Cardiac : There includes coronary artery disease, left ventricular failure and congestive heart failure.
Renal : Renal Failure
Vascular : Dissection of aorta and atherosclearosis are the main vascular complication.
Optic : Hypertensive retinopathy, which has been, graded into 4 grades by Keith wagener and Barber is common.
Effect of HT on organs involved
The pathological changes occurring in these organs are :
Heart :
Sustained HT leads to increased work load and left ventricular hypertrophy. The weight of heart is closely related to the degree of HT not only do the cardiac cell size but there is also an increase in the number of cells.
Progressive changes on other hand increase the muscle mass between the capillaries thus reducing blood supply to the heart. Because of left ventricular wall thickness there is an increase in the pressure gradient from the epicrdium to endocardium , reducing blood supply to the inner portion of the heart muscle Atheromatus changes on the coronary arteries further reduce blood supply causing fibrotic changes and even infarction of heart muscle leading to hypertension heart failure.
Brain :
Medial and initimal hypertrophy is also seen in arteries supplying the brain. There may be degenerative lesions of large vessels e.g. middle cerebral and carotid vessels, which cause thrombotic stroke. In older people tiny aneurysm (Charcot Bouchard aneurysm) have also been seen which cause cerebral hemorrhage. Thus cerebral infarction is secondary to the increased atherosclerosis but cerebral hemorrhage is the result of both, elevated BP and microaneuryzms.
Cerebral Encephalopathy consist of the following symptom complex. Severe HT, disordered consciousness, increase intracranial pressure, retinopathy with Papilloedema and seizures.
Kidneys :
Arteriosclerotic lesions of the afferent and efferent arterioles and the glomerular capillary tufts are the most common renal vascular lesions in HT and results in a decreased glomerular filtration rate and tabular dysfunction. Proteinuria and microscopic haematuria occur because of glomerular lesion and approximately 10% death caused by HT result from renal failure.
Arteries :
Initially there is thickening of the muscular coat, which can add to the increase in peripheral resistance following different stimulas later, there is intimal hypertrophy and generalized degenerative arterial lesions. Although the exact mechanism is not understood there is retention of certain lipoproteins which along with damage to the endothelium from shear forces and several other mechanisms leads to degenerative lesions. The overall lesions are a combination of medial hypertrophy, elastic proliferation, intimal proliferation, lipid deposition, degeneration and thrombotic events.
Retina :
The initial lesion is the irregular caliber of arterioles with localized constriction and dilatation. Due to constriction of arteries the ratio of veins to artery is increased. Micro infarcts may cause cotton wool exudates said to be due to increased axonal fluid transport in normal neurons near the site of the infarct. Rupture of capillaries can cause flame shaped hemorrhages. Swelling of the optic disc (Papilloedema) which is seen in malignant hypertension may not always be associated with hemorrhages and exudates and is due to generalized brain edema.
