Hypertension

A.      Introduction

·         Many people are not even diagnosed with hypertension until certain symptom arise.  Her anecdotal story involves her husband being diagnosed after having an uncontrollable nose bleeding (epistaxis) situation!

·         First off, Hypertension is an abnormal elevation of blood pressure (BP).  It’s a risk factor for many other serious conditions!

·         Today we’ll discuss the pathologic effects of hypertension on the resistance vessels (namely the arterioles and the thickening of these vessels, called arteriosclerosis) and on the heart. 

• Note, that arteriosclerosis includes 3 conditions that involve thickening of the blood vessels.  The first will be discussed today, arteriolosclerosis (dealing w/arterioles) and tomorrow we will discuss atherosclerosis, which underlies many of the diseases discussed in this unit.  The 3^rd disease in this group was not even mentioned, and when I asked Dr. Cleveland she said not to bother even putting it in the notes (b/c anal MD students will memorize it anyways!)

·         There are different ways to classify Hypertension, like primary (essential) and secondary Hypertension and another important distinction is between benign & malignant hypertension.

• Benign Hypertension = persistent, stable, modest elevation of BP over time (like 140/90) à while it is termed “benign”, there is some degree of risk because of a higher BP, but this isn’t as harmful as malignant Hypertension!
• Malignant Hypertension = very severe elevations of diastolic & systolic BP, like 220/120.   This type of Hypertension can get suddenly very worse in a short amount of time, so it’s also called accelerated .

Let’s learn about some pathology associated w/these 2 types of Hypertension, namely arteriolosclerosis:

B.      Arteriolosclerosis

Arteriolosclerosis = characterized by thickening & inelasticity of arteriole walls.  (Remember: the arterioles are the small muscular, resistance vessels in the body).

v      Hyaline arteriolosclerosis

o        More typical in benign Hypertension

o        Arteriolar wall thickens due to increased extracellular matrix (ECM) from smooth muscle injury AND leakage of plasma proteins from the vessel due to endothelial injury.  This thickening will cause narrowing of the blood vessel lumen à narrowing = vascular stenosis à less blood flow to the tissues à tissue ischemia
 

§         When this process of thickening à stenosis à ischemia occurs in the kidney, which is a common place for it to happen, it’s known as benign nephrosclerosis.

§         Histologically, this thickening is amorphous, structure-less, homogeneous, eosinophilic material made from this ECM & plasma proteins.  This term “hyaline” is often used to describe this transluceny, i.e. hyaline membrane, amyloid, thickened keratin layers of this skin.   

o        This thickening of wall is actually common in all of us as we get older, however it is more pronounced and troublesome in patients with hypertension & even diabetics.

v      Hyperplastic arteriolosclersosis

o        More typical in malignant Hypertension.

o        Histologically, there is a concentric, laminar thickening of the vessel wall.  It looks like a swirly target or even an onion skin.  In the kidney this is called malignant nephrosclerosis (you may be able to determine the location of the vessel, for example by the presence of renal glomeruli or other “histological landmarks”.)

o        This causes a narrowing of the lumen, thus constricting blood flow!  Similar to hyaline arteriolosclerosis, there can be tissue ischemia and infarction. 

o        Some other pathological changes may also be present, including:

§         Fibrioid necrosis due to complement activation to make fibrin.  This can lead to an intravascular thrombus to form.  (Note this is different than the other types of necrosis, like coagulative, liquefactive, or caseous necrosis!)

§         Infiltrate of inflammatory cells due to vascular damage, thus called necrotizing arteriolitis.  

Let’s move onto what Hypertension can do to the heart!

C.      Hypertensive Heart Disease

v      Systemic, or Left-Sided hypertensive heart disease

• The adaptive response of the left side of the heart is hypertrophy to work harder against this higher resistance due to thickening.  The cardiac myocytes cannot regenerate to increase their strength, but they can get bigger (hypertrophy).
• This is concentric left ventricular hypertrophy (LVH), b/c it not only involves the free outer wall of the ventricle, but it also involves a hypertrophy of the intraventricular septum!  Everything gets bigger to compensate! 
  • This is different than some other conditions with only selective ventricular hypertophy (although no selective LVH example given in class, she did mention that 2 examples of conditions that will also present with concentric hypertrophy are aortic stenosis & hypertrophic cardiomyopathy).
• If a patient comes in w/ they must have a history of Hypertension, and you must exclude these other conditions to call it systemic hypertensive heart disease.
• The usual thickness is of the ventricle wall is about 1 cm, these hearts can get to 2 cm or more, and they can weigh over 450g (vs. normal heart weight of 300g).
• The walls of the ventricle will also get stiffer with this thickening, which leads to decreased compliance à decreased filling à may lead to left atrial hypertrophy!  In more severe cases, this can lead to heart failure, so Hypertension has serious complications!

v      Pulmonary, or Right-Sided hypertensive heart disease

• This is also called cor pulmonale, which actually means “disease of the heart due to disease in the lungs”!  In this case, you have pulmonary hypertension that causes right sided heart disease.  Diseases intrinsic to the lungs or pulmonary vessels can be important underlying conditions in this pathology.
• Cor pulmonale can be classified as acute or chronic, based on the suddenness of the development of the Hypertension:
   
• Acute cor pulmonale is usually caused by a massive pulmonary thromboembolism in which at least 50% of the pulmonary vascular bed is occluded. 
  • This thrombus is usually from the deep veins of the leg. 
  • If the thrombus lodges in the pulmonary bifurcation, this will suddenly cut off all blood flow to the lungs and cause immediate death (saddle embolism). 
  • This is a medical emergency.
  • In this case, there will not be time for the cardiac myocytes to hypertrophy, so the right ventricular chamber may be dilated, but not usually hypertrophied.
     
• Chronic cor pulmonale develops more slowly over a period of time, like from a chronic obstructive lung disease (i.e. emphysema).  Unlike in the acute cor pumonale, this progresses over time, so the cardiac myocytes are able to adjust & hypertrophy, therefore the right ventricle will be hypertrophied and eventually become dilated.

One other histological note, there may be some pigment in the cardiac myocytes à this is lipofuscin (aka lipochroma).

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