Some Pathological Aspects of Dissecting Aneurysm

Based upon a Dissertation on “Dissecting Aneurysm” given before the Society on Friday, 17th January 1958. The term dissecting aneurysm implies the development of a circulatory pathway between the layers of the vessel wall. It can occur at all ages and in both sexes, being most frequent in men, in the fourth, fifth, and sixth decades, and in women in the eighth and ninth decades. It does not occur in normal arteries. Copyright Royal Medical Society. All rights reserved. The copyright is retained by the author and the Royal Medical Society, except where explicitly otherwise stated. Scans have been produced by the Digital Imaging Unit at Edinburgh University Library. Res Medica is supported by the University of Edinburgh’s Journal Hosting Service: http://journals.ed.ac.uk ISSN: 2051-7580 (Online) ISSN: 0482-3206 (Print) Res Medica is published by the Royal Medical Society, 5/5 Bristo Square, Edinburgh, EH8 9AL Res Medica, Spring 1958, 1(2): 14-17 doi:10.2218/resmedica.v1i2.310 SOME PATHOLOGICAL ASPECTS OF DISSECTING ANEURYSM Based upon a Dissertation on “Dissecting Aneurysm” given before the Society on Friday, 17th January 1958.


SOME PATHOLOGICAL ASPECTS OF DISSECTING ANEURYSM
Based upon a Dissertation on "Dissecting Aneurysm" given before the Society on Friday, 17th January 1958.

By M. J. MACLEAN
The term dissecting aneurysm implies the development of a circulatory path way between the layers of the wall.It can occur at all ages and in both sexes, being m ost frequent in m en, in the fourth, fifth, and sixth decades, and in wom en in the eighth and ninth decades.It does not occur in normal arteries.

Aetiology
The aetiological factors are variable and largely hypothetical but the following theories appear to have substantiating evidence of their authenticity: (1) The m echanical theory.Physical and mental strain causing a sudden increase in blood pressure is sufficient to produce the medial rupture leading to dissecting aneurysm only when the vessel wall is diseased.About 40 per cent, occur after mild exertion, although this as an aetiological factor is disputed by others.Hypertension which m ay be of the essential variety but is usually of renal origin is present in over half the cases.Mechanical injuries such as violence and traumatic accidents probably do not produce dissection.
(2) Congenital deform ities, including coarctation, bicuspid aortic valves, and hypoplasia.16 per cent, of cases of coarctation of the aorta develop dissecting aneurysm .
(3) Pregnancy.In 83 per cent, of one series of investigations, dissection occurred antepartum and thus cannot be attributed to the strains and blood pressure changes occurring during labour.
(4) D iseased aortic wall.Disease of the intima rarely causes dissecting aneurysm and those beginning at atherom atous plaques or ulcers are usually restricted in extent.An abnormal tunica media may arise through disease of the vasa vasorum or be essential in character.The degeneration, which m ay be local or diffuse, is a chromatotrophic or m ucinous process probably involutional or senescent in nature and it m ay progress to cyst formation.There is no connection between syphilitic mesaortitis and dissecting aneurysm and the joint occurrence of the two conditions is m erely coincidental.Since the reaction of hum an tissue to the Treponema pallidum is mainly one of fibrosis, the lesion in the aortic wall is localised rather than generalised.

Pathology
The primary rent in the aneurysm , usually a few centim etres in length, occurs in the aortic intima which is usually normal at the site of the tear.This would suggest that the tear is an effect rather than a cause of dissection.The m ost frequent sites of the tear are, firstly, the ascending aorta, account ing for 50 per cent., of cases of dissection, secondly, the junction of ascend ing and transverse portions for 20 per cent., and thirdly, the junction of transverse and descending portions for 10 per cent., the dissection being in the descending thoracic or abdominal aorta.The length of the dissection

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(3) What factors determine the final course of the dissecting process, either out through the tunica adventitia or back through the tunica intima?Dealing firstly with the mechanics of the initial intimal tear, the influence of an actively contracting hypertrophied left ventricle pro ducing a high systolic blood pressure is evident, and has to be accepted as an important factor in elongating and distending the aorta, especially in its ascending part.Moreover the direction of the blood stream is altered quite suddenly as it passes from ascending to transverse part, and again from transverse to descending portion, so that the wall of the vessel has to withstand a greater strain than elsewhere.This shouid be more marked on the greater curvature of the aorta than on its lesser curvature.The systolic propulsive force which is exerted chiefly longitudinally, parallel to the axis of the lumen, will have greater effect in elongating the vessel if any irregularities are present like atheromatous plaques on the inner sur face which will increase frictional resistance.
Such irregularities are not as common in the ascending aorta as in the transverse and descending portions; but on the other hand primary rupture occurs much more commonly in the ascending aorta than at the junction with the transverse part or in any part of the extrapericardial aorta.This can be attributed to two reasons.Firstly, the longitudinal force is greatest in the ascending portion, as is borne out by the frequency of circumferential tears in this region, for the direction of the linear tear will be perpendicu lar to the direction of the preponderant stretch.Secondly, the abrupt diastolic recoil meeting the resistance of the closed aortic valves is of even greater importance as a factor in producing the primary tear.In diastole on closure of the valve, the longitudinal force is largely converted into a transverse one with consequent lateral stretching of the intrapericardial aorta.Additional factors are the resistance offered by the dis tended pulmonary artery and by the rigid attachment of the pericardium at its reflection, both of these tending to increase the strain which has to be borne by the intrapericardial aorta.
In consideration of the second question, the factors producing the degeneration of the media, we find that the cause of cystic medionecrosis is still unknown.Medionecrosis of the aorta has been produced experi mentally in rabbits using the intravenous injection of diphtheria toxin.Intravenous tyramine injections also produced medial necrosis in some of the animals.Similarly necrosis has been produced in rats by feeding the sweet pea, the toxic component of which is Beta-amino proprionitrile.A medial degeneration has also been produced in guinea pigs and rabbits by deprivation of Vitamin E. Cystic medionecrosis may be found in patients dying from various causes and there is some association with age but none with sex or hypertension.Cystic necrosis may occur without dissection, but appears to be necessary for its development.It may result from exhaustion of the muscle in its efforts to prevent overdistension of the aorta, or an excess of adrenaline might cause spasm of the vasa vasorum, focal ischaemia and necrosis.Whatever the cause the media generally gives way before the intima.
The factors determining the final course of the dissecting process or secondary rupture are (1) weakness of the outer wall, (2) atheromatous plaques weakening the inner wall, and (3) the presence of normal anatomical structures such as aortic branches which tend to hinder continued dissection.Secondary rupture outwards may occur at anv point along the aortic wall, but most frequently into the mediastinum.This occurs in 85 per cent, of cases, the other 15 per cent, dissecting back into the lumen.
The pathogenesis in subjects under the age of forty can generally be attributed to one of the congenital lesions already described.In 50 per cent, of these there is also an in the connective tissue, but it is unlikely that medionecrosis develops long before dissection occurs.
It is not known whether a true cause and effect relationship exists between pregnancy and dissecting aneurysm but, if it does, it may be due to the hormonal changes which may weaken the aortic wall, rendering it more susceptible to dissection.
Hypertension is usually present in those over forty suffering from dissecting aneurysm.Dissection is, however, rare in cases of malignant hypertension, its incidence being 0-2 per cent.(Beaven and Murphy, 1956).These authors report dissection in nine hypertensive patients being treated with methonium drugs, six of whom were in the malignant phase.Since the incidence is greater than would be expected by chance, some workers have suggested that the methonium compounds might play a role in the aetiology of dissecting aneurysm via the wide fluctuations in blood pressure which occur in therapy, these producing additional stress on the aortic wall.This observation is of value since physicians may mistake this complication for a myocardial infarction, withhold hypotensive therapy which may be of some value, and administer anticoagulants which further reduce the remote chance of survival.

Conclusion
In conclusion, the types of patients liable to develop dissecting aneurysm are: 1.Those with coarctation or extreme hypoplasia of the aorta.2. A few patients with atherosclerosis of the aorta with ulceration of the intima which permits dissection to begin at this point.3. Others who develop it through disease of the vasa vasorum of unknown aetiology with weakening of the media.4. In the majority of cases no aetiological factor is found.They present no specific disease of the aorta, in the absence of micro studies.In brief then, no single causative agent or morbid process can be demonstrated as consistently producing the vascular changes leading to dissection.Death in 70 per cent, of cases occurs from rupture externally, and there is little relation between the site of tear, the length of the dissection, and the time of survival.

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