Coronary Atherosclerosis

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Coronary Atherosclerosis

• Prepared by
• Walaa Fathi
• Abed Al Fatah Hassan

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Definition

• Is a disease affecting the arterial blood
  vessel, it is commonly referred to as a
  "hardening" or "furring" of the arteries.
• It is caused by the formation of multiple
  plaques within the arteries.
• Basically it is characterized by intimal
  plaques called "atheromas".

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Pathologically

• The atheromatous plaque is divided into three
  distinct components-
• 1.The atheroma- is the nodular accumulation of a
  soft, flaky, yellowish material at the center of
  large plaques, composed of macrophages nearest
  the lumen of the artery.
• 2. The underlying areas of cholesterol crystals,
  and possibly also.
• 3. Calcification at the outer base of older/more
  advanced lesions.

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Pathogenesis

• 1- The development of focal areas of chronic
  endothelial injury, usually subtle, with
  resulting increased endothelial permeably or
  other evidence of endothelial dysfunction.
• 2- Increased insudation of lipoprotein into the
  vessel wall.
• 3- A series of cellular interactions in these
  foci of injury involving ECs, T lymphocyte, SMCs
  of intimal or medial origin.
• 4- Proliferation of smooth muscle cells in the
  intima with formation of extracellular matrix by
  the SMCs.

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The response-to-injury of atherosclerosis

• - illustration or response to injury of
  atherogenesis in these figure .

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• Those pictures considers AS a chronic
  inflammatory response of the vascular wall to a
  variety of initiating events that can occur early
  in life
• Mechanisms contributes in plaque formation-
  Endothelial dysfunction, Monocyte adhesion,
  Lipid
• and infarction, Smooth muscle proliferation,
  Extracellular matrix deposition, accumulation,
• Thrombosis

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The response-to-injury of atherosclerosis

• 1-Endothelial injury-
• Chronic or repeated endothelial injury is the
  cornerstone of the response to the injury
  hypothesis
• A- Homodynamic disturbances - Disturbances
  perfusion to the tissue
• B- Advance effect of hypercholesterolemia,
  perhaps acting in concert

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• Hyperlipidemia contributes to atherogenesis in
  several ways-
• Chronic hyperlipidemia, particularly
  hypercholesterolemia, may itself initiate
  endothelial dysfunction.
• Lipoproteins accumulate within the intima at
  sites of endothelial injury or dysfunction.
• It provides the opportunity for modification
  of lipid in the arterial wall.

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• Oxidized LDL contributes to atherogenesis in the
  following ways-
• It is readily ingest by macrophages through
  the scavenger receptor that is distinct from the
  LDL receptor
• It is chemo tactic for circulating monocyte
• It increases monocyte adhesion

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• It inhibits the motility of macrophages
  already in lesion.
• It stimulates release of growth factors and
  cytokines.
• It is cytotoxic to endothelial and SMCs.
• It is immunogenic.

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2- Complicated plaques

• In advanced disease, plaques frequently undergo
  patchy or massive calcification, and
• arteries may be converted to virtual pipestems
• Fissuring or ulceration of the luminal surface
  with rupture of the plaque may discharge debris
  into the blood stream (cholesterol emboli)
• Fissuring or ulceration of the luminal surface
  with rupture of the plaque may discharge debris
  into the blood stream (cholesterol emboli)

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• Fissured or ulcerated lesion may develop
  superimposed thrombosis
• Hemorrhage into a plaque may result from loss
  of endothelial integrity (early ulceration),
  leading to progressive influx of blood from
  vessel lumen, or the hemorrhage may arise from
  the perplaque capillaries describe, and may lead
  to its rupture

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Superimposed thrombosis
Advanced atherosclerosis of the abdominal aorta
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3- Rupture

• Although the disease process tends to be slowly
  progressive over decades, it usually remains
  asymptomatic until an atheroma obstructs the
  blood stream in the artery
• This is typically by rupture of an atheroma,
  clotting and fibrous organization of the clot
  within the lumen, coverage the rupture but also
  or over time and after repeated

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4- Stenosis

• Stenosis producing ruptures, resulting in a
  persistent
• usually localized stenosis
• It can be slowly progressive, while plaque
  rupture is a sudden event that occurs
  specifically in atheromas with thinner or weaker
  fibrous caps that have become "unstable

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Fibrous plaque
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Fibro fatty atheroma
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Risk factors

• 1- Age - Is a dominant influence, although early
  lesions of atherosclerosis appear in childhood
• 2- Sex - Males are much more prone to
  atherosclerosis than females. Females are more or
  less sheltered from advanced disease-producing
  atherosclerosis until menopause, unless they are
  predispose by diabetes or hyperlipidemia or sever
  hypertension

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• Familial predisposition - There is well-defined
  to AS and IHD.
• Acquired risk factors - Diabetes, smoking
  hyperlipidemia, hypertension.
• Other factors - Insufficient regular physical
  activity, obesity, high carbohydrate intake.

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Signs and symptoms

• Interfering with the coronary circulation
  supplying the heart or cerebral circulation
  supplying the brain causing stroke or heart
  attack.
• Various heart diseases including congestive heart
  failure and most cardiovascular diseases.
• Peripheral artery occlusive disease (PAOD).

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Signs and symptoms related to cardiovascular
disease

• 1- Chest pain(angina pectoris) - It is typically
  substernal radiating to the left shoulder, arm,
  or jaw
• 2- Subtle, progressive fatigue, weakness, and
  dyspnea (these symptoms usually appear on
  exertion)
• 3- Alteration in mental alertness, inability to
  concentrate, sleep disturbance

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• 4- Myocardial infarction (MI) -The SS of MI
  includes the following -
• Chest pain, unrelieved by rest or medication
• Nausea and vomiting
• Dyspnea
• Orthopnea
• Anxiety, severe apprehension
• Denial
• Dysrhythmias
• Weakness

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Diagnostic parameters -

• 1- Laboratory findings-
• A- Lipid profile - Fasting lipid profiles,
  includes total cholesterol, LDL,HDL, and
  triglycerides
• B- Cardiac enzymes - Creatine kinase (cK)
• C- Leukocytes count and sedimentation rate

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• 2- Other diagnostic test
• A- ECG- A 12- leads ECG is performed to
  determined if the patient with ASHD is having MI.
• B- Exercise stress test - this is recording of
  an ECG during exercise .
• Coronary angiography (cardiac catheterization)
  - catheterization of the RL sides of the
  heart and the coronary arteries is performed to
  define suspected lesion of the coronary anatomy
  in terms of percentage of obstruction .

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Treatment

• 1- thrombolytic
• 2- percutanous transluminal coronary angioplasty
  (PTCA)
• 3- intracoronary stent
• 4- Directional coronary atherectomy (DSA)
• 5- Coronary artery bypass grafting (CABG)

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Nursing diagnosis

• 1- pain related to imbalance exist b/w oxygen
  supply and demand
• 2- Potential for decreased myocardial tissue
  perfusion related to imbalance exist b/w O2
  supply and demand , as evidenced by dysrhythmias
  , or heart failure
• 3- Potential for anxiety related to the diagnosis
  of ASHD, treatment, and possibility of death