Notes by dr Claudio Italiano
Tonight, coming to the hospital, on Radio Uno I learned the news that Italy is the second most long-lived country in the world, thanks to the care that our National Health Service provides to its patients.
However, still today in Italy
100,000 people a year accuse
A patient who suffers from high blood pressure can not remain calm but must know
that he can face problems. Problems are represented by organ damage. It means,
for example, that the heart, the eye, the arterial vessels are subject to damage
due to high pressure values.
They deteriorate and suffer damage sometimes irreversible. To make myself understood, it is clear to all of you that the tires of your car swell to 1.8 -2 ATA, otherwise a tire that is too swollen can explode or not keep the grip on the asphalt.
Why then leave a high pressure inside your vessels? The heart that works against the "post-load" represent high blood pressure, like any muscle, goes into hypertrophy, but this modification of the heart structure is not a useful transformation.
In fact, a hypertrophic heart is an enlarged organ, with dilated cardiac chambers: it can
undergo alterations such as ischemic heart disease and arrhythmias. We can
understand this when we read an electrocardiogram and discover that the "strokes"
of the nib have an excessive dimension that translates into the alterations that
we technically call the Sokolow-Lyon index. But also the eye of a patient with
high pressure undergoes alterations of the arterioles of the fundus of the eye.
We will therefore talk about arterial hypertension and its complications.
In the case of arterial hypertension there are some target organs that are
subject to risk of lesions:
They are:
- the brain
- the eye
- heart
- vessels
Never underestimate the risk of organ damage associated with arterial
hypertension. The writer is a victim of hypertension and, after the umpteenth
service shift, he discovered by chance that the feeling of oppression in the
chest was due to a surge in systolic pressure, in our case up to 200 mmHg. And
we are doctors! So if you go to the doctor or you go to the pharmacy, after
checking the tires of your car, a peek at your blood pressure is essential!
cf >> Hemorrhagic stroke
The brain is subjected to pressure stress, mainly the high diastolic pressure (minimum pressure) to be considered correlated with the risk of stroke. There is a low incidence of stroke in subjects with diastolic <75 mmHg. In general, and for constant increases in diastolic blood pressure of 5, 7.5 and 10 mmHg respectively, there is an increase in the risk of stroke from 34% to 46% and up to 56%. Moreover, the incidence of stroke risk is not very evident in the less developed population, while the diastolic is about 60 mmHg, while it is in those, so to speak, evolved, where other factors such as smoking exist besides hypertension. obesity, hyperfibrinogenemia and hypercholesterolemia.
In China and Japan, hypertension and stroke are common, but coronary artery disease is relatively rare: the difference is in the prevalent levels of cholesterolemia and low-density lipoprotein (LDL). More than 10% of strokes are caused by cerebral hemorrhages that usually develop after rupture of microaneurysms, which appear on the deep penetrating arteries of the cerebral cortex in patients with chronic hypertension. Small aneurysms have been identified in small arteries of 50-200 microns in diameter, at branch points and contracted in the lateral branches of the striated arteries and the penetrating arteries of the cortex.
The density of the lesions is maximum in:
- putamen
- pale globe
- caudate nucleus
- thalamus
- internal cap
Another related lesion to hypertension is an infarct between 0.5 and 15 mm deep
located in the brain. These lesions are evidenced by TAC and are due to
occlusion of one of the same small arterioles that give rise to hemorrhage. The
lesions may show up at the bridge base, or the cerebellar substance as well as
the subcapsular region. Most hypertensive strokes, however, are always due to
atheromatous disease of the extracranial vessels or supraortic trunks, due to
the dormation of atheromatous plaques, where the flow is more turbulent, ie at
the bifurcations. The occlusion of the internal carotid causes a cerebral
infarction in the distribution of the middle or anterior artery or both and the
infarcts can become hemorrhages. Occlusion is always due to a plaque rupture.
Therefore, the treatment of arterial hypertension is at the basis of the
reduction in the incidence of stroke in 40% of fatal and non-fatal cases.
Here's what the retina looks like in
malignant hypertension: note the papilloedema
and very hard exudates described as a macular
star
Even the eye is a target organ of hypertension and exactly the retina is affected by lesion, that is, so to speak, the photographic film of the eye or CCD of our digital cameras! If there are linear or flame retinal haemorrhages associated with diastolic values above 120 mmHg, a diagnosis of accelerated or malignant hypertension can be made. Patients with malignant hypertension have fibrinoid necrosis of the kidney arteries. Blurred vision is a common disorder and other symptoms are occipital headache, exercise dyspnea and weight loss. Hemorrhagic episodes such as epistaxis or hemosperm and encephalopathy may occur in the most severe cases with obtundation and convulsions. The presence of papillaedema means that there is cerebral edema.
The haemorrhages of an eye are not sufficient for diagnosis and can result from a retinal vascular accident such as occlusion of a branch of a retinal vein, which has higher incidence in hypertensive patients. If hemorrhages and papilledema or "staple cotton" stains are present, then areas of infarction of the retinal nerve fiber layer should be considered. The hard exudate, on the other hand, depends on the leakage of plasma from the damaged small blood vessels, with the deposition of high-lipid refractive material.
Also the heart is a target organ of hypertension, since the cardiac pump must work "against pressure", that is against a "post-load", therefore it is not easy to push the blood into the aortic arch which is stressed considerably. The heart works harder and goes towards compensatory concetrial hypertrophy, neither more nor less like that guy who trains his biceps with weights at the gym! But the hypertrophy of the wall for the myocardium is a disadvantage and not an advantage, as it contains in nuce the factors that will determine the heart failure, ie the pump failure. In addition, the wall hypertrophy reduces the compliance of the ventricle in diastole, ie the ventricle fills badly and progressively reduces the performance of the heart, also because the blood perfusion of the enlarged wall is deficient and ischemia is the immediate consequence of what. Ischemia means that there is a reduced flow of stamina and, therefore, oxygen for the myocardium, that is, for the heart muscle with an increased risk of heart attack, especially if the risk factors are also concomitant: smoking, obesity, hypercholesterolemia and hyperfibrinogenemia . Still myocardial hypertrophy predisposes to cardiac arrhythmias and sudden death. In the Framingham study it was shown that heart hypertrophy is an independent risk factor and immature death. The mortality of a subject with hypertrophic cardio-activity over the 12-year follow-up period is 16% and increases to 60% if there is a concomitant stress pattern. At echocardiography it is possible in time to recognize these changes in the myocardium, an investigation that is highly recommended in the subject with mild or moderate hypertension.
The kidney is severely affected by malignant hypertension; in fact, everyone knows that it consists of about one million renal corpuscles, which are in turn made up of a myriad of small vessels and a very sophisticated and delicate blood filtration system. Therefore, renal failure deriving from glomeruli damage is a very frequent occurrence of hypertension and is shown at the beginning with a rise in the values of atrophy and of creatininemia, with the emission of proteins in the urine.
As we know of protein in urine there should not be, because the kidney is equipped with a filter so to speak intelligent, in the sense that it prevents the passage of proteins, red blood cells, white blood cells, albumins, globulins and so on, so the presence of proteinuria or of only albuminuria is an alarm bell: it means that the filter has been ruined and that it has become loosened, letting the good molecules also seep into the waste product represented by the urine. Today, fortunately, there are no longer the old mercurial, but powerful molecules and very manageable, able to protect the kidney.
The main pathological finding of hypertension is the appearance in the kidney of fibrinoid necrosis of small arteries, which tends to be more evident in the afferent glomerular arterioles, but also affects the small interlobular arteries. The appearance of fibrin in the vessel wall probably results from an increased permeability and endothelial damage that allows as we said to plasma proteins and fibrinogen to penetrate the average. There is the concomitant necrosis of smooth muscle cells and lumen thrombosis with loss of functioning glomeruli and the appearance of red blood cells in the urine.
Another lesion is the proliferative endoarteritis of the interlobular arteries that determines an "onion skin" appearance. The fibrin deposition of the vessels in turn causes damage to the circulating erythrocytes, forced to wander between the small vessels affected by the lesions, with the determination of a microangiopathic hemolytic anemia. The haemochromocytometric examination also shows thrombocytopenia. The glomeruli undergo focal necrosis and the glomerular capillaries can break in Bowman's space and in the renal tubules to cause bleeding visible to the naked eye as "mosquito bites" on the surface of the kidney. An increase in renovascular resistances represents an initial etiopathogenetic moment of hypertension damage, then gradually decreases the plasma renal flow, with an increase in renal filtration in the surviving glomeruli until the creatinine clearance is reduced to pathological values.
We talked about the metabolic syndrome, and as we know, is characterized by the
formation of fibrolipid plaques in the arteries of large caliber, being the
basis of heart attack and stroke cerebri. But in the presence of hypertension
the damage is precocious and greater, since it, together with smoking, obesity,
diabetes mellitus, represents a further and serious risk factor. Hypertension
seems to accelerate atherosclerosis, therefore, a process that also depends on
the circulating levels of LDL cholesterol (lipids); it is therefore necessary
that the cholesterol, the bad or LDL, is lowered to 150 mg%, especially if there
are risk factors such as diabetes or smoking. Another aspect of hypertension is
the damage on the large vessels that occurs with a change in the constitution of
the medium that is more evident in the small arteries and arterioles, the
miocytes in the resistance vessels go against the polyploid transformation of
their nucleus with development of collagen tissue, which replaces the elastic
and muscular average. It follows that the vessels become more rigid and this is
technically called "atherosclerotic process".
For the treatment see the page on Hypertension