Synonyms.—Aortic Insufficiency; Aortic Regurgitation.
Definition.—Inability of the aortic valves to properly close an abnormally large aortic opening, or a change in the segments whereby they are shortened by curling of the leaflets, or by calcification.
Etiology.—The predisposing causes of aortic insufficiency are age and sex.
Age.—This is a disease largely of middle or advanced life, though an occasional case is found in early life.
Sex.—Aortic lesions prevail far more frequently in males than females, due to greater exposure, greater dissipation, and greater physical strain or exertion.
Exciting Causes.—Congenital insufficiency is a rare condition, and is due to malformation of the valves, owing to a fusion of two segments, most commonly those behind which the coronary arteries are given off; even this may not, for some time, give rise to incompetency; but the malformed segments invite sclerotic changes, and unless the individual leads a very quiet and careful life, sclerosis of the valve is almost sure to develop.
Acute Endocarditis.—That acute endocarditis occasionally gives rise to aortic lesions, can not be denied, though this lesion usually expends its force upon the mitral valves. When it does occur it is generally the result of necrosis followed by ulceration, and this in turn by early death.
In the young, it may be caused by rheumatic endocarditis, though more often this lesion gives rise to auriculo-ventricular changes. Acute affections, however, give the smaller per cent of cases of aortic lesions, long continued irritation from various sources being the common cause.
Strain.—The frequency with which aortic incompetency is found in strong, able-bodied men, whose occupation entailed long-continued physical exertion, called the attention of the profession to the increased tension the segments sustained during the ventricular diastole. So frequently has this lesion been found in those devoted to athletics, that it is often termed the "athlete's heart." This probably explains the frequency with which a runner falls in a dead faint in the last spurt of a long race.
Syphilis.—That Nemesis which pursues its victim to the grave, and which saps and poisons the vitality of its victim, works its destructive influence upon the aortic valve, and though this is frequently associated with other causes, may of itself produce the lesion. Syphilis is found to a great extent among sailors and soldiers, and the frequency with which this class of men suffer from valvular troubles can not be said to be merely a coincidence.
Alcohol.—Alcohol, by raising the tension in the aortic system, plays no small part as a causal factor, by inducing sclerotic changes in the valve segments.
Uric Acid.—That uric acid has its influence in giving rise to sclerotic changes can not be doubted, since it is a well-known product of various forms of gout and chronic rheumatism, and the etiological bearing of these diseases to valvular changes, is, most likely, largely due to the presence of uric acid. In this way lead poisoning should be considered a factor in producing interstitial changes in the valves, as it favors the accumulation of uric acid.
Aortic incompetency may in rare cases be the result of dilatation of the arch of the aorta near the valves, owing to arterial sclerosis.
An aneurism above the aortic ring would give rise to the same condition. In this case the insufficiency would be relative.
Pathology.—The change of structure in some cases is entirely in the orifice, the valves being normal, but fail to properly close the abnormally large orifice. This is known as relative insufficiency, and is generally caused by an aneurism or arteriosclerosis: according to Burke, there is a gradual enlargement of the aortic orifice from birth, when it is 20 mm. to the age of twenty-one, when it has reached 60 mm., and after remaining quiescent for twenty years, it again undergoes progressive enlargement for another thirty or forty years; yet, notwithstanding these changes, aortic insufficiency from this source is quite rare.
The valvular lesions are quite varied, and as they are progressive in character, other parts of the heart become involved, which may ultimately involve the entire organ. These changes may be noted somewhat in detail, and are as follows: The lesion may be confined to one or two of the semilunar segments, though usually all three are involved. There may be simply thickening of the valves, which render them stiff and less expansive, interfering with their rhythmic closure, and thus permitting slight regurgitation of blood.
More frequently, the segments are contracted and curled, thus imperfectly closing the orifice, the regurgitation being marked. At other times a segment will become adherent to the intima of the aorta, and the diseased segments in rare cases show laceration following a severe strain. The valves may become rigid from calcarious deposits, and appear petrified, the so-called ossification of the valves.
arteriosclerosis of the arch, or atheromatous deposits, may so obstruct the circulation of the coronary arteries that the nutrition of the heart will suffer, followed by degeneration.
Further changes in the heart are slow and progressive and due to regurgitation. The failure of the valves to properly close the orifice permits the blood to flow back into the left ventricle, and there meets the blood coming from the left auricle; as a result of this overdistention, dilatation of the left ventricle follows. The increased volume of blood in the ventricle calls for increased contractile power to expel its contents, and this over-exertion results in compensatory hypertrophy. The hypertrophy in some cases reaches an enormous size, and is known as the cor-bovinum—beef-heart.
Dulles records a case where the heart weighed forty-eight ounces. As a result of this dilatation and hypertrophy of the left ventricle, the trabeculse and papillary muscles become flattened by the intracardial pressure, the auriculo-ventricular opening becomes enlarged, and as a result the mitral valve fails to properly close the opening, and mitral insufficiency is the result. This. leads to dilatation and hypertrophy of the left auricle. The result of this causes engorgement of the lungs, and finally involvement of the right heart. These compensatory changes take place very gradually and with but little effect on the general health, and if no undue or excessive work is required, the patient may live for years with but little inconvenience.
Finally, however, the changes become so marked that the heart fails to properly propel and empty its contents, and engorgement of the lungs follows, cyanosis and dropsy speedily develop, and the case terminates fatally.
Symptoms.—The symptoms include a very wide, range of phenomena, from the mildest to the most pronounced and characteristic. The disease in some cases comes on so insidiously, and the compensatory changes so gradually develop, that the heart is able, if no undue expenditure is called for, to properly perform its function, and the disease is only discovered shortly before death, or in some cases during an autopsy. Most frequently, however, local symptoms develop that draw our attention to this organ, and a careful examination reveals the lesion.
After the hypertrophy becomes marked, great mental excitement or unusual physical exertion is followed by cerebral disturbances, and the patient complains of dizziness, headache, ringing in the ears, flashes of heat, and disturbed vision.
The face may become dusky, and there is throbbing or the arteries. As a result of the cardiac disturbance, there is a sense of oppression, and dyspnea becomes more or less distressing. Pain is a frequent distressing feature, and may be intense, extending down the left arm to the finger-tips, or it may be located under the shoulder-blades or in the joints, especially if rheumatism has preceded the disease.
True angina pectoris occurs more frequently in this than in any other form of valvular disease. In some cases there is marked dilatation of the peripheral vessels, which is accompanied by hot flashes and profuse and exhausting sweats, especially where there has been much disturbance of the pulmonary circulation attended by cough and hemorrhage. These cases have been in some instances mistaken for phthisis.
As the disease progresses and there is failure of compensation, all the symptoms already named are aggravated, and new phases develop. The pulmonary circulation is retarded, engorgement of the lungs follows, respiration is difficult, and cough follows with frequent hemorrhage.
The dyspnea is now a marked feature, and is quite distressing on slight exertion. As night approaches, the breathing seems to be more labored, and the patient, partly through fear and partly from a sense of suffocation, is compelled to pass the night in a chair, not being able to lie down. If there is any mitral disturbance, cyanosis becomes marked, the dyspnea becomes more severe, and dropsy develops, especially of the extremities.
The patient becomes quite anemic, which may partly account for the edema of the extremities. To add to the gravity of the case, a recurring endocarditis not infrequently develops, and would be recognized by the prostration and irregular fever developed.
Symptoms of cerebral, renal, or splenic embolism may arise, and would be recognized by paralysis, renal hemorrhage, and pain in the spleen, with more or less enlargement of the organ.
There seems to be a close relation between mental disturbances and cardiac lesions. These patients not infrequently become nervous and irritable, or melancholic and depressed. Insanity may develop towards the final termination of the disease, with suicidal tendencies, and the patient should be constantly watched after the first appearance of mental disorder.
Physical Signs.—Inspection will reveal a wide and extreme apex beat. This is most marked between the sixth and seventh interspace, and may extend to the anterior axillary line. In children there may be bulging of the precordia. Throbbing of the carotids may be noticed where the pulmonary circulation is disturbed; in fact, the temporal, brachial, and superficial vessels generally, may be seen to pulsate.
Palpation.—If the dilatation is not extensive, a heaving, forcible impulse is felt; but should the dilatation be extreme or the stage of compensation be passed, the impulse is weak and uncertain.
The pulse is characteristic, and was first described by Corrigan, and is often called the "Corrigan" pulse, the water-hammer pulse, the collapsing pulse. It is quick or jerking, and strikes the finger with force, but immediately recedes or collapses. The capillary pulse is frequently seen in aortic insufficiency, and may be noticed by brisk friction on the forehead, after which the hyperemic spot alternately blushes and turns pale.
Percussion.—There is a greater extent of dullness in this than in any other valvular lesion, and extends as low as the eighth interspace, and to the left as far as the anterior axillary line. When the left auricle is hypertrophied, it extends upward and to the left of the sternum. If the right heart has shared in the changes, the dullness extends to the right of the sternum.
Auscultation.—The most characteristic murmur of aortic insufficiency is a prolonged, soft, and somewhat musical or loud murmur, occurring during diastole, and is heard most distinctly in the intercostal space to the left of the sternum or beneath the lower portion of the sternum, extending to the third interspace on the left. It is due to regurgitation of blood from the aorta back into the left ventricle, and is heard with the second heart-sound.
It is heard over a greater distance than any other murmur, and may extend from the lower portion of the sternum to the spinal column. In extreme cases, this murmur may be heard in the carotids, and even in the radials. In many cases there is associated with this bruit a systolic murmur, heard over the aorta, but is shorter and more harsh, and is transmitted upwards to the neck. This sound is due to the roughened condition of the sclerotic change in the aorta, and is heard during the first heart-sound. It is more pronounced over the apex, though it may be transmitted to the arteries of the neck.
In addition to these murmurs, where the mitral orifice is dilated and there is relative insufficiency of the valves, there is a second murmur at the apex, which is most likely produced at the mitral orifice, and is known as the Flint murmur, Austin Flint having called attention to it. This somewhat rumbling sound is usually presystolic, and is no doubt due to the inability of the mitral valve to close the orifice, and as a result, the valve vibrates irregularly between the cross current of blood caused by the backward flow from the ventricle, meeting the forward rush from the auricle. Sometimes a double murmur may be heard in the carotids and subclavians, and occurs at the second sound.
Diagnosis.—That many cases are only recognized during an autopsy might lead one to believe that a diagnosis of the true condition is quite difficult; however, if proper care be made in the physical examination, and the progressive changes that take place be kept in mind, the diagnosis is usually not difficult. In no other valvular derangement do we find so great a hypertrophy of the left ventricle, and such extensive dullness downwards and to the left.
Then the diastolic regurgitant murmur, prolonged, soft, and somewhat musical, is the most characteristic and appreciable of all valvular murmurs, and is heard during the second sound. The characteristic water-hammer, or Corrigan pulse, together with the throbbing carotids and temporal arteries, and the alternate blushing and pallor of the capillaries when the cutaneous surface is rubbed,—all these make the diagnosis comparatively easy. When the lesion is unattended by a bruit, and when other valvular lesions prevail, the diagnosis becomes more difficult, and sometimes impossible.
Prognosis.—Aortic insufficiency does not necessarily mean an early death, and though we may not be able to effect a radical cure, the patient may be made to enjoy life. When the disease comes on insidiously, the compensatory changes enable the heart to do its work satisfactorily, and as long- as hypertrophy equals the valvular derangement, the health is maintained and the patient may even follow quite an active life. With proper instructions as to habits of life and the avoidance of severe physical exertion, the patient may live the allotted time of life. When due to aortic sclerosis, and when atheromatous deposits have taken place, the prognosis is not favorable.