Acute coronary syndromes

Transcription

1 Acute coronary syndromes 1

2 Acute coronary syndromes Acute coronary syndromes results primarily from diminished myocardial blood flow secondary to an occlusive or partially occlusive coronary artery thrombus. Acute coronary syndromes are classified according to electrocardiographic changes into acute myocardial infarction (AMI) ( ST elevation and increase troponins), unstable angina (UA) ( non elevation ST and negative troponins) and non- ST elevation myocardial infarction (NSTEMI) ( increase troponins). 2

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4 ACS present with similar symptoms of chest pain which is not, or only partially, relieved by GTN. ACS arises from the rupture of an unstable atheromatous plaque. This exposes the cholesterol-rich plaque in the intima to the blood, initiating platelet activation and eventual thrombus formation. 4

5 Diagnosis of acute myocardial infarction Diagnosis of AMI is based on patient history, symptoms, ECG findings &lab tests. 1- ECG ECG changes include ST segment elevation, followed by T wave inversion and Q waves development. 5

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7 2- Cardiac enzymes studies: When cardiac cell is injured, enzymes are released into the circulation.the standard enzymes used for lab diagnosis of MI are : 7

8 1-Troponins: Troponins are cardiac muscle proteins which are released following myocardial cell damage and are highly sensitive and specific for myocardial infarction. It can appear in the serum within 6 hr. of infarction & stay elevated in the blood for up to 10 days. 8

9 2- Creatine kinase - MB (CK- MB): The CK-MB isoenzyme is the most specific for diagnosis. It can appear in the serum within 6 hr. of infarction & levels return to normal values within 48 hrs. 9

10 The blood is obtained from the patient at least three times, once at admission & two additional times over the next 12 to 24hrs, in order to measure troponin and CK MB. The troponin will be less sensitive to detect new myocardial damage because it would still be elevated. If early reinfarction is suspected, CK MB concentration determination is the preferred diagnostic test. 10

11 3- Lactate dehydrogenase (LDH): Appears hr. after the onset of chest pain & fall to normal in 7 days.the measurement may be helpful in patients who present with a history of chest pain that began several days before admission.in this patient CK already returned to normal before the patient is evaluated. LDH is compromised of 5 isoenzymes,the heart muscle contains LDH1. So a ratio of LDH1 / LDH2 > 1, may be helpful in distinguishing acute MI from other disorder (like liver disease, hemolysis, leukemia, pulmonary embolism & skeletal muscle disease ). 11

12 4- Aspartate transaminase (AST): Other non specific lab changes include increase in AST appears 6-12 hr. & return to normal in 3-5 days. 12

13 Treatment of acute myocardial infarction Treatment goals : 1- To relief of ischemic chest discomfort. 2-To reduce myocardial infarction by limiting the area affected. 3-To prevent coronary artery reocclusion. 4-To prevent complication, which include: CHF, arrhythmia, recurrent ischemia & reinfarction. 13

14 Pain relief Patients with suspected MI should receive sublingual GTN under tongue and oxygen therapy. Because the pain is associated with sympathetic activation, which causes vasoconstriction, increases the workload of the heart and can exacerbated the underlying conditions. If sublingual GTN fails to relieve the chest pain, IV morphine may be administered together with antiemetic such as prochlorperazine or metoclopramide. 14

15 Antiplatelet therapy An aspirin tablet chewed as soon as possible after the infarct and followed by a daily dose for at least 1 month has been shown to reduce mortality and morbidity. Thienopyridine (Clopidogrel), given in addition to aspirin, can further improve coronary artery blood flow. 15

16 Fibrinolytics It is important to open the occluded artery as quickly as possible by administering a thrombolytic agent. Fibrinolytic agents fall into tow categories: o Fibrin specific (alteplase, tenecteplase and retelpase). o fibrin non- specific (streptokinase). 16

17 They can restore blood flow in an occluded artery if administered within about 6 hrs. of the start of an attack. They cause thrombus dissolution within 30 minutes. All fibrinolytics cause haemorrhage, which may present as a stroke or a gastro-intestinal bleeding. These agents are contraindicate in patients with recent stroke, bleeds, pregnancy and surgery. Patients with exposure to streptokinase, or with history of rheumatoid fever should not receive the drug. 17

18 Unfractionted Heparin or low-molecular weight heparin (e.g. enoxaparin and dalteparin) should administered following Fibrin specific agents. Bivalirudin, a direct thrombin inhibitor, reduces reinfarction rates compared to heparin when given with streptokinase. 18

19 β- blockers : If administered early in the acute phase it may to reduce the area of infarction (limit the amount of myocardial damage ). It also decrease O2 demands &cardiac workload. Unless there are a C/I to their use B-blockers should be given to all patient having MI. ACE-Inhibitors : Useful in patients with signs of heart failure, tachycardia or a history of previous infarction. It should be started with 24 hrs. of diagnosis. Initial doses should be low then titrated as quickly as the patient tolerated. 19

20 Calcium channel blockers: Have coronary &peripheral vasodilatory action,that can elevate some of the coronary vasospasm. CCBs also effective as anti-ischemic agents,it improve coronary blood supply & reduce myocardial oxygen demand. 20

21 Complications of MI: 1-Lethal arrhythmia. 2-Congestive heart failure,mainly left ventricular failure,cause pulmonary congestion. 3-Cardiogenic shock. 21

22 Percutaneous coronary intervention PCI involves the passing of a catheter via the femoral or radial artery and aorta into the coronary vasculature under radio-contrast guidance. Inflation of a balloon at the end of the catheter in the area of the atheromatous plaques opens the lumen of the artery. 22

23 For patients undergoing PCI there is a small risk of death, myocardial infarction and longterm restenosis. This is reduced by Insertion of a coronary artery stent and the use of antiplatelet therapy. 23

24 Antiplatelet and anticoagulant therapy The goal of antiplatelet therapy for patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI) is to reduce the risk of ischaemic events without increasing the risk of bleeding. 24

25 Patients undergoing primary PCI should receive aspirin and clopidogrel as early as possible. Heparin is routinely administered during the PCI procedure. Glycoprotein IIb/IIIa receptor antagonists, particularly abciximab, have been shown to reduce mortality if used during the procedure. These are used in combination with heparin, and a lower ACT ( s) is targeted to reduce bleeding complications. 25

26 Bivalirudin, a direct thrombin inhibitor, has demonstrated less bleeding compared to abciximab and may be useful in those at risk of increased bleeding. 26