Abstract
Introduction
Benjamin Britten, whose centenary we celebrated in 2013, was the greatest English composer of opera since Handel. His major works have never left the repertory and include Gloriana, Peter Grimes and The Turn of the Screw. He died in 1976 from heart failure having had aortic valve surgery three years earlier. The anniversary year of his birth saw an avalanche of performances, films, articles and books, including two new biographies.
The press coverage included speculation about the cause of the heart valve disease that led to his premature death. Paul Kildea’s biography 1 proposed that Britten was suffering from tertiary syphilis. This diagnosis is at variance with the contemporary medical evidence as discussed in Humphrey Carpenter’s earlier biography. 2 This essay examines Kildea’s diagnosis and also poses the question: when should doctors discuss their patient’s illnesses publicly?
The syphilis suggestion
Kildea sets the scene by alluding to the decades of Britten’s youth as being ‘awash with the disease’. He reinterprets Britten’s illness in 1940 when he and Pears were in America as being due to secondary syphilis. The contemporary diagnosis was tonsillitis but complicated by ‘mental perplexities’ to quote Britten himself. Secondary syphilis was nevertheless relatively common in those days and would surely have been recognised by one of the six doctors whom Britten consulted, if that diagnosis had been correct. Kildea hints that Britten’s eminence and the fact that ‘gentlemen of a certain class did not discuss such things … deflected any further probing into his medical history by his doctor in 1960’.
The basis for Kildea’s diagnosis is a conversation that took place between the surgeon, Donald Ross and his friend the cardiologist Hywel Davies in the late 1980s. Davies, who had no involvement in Britten’s care and who practised in America, has also published his account of the conversation in the New Statesman. 3 Davies presents the case for the diagnosis of syphilis in his article but with no medical data. Kildea in his book amplifies the case with statements such as ‘When Ross cut open Britten’s chest and began working on the grossly enlarged heart he discovered the aorta was riddled with tertiary syphilis’. He alleges that the wrong operation was performed, that tests for syphilis were rarely undertaken, and draws a conclusion that has engendered much publicity.
Britten’s cardiac history
Britten was admitted to the National Heart Hospital under the care of the cardiologist Graham Hayward on 2 May 1973. Hayward, like the other senior consultants, visited the hospital once a week. The daily management of Britten’s case was my responsibility. His history included the finding of a heart murmur in infancy following an episode of pneumonia. He had enjoyed an active lifestyle playing vigorous tennis, and swimming, up to six times a day. Aortic regurgitation was detected in 1960 and was complicated by endocarditis in 1968. Subsequently, he remained unwell with fatigue and shortness of breath to such an extent that Peter Pears commented that the effort of composing the opera Death in Venice was killing him. It also seems likely that he was suffering from a cardiac rhythm disturbance. Robert Matthew-Walker 4 in his article on the opera has perceptively pointed out that the opera opens with clarinets a tone apart playing a very irregular rhythm that matched exactly his own arrhythmia. While his was a paroxysm of atrial fibrillation, another possibility would be multiple ventricular ectopics, a common rhythm disturbance in patients with left ventricular volume overload; both arrhythmias were observed later in Britten’s case.
Physical examination confirmed the typical features of a severe aortic valve leak. Screening for syphilis was routine for all patients with leaking aortic valves; neither then nor, as confirmed by Tait during numerous conversations with myself and other doctors, was there any record of a positive result throughout the 1960s. I undertook cardiac catheterisation and demonstrated severe aortic regurgitation with normal coronary arteries. The aorta was dilated but not aneurysmal. The coronary ostia were not narrowed. There was therefore no suggestion of syphilitic aortitis. The left ventricle was dilated, but with ‘vigorous’ contraction as would be expected because Britten’s diastolic blood pressure was only 60 mmHg and his ventricle was therefore working against a very low resistance.
The longstanding aortic valve leak and dilated left ventricle meant that Britten’s heart was not going to recover fully and that his life expectancy was limited, even with successful surgery. We nevertheless considered that valve replacement with a homograft, rather than a mechanical prosthesis with the attendant risks of anticoagulation, offered him the best chance of an improved quality and length of life. Prior to the surgery, we thought that the most likely diagnosis was a congenital bicuspid valve that had become worn and further damaged by endocarditis.
Valve surgery
Donald Ross’ operation report dated 7 May 1973 is detailed and describes the external appearance of the heart as having an enlarged, bulky and flabby myocardium with a distended pulmonary artery root and poorly contracting left ventricle. He describes the appearance of the valve as uncharacteristic but severely regurgitant with a rolled and thickened right coronary cusp. Sumner, the anaesthetic senior registrar, remembers the procedure very well and had an excellent view of the aorta from his position at the head of the operating table. He describes the valve as typically degenerate and calcified; the aortic valve and root were not ‘riddled with syphilis’. The histology of the excised valve showed slight thickening of collagen tissue and also prominence of the zona spongiosa. Vascularity was not increased, and there were no other histological features that suggested infection in the past. The appearances were ‘totally non-specific’, and the suggestion was made that the cause was ‘a myxomatous degeneration of the valve cusps, which has been described in patients with Marfan’s disease, Marfan’s forms frustes or idiopathic’. The use of the word specific in the report is important because it was a euphemism for syphilis in those days; the pathologist is thus telling us that he thought about syphilis but found no supporting evidence.
There is nothing in the operation note to suggest that the procedure was particularly challenging, or that Ross had to ‘stretch the tissue valve to make it fit the syphilitic aorta’ as alleged by Kildea (which would have been a very odd thing to do). Kildea writes: ‘The surgery and mop-up took six hours and was hugely problematic from the outset’. There was a delay in Britten’s return to the ward due to the anticipated difficulty in coming off bypass, then ventricular ectopics and the growing awareness that he had suffered a stroke.
Postoperative course
Britten did not do well after his operation. His stroke affected his speech and right side. This improved with time, but his right hand was permanently affected. He also developed congestive heart failure, not unexpectedly. Since Britten and Hayward did not get on, it was suggested that I should follow him up, which I was privileged to do, visiting him in Aldeburgh regularly. The drugs available to us were limited – digoxin and diuretics, but these did nevertheless bring about relief of congestion. Through the next two years, Britten enjoyed a reasonable quality of life but his fatigue and malaise persisted – primarily due to his damaged left ventricle and also due to a progressive valve leak. Most homograft valves were fine for many years; he was unlucky. Britten’s life was weakened by 1976 and ebbed away peacefully on the night of 3–4 December. I remember his Cheyne-Stokes respiration and Pears and his nurse at his bedside.
Aftermath
Syphilitic infection of the aorta was rare by the 1970s. Grabau found just 15 cases at the Heart Hospital in the previous 10 years. 5 A concealed history of primary or secondary syphilis seems highly unlikely, given the climate of honesty and confidentiality that prevailed in medical circles then, and which was respected by the press. The serological tests for syphilis were not precise but nevertheless they were undertaken, repeatedly, and no positive result was obtained. Many of the preoperative findings were negatives, such as the normal coronary ostia and lack of aneurysmal dilatation of the aorta, but syphilis was very much in the minds of Tait, Hayward and myself before the operation and we found no evidence. Kildea states that Britten was not aware of the diagnosis, but Tait would surely have discussed this possibility with Britten.
Ross was puzzled by the operative appearances. If he had suspected the diagnosis of syphilis in 1973, he would have shared his suspicion with his colleagues. The impact on Britten’s subsequent medical management would have been so great that not to have done so would have been a serious breach of duty. There was no reason to conceal the diagnosis. For all those of us directly involved in Britten’s care to have conspired in a cover up is a ridiculous allegation.
The most persuasive evidence to rebut the suggestion that Britten had tertiary syphilis comes from the histology of the valve. Mucoid degeneration of the aortic valve is now well recognised as a common cause of aortic valve disease and root dilation without the other features of Marfan’s syndrome. Aortic root disease has for some time been more common than primary valve disease in patients undergoing valve replacement for isolated aortic regurgitation. 6 This pathological series is of interest because, among the 268 patients, 15 (6%) had the ‘Marfan syndrome or forme fruste’; none had syphilitic aortitis; the commonest category was ‘cause unclear’. Progressive regurgitation is well described in patients with myxomatous proliferation of the aortic valve. 7 None of us was familiar the pathology of mucoid degeneration in 1973. No wonder Ross was puzzled. The pathology of syphilitic aortitis was well known 8 and we would have recognised that. A speculation about syphilis during a conversation with a friend many years later is not an adequate reason for changing the contemporary diagnosis. The clinical data fit best with the pathologist’s diagnosis, namely an incomplete form of Marfan’s syndrome.
Comment
Kildea’s reliance on a secondary source for his biography has certainly hit the headlines, but the general view now seems to be that the seven pages of speculation have marred what is otherwise a rather good book. Kildea is a notable musician who belongs to an imaginative and creative genre, naturally attracted by a good story, despite my advice some time before publication that he would be irresponsible to publish his account without good supportive evidence.
Britten’s stature as a musician is unaffected by the allegation. The medical conditions of many composers have been a fruitful area of historical research, and the diagnosis of syphilis has not tarnished the reputation of Schubert, for example. In Britten’s case, historians might do better to speculate what he might have written had he had his valve surgery before writing Death in Venice as advised; or was the opera destined to be his final great work?
There must be a time when the long-term interests of the famous are best served by a discussion of their medical details some years after their death, but while the protagonists still possess testamentary capacity. Should Ian Tait and I have set out details of Britten’s medical history some years ago, perhaps at the time of Carpenter’s biography?