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Essential Hypertension* BRmSw 30 October 1965 MEDICAL JOURNAL 1021 Br Med J: first published as 10.1136/bmj.2.5469.1021 on 30 October 1965. Downloaded from Hyperpiesis: High Blood-pressure without Evident Cause: Essential Hypertension* Sir GEORGE PICKERINGt M.D., D.SC., F.R.C.P., F.R.S. Brit. med.J_., 1965, 2, 1021-1026 Benign Hypertension that there is a third factor not in the coronary arteries and not the arterial pressure which contributes to hypertensive heart The benign phase of hypertension offers a great contrast to the disease. Could it possibly be related to advancing years, the malignant phase. The course is long and variable, with the disorder described by William Dock (1945) as presbycardia ? condition often remaining unchanged for years; thus, of As Fig. 12 shows, heart weight and arterial pressure are related Bechgaard's original 1,038 patients, 357 were alive after 20 quantitatively. Since, as Shirley Smith and Fowler (1955) and years (llechgaard et al., 1956). Bechgaard (unpublished) has Hamilton (1956) have shown, heart failure can be relieved and recently reported that 144 were alive after 26 to 32 years. prevented by lowering pressure, and since heart size decreases Uraemia does not occur; bilateral neuroretinopathy does not (Smirk, 1957), there is a strong case for supposing that elevation occur; cerebral oedema does not occur, or occurs only rarely; of arterial pressure is a causal factor in the cardiac changes. patients tend to die of heart failure, cerebral vascular disease, or intercurrent disease. Its nature is clearly different. The malignant phase is characterized by lesions which Cerebral Vascular Disease represent the limit of cardiovascular tolerance, fibrinoid arteriolar necrosis, retinal exudates representing focal vascular Cerebral vascular disease is still something of a morass. It is damage, hypertensive fits of similar origin, left ventricular customary to divide cerebral vascular disease into embolism, failure in response to overloading. While each phenomenon is dependent also on other factors, thus accounting for some 0 variation, few patients fail to exhibit at least two of these phenomena. In the benign phase the relationship between i 20 arterial pressure and the lesions that kill or cripple the patient Uj./ seem to be less close; factors other than arterial pressure intrude more. Hence for a given grade of elevated arterial pressure 0 we have a much greater variability in duration of life and course U z of illness ; so much so that some patients live their full span' and die of unrelated disease. 05 10 z Heart Disease http://www.bmj.com/ It is usual to distinguish two forms of heart disease, arterio- sclerotic and hypertensive, the former with demonstrated I I I I I -I J coronary disease, the latter without. Master's (1953) figures 70 80 90 100 110 showed that women with coronary artery disease tend to have DIASTOLIC BLOOD PRESSURE C Provisional) arterial pressures much above the norm, while in men the FIG. 11.-Risk of coronary heart disease according to level corresponding tendency is slight. Nevertheless, the Framing- of diastolic blood-pressure; Framingham men 45-62, with various serum cholesterol levels. (Kagan and others, 1959. ham studies have displayed that both arterial pressure and Copyright, American Heart Association.) on 25 September 2021 by guest. Protected copyright. plasma cholesterol are related to the future occurrence of myo- cardial infarction in men (Fig. 11). In both the relationship is quantitative; the correlation with arterial pressure is rather 2b0- . low (Dawber et al., 1962). In many patients with cardiac failure associated with elevated 240- arterial pressure and without symptoms of ischaemic heart * 0 disease the coronary arteries are not narrowed after death 220- 0 (Harrison and Wood, 1949). In such patients therapeutic a, reduction of arterial pressure may abolish cardiac failure; the E 200- . E 0 higher the arterial pressure the greater the probability that this 0 will happen. The onset of heart failure is often not precipitated 80- . by a recent rise of arterial pressure. It would seem, therefore, co va 0 60- * Conclusion of the St. Cyres Lecture, delivered to the Institute of I.- Cardiology and the National Heart Hospital, London, at the Royal 0 College of Physicians of London on 23 October 1964. The first 1 40- 0 part was published last week. t Regius Professor of Medicine, University of Oxford. 0 As I read through this I began to wonder what I meant by a full life- 120- 0 span. My mind came round to a patient, age 62, who was sent to me by her doctor to reinforce his advice that she should not cycle six miles (9.6 km.) to work each day. She explained why she did. Eventually I said: " Well, at your age you should retire." The 8 12 1 6 20 24 28 reply came: ' I can't, I have to keep mum and dad." Interested in inheritance, I found from their doctor that dad, aged 90, and HEART WEIGHT (oz.) mum, aged 88, both had diastolics over 130 mm. Hg. This could FIG. 12.-Relationship between systolic blood-pressure and perhaps be said to cosnstitute a full life-span. I allowed the patient heart weight in patients dying of hypertension and renal to cycle to work. disease (Evans, 1921). BReSH 1022 30 October 1965 Hyperpiesis-Pickering MEDICAL JOURNAL thrombosis, and haemorrhage. If we exclude embolism from small arteries 100-300 microns in diameter, particularly on the heart, which is of minor importance in essential hyperten- lateral branches of the striate arteries or on penetrating vessels Br Med J: first published as 10.1136/bmj.2.5469.1021 on 30 October 1965. Downloaded from sion, then it would seem that we are concerned with three quite from the cortex. The muscular tissue of the parent vessel different diseases affecting different sizes of arteries in different terminated abruptly at the point of origin of tlt aneurysm, and ways, and having different relationships with elevation of the remnants of elastica could be seen to extend for a short arterial pressure. All are commonly termed "atherosclerosis," distance into the aneurysm before disappearing. The wall of which confounds the confusion. the aneurysm was composed of connective tissue only, an inner hyaline layer derived from intima fusing with an outer collagenous layer continuous with the adventitia of the parent (a) Nodular Arteriosclerosis vessel. Frequently the aneurysms showed evidence of leaking and thrombosis. Ross Russell's observations suggest that such This disease of larger arteries essentially involves the intima, aneurysms form continuously in patients with elevated pres- where fibro-fatty nodules appear. Thrombosis may close the sures as they grow older. They can produce small haemor- vessel. This is the disease which causes coronary occlusion ; it rhages and small thromboses with local softening which would also causes stenosis and occlusion of the carotid and vertebral resemble the miliary infarcts described by Rosenberg (1940). arteries and the circle of Willis. It has long been known that When the thromboses extend proximally into larger arteries, carotid artery thrombosis may first display itself by transient larger areas of softening may result. Finally, there may be cerebral or retinal ischaemia. Millikan, Siekert, and Shick massive rupture with massive intracerebral haemorrhage. It (1955) suggested that such attacks were embolic. Gunning would seem likely that these intracerebral aneurysms are the et al. (1964) have shown that in patients presenting such attacks missing link between raised arterial pressure and cerebral nodules may be found in the carotid sinus, and that these vascular disease. nodules may present the following layers from lumen to media: fresh platelet leucocyte fibrin thrombus, hyaline fibrin thrombus, Strokes and Hypertension fibrous tissue, and atheroma. The cause of the " atheroma " or nodule of grumous tissue containing cholesterol clefts is still Fig. 9 has shown the relation to be expected from raised uncertain. But there is now quite strong evidence that the arterial pressure at insurance examination, and subsequent nodule grows by deposits of platelet thrombi, ageing, and death from cerebral vascular disease. That these two pheno- becoming incorporated into the wall. Such deposits may mena are related as cause and effect is suggested by Marshall's become detached as emboli friable enough to pass the retinal (1964) observation that when arterial pressure is reduced in and cerebral arteries with no more than transient ischaemia, or patients who have already had strokes further cerebrovascular as emboli stable enough to produce permanent occlusion of episodes are reduced in frequency. Hamilton, Thompson, and cerebral or retinal arteries; both kinds may occur in the same Wisniewski (1964), in a controlled trial, also found a reduced patient. Finally, the thrombus may be big enough to occlude incidence of stroke in symptomless hypertension treated for six the artery where it forms. Thus the symptomatology of this years as compared with controls. disease, so far as it affects the cerebral circulation, is much more variable than was at one time supposed. Dr. Yates very kindly put at my disposal the notes on his Arteriolar Lesions patients with carotid and vertebral artery disease, and I worked The arteriolar lesions of the benign phase consist of fatty out their age-and-sex-adjusted scores. These showed little hyaline subendothelial thickening in the arterioles and elastosis deviation from zero ; that is to say, the arterial pressures in http://www.bmj.com/ in the smaller arteries. These lesions have not been produced these patients were not far removed from those which would experimentally. In man they occur in all kinds of hypertension, have been found in a random sample of the population of though most conspicuously in essential hypertension, and are similar age and sex. This disease, then, is only to a very small generally believed to be consequences of the raised pressure.
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