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HYPERTENSIVE VASCULAR DISEASE/VASCULOPATHY

 The vascular disease of hypertension, by promoting tissue underperfusion and progression of atherosclerosis, contributes to myocardial ischemia and cardiovascular events, heart failure, stroke, nephrosclerosis and chronic kidney disease and peripheral vascular disease

Hypertension (high pressure) can cause significant vessel and end-organ damage. hypertension is a major risk factor for coronary heart disease, cerebrovascular accidents, heart failure, renal failure, and aortic dissection.

Blood pressure is a continuously distributed variable and detrimental effects increase continuously as the pressure rises; thus, no rigidly defined level distinguishes safety from risk, and other concomitant risk factors (e.g., diabetes) can lower the threshold for what is deleterious

DEFINITION

sustained diastolic pressures more than 89 mm Hg or systolic pressures more than 139 mm Hg

Types of hypertensive heart disease

In general, the heart problems associated with high blood pressure relate to the heart’s arteries and muscles. The types of hypertensive heart disease include:

Narrowing of the arteries

Coronary arteries transport blood to your heart muscle. When high blood pressure causes the blood vessels to become narrow, blood flow to the heart can slow or stop. This condition is known as coronary heart disease (CHD), also called coronary artery disease.

CHD makes it difficult for your heart to function and supply the rest of your organs with blood. It can put you at risk for heart attack from a blood clot that gets stuck in one of the narrowed arteries and cuts off blood flow to your heart.

Thickening and enlargement of the heart

High blood pressure makes it difficult for your heart to pump blood. Like other muscles in your body, regular hard work causes your heart muscles to thicken and grow. This alters the way the heart functions. These changes usually happen in the main pumping chamber of the heart, the left ventricle. The condition is known as left ventricular hypertrophy (LVH).

MALIGNANT HYPERTENSION

malignant hypertension is characterized by systolic blood pressure more than 200 mm Hg, diastolic pressure more than 120 mm Hg, renal failure, and retinal hemorrhages.

REGULATION OF BLOOD PRESSURE

Blood pressure is a function of cardiac output and peripheral vascular resistance, which are, in turn, influenced by genetic and environmental factors

  • Cardiac output is determined by myocardial contractility, heart rate, and blood volume. Blood volume is affected by: Sodium load Mineralocorticoids (aldosterone) Natriuretic factors that induce sodium excretion
  • Vascular resistance is determined primarily at the level of the arterioles Vasoconstrictors: angiotensin II, catecholamines, thromboxane, leukotrienes, and endothelin Vasodilators: kinins, prostaglandins, nitric oxide, and adenosine
  • Regional autoregulation occurs when increased blood flow leads to local vasoconstriction; local hypoxia or acidosis can also cause vasodilation
  • Kidneys have a major influence on blood pressure by producing renin in the setting of hypotension.
  • Renin converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II Angiotensin II causes vasoconstriction Angiotensin II also increases blood volume by inducing aldosterone production, which increases renal sodium resorption

MECHANISM OF ACTION

 Sodium homeostasis is a key element of blood volume control, and it is primarily regulated at the level of renal sodium resorption in the distal tubule; this, in turn, is largely influenced by the renin-angiotensin system, which regulates aldosterone production. Although single gene disorders in these pathways are rare causes of hypertension,

 it is apparent that subtle variations in their activity might influence blood pressure in the broader population:

• Mutations in enzymes that influence aldosterone synthesis (11bhydroxylase, 17a-hydroxylase) lead to increased aldosterone production

• Mutations in the renal epithelial Naþ channel protein lead to increased sodium resorption (Liddle syndrome)

PATHOLOGY

Hypertension accelerates the development of atherosclerosis and also causes arteriolar structural changes that potentiate both aortic dissection and cerebrovascular hemorrhage.

 Hypertension is also associated with two forms of small arteriolar disease:

Hyaline arteriolosclerosis is due to endothelial cell (EC) injury, with subsequent plasma leakage into arteriolar walls and increased SMC matrix synthesis. The same lesions occur in diabetic angiopathy due to EC hyperglycemic injury. Microscopically, there is diffuse pink hyaline arteriolar wall thickening, with associated luminal stenosis.

Hyperplastic arteriolosclerosis occurs in malignant hypertension; there is concentric laminated (onion-skin) arteriolar thickening with reduplicated basement membrane and SMC proliferation, frequently associated with fibrin deposition and wall necrosis, called necrotizing arteriolitic.

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