Материал: Internal_diseases_propedeutics._Part_II._Diagnostics_of_cardiovascular_diseases

Pathologic anatomy.

No early pathologic changes occur in primary hypertension.

Large and medium-sized arteries respond to high blood pressure by thickening of the media and disruption of the elastic tissue within their walls. The vessels may become tortuous and dilated and may rupture because of the high pressure in the lumen. If this occurs in the brain, cerebral haemorrhage usually leaves the patient dead or paralysed from a stroke. Hypertension also promotes the formation of atheroma in medium-sized and large arteries, so a stroke may also be caused by occlusion of a cerebral artery by thrombus formed on an atheromatous plaque, or by embolization of atheromatous material from plaques in the extracranial segments of the carotid arteries or aorta. Atheroma formation in the coronary arteries renders hypertensive patients susceptible to angina pectoris, myocardial infarction and sudden death. In smaller arteries and arterioles, hypertension causes prominent thickening of the intima, in addition to medial hypertrophy. In cases of “accelerated” or “maligna nt” hypertension, in which the blood pressure is very high or has risen quickly, these intimal changes can occlude the vessels, producing distal tissue ischemia. This particularly affects the kidneys, causing renal failure. The walls of the small arteries in the brain may be damaged so that their permeability is increased and cerebral edema results, causing hypertensive encephalopathy characterized by headache, confusion, fits and coma. There may also be visual disturbances due to retinal arterial damage, which may be seen on examination of the fundi.

The left ventricle responds to high blood pressure by hypertrophy. Initially, this increases its force of contraction and maintains a normal cardiac output, but eventually the hypertrophied muscle outgrows its oxygen supply and angina and cardiac failure result.

Ultimately, generalized arteriolar sclerosis develops; it is particularly apparent in the kidney (nephrosclerosis) and is characterized by medial hypertrophy and hyalinization. Nephrosclerosis is the hallmark of primary hypertension.

66

Damage of target organs.

Hypertension, particularly long-term existing, leads to viscera damage, called target organs, - heart, vessels, brain and kidneys.

The heart damage in hypertension may declare itself by left ventricular hypertrophy and affecting of coronary vessels with angina pectoris, myocardial infarction development, and also sudden cardiac death. In heart damage progressing the heart failure develops.

Myocardial ischemia may appear not only due to coronary arteries affection (their epicardiac parts), but due to relative coronary insufficiency (unchanged coronary arteries inability to supply with blood hypertrophied myocardium), and due to microvasculopathy.

Vessels damage. Vessels, directly participating in high BP maintenance due to TPR, are themselves one of target organs. Vascular damage is characterized by involving in process retinal vessels, carotids, aorta (aneurysms), and also affecting of small vessels: damage of cerebral vessels (occlusions or microaneurysms) may lead to stroke, renal arteries – to renal functions alteration. Fundi inv estigation allows physician to assess directly vessels changes.

In hypertension vessels narrow, then expose to sclerosis, that is accompanied by microaneurysms and microhemorrhages formation, and also by ischemic damage of blood supplying organs. All these changes may be stage by stage observed on patient's fundus of eye.

Brain damage is characterized by thrombosis and hemorrhages, hypertensive encephalopathy and lacunae formation in brain tissues. Cerebral vessels damage may lead to changes of their walls (atherosclerosis). In various stages of disease these changes may be complicated by stroke due to thrombosis or cerebral vessels rupture with hemorrhage.

Kidneys damage. As early as initial stage of disease there is inclination to renal vessels changes, at first, with some increase, and then decrease of glomerular filtration. Long-term course of hypertension leads to nephroangiosclerosis with significant impairment of renal functions and chronic renal failure development.

Renal functions reflect changes of glomerular filtration rate (GFR). If on initial stage of hypertension GFR is usually normal, on later stages (or in malignant hypertension) it

67

progressively decreases. Furthermore, creatinine blood level and protein urine concentration (microalbuminuria is typical) are the indicators of kidneys involvement in pathologic process.

Hemodynamics

Not all patients with primary hypertension have normal CO (cardial output) and increased TPR. CO is increased, and TPR is inappropriately normal for the level of CO in the early labile phase of primary hypertension. TPR increases and CO later returns to normal, probably because of autoregulation. Patients with high, fixed diastolic pressures often have decreased CO. The role of the large veins in the pathophysiology of primary hypertension has largely been ignored, but venoconstriction early in the disease may contribute to the increased CO.

Plasma volume tends to decrease as BP increases, although some patients have expanded plasma volumes. Hemodynamic, plasma volume, and PRA variations are evidence that primary hypertension is more than a single entity or that different mechanisms are involved in different stages of the disorder.

Renal blood flow gradually decreases as the diastolic BP increases and arteriolar sclerosis begins. GFR remains normal until late in the disease, and, as a result, the filtration fraction is increased. Coronary, cerebral, and muscle blood flow are maintained unless concomitant severe atherosclerosis is present in these vascular beds.

In the absence of heart failure, CO is normal or increased, and peripheral resistance is usually high in hypertension due to pheochromocytoma, primary aldosteronism, renal artery disease, and renal parenchymal disease. Plasma volume tends to be high in hypertension due to primary aldosteronism or renal parenchymal disease and may be subnormal in pheochromocytoma.

Systolic hypertension (with normal diastolic pressure) is not a discrete entity. It often results from increased CO or stroke volume (eg, labile phase of primary hypertension, thyrotoxicosis, arteriovenous fistula, aortic regurgitation); in elderly persons with normal or low CO, it usually reflects inelasticity of the aorta and its major branches (arteriosclerotic hypertension).

68

Hypertension and risk of cardiovascular complications.

Risk factors. Prognosis in patients with hypertension depends not only on BP level. Important meaning have risk factors, divided on main (basic) and additional (Table 7).

Table 7

On risk evaluation main factors are usually used, among additional factors - cholesterol fractions, obesity, impaired glucose tolerance - are chosen.

Stratification of patients by absolute level of cardiovascular risk

Decisions about the management of patients with hypertension should not be based on the level of blood pressure alone, but also on the presence of other risk factors, concomitant diseases such as diabetes, target organ damage, and cardiovascular or renal disease, as well as other aspects of the patient's personal, medical and social situation (Table 8).

Four categories of absolute cardiovascular disease risk are defined (low, medium, high and very high risk) (Table 9). Each category represents a range of absolute disease

69

risks. Within each range, the risk of any one individual will be determined by the severity and number of risk factors present. So, for example, individuals with very high levels of cholesterol or a family history of premature cardiovascular disease in several first-degree relatives will typically have absolute risk levels that are at the higher end of the range provided. Similarly, individuals with other risk factors listed in Table 8 may also have absolute risk levels that are towards the higher end of the range for the category.

How well these estimates predict the absolute risk of cardiovascular disease in Asian, African or other non-Western populations is uncertain. In those countries CHD incidence is relatively low and heart failure or renal disease is more common.