Good presentation

1. Arteriosclerosis and
documented vascular risk
Presenters: Dr. Abubakar Ali & Dr. Hanaa Sheikh
Supervisor: Dr. Mohammed Prosper (Cardiologist )

2. Outline
• Introduction
• Types of arteriosclerosis
• Risk factors and etiology
• Pathogenesis
• Clinical features
• Differential diagnosis
• Diagnosis
• Treatment
• References

3. Introduction
• Arteriosclerosis is a group of vascular diseases
that involve the thickening and loss of
elasticity of the walls of arteries.
• Arteriosclerosis (arterio- meaning artery and -
sclerosis meaning hardening).
• It’s a general medical term that refers to your
normally flexible artery walls becoming hard
or stiff.
• Arteriosclerosis is a gradual process that
occurs over many years.

4. Epidemiology
• Prevalence of atherosclerotic cardiovascular disease stratified by low-density-
lipoprotein cholesterol and associated treatment patterns within the nations of
the United Kingdom Prevalence ranged from 6.58% in England to 8.26% in
Northern Ireland (C.L. Morgan et al 2022).
• the overall prevalence of clinical ASCVD among the included Korean adult
patients per 1000 individuals was 98.25 in 2014 and 101.11 in 2015 (Hyungtae
Kim et al 2019)
• Prevalence and risk factors for subclinical atherosclerosis amongst adults living
with HIV in University of Abuja Teaching HospitalOverall prevalence of subclinical
atherosclerosis was 43.32% (62.25% in ART-experienced) (Taiwo Adedokun et al
2023).

5. Types of arteriosclerosis
 There are three major types of arteriosclerosis:
1. Atherosclerosis
2. Arteriolosclerosis
3. Mönckeberg Medial Calcific Sclerosis

6.  Atherosclerosis
• Atherosclerosis is a form of arteriosclerosis in which deposits of fats,
cholesterol, and other substances form on the walls of an artery.
• The accumulation of these deposits, called plaque, causes the blood
vessel to narrow.
• High cholesterol, obesity, smoking, diabetes, and hypertension (high
blood pressure) are all contributing risk factors.
• An atherogenic lipoprotein phenotype has been defined as the
presence of a predominance of small, dense LDL particles,
hypertriglyceridemia, and low plasma HDL cholesterol concentration.

7. • This lipoprotein phenotype, which is strongly linked to obesity, insulin
resistance, hypertension, and abnormalities in postprandial
lipoprotein metabolism, is similar to the so-called metabolic
syndrome in that both are associated with a cluster of atherogenic
and thrombotic risk factors.
• Atherosclerosis is the underlying cause of most cases of myocardial
infarction, ischemic stroke, and peripheral arterial disease.
• It is also a major cause of chronic heart failure and vascular dementia.
• Atherosclerosis, which is a chronic inflammatory response to the
accumulation of lipid in the artery wall, is characterized by clinically
silent intimal plaques that develop in arteries for years and even
decades.

8. • When severe, atherosclerosis can lead to coronary artery disease
(CAD), a major cause of heart attack and stroke.
• Atherosclerosis occurring in the blood vessels of the kidneys can
cause a condition known as renal artery stenosis. Atherosclerosis in
the vessels that carry blood from the heart (particularly those of the
lower limbs) is referred to as peripheral artery disease (PAD).

9. RISK FACTORS
• Aging
• Smoking
• Physical inactivity
• Obesity
• Positive family history
• Diabetes mellitus
• Hypercholesterolemia
• Hypertension
• Estrogen, oral contraceptive pills
• Diet
• Hypothyroidism
• Obstructive liver disease

10. PATHOPHYSIOLOGY
• Endothelial cells of arteries are damaged by HTN, smoking, DM,
hypercholesterolemia
• Damaged endothelial increase permeability of LDL to inter
internal layer of arterial wall
• White blood cells like Monocytes which moves in blood vessels
can be attached by adhesion protein molecule produced by the
damaged endothelial cell and undergo morphological changes
and inter in by diapedesis.
• Then it produce free radicles which in contact by LDL and
becomes oxidized and cause positive feedback of immune cell
which cause to produce more modified LDL molecules.

11. • So macrophage and tunicate internal start to engulf modified LDL
molecules and cause production of form cells and saturated with LDL
particles and in excess amount it cause Form appearance
• Later on Form cells die and release content which are quickly
engulfed by near WBC and the area begin to form a plaque and
covered by endothelial cells
• Plaque accumulates calcium salts over time will harden and called
Atherosclerosis
• When endothelial cells of plaque compromise blood clots will form
on vessel wall and thrombus will form and when it loose it will form
embolus

12. PATHOPHYSIOLOGY

18. Clinical presentation
• It is possible to have arteriosclerosis for many years without
experiencing symptoms.
• Studies have suggested that even asymptomatic peripheral arterial
disease (PAD) is associated with increased CAD mortality.
• Warning signs of a clogged artery are usually felt when arteries are
severely narrowed.
• Symptoms of arteriosclerosis depend on which blood vessel is
occluded
 Coronary Arteries: myocardial infarction and angina
 Cerebral Arteries; stroke

19.  Peripheral Arteries
• Signs and symptoms of peripheral artery disease (PAD) include:
• Leg pain
• Difficulty walking
• Change in leg color
• Coldness in the lower leg or foot
• Poor wound healing
• Aortoiliac disease manifests as pain in the thigh and buttock, whereas
femoropopliteal disease manifests as pain in the calf.
• Erectile dysfunction (ED) has been linked as a potential early indicator
of both CAD and PVD.

20. • Leriche syndrome is a clinical syndrome described by intermittent
claudication, impotence, and significantly decreased or absent
femoral pulses.
• This syndrome indicates chronic peripheral arterial insufficiency due
to narrowing of the distal aorta.
• Advanced PVD may manifest as mottling in a "fishnet pattern" (livedo
reticularis), pulselessness, numbness, or cyanosis.
• Paralysis may follow, and the extremity may become cold; gangrene
eventually may be seen.
• Poorly healing injuries or ulcers in the extremities help provide
evidence of preexisting PVD.

21.  Renal Arteries
• Symptoms of acute renal arterial occlusion of the kidneys include:4
• Back pain, Decreased urine output
• Blood in the urine, Flank or side pain
• Symptoms of high blood pressure such as headache, changes in
vision, and swelling

22.  Intracranial large artery atherosclerosis:
• Atherosclerotic stenosis of the major intracranial arteries, also known
as intracranial atherosclerosis (ICAS) or cerebral atherosclerosis, is an
important cause of ischemic stroke.
• Epidemiology of ICAS in the United States, accounts for approximately
8 to 10 percent of ischemic stroke and may account for 30 to 50% of
ischemic stroke in Asian populations (Mattioni A et al 2014).
• The manifestations of ischemia due to intracranial large artery
atherosclerosis are not specific, as the same stroke syndromes may
arise from other sources of ischemia, including cardiac embolism,
artery-to-artery embolism from extracranial large artery stenosis, and
small vessel disease.

24. Diagnostic Approaches in Atherosclerosis
• Gold standard of diagnosis: angiography
• Electron-beam CT: “coronary calcium score” – assessment for total
plaque burden
• Doppler ultrasound: used to detect renal or carotid lesions,
assessment of intima-media
thickness.
• Intravascular UltraSound (IVUS) unique information on plaque
structure, volume and area
• D dimer, C-reactive protein
• Lipid profile

27. PRINCIPLES OF ANTIATHEROSCLEROTIC
THERAPY
• Current treatment of atherosclerosis aims to control risk factors and
to maintain or restore perfusion in affected arteries.
• To date, firmly established interventions include smoking cessation,
dietary and pharmacologic reduction of LDL cholesterol, and
management of blood pressure.
• Available data also strongly support intervention directed toward
hyperglycemia, hypertriglyceridemia, obesity, and physical inactivity.
• Cholesterol-lowering statins clearly reduce atherosclerotic lesions and
inhibit their progression.

28. • Statins also prevent nitroglycerin-induced endothelial dysfunction and
nitrate tolerance, and they inhibit immune activity and inflammation.
• Aspirin and other inhibitors of platelet aggregation, β-adrenergic
receptor blockers, and angiotensin-converting enzyme inhibitors or
angiotensin II antagonists are also part of the routine secondary
prevention of coronary heart disease.
• Inhibitors of platelet aggregation are widely used for secondary
prevention of atherosclerotic cardiovascular disease.

30.  Mönckeberg Medial Calcific Sclerosis
• Mönckeberg medial calcific sclerosis is a rare condition in which
calcium accumulates in the middle muscular layer of an artery.
• Older age is the major contributing factor given that most people over
65 will experience some level of calcification in blood vessels.
• The exact cause of Mönckeberg medial calcific sclerosis remains
unknown. What scientists do know is that the incidence is higher in
people with diabetes, CKD, lupus, and hypervitaminosis D (toxic levels
of vitamin D)—all of which are associated with calcium imbalance.

31.  Arteriolosclerosis
• Arteriolosclerosis is similar to atherosclerosis except that it occurs in
smaller arteries and arterioles, While atherosclerosis affects medium
or large arteries.
• The risk of arteriolosclerosis is higher in people with uncontrolled
diabetes and hypertension, both of which can inflict significant
damage on smaller blood vessels.
• Aging is also a contributing factor, as is the use of certain drugs
(like calcineurin inhibitors).

32. PERIPHERAL VASCULAR DISEASE
• Is defined as a clinical disorder in which there is a stenosis or occlusion in the blood
vessels of the limbs.
• They are 2 types of peripheral vascular diseases
a. Functional PVD : doesn’t involve defects of blood vessel’s structure,
often related with symptoms of spasm.
b. Organic PVD :It involves structural changes in blood vessels.
Example; inflammation and tissue damage
Arteriosclerosis is a type of organic peripheral vascular disorder

33. PERIPHERAL ARTERY DISEASES
• Is defined as a clinical disorder in which there is a stenosis or occlusion in the
aorta or the arteries of the limbs.
• Atherosclerosis is the leading cause of PAD in patients >40 years old.
• Other causes include thrombosis, embolism, vasculitis, fibromuscular
dysplasia, entrapment, cystic adventitial disease, and trauma.
• The highest prevalence of atherosclerotic PAD occurs in the sixth and seventh
decades of life.

34. CLINICAL EVALUATION
• Fewer than 50% of patients with PAD are symptomatic
• Most patients with peripheral arterial disease have coexistent coronary artery
and cerebrovascular disease
• Slow or impaired gait
• Intermittent claudication (defined as pain, ache, cramp, numbness, or a sense of
fatigue in the muscles) it occurs during exercise and is relieved by rest
• Symptoms are far more common in the lower than in the upper extremities
because of the higher incidence of obstructive lesions in the former region
• Critical limb ischemia may develop

35. CLINICAL EVALUATION
• Rest pain or a feeling of cold or numbness in the foot and toes
• Decreased or absent Pulses distal to the obstruction
• Presence of bruits over the narrowed artery
• Muscle atrophy.
• More severe disease, hair loss, thickened nails, smooth and shiny skin, reduced
skin temperature, and pallor or cyanosis are common physical sign
• Ulcers or gangrene
• Peripheral edema
• Ischemic neuropathy can result in numbness and hyporeflexia

36. INVESTIGATIONS
1. The history and physical examination are
often sufficient to establish the diagnosis of
PAD
2. Ankle: brachial index, or ABI
Values of 1.00–1.40 in normal
individuals.
Values of 0.91–0.99 are considered
“borderline,”
Values of <0.90 are abnormal and
diagnostic of PAD.
Values of >1.40 indicate non
compressible arteries secondary to vascular
calcification.
3. Laboratory test (blood sugar ,RFT, FBC, ESR)
4. Duplex ultrasonography (which combines
B-mode imaging and Doppler flow velocity
waveform analysis)
5. Transcutaneous oximetry, and stress testing
(usually using a treadmill)
6. Magnetic resonance angiography (MRA)
7. Computed tomographic angiography (CTA)
8. Conventional catheter-based angiography

38. INVESTIGATIONS

42. PROGNOSIS
• Approximately one-third to one-half of PAD develop coronary artery
• Patients with PAD have a 15–25% 5-year mortality rate and a two- to six-fold
increased risk of death from coronary heart disease.
• Approximately 75–80% of non-diabetic patients who present with mild to
moderate claudication remain symptomatically stable.
• Measurement of ABI is useful for detecting PAD and identifying persons at risk for
future atherothrombotic events.
• Approximately 1–2% of the group ultimately develops critical limb ischemia each
year
• Approximately 25–30% of patients with critical limb ischemia undergo
amputation within 1 year
• The prognosis is worse in patients who continue to smoke cigarettes or have
diabetes mellitus

44. FIBROMUSCULAR DYSPLASIA
• Is a heterogenous group of non-atherosclerotic, non-inflammatory arterial
changes, causing some degree of vascular stenosis, occlusion, or aneurysm
• Is a hyperplastic disorder that affects medium-sized and small arteries
• It occurs predominantly in females
• Classified in 1. intimal fibroplasia (also classified as focal)
2. medial dysplasia (multifocal).Is most common
It also divided into medial fibroplasia, perimedial fibroplasia,
and medial hyperplasia
3. adventitial hyperplasia

45. • It occurs in fibromuscular layer of arteries (intima) and involve media
and adventitial layers of arterial wall
• It can have beading, narrowing, aneurism and dissection
• The causes is not unknown
• Risk factors a) congenital
b) smoking
c) connective tissue diseases
d) hormones
Fibro muscular dysplasia may affect the :-
Renal arteries (60 to 75%),
Carotid and intracranial arteries (25 to 30%),
Intra-abdominal arteries (9%),
External iliac arteries (5%).

46. Clinical Evaluation
Is usually asymptomatic and when occurs varies by location
• Increased blood pressure
• Headache
• Claudication
• Femoral bruits
• Decreased femoral pulses
• TIA or Stroke

47. INVESTIGATIONS
• Duplex ultrasound
• CTA/MRA
• Catheter-based angiography

48. TREATMENT
• Smoking secession
• Control HTN
• Control DM
• Regular supervise exercise
• Statins therapy
• Antiplatelets
• Baloon angioplasty (PTA)
• Surgery (brain aneurism) depends on size, location, and severity.

49. ACUTE LIMB ISCHEMIA
• It occurs when arterial occlusion results in the sudden cessation of
blood flow to an extremity.
• The severity of ischemia and the viability of the extremity depend on
the location and extent of the occlusion and the presence and
subsequent development of collateral blood vessels.

50. CAUSES
• Embolism (most common sources of arterial emboli are the heart,
aorta, and large arteries)
• Thrombus in situ
• Arterial dissection
• Trauma.

51. CLINICAL FEATURES
• The symptoms of an acute arterial occlusion depend on the
location, duration, and severity of the obstruction
• Often severe pain, paresthesia, numbness, and coldness develop in
the involved extremity within one hour.
• Paralysis may occur with severe and persistent ischemia
• Physical findings include loss of pulses distal to the occlusion,
cyanosis or pallor, mottling, decreased skin temperature, muscle
stiffening, loss of sensation, weakness, and/or absent deep tendon
reflexes.

52. CLASSIFICATION OF ACUTE LIMB ISCHEMIA

53. INVESTIGATIONS
• Doppler assessment of peripheral blood flow
• MRA
• CTA
• Catheter-based arteriography

54. TREATMENT
• Anticoagulation with intravenous heparin to prevent propagation
of the clot and recurrent embolism
• In cases of severe ischemia of recent onset, particularly when
limb viability is jeopardized, immediate intervention to ensure
reperfusion is indicated
• Catheter-directed thrombolysis/thrombectomy
• Surgical thromboembolectomy
• Arterial bypass procedures

55. Are used to restore blood flow to the ischemic extremity promptly,
particularly when a large proximal vessel is occluded
• Intraarterial thrombolytic therapy with recombinant tissue
plasminogen activator, reteplase, or tenecteplase is most effective
when acute arterial occlusion is recent (<2 weeks) and caused by a
thrombus in an atherosclerotic vessel, arterial bypass graft, or
occluded stent.

56. TREATMENT
• Percutaneous mechanical thrombectomy using devices that employ hydrodynamic
forces or rotating baskets to fragment and remove the clot
• Surgical revascularization is preferred when restoration of blood flow must occur
within 24 h to prevent limb loss or when symptoms of occlusion have been
present for >2 weeks.
• Amputation is performed when the limb is not viable, as characterized by loss of
sensation, paralysis, and the absence of Doppler-detected blood flow in both
arteries and veins.
• Long-term anticoagulation is indicated when acute limb ischemia is caused by
cardiac thromboembolism. Emboli resulting from infective endocarditis, the
presence of prosthetic heart valves, or atrial myxoma often require surgical
intervention to remove the cause

57. Critical Limb Ischemia/Amputation
• Critical limb ischemia (CLI) (or chronic limb-threatening ischemia16) is
a severe form of PAD and is usually defined as PAD with rest pain,
nonhealing wounds, or tissue loss.
• A systematic review has reported that the 1-year cumulative
incidence for each of mortality and amputation is ≈20% among
patients with CLI (Abu Dabrh AM et al 2015).

59. REFERENCES
1. Oxford Handbook of Cardiology
2. NMS Medicine 7TH edition
3. UpToDate 2023
4. Kumar and Clacks Clinical Medicine 9th edition
5. Davidsons principle and practice of medicine 22nd edition
6.
Guidelines – EAS European Atherosclerosis Societyhttps://eas-
society.org › publications › guidelines
7. 2019 ACC/AHA Guideline on the Primary Prevention of ...AHA
Journalshttps://www.ahajournals.org › CIR.0000000000000678U