Background A large volume of literature has documented racial disparities in the delivery of cardiovascular care in the United States and that decreased access to procedures and undertreatment lead to worse outcomes. A lack of diversity among physicians is considered to be a major contributor. The fellowship training program in cardiovascular medicine at The Ohio State University Medical Center had never trained a fellow from a minority group underrepresented in medicine (URM) before 2007. Intervention In 2005, the fellowship made it a priority to recruit and match URM candidates in an effort to address the community's lack of diversity and disparities in cardiovascular care. Methods Program leaders revised the recruitment process, making diversity a high priority. Faculty met with members of diverse residency programs during visits to other institutions, the focus of interview day was changed to highlight mentorship, additional targeted postinterview communications reached out to highly competitive applicants, and a regular mentoring program was constructed to allow meaningful interaction with URM faculty and fellows. Results Since these changes were implemented, the program has successfully matched a URM fellow for 5 consecutive years. Such candidates currently make up 4 of 16 total trainees (25%) in the fellowship in cardiovascular medicine. Conclusions The cardiovascular medicine fellowship training program at The Ohio State University was able to revise recruitment to attract competitive URM applicants as part of a concerted effort. Other educational programs facing similar challenges may be able to learn from the university's experiences.

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A 53-year-old woman with a history of hypertension was referred for an echocardiogram by her primary care physician after an unspecified abnormal ECG. The echocardiogram showed normal left ventricular size and function; however, an isolated cleft posterior mitral valve leaflet was identified with concomitant bileaflet prolapse and mild mitral regurgitation. She was subsequently referred to a cardiologist for clinical evaluation. Cleft mitral valve leaflet (CMVL) is an uncommon congenital cause of mitral regurgitation. Clefts, defined as slit-like holes or defects, are hypothesized to be a result of incomplete expression of an endocardial cushion defect which most commonly involves the anterior mitral valve leaflet with a paediatric incidence of 1:1340. Clefts affecting only the posterior mitral valve leaflet are extremely rare with only four cases being reported in the medical literature. Important co-existing anomalies with either posterior and/or anterior CMVL include counterclockwise rotation of the papillary muscles, the presence of an accessory papillary muscle or mitral valve leaflet, atrial septal defects, and mitral valve prolapse. Regurgitation from CMVL can lead to important physiological and anatomical changes within the cardiac system. Regurgitation results from blood flow directly through the cleft itself or from malcoaptation from accessory chordae with or without papillary muscle distortion. Significant chronic mitral regurgitation elevates left atrial filling pressures and leads to chamber enlargement and eccentric left ventricular hypertrophy. Early detection through two-dimensional echocardiography can provide accurate anatomical images of the various mitral valve structures and identify associated congenital anomalies. Early surgical correction is preferred before mitral regurgitation causes unfavourable remodelling. Most mitral valve cleft defects can easily be repaired by suturing the edges of the cleft. If a cleft resection leads to limited residual valve tissue, the leaflet of the mitral valve can be reconstructed using an autologous pericardial patch pre-treated with buffered glutaraldehyde. Posterior CMVL is an uncommon but clinically important cause of mitral insufficiency. Early recognition of this rare clinical entity and possible co-existent anomalies can identify the patients who would benefit from surgical intervention before compensatory left ventricular remodelling and contractile dysfunction develop.