Pathogenetic Factors and Vascular Wall Injury
The development of the disease is determined by a triad of factors: chronic psycho-emotional stress, genetic cell membrane defects (with impaired transport of $Ca^{2+}$ and $Na^{+}$ ions), and hereditary alterations of the pressure-natriuresis mechanism. Lipid metabolism imbalance (elevated LDL and VLDL with decreased HDL) further accelerates atherosclerotic processes.
The morphogenesis of hypertensive macroangiopathy in the aorta, large, and medium-sized arteries includes successive phases:
- Hyperelastosis: Initial thickening of the elastic framework;
- Elastofibrosis: Proliferation of connective tissue;
- Endothelial injury with the development of arteriosclerosis.
Circular fibrous plaques severely narrow the lumen of the aorta, coronary, carotid, renal, and cerebral arteries. The stiffening of the walls leads to baroreceptor failure, which establishes a "vicious cycle" that stabilizes high blood pressure.
Stages of Morphogenesis in the Benign Form
The benign course of the disease is divided into three clinicomorphological stages:
- Transitory (preclinical): Characterized by functional vascular spasm without marked organic changes.
- Vascular: Accompanied by progressive hyalinosis of arterioles and atherosclerosis of muscular-elastic and elastic-type arteries.
- Organ stage: Leads to secondary remodeling of organs due to impaired intra-organ blood flow.
Cardiac Changes
In response to the workload, left ventricular myocardial hypertrophy develops, leading to a sharp increase in organ weight up to 900–1000 g (cor bovinum or "bovine heart"). The wall thickness reaches 2–3 cm. Subsequently, hypoxia and cardiomyocyte dystrophy cause diffuse small-focal cardiosclerosis, culminating in myogenic chamber dilation (eccentric hypertrophy).
Organ Pathology and Acute Complications
Chronic blood flow disturbances cause atrophic and sclerotic changes in target organs:
- Arteriolosclerotic nephrosclerosis: Hyalinosis of afferent arterioles and glomeruli develops, along with tubular atrophy and renal stromal sclerosis. The organ shrinks, and its surface becomes fine-grained. The process is always bilateral and results in a primary contracted kidney (arteriolosclerotic nephrocirrhosis), progressing to chronic kidney disease.
- Hypertensive retinopathy: Characterized by hyalinosis of retinal vessels, papilledema ("choked disc"), focal retinal detachment, and hemorrhages.
Acute lesions occur during hypertensive crises against the background of vasospasm, thrombosis, or vascular wall necrosis. The most frequent causes of fatal outcomes are acute myocardial infarction, stroke, acute kidney injury, and aortic dissection.
Features of Malignant Hypertension
The malignant variant is not a separate nosology, but rather an extremely aggressive form of the disease. It most frequently affects men aged 30–50 years and is accompanied by a sharp rise in blood pressure (up to 220/140 mmHg).
- Main morphological criterion: Fibrinoid necrosis of arterioles.
- Vascular changes: Development of microaneurysms and their subsequent rupture.
- Dynamics: Rapid progression with frequent hypertensive crises and rapidly progressive organ failure.