THE BLOOD VESSELSManar hajeer, MD

University of Jordan

Faculty of medicine, pathology department.

Vascular pathology:1- Narrowing or complete obstruction of

vessel lumina, either progressively (e.g., by atherosclerosis) or precipitously (e.g., by thrombosis or embolism).

2- Weakening of vessel walls, causing dilation and/or rupture.

AIMS:

Atherosclerosis. Hypertensive vascular disease. Aneurysms. Aortic dissection.

ATHEROSCLEROSIS

Characterized by intimal lesions called atheromas (atherosclerotic plaques) that protrude into vascular lumina.

Atherosclerotic plaque consists of raised lesion with soft yellow core of cholesterol covered by a firm, white fibrous cap.

COMPLICATIONS OF ATHEROMAS:

1. Obstructs blood flow. 2. weakens the underlying media. 3. Rupture, causing acute catastrophic vessel thrombosis.

EPIDEMIOLOGY :

I. Major constitutional risk factors

A-Age :

Has a dominant influence.

Accumulation of atherosclerotic plaque is a progressive process, but it does not usually become clinically manifest until lesions reach a critical threshold.

Between ages 40 and 60, the incidence of myocardial infarction in men increases fivefold.

B- Gender

- Premenopausal women are relatively protected against atherosclerosis.

- After menopause, the incidence of atherosclerosis-related diseases increases and with greater age eventually exceeds that of men.

C- Genetics

- In some instances it relates to familial clustering of other risk factors , such as hypertension or diabetes.

- Also familial hyperlipidemia , specifically hypercholesteremia.

II. Major modifiable risk factors

1- Hyperlipidemia

The low-density lipoprotein (LDL) cholesterol ("bad cholesterol"); has an essential physiologic role delivering cholesterol to peripheral tissues. In contrast, high-density lipoprotein (HDL, "good cholesterol") mobilizes cholesterol from atheromas and transports it to the liver for excretion in the bile.

Consequently, higher levels of HDL correlate with reduced risk of atherosclerosis.

High dietary intake of cholesterol and saturated fats (present in egg yolks, animal fats, and butter, for example) raises plasma cholesterol levels.

Diets low in cholesterol and/or with higher ratios of polyunsaturated fats lower plasma cholesterol levels.

Omega-3 fatty acids (abundant in fish oils) are beneficial.

(trans)unsaturated fats produced by artificial hydrogenation of polyunsaturated oils (used in baked goods and margarine) adversely affect cholesterol profiles.

Exercise raises HDL levels, whereas obesity and smoking lower it.

2. Hypertension:

Both systolic and diastolic levels are important.o On its own, hypertension can increase the risk of IHD by

approximately 60% in comparison with normotensive populations.

o Left untreated, roughly half of hypertensive patients will die of IHD or congestive heart failure, and another third will die of stroke.

3- Cigarette Smoking: A well-established risk factor in men, and an increase in

the number of women who smoke probably accounts for the increasing incidence and severity of atherosclerosis in women.

Prolonged smoking of one pack daily increases the death from IHD by 200%. Smoking cessation reduces that risk substantially.

4- Diabetes Mellitus:

- The incidence of myocardial infarction is twice as in non-diabetic individuals.

- There is also an increased risk of strokes.

- There is 100 fold increased risk of gangrene of the lower extremities.

PATHOGENESIS

Atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury.

Endothelial Injury and dysfunction:

Endothelial loss by mechanical denudation, hemodynamic forces and other factors results in intimal thickening; and in the presence of high-lipid diets, typical atheromas ensue.

Inflammation :

Inflammatory cells and mediators are involved in the initiation, progression, and the complications of atherosclerotic lesions.

CAUSES OF ENDOTHELIAL INJURY AND DYSFUNCTION

(hypertension, hyperlipidemia, hyperglycemia, smoking, hemodynamic factors).

Lipids: Impair endothelial cell function by increasing local production of reactive oxygen species. Lipoproteins when oxidized accumulate within the intima, and the oxidized LDL is ingested by macrophages.

ATHEROSCLEROTIC PLAQUES

The key processes in atherosclerosis are intimal thickening and lipid accumulation.

Plaques cause intimal thickening and impinge on the lumen of the artery and grossly appear white to yellow .

Atherosclerotic lesions are patchy, involve only a portion of the arterial wall ; in early lesions.

DISTRIBUTION OF PLAQUES

In humans, the abdominal aorta is typically much more frequently involved than the thoracic aorta.

In descending order, the most extensively involved vessels are the lower abdominal aorta, the coronary arteries, the popliteal arteries, the internal carotid arteries, and the vessels of the circle of Willis.

Vessels of the upper extremities are usually spared, as are the mesenteric and renal arteries except at their ostia.

COMPLICATIONS OF ATHEROSCLEROSIS

1.Rupture, ulceration or erosion of atheromatous plaques induce thrombus formation and such thrombi can partially or completely occlude the lumen and lead to ischemia .

2.Atheroembolism.

3.Aneurysm formation.

SYMPTOMATIC ATHEROSCLEROTIC DISEASE

a. Coronary arteries causing , Myocardial infarction (heart attack),

b. Cerebral vessels causing cerebral infarction (stroke),

c. Lower extremities: peripheral vascular disease (gangrene of the legs)

d. Aortic aneurysms,

PRIMARY PREVENTION PROGRAMS

Aims:

a. Delaying atheroma formation.

b. Encouraging regression of established lesions in persons who have not yet suffered a serious complication of atherosclerosis.

PRIMARY PROGRAMS INCLUDE:

a. Cessation of cigarette smoking.

b. Control of hypertension.

c. Weight loss, exercise.

d. Lowering LDL blood cholesterol levels while increasing HDL ( by diet or statins).

SECONDARY PREVENTION PROGRAMS

Are to prevent recurrence of events such as myocardial infarction or stroke in symptomatic patients and involves:

a. The use of aspirin (anti-platelet agent),

b. Statins,

c. Beta blockers (to limit cardiac demand),

d. Surgical interventions (e.g., coronary artery bypass surgery, carotid endarterectomy).

- These can successfully reduce recurrent myocardial or cerebral events.

HYPERTENSION

Elevated blood pressure is called hypertension, it is one of the major risk factors for atherosclerosis.

Pathogenesis of Hypertension

1- 90% to 95% of hypertension is idiopathic (essential) which is compatible with long life, unless a myocardial infarction, or stroke supervenes.

2. Secondary hypertension (5%):

a. Renal diseases.

b. Narrowing of the renal artery by atheroma (renovascular hypertension).

c. Endocrine causes: diseases of the adrenal glands, such as primary aldosteronism, Cushing syndrome or, pheochromocytoma.

MALIGNANT HYPERTENSION

A rapidly rising blood pressure (>200\120 mmHg) that if untreated leads to death within 1 or 2 years.

Complicates 5% of hypertension cases. The clinical syndrome is characterized by:

1. Severe hypertension (diastolic pressure over 120mmHg),

2. Renal failure.

3. Retinal hemorrhages with or without papilledema

1. ESSENTIAL HYPERTENSION

- Alterations in renal sodium homeostasis and/or vessel wall tone underlie essential hypertension.

- Both increased blood volume and increased peripheral resistance contribute to the increased pressure.

- Results from an interplay of genetic and environmental factors (stress, obesity, smoking, physical inactivity, and heavy consumption of salt) affecting cardiac output and/or peripheral resistance.

VASCULAR PATHOLOGY IN HYPERTENSION

a- It accelerates atherogenesis.

b- It induces degenerative changes in the walls of arteries that potentiate aortic dissection and hemorrhagic stroke .

c. It is associated with small vessel disease: Hyaline arteriolosclerosis and hyperplastic arteriolosclerosis.

1. HYALINE ARTERIOLOSCLEROSIS

Consists of pink hyaline thickening of the walls of arterioles with narrowing of the lumen.

Is seen frequently in elderly patients, whether normotensive or hypertensive, but more generalized and severe in patients with hypertension.

Also common in diabetics.

2. HYPERPLASTIC ARTERIOLOSCLEROSIS.

- Related to more acute or severe elevations of blood pressure

- It is characteristic of (but not limited to) malignant hypertension.

- Associated with acute cerebral and/or renal injury.

- It is associated with onion-skin thickening of arterioles with luminal narrowing.

ANEURYSM

Is a localized abnormal dilation of a blood vessel or the heart, and its types:

1.True aneurysm:

- It involves all three layers of the arterial wall (intima, media, and adventitia) (Examples: :Atherosclerotic, syphilitic or the attenuated wall of the heart “ventricular aneurysms”)

2. False aneurysm ( pseudoaneurysm)

- Is a breach in the vascular wall leading to an extravascular hematoma that communicates with the intravascular space ("pulsating hematoma").

- Example: Ventricular ruptures after myocardial infarctions that are contained by a pericardial adhesion .

Both true and false aneurysms can rupture, often with catastrophic consequences.

Causes of aneurysms:

1. The main cause of aortic aneurysms is atherosclerosis.

2. Vasculitis .

3. Mycotic aneurysm: Infection of a major artery that weakens its wall, can originate from:

a. Embolization of a septic thrombus, as a complication of infective endocarditis.

b. Extension of an adjacent suppurative process.

ABDOMINAL AORTIC ANEURYSM (AAA)

- Atherosclerosis, is the most common cause of aneurysms.

- Atherosclerotic plaques compress the underlying media and also compromise nutrient and waste diffusion from the vascular lumen into the arterial wall.

- The media consequently undergoes degeneration and necrosis, thus allowing the dilation of the vessel.

Atherosclerotic aneurysms occur most frequently in the abdominal aorta (often abbreviated AAA), but the common iliac arteries, the aortic arch, and descending parts of the thoracic aorta can also be involved.

THE CLINICAL CONSEQUENCES OF AAA :

1. Rupture into the peritoneal cavity with massive fatal hemorrhage.

2. Obstruction of a vessel resulting in ischemic injury- renal (kidney infarction), mesenteric (GI tract infarction).

3. Embolism from atheroma or thrombus.4. Compression of a ureter .5. An abdominal mass (often palpably pulsating) that

simulates a tumor .

The risk of rupture is related to the size of the aneurysm, varying from nil for AAAs of 4cm or less to 25% per year for aneurysms larger than 6 cm.

- Aneurysms of 5 cm or more are managed aggressively, usually by surgery.

AORTIC DISSECTION

- Is a catastrophic event ,whereby blood split apart the laminar planes of the tunica media to form a blood-filled channel within the aortic wall.

- This channel often ruptures through the adventitia and into various spaces where it causes either:

1. Massive hemorrhage.2. Cardiac tamponade (haemorrhage into the pericardial

sac).

CAUSES:

1. Men aged 40 to 60 years with hypertension (more than

90% of cases)2. Younger patients with systemic or localized

abnormalities of connective tissue affecting the aorta (e.g., Marfan syndrome)

3. Iatrogenic, complicating arterial diagnostic catheterization.

4. Rarely, dissection of the aorta or other branches, including the coronary arteries, occurs during or after pregnancy.

Dissection is unusual in the presence of atherosclerosis or other causes of medial scarring, such as syphilis, because the medial fibrosis inhibits propagation of the dissecting hematoma.

Regardless of the underlying etiology that causes medial weakness, the trigger for the intimal tear and initial intramural aortic hemorrhage is not known in most cases.

Nevertheless, once the tear has occurred, blood flow under systemic pressure dissects through the media, augmenting progression of the medial hematoma.

Accordingly, aggressive pressure-reducing therapy may be effective in limiting an evolving dissection.