George Burch was a prominent American cardiologist and contributed extensively to the knowledge of the heart disease, particularly in the field of electrocardiography. He held the position of Chairman of the Department of Medicine at Tulane University.
In 1963, Burch in collaboration with Pasquale and Phillips reported a case series in which two patients presented with new onset systolic murmur of mitral regurgitation following extenisve anteroseptal myocardial infarction. Both these patients expired at ten days and 5 months respectively after the initial presentation from congestive heart failure. Autopsy examination, in both cases, showed extensive anteroseptal scar tissue. Furthermore, papillary muscles and chordae tendinae were not ruptured in either cases.
Following these observations, Burch et al postulated several hypotheses to describe the mechanism of mitral regurgitation after myocardial infarction in the absence of papillary muscle rupture. They introduced the concept of "papillary muscle dysfunction."
In the conclusion of their article, these authors commented:
"A syndrome is described which should be considered in the differential diagnosis of precordial systolic murmurs which develop suddenly after myocardial infarction. The syndrome is considered to develop as a result of infarction of a papillary muscle. Failure of the infarcted papillary muscle to contract during systole results in mitral regurgitation and an associated apical systolic murmur...The syndrome of mechanical dysfunction of a papillary muscle was extended to include instances in which the normal spatial relationship between a papillary muscle and the mitral cusps is altered by an aneurysm of the left ventricle or fibrosis and contraction of a papillary muscle. In these instances the murmur of mitral regurgitation should begin with the first heart sound at the apex."
In this article, Burch et al reported the occurrence of mitral regurgitation after myocardial infarction without papillary muscle rupture. They postulated several hypotheses to explain the mechanism of mitral regurgitation including the lack of contraction of infarcted papillary muscle which would lead to mitral valve prolapse. During the last two decades, experimental and sophisticated imaging studies have not confirm this hypothesis and have shown that following a myocardial infarction, left ventricle remodels and transforms from a normal elliptical shape into a more spherical shape. This modification of the left ventricular geometry leads to an apical and lateral displacement of papillary muscles (mostly the postero-medial papillary muscle) causing a tethering of the mitral leaflets. This apical tenting of the leaflets prevents their free margin to reach the plane of the annulus, reduces significantly the surface of coaptation during systole and produces mitral regurgitation.
As mentioned above, they also provided an explanation for the frequent finding of mitral regurgitation in patients with myocardial infarction and aneurysm of the free wall of the left ventricle. In this clinical setting, their hypothesis is extremely close to our current knowledge and these authors should be recognized for their important original contribution to our knowledge of the mechanism of ischemic mitral regurgitation.