Hypertension and Cerebrovascular Diseases

Introduction 

Arterial hypertension (HPN) is, after age, the most powerful risk factor for stroke. Hypertensive persons have a 4-5 fold increase of stroke risk, as compared to normotensive and this increased risk operates for both ischemic and hemorrhagic strokes. In addition, acute elevation of blood pressure can lead to a third type of cerebrovascular disease that is the hypertensive encephalopathy.

Hypertension and ischemic strokes 

Ischemic strokes constitute two-thirds to three-quarters of all strokes; their most common causes are atherosclerosis, lipohyalinosis (previously called arteriosclerosis), and embolisms of cardiac origin. Hypertension plays a causal or aggravating role in all these three etiologies. 

Hypertension is a major risk factor for ischemic strokes associated with atherosclerosis. Eighty-five percent of patients suffering from this type of stroke are hypertensive. Since the Framingham study, HPN is considered to be a major risk factor of atherosclerosis for all body arteries. It is however, the most important risk factor for cerebral arteries, while it comes after dyslipidemia for coronary arteries and after diabetes and cigarettes smoking for lower limbs arteriopathy. Not only extracranial arteries stenoses and occlusions are more frequent in hypertensive than normotensive persons, but HPN drives also atherosclerosis into small intracranial arteries that are not usually affected by this disease. 

The role of hypertension in lipohyalinosis is even more important. This disease affects the small perforating cerebral arteries of less than 0.3 mm of diameter. The wall of these arteries becomes disorganized with segmental narrowings and dilatations and hyaline degeneration. The occlusion of these arteries leads to small deep cerebral infarcts called lacunes. In his original description of lacunes in 1965, CM Fisher reported 114 autopsy cases. One hundred eleven of these patients were hypertensive before their death. The cerebral deep perforating arteries have the particularity of arising directly from large pericerebral arteries. They are therefore likely, in the absence of successive ramifications, to be under high physical strain leading to their degeneration in hypertensive patients. 

Hypertension is also an indirect risk factor for ischemic strokes resulting from cardio-embolism, as it is a well established risk factor for the three main cardiac sources of embolisms i.e. non-valvular atrial fibrillation, myocardial infarction and congestive cardiomyopathy. 

Finally, and as a logical consequence of the major role of HPN in ischemic strokes in general, it is considered to be the first risk factor for vascular dementia, whether it is due to multiple infarcts or to Binswanger’s disease. 

Hypertension & Hemorrhagic strokes 

Arterial Hypertension is considered to be the direct cause of approximately two-thirds of cerebral hemorrhages. Most of these hemorrhages occur in the regions of basal ganglia, thalami, pons and cerebellar white matter. In this regard, it is remarkable that hypertensive cerebral hemorrhages and lacunar infarcts are usually located in the same brain regions i.e. in the territories of perforating cerebral arteries. These arteries, in normal individuals, can tolerate a pressure up to 1500 mm Hg before they rupture. However, when they are affected by lipohyalinosis in chronically hypertensive patients, micro-aneurysms appear in their walls and they become very fragile. Their rupture will lead to cerebral hemorrhages and their occlusion to lacunar infarcts. 

Most of subarachnoid hemorrhage cases are due to rupture of saccular aneurysms. These arterial wall anomalies are probably due to congenital defects in arterial wall media and elastic layers, but HPN is known to accelerate their development and contribute to their rupture. In more than 50% of cases, aneurysmal rupture occurs during an exercise or a condition where blood pressure (BP) tends to rise acutely. 

However, finding a high BP after a cerebral or a subarachnoid hemorrhage does not necessarily mean that the patient has been hypertensive. High blood pressure can be simply due, in these cases, to the Cushing effect where a sudden rise in intracranial pressure with distortion or compression of the brainstem can provoke an acute rise in blood pressure. 

Hypertensive Encephalopathy 

The term “hypertensive encephalopathy” is used to describe acute, usually reversible, brain changes associated with an acute rise of BP in the absence of major cerebral hemorrhage or infarct. It is probably due to a dysfunction of the autoregulation system of cerebral blood flow. This flow is around 50 ml/100 g brain tissue/ min and is constant despite blood pressure changes as long as the mean BP (2max +1 min divided by 3) is between 60 and 130 mmHg. The autoregulation curve is however, shifted to the right in hypertensive patients where its respective limits are higher. When there is an acute rise in BP, over the autoregulation limits, there is a first reaction of hyper-regulation with arterial spasm, and scattered small ischemic changes. In a second phase, or if the blood pressure continues to rise, there is a complete failure of the system with vasoplegia, exudations, micro-hemorrhages and cerebral edema. For an unknown reason, most of these changes occur in the parieto-occipital white matter and lead to the so-called “posterior leukoencephalopathy syndrome”. And because the autoregulation curve is shifted to the right in chronic hypertension, hypertensive encephalopathy is rare in hypertensive patients unless their blood pressure reaches very high numbers. It is more common in normotensive persons who have an acute rise in BP, such as young individuals with acute nephritis or young women with eclampsia. A rapid correction of BP numbers in these cases usually leads to rapid improvement in clinical condition 

In conclusion, hypertension is associated with various cerebrovascular disorders. Its early detection and control are definitely the most effective measures for stroke prevention, both at primary and secondary levels. The historical decline of stroke incidence that was observed between 1950 and 1980 was probably due to this detection and control. The two recent studies HOPE and PROGRESS suggest that some of the ACE inhibitors will have a greater effect in continuing this trend

 

            Adnan Awada, MD, FAAN

            Head, Neurology Section

            King Fahd National Guard Hospital, Riyadh