1. ST-Elevation Myocardial Infraction Ruaa Jazzari Jihan Azar Mohammad abu Awad Abdallah Al.Kharouf

2. Definition Ischemic heart disease (IHD) also known as coronary artery disease, is defined as : reduction in blood supply into the heart in a way it dosent cover its demands ; Total or partial obstruction can lead to ischemia. IHD could be : -Angina -Acute coronary syndromes (ST and Non-ST MI)

3. Acute Coronary syndromes (ACS’s) are classified according to ECG into : -ST segment elevation MI - Non-ST Segment elevation ACS which includes : A.Non-ST MI B. Unstable angina.

4. ST-segment elevation MI

5. Epidemiology Around 81 million American adults: >1 type of cardiovascular disease (CVD) As an estimate, 2,400 Americans die of CVD each day average of 1 death every 33 seconds In 2004, CHD was responsible for 52% of CVD deaths Common initial presentation: women: angina men: myocardial infarction

6. Etiology/Pathophysiology Coronary atherosclerotic plaque formation leads to imbalance between O2supply & demand of myocardial ischemia Important measures in understanding the rationale for the selection and use of pharmacotherapy for IHD: The determinants of myocardial oxygen demand (MVO2) Regulation of coronary blood flow The effects of ischemia on the mechanical and metabolic function of the myocardium Ischemia: lack of O2, decreased or no blood flow in myocardium Anoxia: absence of O2to myocardium

7. The major components of a well-developed intimal atheromatous plaque overlying an intact media.

9. Determinants of myocardial oxygen demand (MVO2) - HR - contractility - intramyocardialwall tension during systole (most important) Determinants of ischemia: - resistance in vessels delivering blood to myocardium - MVO2 Etiology/Pathophysiology

11. The cause of MI in more than 90% of patients is rupture, fissuring or erosion of an unstable atherosclerotic plaque. A clot forms on top of the ruptured plaque. Exposure of collagen and tissue factors induces platelets adhesion and activation. Which promote the releasing of Thrmoboxane A2 and ADP from platelets producing vasoconstriction and platelet activation. A change in the conformation of Glycoprotiens IIB/IIIA surface receptor of platelets occures that cross-links platelets to each other through fibrinogen bridges.

12. Activation of the extrensic coagulation cascade occurs as a result of exposure of blood to the thromogenic lipid core and endotheluim, which are rich in tissue factor. This leads to formation of fibrin clot composed of fibrin strands, cross-linked platelets, and trapped RBC’s. Ventricular Remodeling occurs after MI and is characterized by left ventricular dilationand reduced pumping function, leading to cardiac failure

14. Constitutional risk factors in IHD: - Age - Gender - Genetics Modifiable risk factors in IHD: - Hyperlipidemia - Hypertension - Cigarette smoking - Diabetes mellitus

15. Additional risk factors: - Inflammation - Hyperhomocystinemia - Metabolic syndrome - Lipoprotein (a) levels - Factors affecting hemostasis - Other factors

16. Acute plaque change Plaque rupture is promptly followed by partial or complete vascular thrombosis resulting in acute tissue infarction (e.g., myocardial or cerebral infarction). Plaque changes fall into three general categories: -Rupture/fissuring, exposing highly thrombogenic plaque constituents-Erosion/ulceration, exposing the thrombogenic subendothelial basement membrane to blood-Hemorrhageinto the atheroma, expanding its volume

17. The events that trigger abrupt changes in plaque configuration are complex and include: - Intrinsic factors (e.g., plaque structure and composition) - Extrinsic factors (e.g., blood pressure, platelet reactivity)

19. Etiology/Pathophysiology Regulation of coronary blood flow Coronary blood flow: inversely related to arteriolar resistance directly related to coronary driving pressure Anatomic Factors: EpicardialVs intramyocardial Extent of functional obstruction important limitation of coronary blood flow severe stenosis(> 70%) ischemia & symptoms at rest

20. Metabolic Regulation Changes in O2 balance lead to rapid changes in coronary blood flow a number of mediators may contribute to these changes, the most important ones are: adenosine other nucleotides nitric oxide prostaglandins CO2 H+

21. Complication of MI Cardiogenic shock HF Valvular dysfunction Arrhythmias Pericarditis Stroke secondary to LV thrombus embolization Venous thromboembolism LV free-wall rupture

22. Clinical Presentation Predominant symptom is midline anterior chest discomfort (Usually at rest), sever new onset angina, or increasing angina that lasts for more than 20 min. Discomfort may radiate to the shoulder, down the left arm to the back or to the jaw. Accompanying symptoms may include nausea, vomiting, diaphoresis and shortness of breath No specific features indicate ACS’s on physical examination. However, patients with ACS’s may present with signs of acute HF or arrhythmias.

23. Diagnosis Obtain 12-lead ECG within 10 min of presentation. Key findings indicating myocardial ischemia or MI are ; ST-segment depression, T-wave inversion. Appearance of a new left bundle-branch block with chest discomfort in highly specific for acute MI. Some patients with myocardial ischemia have no ECG changes so biochemical markers and other risk factors for CAD should be assessed.

24. ST-Segment depression Myocardial infarction T-Wave inversion Myocardial infarction

25. Biochemical markers of myocardial cell death are important for confirming diagnosis of acute MI. Diagnosis is confirmed with detection of rise and/or fall of cardiac biomarkers (Cardiac troponin preferred) with at least one value above 99 th percintile of the upper reference limits and at least on of the following :

26. Symptoms of ischemia New significant ST-segment-T-wave changes or new left bundle branch block. Pathological Q-waves Imaging evidence of new loss of viable myocarduim or new regional wall motion abnormality

27. Patient symptoms past medical history, ECG and biomarkers are used to stratify patients into low, medium or high risk of death MI or likelihood of failing pharmacotherapy and needing urgent coronary angiopathy and percutaneous coronary intervention (PCI).