Organ complications of hypertension
Hypertension-related vascular injuries: Most vascular injuries in hypertensive patients are directly dependent on the severity of hypertension
These injuries can induce the development of tissue damage, both haemorrhagic and ischaemic.
The vascular changes in the hypertensive are: arteriolar thickening, arteriosclerosis, arteriolar necrosis, arterial and microvascular aneurysms, fibromuscular hyperplasia of the media.
Arteriolar thickening underlies the increase in peripheral vascular resistance characteristic of hypertension
Through this vascular structural change, the stress exerted on the individual myocellular decreases, the capacity for further vasoconstriction remains, which protects the tissue from the risk of hyperperfusion by shifting the upper limit of autoregulation to higher levels, but exposes it to the risk of hypoperfusion due to abrupt pressure drops below the lower limit of autoregulation.
Atherosclerosis is promoted by hypertension through different mechanisms, all the more so if other risk factors coexist, while arteriolar necrosis is typical of the malignant phase.
Aneurysms of the aorta expose one to the risk of fatal dissection, while small aneurysms of the cerebral arteries are sites of rupture and cause cerebral haemorrhage. Documentation of the existence of atherosclerotic vasculopathy is useful for risk stratification as well as for therapeutic purposes and makes use of common ultrasonographic and radiological methods.
Hypertension and left ventricular hypertrophy
In essential hypertension, the heart may initially appear normal on objective examination, and on instrumental investigations (ECG, echocardiogram and chest X-ray).
With the passage of time, the chronic haemodynamic overload caused by arterial hypertension promotes an increase in the volume and number of myocardiocytes through increased left ventricular parietal stress.
In addition to haemodynamic overload, activation of the sympathetic nervous system, circulating and tissue renin-angiotensin system, growth factors and genetics also contribute to the pathogenesis of hypertrophy.
The increase in myocardial mass normalises the stress on the single cell.
Hypertrophy of the left ventricle is a frequent autopsy finding in the hypertensive patient.
The echocardiogram is the most precise examination to document the existence of left ventricular hypertrophy in vivo.
It is arbitrarily defined as an increase in left ventricular mass greater than 131 g/m2 in males and 100 in females.
Left ventricular mass correlates with tensor levels, both ‘random’ and ‘ambulatory’.
The presence of left ventricular hypertrophy is associated with a poorer prognosis, due to the increased risk of arrhythmias, myocardial infarction, stroke, sudden death and lower limb obliterative arteriopathy.
The hypertrophy of the left ventricle is partly corrected by antihypertensive therapy, conducted over long periods.
Hypertensive retinopathy
The retina is the only part of the body in which the resistance arterioles can be directly observed.
Examination of the fundus oculi is therefore of fundamental importance in the hypertensive person to document the effects of the disease on the vascular bed.
The first classification of hypertensive retinopathy is that of Keith, Wagener and Baker (1939).
It has the historical merit of having identified some elementary lesions, but it is currently outdated in its description of the lesions themselves, because some of them are common to both hypertension and atherosclerosis and because different lesions often coexist and are not expressions of different stages of the disease.
The changes found in hypertensives are: increased arterial tortuosity, increased axial reflex with ‘silver thread’ arteries, arteriovenous crossings or compressions, ‘flame’ haemorrhages, soft or cottony exudates, hard and shiny exudates, papilledema.
Increased arterial tortuosity and ‘silver thread’ arteries are linked to both hypertension and ageing. Increased axial reflex is an expression of thickening of the vessel wall.
Crossings between arteries and veins are commonly seen in the normal retina, but when the arteriolar wall is thickened, the veins are compressed and appear occluded.
Soft exudates are an expression of retinal infarcts, while hard exudates consist of lipid deposits.
Papilla oedema is a swelling of the optic disc associated with cerebral oedema.
The specific changes in hypertension are: calibre alterations (vasospasm alternating with vasodilatation, diffuse vasospasm with increased ratio of vein to artery calibre), cottony exudates and flame haemorrhages, papilla oedema and optic disc swelling. Keith, Wagener and Baker’s classification identifies the following grades:
- Grade I: modest vascular changes
- Grade II: silver thread changes, tortuosity and arteriovenous compressions
- Grade III: retinal haemorrhages and cottony spots and/or hard, shiny exudates
- Grade IV: retinal haemorrhages, exudates and papilledema.
In a hypertensive patient, more advanced retinal changes only appear in the presence of diastolic pressure above 125 mmHg, which has persisted for some time or has increased rapidly.
The diagnosis of advanced hypertensive retinopathy, with haemorrhages and exudates, and papilla oedema, requires the prompt institution of antihypertensive therapy.
Hypertensive nephropathy: hypertension is a cause and consequence of many renal diseases
Systemic arterial hypertension is probably the most important risk factor for the progressive decline in renal function, which occurs due to continuous nephron loss.
On the other hand, most normotensive patients who present with renal disease develop hypertension that worsens as renal function progressively declines.
Progressive glomerular sclerosis is the final event common to many kidney diseases without distinguishing characteristic macroscopic and microscopic anatomopathological features.
It follows that once the kidney is in terminal failure, the primary cause is unrecognisable both anatomopathologically and clinically.
This is why in the terminal phase it is often difficult if not impossible to distinguish hypertensive nephropathy from hypertension resulting from renal disease.
The incidence of hypertensive nephropathy, defined as terminal renal failure in which long-standing hypertension is the sole aetiological agent, is unknown.
However, most hypertensive patients today do not have severe renal complications.
Nevertheless, it is currently believed that hypertension is, after diabetes, the second leading cause of end-stage renal failure and accounts for almost 50 new cases of end-stage renal failure per year per million inhabitants.
The number of hypertensives arriving at dialysis or transplantation is steadily increasing, especially following the reduction in cardiac and cerebrovascular mortality.
From an anatomopathological point of view, hypertensive nephrosclerosis is characterised by shriveled kidneys with an irregular and coarsely granular surface.
The arterioles show thickening and fibrosis, splitting of the internal elastic lamina and jalinisation.
The glomerular damage is focal and manifests itself with glomerular collapsing and sclerosis; the tubule is atrophic.
Hypertensive nephropathy is probably caused by multiple mechanisms including ischaemia with glomerular hypoperfusion (particularly in patients with nephrovascular hypertension), glomerular hypertension (resulting from inappropriate vasoconstriction of the afferent arteriole) hypercholesterolaemia, endothelial dysfunction with intracapillary thrombosis, increased passage of macromolecules in the mesangium and Bowman’s capsule, which stimulates synthesis of matrix components and tubular damage.
From a clinical point of view, the diagnosis of hypertensive nephropathy is mostly presumptive
Urine examination allows other causes of nephropathy to be ruled out: the presence of a modest proteinuria (1.5-2 g/day) without cylindruria is, however, common.
Some hypertensives have a higher than normal urinary albumin excretion (15 mg/min), but this is not detectable with the standard stick examination.
The presence of microalbuminuria (range 30-300 mg/min) is accompanied by increased cardiovascular risk and is probably an expression of multidistrict endothelial damage.
Diagnostic radiology does not help in the definition of hypertensive nephropathy but allows other causes of renal disease to be ruled out.
Biopsy examination is often of little use. The diagnosis of hypertensive nephropathy is therefore often presumptive and only an adequate follow-up of hypertensive patients will make it possible to document its true incidence in the population and the long-term effects of antihypertensive therapy.
Cerebral complications related to hypertension
The risk of death and permanent neurological damage from cerebrovascular disease increases progressively with age, and in the elderly cerebrovascular accidents account for 20% of the causes of death.
In stroke survivors, permanent neurological damage represents an individual and social cost that is difficult to calculate.
Hypertension is the main risk factor for vascular cerebropathy, but hypertension therapy, as it has been conducted so far, has only reduced the number of cerebrovascular accidents in the population by 40%.
This suggests that the control of hypertension is still inadequate, that the antihypertensive drugs used so far have undesirable effects that mitigate their potential benefits, and that not all cardiovascular risk factors are yet fully understood.
The cerebral diseases associated with high blood pressure are: atherothrombotic cerebral infarction, cerebral thromboembolism, cerebral haemorrhage, subarachnoid haemorrhage, and transient ischaemic attack.
Stroke is the most frequent brain injury in white hypertensives with moderate and mild hypertension.
However, the overall risk of stroke in a hypertensive person is about half that of myocardial infarction.
The incidence is about 2% per year in patients with moderate hypertension and 0.5% in patients with mild hypertension
The most frequent cerebrovascular accidents are cerebral infarctions.
They originate from atherothrombosis of the large intracranial vessels and manifest clinically as overt strokes, lacunar infarcts and transient ischaemic attacks.
Although multifactorial in origin, atherothrombotic cerebral infarction is three times more frequent in hypertensives than in the normotensive, in both sexes and at all ages.
The risk increases with both increasing systolic and diastolic blood pressure.
Thromboembolism originates from thrombi in the left ventricle or left atrium if atrial fibrillation coexists.
Another source of embolus is an ulcerated plaque of the extracranial carotid arteries.
The clinical picture is that of an overt stroke or transient cerebral ischaemic attack.
Cerebral haemorrhage is a frequent complication of severe hypertension, especially in the black race.
It is mostly caused by ruptured intracerebral microaneurysms.
Subarachnoid haemorrhage is due to ruptured sacciform aneurysms of the Willis polygon, mostly on a malformative basis.
There is no definite documentation of the role of hypertension in the pathogenesis of rupture, but treatment of hypertension prevents recurrences.
Diagnosis of cerebrovascular complications of hypertension is primarily anamnestic and clinical but also takes advantage of neuroradiological and ultrasonographic methods.
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