HYPERTENSION

In medically advanced countries, hypertension is the most common serious chronic disease, affecting about a half of the population over 50 years of age. Arterial hypertension is defined clinically as borderline when it riches 140/90 mm Hg and hypertensive when 165/95 mm Hg.

There is elevation of systolic pressure alone, (systolic hypertension) or elevation, of both systolic - and diastolic pressure (diastolic hypertension), both have an increased risk of serious complications, but diastolic hypertension is more dangerous.

Hypertension is classified into two types:

1. In 90-95% of all cases of hypertension, no cause can been established – such cases are called essential or idiopathic or primary.

2. In only 5-10% of all cases of hypertension is any disease, which may be associated with disturbance of these mechanisms detectable – such cases are secondary hypertension. Examples:

·        Kidney diseases.

·        Hyperfunction of adrenal cortex (Cushing ‘s syndrome – corticosteroid excess).

·        Tumor of adrenal medulla (pheochromocytoma) – catecholamine excess.

·        Hypertension occurs in toxemia of pregnancy.

·        This hypertension comprises 5-10% causes of disease.

If these causes of secondary hypertension were eliminated, hypertension disease would be cure.

According to the clinical course, both types of hypertension may be benign or malignant.

1. Benign hypertension is moderate elevation of blood pressure and the rise is slow as the years pass. About 90% of patients of hypertension have benign disease.

2. Malignant hypertension is marked and rapid increase of blood pressure to 200/140 mm Hg or more and the patients have papilledema, hemorrhages and hypertensive encephalopathy.

All the above mechanisms are essentially vaso-constrictor. The possible roles of vaso-dilator mechanisms – for example the effect of nitric oxide on vascular smooth muscle – are being currently researched.

The increased peripheral resistance resulting in sustained hypertension may arise from:

1. Increased sympathetic tone.
2. Increased release of renin and generation of angiotensin.
3. The presence of vasoconstrictive substances in the circulation.
4. Increased sodium load and extracellular fluid load, and finally.
5. A postulated excessive responsiveness to the other factors.

Morphology

·        It is important to realize that the central lesion in most cases of hypertension is a decrease in the size of the lumen in small muscular arteries and arterioles, the resistance vessels that control the flow of blood through the capillary bed.

·        The lumen may be restricted by active contraction of the vessel wall, an increase in the structural mass of the vessel wall, or both.

·        The morphologic changes associated with moderate elevations of blood pressure are too subtle to be detected by simple histological studies. Small muscular arteries show segmental dilatation as a result of necrosis of smooth muscle cells.

·        The combination of cell necrosis and deposition of plasma proteins in the vessel wall is termed fibrinoid necrosis.

·        The period of acute injury is rapidly followed by smooth muscle proliferation and a striking increase in the number of layers of smooth muscle cells, which yields the so-called onion-skin appearance. Taken together, these changes are labeled malignant arteriosclerosis or malignant arteriolosclerosis, depending on the size of the vessels affected.

Clinical-morphological stages

1.       Subclinical stage occurs by hypertrophy of muscular layer and elastic structures of arterioles and small-sized arteries, spasm of arterioles. At this stage the hypertrophy of the left ventricle of heart begins.

2.       A stage of general changes of arteries begins as arterial pressure increases. Arteriolar walls permeability is increased, it results in plasmatic impregnation and hyalinosis. Elastic, muscular-elastic and muscular arteries walls undergo elastofibrosis and atherosclerosis. Elastofibrosis is characterized by a hyperplasia and breaking of internal elastic membrane and spreading of connective tissue. Atherosclerotic changes in case of hypertension are more extensive, the process reaches small-sized arteries of muscular type, plaques are more often circular, that cause acute mechanical stenosis of the vessel.

3.       The stage of secondary changes of organs is developed in connection with changes of arteries and insufficiency of the intraorganic blood circulation. These changes develop slowly, that results in atrophy of parenchyma and sclerosis (it’s characteristic of benign hypertension), quickly (spasm, thrombosis, fibrinoid necrosis) and causing infarctions and hemorrhages (it’s characteristic of malignant hypertension).

The main clinical-morphological forms of essential hypertension

1. Cardiac form

·        Hypertensive heart disease or hypertensive cardiomyopathy is the disease of the heart resulting from systemic hypertension of prolonged duration and manifesting by left ventricular hypertrophy.

·        Often hypertension predisposes to atherosclerosis. The arterial changes and vascular complications increase with the severity and duration of the hypertension, but are modified by genetic factors, environmental factors, sex (females tolerate hypertension better), and associated diseases.

·        Macroscopically, the most significant finding is marked hypertrophy of the heart, especially of the left ventricle. Weight of heart reaches 1 kg, thickness of left ventricle walls is up to 3 cm, the papillary muscles are rounded and prominent, and the cardiac chamber is small (concentric hypertrophy). But when decompensation and cardiac failure develop, there is eccentric hypertrophy (myogenic dilation) with thinning of the ventricular wall and dilation of the left ventricular and atrial cavities.

·        There may be dilatation and hypertrophy of right heart as well. Heart is called “cor bovinum”.

2. Cerebral form (Cerebrovascular diseases.

It is characterized first of all as impairment of cerebral blood circulation. This hypertension can result in two main types of parenchymal diseases of the brain:

1) Ischemic brain damage (hypoxic encephalopathy and cerebral infarction).

·        The pathologic appearance of the brain in hypoxic encephalopathy varies depending on the duration and severity of hypoxic episode and the length of survival.

·        Macroscopically, there is focal softening. The area supplied by distal branches of the cerebral arteries suffers from the most severe ischemic damage and may develop border zone or watershed infarcts in the adjacent zones between the territories supplied by major arteries.

·        Microscopically, the nerve cells die and disappear and are replaced by reactive fibrillary glia.

·        Cerebral infarction is a localized area of tissue necrosis caused by local vascular occlusion.

·        Cerebral infarction may be anemic or hemorrhagic.

·        Macroscopically, an anemic infarct becomes evident 6 - 12 hours after its occurrence. The affected area is soft and swollen and there is blurry of junction between gray and white matter. Within 2-3 days, the infarct undergoes softening and disintegration.

·        A hemorrhagic infarct is red and superficially resembles a hematoma. It is usually the result of fragmentation of occlusive arterial emboli or venous thrombosis.

2) Intracranial hemorrhage (intracerebral and subarachnoid hemorrhage).

·        Hemorrhage into the brain of patient with hypertension is intracerebral hemorrhage, which is usually of hypertensive origin due to rupture of microaneurysm.

·        The common sites of hypertensive intracerebral hemorrhage are the region of the basal ganglia, medulla and cerebellum cortex.

·        About 40% of patients die during the first 3-4 days of hemorrhage, mostly from hemorrhage into the ventricles.

·        The outcome of intracerebral hemorrhage is cyst formation. Patients can be paralyzed.

3. Renal form

·        Renal form is characterized by chronic arteriolo-sclerotic nephrosclerosis.

·        Kidneys have a term “primary shrunken kidneys”.

·        Macroscopically, both kidneys are affected equally and are reduced in size and weight, often weighting about 6 gm. The capsule is connected densely to the cortical surface. The surface of the kidney is finely granular and shows V-shaped areas of scarring. The cut surface shows firm kidney and narrowed cortex.

·        Microscopically, there are primary diffuse vascular changes, which produce parenchymal changes and secondary as a result of ischemia. There is variable degree of atrophy of parenchyma; these include glomerular shrinkage, deposition of collagen in Bowman's space, periglomerular fibrosis.

·        Clinical features are variable, elevation of the blood pressure with headache, dizziness, and palpitation.

·        Renal failure and uremia may occur.

·        In case of malignant hypertension can develop as hypertonic crisis - acute increase of arterial pressure in communication (connection) with spasm of arterioles.

·        Morphological appearance of hypertonic crisis: plasmatic impregnation or fibrinoid necrosis of arteriolar walls.

The causes of death among hypertensive patients are the following:

·        Congestive heart failure.

·        Coronary artery disease.

·        Cerebrovascular accidents.

·        Uremia.

·        Causes unrelated to hypertension. The cardiac complications therefore account for 36% of the death.