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Acute Coronary Syndrome ACS

Prof. M. Adel. Definition . (ACS) is a set of signs and symptoms(syndrome) related to a range of acutemyocardial ischaemic states, which include: unstable angina, non-ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI).. Prof. M. Adel. Classification of ACS.

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Acute Coronary Syndrome ACS

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    1. Prof. M. Adel Acute Coronary Syndrome (ACS) Objectives: Definition . Classification Diagnosis Treatment modalities. Clinical implications of drugs used in ACS. Highlight the importance of analgesics (morphine), aspirin, clopidogrel,nitroglycerine, ACE-I, beta-blockers & anticoagulants

    2. Prof. M. Adel Definition (ACS) is a set of signs and symptoms (syndrome) related to a range of acute myocardial ischaemic states, which include: unstable angina, non-ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI).

    3. Prof. M. Adel Classification of ACS

    4. Prof. M. Adel Signs and symptoms Chest pain as tightness around the chest and radiating to the left arm and the left angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well as shortness of breath. In many cases, the sensation is "atypical", with pain experienced in different ways or even being completely absent (which is more likely in female patients and those with diabetes). Some may report palpitations, anxiety or a sense of impending doom and a feeling of being acutely ill.

    5. Prof. M. Adel Diagnosis Electrocardiogram Elevated in the ST segment, new left bundle branch block ? acute heart damage (MI), ? treatment for a heart attack in the form of angioplasty or thrombolysis immediately. In the absence of such changes, it is not possible to immediately distinguish between unstable angina and NSTEMI. Thus troponins are therefore usually tested 6 and 12 hours after the onset of pain.

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    7. Prof. M. Adel NSTE-ACS The treatment of patients is directed to : Alleviate pain and anxiety, Prevent or limit progression to acute myocardial infarction. Prevent recurrences of ischemia.

    8. Prof. M. Adel Treatment includes: Aspirin reduces the risk of complications by more than 50%. Low molecular weight heparin (anoxaparin): is also effective and the combination of heparin and aspirin is more effective than aspirin alone. Clopidogrel treatment within 24 hours has been shown to decrease cardiac death, myocardial infarction or stroke. Combination with low-dose aspirin should be continued for up to 12 months after the most recent acute episode of non-ST segment-elevation ACS and then low-dose aspirin alone is recommended.

    9. Prof. M. Adel Nitrates (sublingual, oral or intravenous): for ongoing pain whilst waiting for more definitive procedures and may overcome superimposed coronary artery spasm. opioids (morphine) if the pain persists. Beta-blockers improve outcome and can reduce the severity and frequency of attacks. Calcium antagonists, e.g. diltiazem, verapamil, are used for patients who cannot tolerate a beta-blocker or in addition to a beta-blocker. Verapamil should not be combined with a beta-blocker.

    10. Prof. M. Adel ACE inhibitor: reduce mortality and should be started as an inpatient unless contraindicated. An insulin sliding scale should be used for patients with diabetes mellitus or a raised blood glucose.

    11. Prof. M. Adel Management of Cocaine associated ACS It should be manged in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early.

    12. Prof. M. Adel Fibrinolytic Drugs (Thrombolytics) Mechanism: they activate the conversion of plasminogen to plasmin, which in turn converts fibrin into soluble products. Plasminogen ? plasmin Fibrin soluble product

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    16. Prof. M. Adel NB: Streptokinase, anistreplase and urokinase are non fibrin-selective i.e. they activate plasminogen in thrombi & circulation. So, they increase the risk of bleeding. Pro-urokinase and altiplase are fibrin-selective i.e. their action is more localized on the plasminogen of the thrombi and less likely to produce bleeding.

    17. Prof. M. Adel A/E: Bleeding. Arrhythmias. Hypotension. Streptokinase may loses its effect or causes allergy if antibodies was formed against it.

    18. Prof. M. Adel Antiplatelet Drugs Aspirin: Aspirin irreversibly inhibit COX (up to the life-time of the platelets 8-10 days). Both PGI2 and TXA2 synthesis are inhibited. Aspirin in small dose 75-100 mg/day inhibits TXA2 synthesis without significant effect on the endothelial PGI2. Toxicity: peptic ulcer bleeding in patients > 60 years.

    19. Prof. M. Adel Clopidogrel It is a thienopyridine derivative. It irreversibly inhibits the P2Y12 purinergic receptor on platelets, thereby blocking ADP-mediated platelet activation. Usually given in combination with aspirin because of their complementary mechanism of action. Toxicity : bleeding, dyspepsia, and rashes.

    20. Prof. M. Adel Low molecular weight heparin (LMWHs) enoxaparin Low molecular weight fractions of heparin. It inhibits activated factor X. It has minimal bleeding tendency and it has a long t 1/2. It is given s.c or i.v once/day. No laboratory monitoring is required.

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    29. Prof. M. Adel Prevention of ACS Primary prevention of atherosclerosis by: Healthy eating. Exercise. Treatment for hypertension and diabetes. Avoiding smoking. Controlling cholesterol levels); in patients with significant risk factors, Aspirin has been shown to reduce the risk of cardiovascular events.

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