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The normal mitral valve provides unidirectional flow from left atrium (LA) to left ventricle (LV) in a smooth and efficient fashion. Mitral incompetence allows backward flow into the LA, requiring the LV to pump additional volume to compensate for that lost to regurgitation (MR). In its compensated state, even severe chronic MR is remarkably well tolerated at least for short periods of time. Patients are often totally asymptomatic, and many can achieve normal results during cardiopulmonary stress testing, objective proof that symptom absence is based upon true physiological compensation for the existing pathological state.1 How does the LV accomplish this feat? Logically, it must be able to generate adequate forward stroke volume at physiological filling pressure, lest the patient would develop dyspnoea on exertion.
Stroke volume is dependent on innate LV volume (elephants have bigger stroke volumes than mice), contractility, preload and afterload. Three of the four of these properties, volume, preload and contractility, are fairly straightforward. LV remodelling in chronic MR is unique, leading to an enlarged thin-walled chamber.2 Both in man and in the experimental animal, this remodelling leads to increased LV compliance (an unusual occurrence in cardiology) and enhanced LV filling, the mechanism whereby the large diastolic volume of MR is accommodated at near-normal filling pressure.3 Obviously, this same remodelling increases total LV volume, so that normal ejection creates increased total stroke volume in turn maintaining forward stroke volume in the normal range. Volume expansion of …
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