ARTEROSCLEROSIS

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ARTEROSCLEROSIS

The normal artery consists of three


distinctive layers
• The intima,
• the innermost layer comprising a single layer of
endothelial cells on the luminal surface
• The media, a tube of vascular smooth muscle cells
(VSMCs) and their extracellular matrix shown in this
slide
• The adventitia, the outer protective layer comprising
loose connective tissue containing blood vessels and
nerves which supply the artery itself.1,2
• The endothelial cells of the intima have a number of
important functions; forming a non-thrombotic, non-adherent
surface, acting as a semi-permeable membrane, synthesising
and releasing chemical mediators, maintaining the basement
membrane, and modifying lipoproteins as they cross into the
artery wall.
• The VSMCs of the media contract and relax to alter the lumen
diameter of the vessel in response to a variety of circulating
and local stimuli, regulating vascular tone, blood flow and
blood pressure. This is effected through the production of a
number of vasoactive substances including prostaglandins,
endothelin and nitric oxide (NO).
NORMAL ARTERIAL WALL
Pathogenesis of Atherosclerotic Plaques

Endothelial damage

Protective response results in production of


cellular adhesion molecules

Monocytes and T lymphocytes attach to


‘sticky’ surface of endothelial cells

Migrate through arterial wall to subendothelial space

Macrophages take up oxidised LDL-C

Lipid-rich foam cells

Fatty streak and plaque


Risk Factors Associated with Impaired
Endothelium Dependent Vasodilatation
• Dyslipidaemia
• Hypertension
• Diabetes Mellitus
• Cigarette Smoking
• Aging
• Menopause
• Family History of premature CAD/1st degree rel

• Risk factors cause endothelial damage and do so rapidly


Less Reliable but Probable Risk
Factors
• Physical inactivity
• Excess alcohol ingestion
• Insufficient fruits and vegetables in the diet
• Emotional stress
• Elevated cardiac CT scan calcium scores
• Positron emission tomography (PET) scanning
Types of Atherosclerotic Plaque
• Fatty streak
• Fibrous plaque
• Complex (Complicated) plaque
• Ulcerative lesions
• Intraplaque haemorrhage
Stable vrs Vulnerable Plaques

• Vulnerable plaques are characterised by thin fibrous caps, a core


rich in lipid and macrophages, and less evidence of smooth muscle
proliferation. In contrast, the stable plaque has a relatively thick
fibrous cap protecting the lipid core from the contact with blood.

• Vulnerable plaques are prone to rupture and ulceration, followed


by rapid development of thrombi. The size of the plaque does not
appear to predict whether a plaque is prone to rupture, indeed
clinical data suggest that stable plaques more often show luminal
narrowing detectable by angiography than do vulnerable plaques.
At sites of lesion disruption, smooth muscle cells (SMCs) are often
‘activated’, as detected by their expression of the transplantation
antigen HLA-DR.
Stable vrs Vulnerable Plaques

• Rupture usually occurs at sites of thinning (particularly


at the shoulder area of the plaque) and is associated
with regions where there are relatively few SMCs but
abundant macrophages and T cells. Rupture is
associated with greater influx and activation of
macrophages, accompanied by release of matrix
metalloproteinases that are involved with the
breakdown of collagen.1
The Vulnerable Atherosclerotic Plaque

SMC – smooth muscle cell


HDL-DR – transplantation antigen indicating ‘activation’ of SMCs Libby P. Circulation 1995;91:2844-2850.
ACUTE CORONARY SYNDROME (ACS)
• Acute coronary syndrome is made up of
• Myocardial infarction (STEMI OR NSTEMI)
• Unstable angina
DIAGNOSING ACS
• The diagnosis of ACS depends upon
• The characteristics of the chest pain (if present) and the specific
associated symptoms
• Abnormalities on electrocardiogram (ECG) and
• Levels of serum markers of cardiac injury.
WHEN TO SUSPECT ACS
• Clinicians should consider the possibility of ACS in any adult who
presents to the emergency department complaining of chest
discomfort or dyspnea.
• A personal or family history of ACS or
• other cardiovascular disease, older age, diabetes, dyslipidemia,
cigarette smoking, hypertension, or
• cocaine use all increase the likelihood.
WHEN TO SUSPECT ACS
• Pain from coronary-related ischemia is more often characterized as
non-focal chest discomfort or pressure rather than pain, is generally
gradual in onset, and is exacerbated by activity
• Discomfort that radiates, particularly to either or both arms, should
increase suspicion for ACS.
WHO Criteria for Acute MI
• STEMI
• Chest pain or classic symptoms ≥30min
• ST ↑of .1mV in 2 contiguous leads or new LBBB
• ↑Cardiac enzyme levels
• NSTEMI
• Chest pain or classic symptoms ≥30min
• ST ↓ or T inv
• ↑Cardiac enzyme levels
ECG
• Usually, the ST segment (between the S wave and T wave) is
isoelectric, i.e. there is no deviation from baseline. This segment
should be at the same level as the other isoelectric parts of the ECG,
such as the segment between the T and P waves
• An elevated ST segment could be a normal variant (e.g. “high take
off”)
• ST-Elevated Myocardial Infarction (STEMI) should be considered a
medical emergency
• A normal ECG (without ST elevation) does not exclude the possibility
of myocardial infarction.
ECG
Important definitions
• Angina: Discomfort in the chest with or without radiation to the arms,
neck or back which is caused by myocardial ischemia and can se
associated with a disturbance of myocardial function but not with
necrosis
• Ischemia: Recurrent chest discomfort considered to be probable or
definite angina that is at least 10min in duration
Unstable Angina
• Sudden acceleration in the severity of previously stable angina, rest
angina or post-MI angina
• Pathologically characterized by incomplete or transient coronary
artery occlusion
• Initial thrombus platelet-derived with vaso-constrictive response
UA Definition
• Angina pectoris or equivalent ischaemic discomfort with at least one
of 3 features
• It occurs at rest or with minimal exertion usually lasting >10 min
• It is severe and of new onset (i.e. within the prior 4-6wk)
• It occurs with a crescendo pattern ( i.e. distinctly more severe, prolonged, or
frequent than previously
Biochemical Markers
Molecular First Duration of Sensiti Specifi
Protein mass (kD) detection detection vity city

Myoglobin 16 1.5–2 h 8–12 h +++ +

CK-MB 83 2–3 h 1–2 d +++ +++

Troponin I 33 3–4 h 7–10 d ++++ ++++

Troponin T 38 3–4 h 7–14 d ++++ ++++

CK 96 4–6 h 2–3 d ++ ++
Cardiac Biomarkers
• Positive Cardiac Markers
• cTnI>0.1, CK-MB>5, CK> 266
• CK, CK-MB every 8h x3d
• cTnI X1 (at least 3h after the onset of chest discomfort)
• CTnI
• cTnI begins to increase 3h after ischaemia, peaks at 14-18h and remains
elevated for 5-7days
• cTnI levels 1.0-1.6: About 1/3 of patients previously diagnosed as unstable
angina because of normal CK-MB levels actually have elevated cTnI levels and
therefore are experiencing a micro MI
APPROACH TO A PATIENT WITH
SUSPECTED ACS
Immediate General Treatment
• O2
• Aspirin 300mg
• Nitroglycerin (0.4mg SL or spray)
• Morphine (if pain not relieved by NTG)

(Memory MONA)
Bed rest
Nursing
• Telemetry Monitoring
• HR every 2h and rhythm every 4h or as patient condition warrants
• O2
• O2 sat every 4h. Delivery via nasal prongs for 2-3h. Continue if low arterial sat (<90%)
• Activity level
• Bedrest with commode privileges for 12 h
• If haemodynamically stable progress activity as tolerated with ambulation to the bathroom, bathing,
and light ambulation
• A patient with an uncomplicated Mi is likely to return to prior activities within 2 weeks
READING ASSIGMENT
• Atrial Fibrillation
• Infective Endocarditis
• Deep Vein Thrombosis

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