Cardiovascular Pathology


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Cardiovascular Pathology

Philip R. Faught, M.D.



  • Simply means hardening (sclerosis) of arteries

  • May affect small arteries/arterioles (arteriolosclerosis)

  • A rare type is fibromuscular dysplasia

  • The big one is atherosclerosis

Clinical Consequences of Arteriosclerosis

  • Ischemia of distal organs/tissues:

    • Myocardial infarct

    • Brain infarct (stroke)

    • Small bowel and kidney infarcts
    • Gangrene of lower extremities

  • Abdominal aortic aneurysm


Ischemia in general is worse than hypoxia. With ischemia, tissues are hypoxic and cellular waste products are not removed. Some degree of adjustment to pure hypoxia is possible, e.g. accommodation to high altitude.

Fibromuscular Dysplasia

  • The Wall Street Journal says many medical schools do not address this!

  • Refers to focal/segmental thickening of the walls of medium to large muscular arteries (usually medial, arteries may have a “string of beads” appearance)

  • Can affect renal, splanchnic, carotid, vertebral arteries

  • F > M, typical age 20 to 50 years

  • Can be asymptomatic or cause hypertension, headaches, dizziness, tinnitus (depending on the artery involved), even with aneurysm formation or rupture or stroke if severe

  • Condition is developmental and familial in some cases

  • Treatment may be antihypertensive and antithrombotic meds or angioplasty if necessary

Notes: The Wall Street Journal, June 27 & 28, 2009, ran a front page story about missed diagnoses of this disorder. Missed diagnoses of rare (or fairly rare) diseases make for great lay press stories (eg. celiac disease). FMD may present with bizarre clinical manifestations depending on what organ/tissue is ischemic, leading to incorrect or non-diagnoses. Robbins, 9th ed. has a paragraph on FMD in the blood vessel chapter and another in the kidney chapter, the latter organ being the one most commonly affected by FMD. Diagnosis is by thinking of it and obtaining imaging studies. A bruit over a large artery in the neck or abdomen may occur (although atherosclerosis is a more common cause of this).


  • This is the most significant type of arteriosclerosis, and is responsible for approximately half of deaths in the Western world

  • It primarily affects the aorta and the larger elastic and muscular arteries (the arteries that have names that you know)

Involved Arteries in Atherosclerosis

  • Aorta, abdominal > thoracic; worse around major ostia

  • Popliteals, internal carotids, Circle of Willis

  • Coronaries

  • Usually spared are the upper extremity arteries, mesenteric & renals except at ostia

  • Pulmonary arteries not involved except with severe pulmonary hypertension; veins not involved

Note: If the ascending thoracic aorta is severely involved, the causes include diabetes mellitus, hyperlipidemia type II, and syphilis.

Basic Lesion: The Atherosclerotic Plaque

  • Start out as small intimal plaques  get larger  more numerous  coalesce

  • Plaques are typically patchy and eccentric

  • Plaques secondarily compress and thin the media

  • Plaques consist of varying amounts of lipid and fibrous tissue

  • Some compensatory dilatation of the vessel may occur (up to a point)


The three principle components of the plaque are:

Cells: Modified smooth muscle cells, macrophages recruited from blood, monocytes, and T lymphocytes

Lipid: Intra- and extracellular. Mostly cholesterol and cholesterol esters

Other extracellular stuff: Collagen and elastin, proteoglycans, calcium

Proportions vary in different plaques. Plaques may be mainly fibrous without much central lipid.

Complicated Atherosclerotic Plaques

  • Calcification – may be extensive

  • Focal rupture or ulceration – may be accompanied by:

    • Hemorrhage into plaque

    • Thrombus formation on plaque

    • Escape of lipid from plaque  cholesterol emboli (atheroemboli)

  • Weakening of media  aneurysm formation


Thrombus may occlude the lumen  infarct, or may cause thromboemboli. Hemorrhage into a plaque may also cause occlusion of lumen & hematoma formation in vessel wall.

The Fatty Streak

  • Yellow, minimally raised intimal lesions seen in children & young adults

  • Microscopically see lipid-laden macrophages in the intima – streaks go away as AS takes over

  • Location of streaks is similar (not identical) to later AS plaques

  • Relationship to later AS is complex and unclear


Both fatty streaks and atherosclerotic plaques are related to increased blood lipids and smoking. Fatty streaks may be seen in populations where atherosclerosis is not prevalent.

Epidemiology of Atherosclerosis

  • Ubiquitous in N. America, Europe, Australia, New Zealand, Russia, other developed nations

  • Much less prevalent in Central & S. America, Africa, Asia

  • Japanese who immigrate to U.S. & adopt U.S. diet & life style acquire U.S. predisposition


Age: Starts in childhood & progresses over decades. Early AS is a common autopsy finding in teens & 20s, but not clinically significant until middle age or later when AS causes symptoms/organ injury.

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