Valvular-ventricular interaction: the importance of the mitral chordae tendineae in terms of global left ventricular systolic function.
While conventional mitral valve replacement (MVR) for patients with chronic mitral regurgitation has been associated with relatively high operative mortality rates and incidence of late postoperative left ventricular (LV) failure and death, chordal-sparing mitral valve operations (valve repair/reconstruction or MVR with preservation of the chordae tendineae) subjectively appear to portend lower operative morbidity and mortality rates, better functional results, and improved long-term survival rates. Such empirical clinical observations have provided the basis for the concept of valvular-ventricular interaction, namely, that the intact mitral chordae are important mediators of more efficient and forceful ventricular contraction that enhances LV performance. This paper reviews the pertinent basic physiology and dynamics of the chordae tendineae and papillary muscles and examines critically the available experimental and clinical data regarding valvular-ventricular interaction. The problems inherent in quantifying LV contractility are central to this discussion and are also examined. While earlier experimental studies have produced conflicting results, more recent experiments utilizing load-independent measures of ventricular performance (particularly in isovolumic preparations) have conclusively demonstrated the importance of chordal integrity for optimal LV systolic function in normal animal hearts. The balance of the clinical evidence is also suggestive (although by no means conclusive) regarding the importance of valvular-ventricular interaction. Recent experimental evidence suggests that the mitral chordae enhance LV systolic function by means of regional afterload reduction. The mechanism(s) responsible for valvular-ventricular interaction, however, remains incompletely characterized at the present time, which underscores the urgent need for further experimental and, most importantly, clinical studies.
Sarris
G E
GE
Department of Cardiovascular Surgery, Stanford University School of Medicine, California.
Miller
D C
DC
D000818:Animals; D006348:Cardiac Surgical Procedures / Q000379:methods / Q000401:mortality; D002815:Chordae Tendineae / Q000502:physiology* / Q000601:surgery; D004195:Disease Models, Animal; D004285:Dogs; D005069:Evaluation Studies as Topic; D006439:Hemodynamics; D006801:Humans; D008944:Mitral Valve Insufficiency / Q000503:physiopathology / Q000601:surgery; D009200:Myocardial Contraction / Q000502:physiology; D010210:Papillary Muscles / Q000502:physiology*; D015996:Survival Rate; D013552:Swine; D016277:Ventricular Function, Left / Q000502:physiology*