myocardial infarction report

7/31/2019 Myocardial Infarction Report

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Report Outline


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Etymology

Myocardium heart muscle

Infarction tissue death dueto Oxygen starvation(ischemia)


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Incidence Rate

WHO (2010):

Leading cause of NCDdeaths in 2008 were CVD

Approximately 17 milliondeaths or 48% of all NCDdeaths


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Incidence Rate

DOH (2010):

Diseases of the heart ranked1st in the list of diseases

that cause death (NCD and CD)

Approximately 63,000 death or

24% of all NCD and CD death


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Precipitating Factors

Age

Family History Sex : Male


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Predisposing Factors

Hypertension

High levels of LDL and lowlevels of HDL

Smoking

High in saturated fat diet


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S/Sx

Sweating

Varying degree of chest pain radiates to the jaw, neck, leftarm, back and epigastrum;

lasts 20 minutes Anxiety


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S/Sx

Fainting

Light-headedness

Shortness of breath (Dyspnea)

*Approx. of all MI patients

experience warning symptoms likeAngina Pectoris prior to infarction


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Summary of Mechanisms Involved in the Causation

of Myocardial InfarctionDevelopment of atherosclerosis

(usually polygenic)

Plaque rupture

Formation of large thrombus in a coronary

artery


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Diagram :

1. occlussion of a branch of the left coronary artery

2. myocardial infarction resulting from #1 at the anterior wall of the heart


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of Myocardial InfarctionDeprivation of blood supply (ischemia) to an

area of the myocardium

Shift to anaerobic glycolysis decreased

synthesis of ATP, depletion of adenine

nucleotide pool

Increase of NADH due to inactive terminal

electron transport chain: due to lack of oxygen


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of Myocardial InfarctionAccumulation of lactic acid and other

metabolites in myocardial muscle, causing

increased cellular osmolarity and altered

membrane permeability

Decrease in Ph in heart muscle cells

Increasingly inefficient contraction of heart

muscle


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of Myocardial InfarctionCessation of contraction

Activation of membrane phospholipases,degradation of proteins by proteases, influx of

Ca nucleotide pool

Death of affected area of heart muscle


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Management:

Treatment with Drugs

Vasodilator gives immediate

relief from pain

Beta-blockers decreases the

need of heart for extra metabolicOxygen during stressful condition


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Surgical Treatment

Aortic-Coronary Bypass divert

or shunt the flow of blood


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Coronary Angioplastyreconstruction of damaged

blood vessels

Surgical Treatment


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Lecture Objectives

Discuss significant enzymes inMyocardial Infarction.

Enumerate and differentiatesignificant Isoenzymes.

Discuss other protein cardiacmarkers.


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What are the significant

enzymes in diagnosis of MI?

Lactate dehydrogenase (LDH)

Creatine Kinase (CK)


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Cytoplasmic enzyme

Tetramer of 2 subunitsH (for heart) and M (for muscle)

Produce 5 isoenzyme


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Isoenzyme

HHHH (LDH-1) heart and RBC

17-27% of the normal serum total.

HHHM (LDH-2) heart, RBC, renal cortex


HHMM (LDH-3) variety of organs18-25% of the normal serum total.


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HMMM (LDH-4)variety of organs


MMMM (LDH-5)liver and skeletalmuscle



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Lactate dehydrogenase

Flipped LD ratio

LDH 1 > LDH 2

rise within 12-24 hours

peaks within 48-72 hours

remains elevated for 10-14 days.


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Creatine Kinase

transfer of energy in musclemetabolism

comprised of two subunits

the B (brain) and the M (muscle)

resulting the 3 CK isoenzyme.


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CK-BB (CK-1) brain , smooth muscles

CK-MB (CK-2)35% in cardiac muscle

CK-MM (CK-3) muscles, normalserum.


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Creatine kinase

rise within 4-6 hours

peak at 24 hours return to baseline by 48-72

hours


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Enzyme Rise Peak Decline

LDH 12-24 hours 48-72 hours 10 -14 days

CK 4-6 hours 24 hours 48-72 hours


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Other significant protein in diagnosingMyocardial Infarction


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Troponin

marker of all heart muscle damage

Not present in normal serum

Regulatory complex of 3 protein

TnT (tropomyosin binding complex)

TnI (Inhibitory subunit binds to actin)

TnC (Calcium binding subunit)


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Troponin T

Early and late diagnosis of AMI

Rise within a few hours

Peak by day 2

Elevated beyond 7 days


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Troponin I

Only found in the myocardium

Specific for cardiac disease

Rise within 4-6 hours

Peaks at 12-18 hours

Elevated until 7 days


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Myoglobin

Heme-containing protein

Related to muscle mass and activity

Lack specificity to myocardium

Cleared by renal filtration


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Myoglobin

2-3 hours following onset of MI,

peaks about 6 hours

returns to baseline after 24 hours


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Therapeutic Enzymes

Outline:Enzymes that have therapeutic

value to MI.

What other drugs can be used for MI?

Reperfusion Injury and its relevance tothrombolytic therapy


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Therapeutic Enzymes

Thrombolytics: also known asplasminogen activators or fibrinolytic

drugs

Streptokinase

UrokinaseTissue PlasminogenAcivator


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Thrombolytics:

Streptokinase

- Protein secreted by several species ofstreptococci-onset is immediate; long-acting(duration is about 12 hours, but canbe as long as 24 hours)


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Thrombolytics:

Urokinase

-Produced in renal parenchymal cells- almost same function as

streptokinase- onset is same with streptokinase


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Thrombolytics:

Tissue Plasminogen Activator (TPA)

- Synthesized in the endothelial cells- most commonly used thrombolytic

- tPA (Alteplase): onset is immediate;effects may linger up to 4 hoursafter infusion


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Thrombolytics:


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Thrombolytics:

Important To Note:

- efficiency depends on the ageof the clot

- administration of any anticoagulant or

antiplatelet drugs is contraindicatedwithin 24-48 hours


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- thrombolytics administration iscontraindicated to known surgerywithin 10 days, or any known case

of internal bleeding

Other anti thrombotic


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Other anti-thromboticdrugs:

Anti-platelet drugs

Anticoagulant drugs


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Anti-platelet drugs:

Aspirin

-Inhibits platelet cyclooxygenase

- Side Effects: GI side effect (ulceration),

risk for bleeding


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A i l l d


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ADP-receptor antagonist:-Prevents ADP from attaching to receptor;platelet clumping

-Ticlopidine, Clopidogrel- may cause thrombocytopenia & neutropenia(Ticlopidine)


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ADP-receptorantagonist

A i l l d


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Glycoprotein IIb/IIIa receptor inhibitor:

-Prevent cross-linking of platelets- used by specialists; not used in anoutpatient setting

- may cause major bleeding, thrombocytopenia-Abciximap

A i l l dGlycoprotein IIb/IIIa receptor inhibitor:


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Anti-platelet drugs:y p / p


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- Sites of platelet

inhibitors

TXA2 Inhibitors X

A ti l t D


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Anticoagulant Drugs:

- Used as blood thinner

Intravenous Heparin Oral Anticoagulant (Warfarin)

R f i I j


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Reperfusion Injury

Refers to myocardial, vascular or

electrophysiological dysfunction

factors that contribute to reperfusion injury:- damage to cellular and organelle

membranes, including mitocondria- myocyte hypercontracture


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- free radical formation

- leukocyte aggregation andinflammatory mediators

- endothelium damage

R f i I j


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Reperfusion Injury:

Clinical manifestations:

- Arrhythmias

- microvascular dysfunction(No reflow phenomenon)

- myocyte death

R f i I j


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Reperfusion Injury:

Potential Therapies:

- No clear solutions yet; management- combination of techniques for rapid

reperfusion, use of antioxidants,neutrophil inhibitors

myocardial infarction report

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