or nonfatal MI by 46% at 6 months Benefit not seen at 7 days, but became apparent after 10 days of therapy (the time required for full antiplatelet activity) An alternative for patient with asprin intolerance
Slide 35 - Unstable Angina Anti-Platelet Therapy Clopidogrel CAPRIE(Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) 19,000 patients randomly assigned to clopidogrel(75 mg/d) or to Aspirin(325mg/d) There are 8.7% reduction in the combined incidence of stoke, MI, or death(P≑0.043) Patients with MI did better with aspirin Patients with PVD or stroke did better with clopidogrel
Slide 36 - Unstable Angina Anti-Platelet Therapy GP IIb/IIIa inhibitors Abciximab (monocional antibody) Eptigibatide (peptidic inhibitor) Lamifiban and tirofiban (non-peptides) direct occupancy of the GP Iib/Iia receptor by a monoclonal antibody or by synthetic compounds mimicking the RGD sequence for fibrinogen binding prevents platelet aggregation
 

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