Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5812573 | Medical Hypotheses | 2012 | 4 Pages |
Abstract
It is hypothesized that an increased EF in HFpEF patients has a role in augmenting cardiac output (CO) especially during exercise. Normal mechanisms for increasing CO are restricted in HFpEF. For e.g., recruiting the Frank-Starling mechanism is limited by a thick left ventricle (LV) which is stiff and distends, however with greater than normal filling pressure. Increasing heart rate and decreasing systemic vascular resistance during exercise was shown to be significantly restricted in HFpEF. It is hypothesized that a “greater than normal” EF in HFpEF translates into a more forceful contraction, storing elastic energy (during systole) in the myocardial tissue. When systole terminates, as the contractile elements detach, the stored energy is utilized for rapid relengthening of the contractile elements of the myocardium, before mitral valve opening. The abrupt expansion of the LV decreases LV pressure to a minimum, thereby increasing the pressure gradient between the left atrium and LV. The latter pressure gradient accounts for an efficient early LV filling. Using the energy stored during systole in favor of early LV filling is referred to as elastic recoil (ER, also termed: diastolic suction). ER is especially important when heart rate is increased, resulting in a short time window for LV filling. The mechanism of ER is hypothesized to account for maximizing the potential for early LV filling. A systematic review of the literature is needed to verify that the observation is true, and further studies to support this hypothesis.
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Authors
Guy Dori, Michael Rudman, Oscar Lichtenstein, Jorge E. Schliamser,