ST-Elevation Myocardial Infraction

Ruaa JazzariJihan Azar Mohammad abu AwadAbdallah Al.Kharouf

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)

• 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 .

ST-segment elevation MI

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

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

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

• 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

• 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.

• 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

• Constitutional risk factors in IHD:- Age- Gender- Genetics

• Modifiable risk factors in IHD:- Hyperlipidemia- Hypertension- Cigarette smoking- Diabetes mellitus

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

• 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

• 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)

Etiology/Pathophysiology Regulation of coronary blood flow

• Coronary blood flow: inversely related to arteriolar resistancedirectly 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

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+

Complication of MI

• Cardiogenic shock • HF• Valvular dysfunction• Arrhythmias• Pericarditis • Stroke secondary to LV thrombus embolization • Venous thromboembolism • LV free-wall rupture

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 .

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 .

ST-Segment depression Myocardial infarction

T-Wave inversion Myocardial infarction

• 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 99th percintile of the upper reference limits and at least on of the following :

• 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

• 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).