Atherosclerosis and Hypertension

The learning outcomes for this lecture are basically a paragraph, so I'm going to divide this post into talking about atherosclerosis and hypertension separately, and then divide those sections into various different components.

Atherosclerosis

Aetiology and predisposing factors

There are many different predisposing factors for atherosclerosis. Non-modifiable factors include age (older people are more at risk), sex (males are more at risk), and a family history of atherosclerosis. Modifiable risk factors include high lipid levels, high blood pressure, smoking, and uncontrolled diabetes. There may also be many other risk factors other than those that I just listed. Having multiple risk factors can increase your risk of atherosclerosis even further.

Pathogenesis and pathophysiology

In atherosclerosis, artery walls thicken and harden as a result of the formation of atheromas or plaques. The formation of a plaque is also known as atherogenesis. Atherosclerosis is a sub-type of arteriosclerosis, which refers to basically anything that can cause the arteries to harden. (Arteriosclerosis is not to be confused with arteriolosclerosis, which is where arterioles- not arteries- become thickened and hardened. Arteriolosclerosis is generally not the result of atherosclerosis.)

The onset of atherosclerosis can be slow or sudden, and the extent of blockage by the atheroma can be partial or complete. Blockage of the blood vessel reduces the blood supply to the tissues. Formation of atheromas causes the artery wall to weaken and increases the risk of thrombus (clot) formation.

One hypothesis for the formation of atheromas is the response to injury hypothesis. This hypothesis states that damage to the endothelium, as may occur due to high blood pressure, smoking, or some other aetiological factor, may cause the endothelium to become dysfunctional. Over time, lipoproteins can accumulate in the vessel wall. Other changes may happen as well, such as the invasion of monocytes (which turn into macrophages and then into foam cells as they consume lipids), adhesion of platelets, recruitment of smooth muscle cells from the tunica media, and so on.

It is also important to note that atherosclerosis only affects arteries and not veins. However, a vein used a bypass grant can become "arterialised" and develop atheromas. Atheromas are also unlikely to affect arteries that are not under much pressure, such as the pulmonary arteries and upper limb arteries.

Classification scheme

Atherosclerotic lesions can be assigned a class from Type I to Type VI, depending on severity. Type I is the initial lesion and as the lesion progresses, it can move up through to Type VI. Only type IV onwards are considered to be atheromas (though type III is considered an intermediate, or pre-atheroma stage).

Morphological changes and clinical features

A Type II lesion is also known as a fatty streak. Many people can get fatty streaks, even children, but they can regress and do not all progress to the atheroma stage.

A Type V lesion is a fibroatheroma. It is made up of a soft lipid core with a fibrous cap and usually only involves part of the circumference of the wall.

Complications and clinical sequelae

There are many different complications of atheromas. Some atheromas become calcified, increasing the risk of myocardial infarction (heart attack) and death. Atheromas may also release atheroemboli (basically pellets of cholesterol) that may go on to occlude smaller downstream vessels. Another complication is that they might rupture, resulting in formation of a thrombus that may embolise and occlude a downstream artery. Bleeding may also occur into the atheroma, causing the atheroma to expand and block the artery. Finally, atheromas may lead to formation of an aneurysm as the artery wall has weakened.

Atherosclerosis has consequences in many organs in the body. In the heart, atherosclerosis can lead to angina, myocardial infarction, and even sudden death. In the brain, atherosclerosis can lead to transient ischaemic attacks (TIAs) and stroke. In the peripheral arteries, atherosclerosis can lead to pain, ulcers that won't go away, and gangrene. Depending on which arteries are blocked, it may also have other consequences such as impotence. Atherosclerosis, as mentioned before, can also cause aneurysms, particularly in the abdominal aorta.

Systemic hypertension

Aetiology and predisposing factors

Most cases of hypertension are idiopathic, meaning that we don't know what caused the hypertension. However, hypertension can also be a result of a problem elsewhere in the body, such as an endocrine disorder or renal failure. Hypertension may also be due to pregnancy or certain medications.

Pathogenesis and pathophysiology

Some patients with hypertension may develop hypertensive emergency, in which there is a severe rise in blood pressure. The high blood pressure can damage organs, particularly those with small vessels, such as the kidneys and retina.

Classification scheme

Hypertension can lead to arteriolosclerosis (hardening and thickening of arterioles). There are two main types of arteriolosclerosis: hyaline arteriolosclerosis and hyperplastic arteriolosclerosis.

Morphological changes and clinical features

In hyaline arteriolosclerosis, the tunica media is thickened because the high pressure causes eosinophilic hyaline material to leak into the arteriolar wall. There may also be smooth muscle hypertrophy and fibrosis. The lumen of the arterioles is narrowed, resulting in ischaemia (reduced blood flow) to organs.

Hyperplastic arteriolosclerosis pretty much only happens in severe hypertension. It is a proliferation of smooth muscle cells that looks like an onion skin under the microscope. In hyperplastic arteriolosclerosis, the lumen is severely narrowed.

Complications and clinical sequelae

The complications of hypertension and the resulting arteriolosclerosis are similar to that of atherosclerosis: less blood reaches organs, causing ischaemia and damage to those organs. Also, since the blood pressure is higher, the heart has to pump harder, resulting in hypertrophy of the heart. This might sound good, but eventually the heart might grow to the point that the coronary arteries can't adequately supply it any more, resulting in tissue death.