Tricuspid Stenosis- A Simple Diagnostic .

Sign *

HARRY VESELI.? M.D.

Near,, Yorli, .New York

F OR a long time the occurrence of tri- cuspid valvular disease had been con- sidered rare and its clinical recognition

almost impossible. Studies’-8 during the past ten years, however, have added much to our knowledge of this valvular lesion. It has been shown that the condition is not so rare and that its clinical diagnosis can often be made. Nevertheless the definitive diagnosis of a tricuspid lesion, and spe- cifically of tricuspid stenosis, is still difficult at the bedside. The following observations are recorded to describe a new clinical sign which is simple to elicit and indicative if not pathognomonic of tricuspid stenosis.

CASE REPORT

P. S., a forty-four year old white man, dress operator, was admitted to the medical service of Beth Israel Hospital. There was no history of polyarthritis or chorea but he was known to have had a cardiac condition for twenty-five years. This was asymptomatic for twenty-two years during which time he worked regularly. During the three and a half years prior to ad- mission he attended the cardiac clinic of the hospital because of dyspnea, orthopnea and slight cough, some lack of his usual endurance and weakness. He also had been having attacks of precordial distress, sensations of internal pressure of moderate severity, lasting ten to twenty minutes each two to five times a week; these were not especially related to exertion but caused him to stop work temporarily. For two to three months before admission these symp- toms grew worse and he had frequent attacks of paroxysmal nocturnal dyspnea. His sputum was often blood-tinged.

Physical examination revealed him to be well

developed and well nourished, slightly dyspneic and slightly cyanotic. His temperature was normal. The sclerae were not icteric. The heart percussed enlarged to the left and downward. The apical impulse was felt 12 cm. from the midline in the fifth intercostal space. A systolic thrill was felt over the base especially over the aortic area. The following murmurs were heard: at the apex a loud, rough systolic and a less rough diastolic and presystolic; at the base a loud, rough systolic and a faint, blowing, early diastolic, loudest over the aortic area; at the tricuspid area (just to the right of the lower sternum) a rough, moderately loud diastolic murmur; a thrill was not felt over this area. A2 equalled Pz and was not accentuated. The rate was 80 to 90 per minute and regular. The radial pulses were small. The blood pressure was 135/90. With the patient in the sitting position the neck veins were distended and were seen to have fairly marked pulsations. When these pulsations, felt over the right carotid and jugular area, were correlated with the heart sounds they did not seem to be systolic in time. With the index finger of the left hand placed over the right jugular pulse near the base of the neck and the index finger of the right hand placed in the suprasternal notch, the impulses felt under both hands were quite forceful but not synchronous; the jugular came just before the one in the suprasternal notch. The latter was systolic and due to the pulsation of the dilated aorta and innominate artery; the former, venous and presystolic, apparently was produced by the contracting hypertrophied right atrium.

Over the lung bases, right and left, a few rales were heard on inspiration. The respiratory rate was 32 per minute. The liver was enlarged to three fingerbreadths below the costal margin and gave an impulse synchronous with the heart beat. The spleen was not palpable. There

* From the Medical Service of Beth Israel Hospital, New York, N. Y.

OCTOBER, 1949 497

Tricuspid Stenosis- Resell

was slight pretihial edema; no clubbing was present.

Laboratory data were as follows: The urine showed l-l- albumin. The hemoglobin was 15.0 Gm. (per cent); erythrocytes 5,630,OOO per c.mm. of blood. The blood Wassermann test was negative. The erythrocyte sedimentation rate was 5 mm. in forty-five minutes. N.P.N. of the blood was 39 mg. per cent. The venous pressure was equal to 17 cm. of water. The patient was not cooperative enough accurately to record the circulation time.

The teleroentgenogram revealed the cardiac silhouette to be markedly enlarged and fluoro- scopy disclosed enlargement of all chambers, dilatation of the aorta and calcification of the aortic valve. The electrocardiogram was typical of the pattern associated with left ventricular strain.

The diagnosis was rheumatic heart disease, enlarged heart, mitral stenosis, mitral insuffi- ciency, aortic stenosis, aortic insufficiency and tricuspid stenosis; regular sinus rhythm and class IV (classification of New York Heart Association).

There was considerable improvement in response to cardiac therapy but after ten days he insisted on leaving the hospital. One month later he was readmitted and stated he had been confined to bed at home most of that month and had taken his medication, 0.2 Gm. digitalis, daily. However, the dyspnea. orthopnea and weakness increased. There were occasional chest pains as before. His physician finally advised him to return to the hospital. This time he appeared very tired, dyspneic and slightly orthopneic. There was some cyanosis of the face and nail beds. Jaundice was not present. The physical findings were about the’same as re- corded one month before on the previous admission. There were more rales at both lung bases.

The neck veins were distended and pulsations were visible. The strong presystolic pulsation felt in the jugular area was again noted to “see- saw” with the systolic impulse felt in the supra- sternal notch. The enlarged liver and its pulsa- tions were felt. The diastolic murmur was again heard to the right of the lower sternum. Icterus index was 10. The electrocardiogram revealed no significant changes from the one previously described. Because of a rise in temperature to 101~.” on the second day a blood culture was taken but found sterile. The patient this time

failed to respond to therapy; symptoms in- creased and rales at the lung bases became more numerous. The temperature rose to 103O~. on the fourth day and the patient succumbed on the next, the fifth day of the second admission, apparently of cardiac failure and possible hypostatic pneumonia or pulmonary infarction.

Postmortem examination was performed by Dr. Henry Brody. The veins in the neck were unusually distended, sufficiently so on the left to make prominent one of the valves in the external jugular vein. The pericardial sac was markedly distended, containing 300 cc. of clear, light yellow fluid. The pericardial surfaces were smooth and glistening. The heart weighed 800 Gm.; it was roughly quadrilateral, measuring 16 by 16 cm. The anterior surface was made up almost equally by the right and left ventricles. The tips of the auricular appendages, both right and left, also appeared in the anterior view. The right atrium showed marked roughening and thickening of its epicardial surface. The diame- ter was but slightly increased; the trabecular markings were very prominent. A very small organized thrombus was present in the tip of the auricular appendage. The tricuspid valve was partly stenosed, not admitting two fingers. It was roughly elliptical, the axes measuring 2 and 1 cm., respectively. There was complete fusion of the valves at the commissures so that the individual cusps could not be distinctly recognized. The valve was thickened, irregu- larly nodular and somewhat stiffened. The chordae tendinae were only slightly thickened. They did not appear shortened. The right ventricle was small. The columnae carneae appeared moderately rounded. The chamber was filled with a large amount of postmortem clot.

From the ventricular aspect the thickening and deformity of the line of closure of the tri- cuspid valve were quite prominent. The right ventricular myocardium measured, 5 mm. in thickness in the region of the outflow tract. The circumference of the pulmonic valve was 6 cm. The posterior cusp in its left half was folded so that the normal free edge was adherent to the pulmonic surface of the valve. The new edge so formed was thick and showed a number of pin- head, glistening, grayish-white nodules. There was some thickening of the adjacent left cusp. The pulmonary artery showed only small, early atheromatous plaques. The left atrium was slightly dilated, its wall rather markedly thick-

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Tricuspid Stenosis-b’esell 499

ened. The foramen ovale was closed. The left auricular appendage was negative. There was some ridging and wrinkling of the atria1 endo- cardium posteriorly. The mitral valve was narrowed, forming a somewhat curved slit slightly less than 3 cm. in length. Its ring was completely calcified, forming knobby protru- sions into the lumen. On the endocardium were seen a number of smaller than pinhead, glisten- ing nodules.

The left ventricle showed some degree of dila- tation. The columnae carneae were definitely flattened. There was very marked hypertrophy of the wall, reaching a thickness of 18 mm. From the ventricular surface the marked stenosis and insufficiency of the valve was very striking. The chordae tendineae were markedly thickened but appeared stretched rather than flattened. A small moderator band was present, extending from the anterior surface to the mid-portion of the interventricular septum. There was marked graying and thickening of the endocardium of the interventricular septum immediately below the aortic valve. The aortic valve could best be viewed from above. The size of the lumen was entirely fixed due to calcification of the valve cusps. The lumen was almost circular with an approximate diameter of 11 mm. The cusps and their commissures were markedly thickened, calcified and showed many calcific protruber- antes. The calcification along two of the com- missures extended up the aorta for a distance of less than 1.5 cm. The wider of the two was 1.4 cm. Above these the ascending portion of the aorta was relatively free of any change except for a band of yellow atheroma-like deposit, 1 cm. wide and 5 cm. in length. There was also an area about 1 cm. in diameter which showed small, glistening, reddish elevations. The coro- nary orifices were not involved in the calcific process. The coronary arteries in their first portions were markedly sclerotic and in places calcified. There was, however, no serious im- pairment of the lumen at any point, and no ulcerations or thrombi.

In the lungs there were a few, small, fresh hemorrhagic infarcts at both bases; the pul- monary arteries showed practically no athero- sclerotic change. There were 100 cc. of light orange, clear fluid in the right pleural cavity and less than 200 cc. in the left.

The liver weighed 1,180 Gm. ; it measured 22 by 18 by 7 cm. Its markings were somewhat accentuated; lobulations were distinct.

OCTOBER, 1949

Microscopically, sections of the heart showed no evidence of active rheumatic inflammation. Perivascular, mostly acellular scars were numer- ous. The endocardium showed fibrous thicken- ing; the muscle fibers showed hypertrophy. Sections of lung, liver, spleen and kidney showed chronic passive congestion.

COMMENT

Venous phenomena are usually men- tioned in descriptions of tricuspid valvular disease. The veins of the body are engorged and dilated and the pressure therein in- creased. The veins in the neck are of particular concern. The prominent “a” wave in the jugular sphygmogram has been frequently referred to, as has the presystolic impulse in the veins of the neck and in the liver. The marked and chronic systolic pulsations of the deep jugular veins, a “vigorous pulsation raising the sternocleido- mastoid,” has been emphasized by White and Cook3s6 although they also indicated the absence of notable pulsation in the neck veins and liver in some cases.

Mackenzie9 told of one case in which a large wave was sent back from the hyper- trophied auricle with such force that it caused the valves in the jugular and sub- clavian veins to close with a snap which he heard over these veins as a clear, sharp sound preceding the first heart sound.

Some believed that without knowing the time of the pulse waves in the neck (or liver), the clinical diagnosis of tricuspid stenosis was not warranted. Wolferth8 em- phasized that the characteristic impulse in the veins in the neck in tricuspid stenosis should be presystolic. Crighton Bramwell has indicated the diagnostic value in tri- cuspid stenosis of a powerful auricular impulse which he recorded in the jugular sphygmogram. lo With auricular fibrillation the presystolic impulse is lost, and in nodal rhythm its timing is different.

In our case, demonstrated at necropsy to have tricuspid stenosis, a marked pre- systolic impulse was felt over the right jugular vein just above the clavicle and over the sternocleidomastoid muscle. This

500 Tricuspid Stenosis- Vesell

FIG. 1. Position of hands to elicit impulses over the jugular vein and episternal notch.

was of surprising force for a venous pulse. It was easily timed by comparison with the systolic aortic impulse in the episternal notch palpated by the index finger of the other hand. (Fig. 1.) A see-saw movement was conveyed to the two palpating fingers by the two vascular pulsations. The strong presystolic venous impulse over the jugular vein was considered caused by the contrac- tion of the hypertrophied right atrium; this impulse was well transmitted to the neck because of the obstruction at the stenotic tricuspid orifice causing a damming-back action, the right atrium being unable to empty itself readily. Transmission of the impulse was also aided by the increased venpus distention and increased pressure in

the large veins central to this area. We have never felt a presystolic impulse in the jugular vein in congestive heart failure without tricuspid stenosis. The systolic im- pulse in the episternal notch due to the pulsation of the adjacent dilated aorta and innominate artery was undoubtedly modi- fied by the aortic valvular disease present. It is increased by the insufficiency of the valve though decreased by the stenosis, lesions which accompany most cases of tricuspid stenosis.

SUMMARY

A simple sign characteristic of tricuspid stenosis is described. A case of tricuspid stenosis with necropsy findings is reported in which this sign led to the correct ante- mortem diagnosis.

REFERENCES

1. ALTSCHULE, M. D. and BUDNITZ, E. Rheumatic disease of the tricuspid valve. Arch. Path., 30: 7, 1940.

2. ALTSCHULE, M. D. and BLUMGART, H. L. The circulatory dynamics in tricuspid stenosis. Am. Heart J., 13: 589, 1937.

3. COOKE, T. and WHITE, P. D. Tricuspid stenosis- with particular reference to diagnosis and progno- sis. Rd. Heart J., 3: 147, 1941.

4. DRESSLER, W. Clinical Cardiology. New York and London, 1942. Paul B. Hoeber.

5. FRIEDLANDER, R. D., and KERR, W. J. The clinical diagnosis of tricuspid stenosis. Am. Heart J., 11: 357, 1936.

6. GARVIN, C. F. Tricuspid stenosis-incidence and diagnosis. Arch. Int. Med., 70: 104, 1943.

7. SMITH, J. A. and LEVINE, S. A. The clinical features of tricuspid stenosis. Am. Heart J., 23: 739, 1942.

8. WHITE, P. D. and COOKE, W. T. The recognition and significance of marked and chronic systolic pulsation of the deep jugular veins. Tr. 8. Am. Physichns, 54: 199, 1939.

9. MACKENZIE, SIR JAMES. Diseases of the Heart. 3rd ed., p. 337. London, 1921. Henry Frowde and Hodder and Stoughton.

10. BRAMWELL, C. and KING, F. The Principles and Practice of Cardiology. P. 151. London, 1942. Oxford University Press.

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