Original descriptions of the classic signs of aortic valve insufficiency☆

Introduction 

The valves of the heart and their diseases have generated interest since ancient times. The early observations regarding valvular deformities were confined to morbid changes with no reference to hemodynamic significance (1). Galen (130–200 AD) wrote “the general purpose of the valves is to prevent a reversal of flow of any sort. For nature does not want to tire the heart with unnecessary work, nor commit the error of putting anything at a place from any place which she intends to take it away again or lead it away from a place where its presence is necessary” (2). da Vinci (1452–1519) depicted, by diagrammatic illustration, how the aortic valve normally functions to prevent aortic insufficiency (3). The classic clinical signs of aortic insufficiency indicating hemodynamic disturbances were described later.

Corrigan’s pulse 

Although the name of Corrigan (1802–1880) is linked to other entities such as Corrigan’s cirrhosis (fibrous phthisis) and Corrigan’s cautery (button cautery), his description of “Corrigan’s pulse” has assured his immortality in medical history. In 1832 he published a paper in the Edinburgh Medical and Surgical Journal on “Patency of the Mouth of the Aorta or Inadequacy of the Aortic Valve,” in which he described the typical pulse of aortic insufficiency (4). This article contained three illustrations showing the morbid appearance of these valves. Though not appreciated by his colleagues early in his career, he later became the most popular doctor in Ireland. When this article was written, Corrigan honestly believed that it was the first published work on the subject. Hope (1801–1841) took violent exception to the assumption and claimed the discovery of aortic insufficiency as his own, made in 1826 (5). Hope claimed that he had taught this at St. Bartholomew’s Hospital in 1826 and at La Charite, Paris, in 1827. Hope, in 1831, had described the “jerking pulse” of aortic insufficiency. More noteworthy cases of this condition had been observed earlier than Hope’s description, however.

Cowper (1666–1709), in 1705, and de Vieussens (1641–1716), in 1715, described the clinical aspects of aortic insufficiency, but they did not attempt to discover the pathological cause. Cowper described the characteristic bounding pulse of aortic insufficiency (6). de Vieussens, a Montpellier physician, described the pulse of aortic insufficiency as “very full, very fast, hard and unequal, and so strong, the arteries on both sides struck the ends of my fingers just as a cord would have done which was very tightly drawn and violently shaken” (7). In 1822, Cuming reported signs and symptoms of a case of aortic insufficiency, proved at autopsy, in the Dublin Hospital Reports (8). Hodgkin (1798–1866) presented two papers, in 1827 and in 1829, before the Hunterian Society, in which he showed knowledge of the chief signs of aortic insufficiency by describing cases of protrusion of aortic valve cusps into the left ventricle instead of effectually closing the valve against a reflux of blood (9). He noticed inordinately violent arterial action and a remarkable thrill in the pulse, which was regular. However, none of the accounts mentioned equals that of Corrigan for completeness and masterful description, correlating signs of the disease with an understanding of the underlying valvular pathophysiology. He wrote:

What is deficient in general symptoms from their obscurity is, however, amply supplied by the certainty of the physical and stethoscopic signs, which may be referred to the three following indications, 1st, Visible pulsation of the arteries of the head and superior extremities. 2nd, Bruit de souffle in the ascending aorta, in the carotids, and subclavians. 3rd, Bruit de souffle and fremissement, or a peculiar rushing thrill felt by the finger, in the carotids and subclavians. In conjunction with these may be reckoned the pulse, which is invariably full. When a patient affected by the disease is stripped, the arterial trunks of the head, neck and superior extremities immediately catch the eye by their singular pulsation. At each diastole the subclavian, carotid, temporal, brachial and in some cases even the palmar arteries, are suddenly thrown from their bed, bounding up under the skin. But when the semilunar valves, from any of the causes enumerated, become incapable of closing the mouth of the aorta, then after each contraction of the ventricle, a portion of the blood just sent into the aorta, greater or less, according to the degree of the inadequacy of the valves, turns back into the ventricle. Hence the ascending aorta and arteries arising from it, pouring back a portion of their contained blood, become after each contraction of the ventricle, flaccid or lessened in their diameter. While they are in this state, the ventricle again contracts and impels quickly into these vessels is thus marked by so sudden and so great an increase of size as to present the visible pulsation which constitutes one of the signs of the disease. That this visible pulsation of the arteries is owing to the mechanical cause here assigned is made evident by several circumstances. It is most distinct in the arteries of the head and neck, which empty themselves most easily into the aorta, and of course into the ventricle. In the arteries of the lower extremities, of even larger size than those which present it about the head and neck, it is not seen to any comparative degree, and most generally not at all while the patient is standing or sitting. It is much more marked in the arteries of the head and neck in the erect than in horizontal posture; and a patient suffering under the disease himself, first pointed out a circumstance which is convincing of its being produced as asserted. He would increase the pulsation of the brachial and palmar arteries in a most striking degree by merely elevating his arms to a perpendicular positions above his head. He thus enabled the brachial and palmar arteries to empty themselves more easily back upon the aorta. They became flaccid, and then, on the next contraction of the ventricle, their diastole became comparatively greater, and their visible pulsation of course more marked. (4)

De Musset’s sign 

de Musset (1810–1857) was a French writer. “de Musset” is the only eponym of aortic insufficiency attributed to a patient and not to a physician (10). This sign was originally described by the poet’s brother, Paul, who wrote the biography of the more famous Alfred. In his original description, Paul wrote:

One morning in month of March (of 1842), during the lunch, I observed the head of Alfred was showing a slight bobbing which was involuntary, seemingly occurring with each heart beat. He asked my mother and me why we were looking at him with such an air of astonishment. We told him what we saw. ‘I did not think you could see it’ he replied, ‘but I will reassure you.’ He pressed on his neck with his thumb and index finger and in a moment his head stopped bobbing with each heart beat. ‘You see,’ he said to us ‘this dreadful malady is cured by a method, which is not only simple but inexpensive as well.’ Mother and I were reassured in our ignorance, not realizing that this was the first sign of a serious affliction which would take his life just fifteen years later (10).

de Musset contracted syphilis as a young man, which led to aortic aneurysm and aortic insufficiency. Paul’s work was published in 1877 but the eponym was not offered to the medical literature until 1900, when Delpeuch proposed it (11).

Hill’s sign 

Hill (1866–1952) was a British physiologist. He was involved in the sphygmomanometric measurement of the systolic blood pressure by palpation of the brachial artery and the dorsalis pedis or posterior tibial artery (12). Though the finding of a greater systolic blood pressure in the leg than the arm in aortic insufficiency came to be known as Hill’s sign, by his own account he was not the first to notice this. He wrote:

Up to this point we had never found any difference between leg and arm readings of young men placed in the horizontal position. The arteries of the legs thicken with age, and have stiffer walls than those of the arms owing to high hydrostatic pressure of the blood in the standing posture, and thus we should expect a difference in reading to appear with advancing age if it were due to better conductance. Holtzmann, acting on the suggestion of one of us, made some independent observations of a similar kind and like result, in the London Hospital. He also tried the pressure in 2 or 3 cases of aortic regurgitation, and told us that he found a noticeable difference between arm and leg reading in such. Following up this interesting observation, we found that in all cases of aortic regurgitation there is this marked difference, which is not abolished by the method of oscillating the pressure up and down near the obliteration pressure. So marked is this difference that we believe we could pick out cases of aortic regurgitation by it alone. (12)

Hill described the sign, which now bears his name, in 10 cases of aortic insufficiency, and 2 years later he wrote another paper with more explanation of systolic popliteal-brachial gradient in aortic regurgitation.

Austin Flint’s murmur 

Flint’s name has been handed down to posterity linked with the names of Laennec, Skoda and Auenbrugger. Laennec described the classic art of auscultation in Europe, Skoda introduced Laennec’s method of auscultation into medical practice, and Auenbrugger described percussion of the chest. Flint (1812–1886) has a special place in the history of medicine in America. He was a gifted teacher, founder of two medical schools and professor in six medical schools. He was a prolific writer and outstanding clinician. He was born in Petersham, Massachusetts. On graduation from Harvard Medical School in 1833, he commenced medical practice in Northampton and Boston. In 1836, Flint moved to Buffalo and stayed there for 20 years. At the age of 35, Flint became the first professor of the Theory and Practice of Medicine at Buffalo Medical College. He was on the faculties at three different institutions between 1856 and 1860. Each summer he was in Buffalo and in the winter he taught at New Orleans Medical College as Professor of Clinical Medicine and was visiting physician at Charity Hospital, a position he held until 1861. While at Charity Hospital, Flint described the heart murmur for which he is best remembered (13). His original description published in 1862 is as follows:

In some cases, in which free aortic regurgitation exists, the left ventricle becoming filled before the auricles contract, the mitral curtains are floated out and the valve closed when the mitral current takes place and under the circumstances, this murmur may be produced by current just named, although no mitral lesion exists. A mitral direct murmur, then, may exist without mitral contraction and without any mitral lesions, provided there be aortic lesions involving considerable aortic regurgitation. This murmur by no means accompanies aortic regurgitation lesions as a rule. The circumstances, which may be required to develop, functionally, the latter murmur, in addition to the amount of aortic regurgitation, remain to be ascertained. Probably enlargement of the left ventricle is one condition. (14)

Duroziez’s double intermittent murmur 

Duroziez (1826–1897) was born in Paris in 1826 and received his doctor’s degree in 1853. While still a medical student he won the Corvisart Prize for a dissertation on the therapeutic properties and physiological action of digitalis. In 1856 he became chief of the Clinic at the Charite, and in 1870 served as an army surgeon in the Franco-Prussian war. In 1882 he was elected president of the Society of Medicine, and in 1895 was made Chevalier of the Legion of Honor. Duroziez is remembered for his description of pure mitral stenosis (“Duroziez’s disease”), the presystolic rumble and reduplication of the second heart sound, but especially for his description of the double femoral murmur (“Duroziez’s sign”) in aortic insufficiency. He described this femoral double intermittent murmur in 1861. He wrote:

There are 2 ways of producing the double murmur, with the stethoscope or with the hand. (The first method) One gradually presses the instrument as if to obliterate the (femoral) artery; at a certain moment, the double murmurs appears; (The second method) Or else this, which can be done only when the diastolic component is easy to find; one can simply lay the stethoscope on the (femoral) artery; then in sequence, press with the hand, in succession, first upstream (2 cm above) and then downstream (2 cm below) of the stethoscope. The upstream pressure produces the systolic murmur and the downstream pressure produces the diastolic component,clearly proving that the diastolic component is produced by the blood flowing backwards from the artery of the leg. (15)

Quinke’s sign 

Quinke (1842–1922) published his classic paper on the capillary pulsation when he was 26 years old and was an assistant in the Medical Clinic in Berlin. Even though Quinke’s capillary pulsation has been listed as a classic peripheral sign of aortic incompetence, Quinke himself acknowledged presence of the capillary pulsation with a wide pulse pressure. He wrote:

A large and rapidly falling pulse is seen especially in aortic insufficiency, and for this reason the capillary pulse is especially clear in this condition. Even in a horizontal position of the hand, we see a very clear and rapid appearance and disappearance of the margin between the red and white zone and also with a uniform coloration of the nail and lighteninglike and evanescent reddening. It is, in general, impossible to state upon which fingernail the phenomenon is clearest, but usually, it seems to me, the index finger is the best in the area between the whitish, clear zone and red, injected zone of the capillary system of the nailbed, in the majority of persons examined there is with each heart beat a forward and backward movement of the margin between the red zone and clear white zone, and one can convince himself that the increase in redness follows a moment later than the apex beat and is still clearly systolic and rather rapid; while the backward movement of the edge of the redness seems to take place more slowly (16).

The original descriptions of the signs of aortic valve insufficiency not only have historical significance but also a utility in current practice. The purpose of a good physical examination is to find the patients who need to have a more sophisticated workup, and the physical signs of valve insufficiency serve this purpose well.