Br Heart J 1980; 43: 470-3

Left vocal cord paralysis and dysphagia inmitral valve diseaseA A MORGAN, A J MOURANT

From University College Hospital, London; and the Cardiac Department, The London Hospital,London

SUMMARY Two cases of severe mitral stenosis with both hoarseness, caused by left vocal cord palsy,and dysphagia are described. This combination in the same patient has not, to our knowledge, beenpreviously described.

Previous studies have firmly established that vocal cord paralysis in mitral stenosis is a result ofcompression of the left recurrent laryngeal nerve as it passes around the aortic arch. It is suggestedthat dysphagia may also develop as a result of neurological damage, in this case to autonomic nerve

plexuses supplying the oesophagus, leading to abnormal peristalsis and enabling external compressionby a tense left atrium sufficient to cause symptoms.

Left vocal cord paralysis and dysphagia are un-common complications of mitral valve disease.Since first described by Ortner,' studies haveindicated that left recurrent nerve palsy occursin less than 1 per cent of patients with mitralstenosis.' Dysphagia has been reported in only asmall number of patients.'-6

After an extensive search of the world's publica-tions we have been unable to find any reportedcases of mitral stenosis with both hoarseness,Received for publication 27 July 1979

a

caused by left recurrent laryngeal nerve palsy, anddysphagia. We report two such patients and discussthe mechanisms by which the abnormalities mayarise.

Case 1

This patient developed palpitation at the age of 55,when she was found to have mitral stenosis withatrial fibrillation; there was no history of rheumaticfever. The palpitation settled with digoxin, and she

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Fig. 1 Radiological investigations in case 1. (a) Chest x-ray, showing conspicuous cardiomegaly with gross left atrialenlargement. (b) Barium swallow (right anterior oblique projection) showing backward displacement of the oesophagusaround the enlarged left atrium. (c) Hilar tomography during the barium swallow showing delayed passage of contrastmaterial at the angle of tracheal bifurcation and pronounced upward displacement of the left main bronchus.

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remained well for 10 years when mild effortdyspnoea developed. Five years later she becamehoarse, and subsequent laryngoscopy revealedcomplete paralysis of the left vocal cord. Over thenext two years she noticed difficulty in swallowingsolid foods, which felt to her as if they were stickingin the middle of her chest. She had also becomemore breathless with effort and slept with fourpillows to avoid orthopnoea.On examination, she was in atrial fibrillation with

a slight increase in jugular venous pressure, rightventricular enlargement, and the auscultatoryfindings of severe mitral stenosis. The electrocardio-gram was compatible with these findings. Her chestx-ray film showed distinct cardiomegaly (Fig. la).At cardiac catheterisation the indirect left atrialpressure was 30 mmHg (mean) and she was foundto have an end-diastolic gradient across the mitralvalve of 15 mmHg and a pulmonary artery pressureof 90/40 mmHg. Left ventricular angiographyshowed trivial mitral reflux. Finally, barium studiesshowed considerable backward displacement of theoesophagus with delayed passage of dye through themid-portion (Fig. lb), and hilar tomography during

the barium examination indicated gross wideningof the angle of tracheal bifurcation (Fig. lc).A diagnosis of severe mitral stenosis with pul-

monary hypertension was made. She declinedoperation and is being treated with digoxin anddiuretics.

Case 2

At the age of 41 this housewife underwent mitralvalvotomy because of increasing breathlessnesssecondary to mitral stenosis. There was no historyof rheumatic fever. Ten years later she sustained aleft hemiplegia from which she made a completerecovery. She was virtually asymptomatic for afurther three years, when effort dyspnoea and ankleoedema developed, and two years later she wasadmitted to hospital in acute pulmonary oedemawhich improved with diuretic treatment. Sheunderwent cardiac catheterisation when severemitral stenosis with a gradient of 15 mmHg wasfound. Pulmonary artery pressure was 55/20 mmHg,with mean indirect left atrial pressure of 20 mmHg('v' wave, 30 mmHg). Angiography disclosed trivial

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Fig. 2 Radiological investigations in case 2. (a) Penetrated PA chest x-ray film showing cardiomegaly, left atrialenlargement, prominent left pulmonary artery, and upward displacement of the left main bronchus. (b) Barium swallow(right anterior oblique projection) showing compression and backward displacement of the oesophagus.

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Morgan, Mourant

mitral regurgitation and slight aortic regurgitation;left ventricular contraction was normal. She de-clined operation but subsequently became increas-ingly breathless with effort and developed bothdysphagia and hoarseness. At laryngoscopy the leftvocal cord was noted to be completely paralysed.

She was readmitted to hospital. The venouspressure was slightly raised and both ventricles wereclinically enlarged. Auscultatory findings were ofsevere mitral stenosis and slight aortic regurgitation.The electrocardiogram showed right axis deviationwith digoxin effect and her chest x-ray film showedsevere cardiomegaly with left atrial enlargement andupward displacement of the left main bronchus(Fig. 2a). At barium swallow oesophageal displace-ment and compression were shown (Fig. 2b).

She underwent mitral valve replacement surgerywith a Bjork-Shiley prosthesis and her post-operative progress was uneventful, though she wasstill hoarse when examined six weeks later. Shedied suddenly two months after operation but therewas no necropsy.

Discussion

Left vocal cord paralysis in mitral stenosis is causedby compression of the left recurrent laryngeal nervebetween the aortic arch and the pulmonary artery7

which is displaced upwards by the enlarged leftatrium (Fig. 3a). Enlarged tracheobronchial lymphnodes may be an additional contributory factor.8The mechanisms of dysphagia in association withmitral valve disease are less certain. Normalswallowing is controlled and co-ordinated byautonomic nerve plexuses in the oesophagus. Theseplexuses derive their nerve supply from the vagusnerves and thoracic sympathetic outflow; fibresform the posterior pulmonary plexuses from whichfour or five cords pass posteriorly to the middle ofthe oesophagus. The cords then divide into theoesophageal plexus which supplies afferent andefferent fibres (Fig. 3b). During normal peristalticcontraction, pressure within the oesophageal lumenreaches peak values of 40 to 80 mmHg.9

In severe mitral stenosis the enlarged left atriumdisplaces the oesophagus, usually backwards andto the right.5 6 Pressure within the left atrium isincreased and may interfere with normal oeso-phageal peristalsis sufficient to cause dysphagia,though the maximum pressure applied to the oeso-phagus by the left atrium is never likely to exceedpeak intra-oesophageal pressure during activeperistalsis. However, autonomic nerve fibresstretched between the posterior pulmonary plexusesand the oesophagus may themselves be damaged,resulting in abnormal oesophageal peristalsis and

a UFig. 3 Normal anatomical relations of the left atrium (drawn by J Abbott). (a) Anterior view showing the leftrecurrent laryngeal nerve passing around the aortic arch, behind the ligamentum arteriosum and above the leftpulmonary artery and left main bronchus. (b) Posterior view showing division of the vagus nerves into posteriorpulmonary plexi, from which fibres pass over the left atrium to the oesophagus.

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an increased likelihood to dysphagia developing asa result of external compression from the enlargedand tense left atrium.The two patients described in this paper

developed both hoarseness and dysphagia as theseverity of the mitral valve disease increased. Ineach case hoarseness was found at laryngoscopy tobe caused by left vocal cord paralysis. Dysphagiawas not sufficient to cause extreme difficulty inswallowing in either patient though both describedthe sensation of food sticking at mid-thorax level.Barium swallow showed conspicuous oesophagealdisplacement around an enlarged left atrium in eachpatient, and there is no doubt that the degree ofdisplacement would have been sufficient to stretch,and possibly damage, nerves supplying the oeso-phageal plexus.

We thank Dr W Brigden for permission to reportthese cases under his care and for his help inthe preparation of this paper.

References

'Ortner N. Recurrenslahmung bei Mitralstenose. WienKlin Wochenschr 1897; 10: 753-62.2Wood PH. Diseases of the heart and circulation, 3rd ed.London: Eyre & Spottiswoode, 1968: 624.3Bloomfield AL. Dysphagia with disorders of the heartand great vessels. Am J Med Sci 1940; 200: 289-99.4Dines DE, Anderson MW. Giant left atrium as a causeof dysphagia. Ann Intern Med 1966; 65: 758-61."le Roux BT, Williams MA. Dysphagia megalatriensis.Thorax 1969; 24: 603-6."Whitney B, Croxon R. Dysphagia caused by cardiacenlargement. Clin Radiol 1972; 23: 147-52.7White PD. Heart disease, 3rd ed. New York: Macmillan,1947: 615.8Dolowitz DA, Lewis CS. Left vocal cord paralysisassociated with cardiac disease. Am J Med 1948; 4:856-62.9Earlm R. Clinical tests of oesophagealfunction. London:Crosby Lockwood Staples, 1976: 42.

Requests for reprints to Dr A J Mourant, CardiacDepartment, The London Hospital, Whitechapel,London El 1BB.

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