Traite clinique et pratique des maladies du coeur et de la crosse de l'aorte. Paris. J.B. Bailliere, 1883.
Diagnostic et traitement des maladies du coeur. Paris, Asselin & Cie., 1883.
During the second half of the 19th century, textbooks on diseases of the heart were published with a greater frequency in England and France.
In England, Walsh and Stokes wrote comprehensive textbooks with extensive sections on valvular heart diseases which included original contributions. These authoritative works have already been discussed. Another important contributor was Sir Byrom Bramwell, who published his "Diseases of the heart and thoracic aorta" in 1884. The chapter of Bramwell's monograph on endocarditis is described in the Disease Specific Approach section. During that period, other outsanding physicians such as Fothergill, Balfour and Broadbent published their own textbook on cardiac diseases. Their works, however, had limited impact in enhancing our understanding of mitral valve pathology.
In France, two important contributors were Michel Peter and Constantin Paul who published their cardiology textbook in 1883. Paul's monograph was translated into English in 1884.
Michel Peter wrote a comprehensive chapter on mitral valve disease which included the state-of-the-art knowledge of his days. He also incorporated the graphic methods of Marey and discussed extensively the findings of sphygmography in patients with mitral valve stenosis or regurgitation.
An interesting part of this chapter is the discussion regarding functional mitral regurgitation. Peter believed that the latter was caused by the lack of contraction of the left ventricle ( "ATONIE du muscle ventriculaire gauche"). He was of the opinion that this ventricular dysfunction was often a temporary phenomenon. Peter strongly disagreed with the alternative hypothesis which was expressed by some of his colleagues. In his monograph, he wrote:
"...some have tried to demonstrate that the reason for insufficiency [functional mitral insufficiency] is the dilatation of the ventricle; as the chordae tendinae could not develop parallel to the ventricular dilatation, they would become too short and at the time of systole they would prevent the upward motion and the coaptation of the leaflets, leading to mitral insufficinecy. I personally believe, that this murmur of mitral insufficiency is not due to the dilatation of the orifice.., or to the dilatation of the ventricle, but it results in reality from the lack of contraction of the left ventricular muscle..."
This explanation that Peter refuted is the foundation ,nowadays, for the pathophysiology of mitral valve regurgitation in dilated and ischemic cardiomyopathy.
Peter's chapter on "mitral valve lesions" beautifully illustrated is displayed here.
Constantin Paul also devoted an extensive section of his valuable monograph to mitral valve disease. He placed a great emphasis on physical diagnosis, particularly cardiac auscultation. He reviewed in detail the work of his predecessors that elucidated the mechanism and timing of murmurs in mitral valve disease. Similarly to Peter, he used Marey's sphygmograph to study the radial pulse in patients with mitral valve stenosis or regurgitation. He described the symptoms associated with mitral valve disease and reviewed the evolution and prognosis of this affection.
Paul reviewed in detail the anatomical lesions in the setting of mitral stenosis or regurgitation. He performed numerous autopsy examinations in patients with mitral regurgitation and left ventricular dilatation and expressed Peter's opposite view. In his monograph, Paul wrote that in patients with mitral regurgitation due to left ventricular dilatation it was important to analyse valvular lesions through the ventricular cavity. He then continued that in this scenario, papillary muscles were separated, leading to a displacement and separation of chordae tendinae. He also stressed that in the setting of cardiac enlargement, the deformation of the posterior wall would lead to a transverse deformation of the mitral orifice with an anterior leaflet which becomes short and a posterior leaflet that does not function any longer. Paul's explanation of the mechanism of mitral regurgitation in patients with enlarged heart was rediscovered and reconfirmed more than a century later using sophisticated imaging modalities.