Faculty Bibliography

PURPOSE OF REVIEW: Functional mitral regurgitation (FMR) is a common complication of left ventricular dysfunction. It is now recognized as an important clinical entity and an independent predictor of poor prognosis in cardiomyopathy patients. In this review, we provide a comprehensive summary of the pathophysiology, latest imaging modalities, and diagnostic criteria for FMR. Additionally, we discuss the recent literature on the continuously evolving surgical and percutaneous treatment options. RECENT FINDINGS: The criteria for quantification of FMR on echocardiography were updated and are distinct from organic mitral regurgitation in the most recent American College of Cardiology/American Heart Association 2014 valve guidelines. Furthermore, the evolving role of MitraClip for potential treatment of FMR offers exciting prospects to treat high-risk symptomatic patients. SUMMARY: Our review serves to consolidate the current diagnostic and treatment modalities for FMR and provide a contemporary resource for clinicians while treating patients. Additionally, we identify the gaps present in our knowledge of FMR to guide further clinical investigation.

Metabolic syndrome (MS) is commonly associated with left ventricular (LV) diastolic dysfunction and LV hypertrophy. We sought to examine whether preclinical LV diastolic dysfunction can occur independent of LV hypertrophy in MS. We recruited 90 consecutive participants with MS and without cardiovascular disease (mean age 46 years, 78% women) and 26 controls (no risk factors for MS; mean age 43 years, 65% women). Participants underwent echocardiography with tissue Doppler imaging. In age- and gender-adjusted analyses, MS was associated with higher left atrial (LA) diameter, higher LV mass, lower E/A ratio, and lower mean e' (p <0.001 for all). These associations remained significant after further adjusting for blood pressure, antihypertensive medication use, and body mass index. After adjusting for LV mass, MS remained independently associated with higher LA diameter, lower E/A ratio, and lower mean e' (p ≤0.01 for all). Specifically, subjects with MS had a 1.8 cm/s lower mean e' compared with controls (p = 0.01). Notably, differences in mean e' between those with and without MS were more pronounced at younger ages (p for interaction = 0.003). In conclusion, MS was associated with preclinical LV diastolic dysfunction independent of LV mass, as reflected by higher LA diameter, lower E/A ratio, and lower mean e'. This suggests that MS can lead to the development of diastolic dysfunction through mechanisms independent of hypertrophy. Differences in diastolic function were more pronounced at younger ages, highlighting the potential importance of early risk factor modification and preventive strategies in MS.