Download ST-Elevation Myocardial Infaraction

ST-Elevation Myocardial
Infraction
Ruaa Jazzari
Jihan Azar
Mohammad abu Awad
Abdallah 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.
Etiology/Pathophysiology
• 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
• 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 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
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
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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).