LAUSR

In a normal heart, the passive leg lifting maneuver (LLM) will result in an increase in myocardial contractility, according to the mechanistic concept of the Frank-Starling law. With the progression of myocardial disease this ability is impaired and the myocardial functional reserve (mFR) is reduced (Figure1 – Panel A). The variation of left ventricular global longitudinal strain (as an index of contractile function) with LLM may thus represent a marker of left ventricular mFR. To assess the variation of left ventricular global longitudinal strain (LV GLS) with LLM as a marker of mFR in a healthy population and in patients with myocardial disease (hypertrophic myocardiopathy - HCM and systolic dysfunction patients – SystDysf. We evaluated the variation of LV GLS by 2-dimensional Speckle Tracking Echocardiography (2D-STE), in response to passive LLM, in a population of 103 individuals (54 healthy individuals, 28 HCM patients and 21 left ventricular SystDysf patients). Clinical, demographic and echocardiographic parameters (including LV longitudinal mechanics obtained with 2D-STE before and after LLM) were described. The population had a mean age of 46±18 years and 55% were women. Increased venous return to the heart during LLM was confirmed by an increase in the maximal diameter of the inferior vena cava (15,1±3,6 vs 20,6±3,8 mm, p<0.001). There was a significant variation of LV GLS in healthy individuals submitted to LLM (−20,58±3,0 vs −21,5±2,6%, p=0,02, Δ 0,6%, 95% CI 0,1–1,1%). Regarding the HCM and SystDysf groups, no significant change in LV GLS was observed with LLM (−13,2±2,8 vs −12,3±2,9%, p=0,12, Δ +0,6%, 95% CI −1,4 to 0,18% and −10,2±2,5 vs 10,2±2,7%, p=0,79, Δ 0,08%, 95% CI −0,7 to 0,5%, respectively). Figure 1 (Panel B) To our knowledge, this is the first report describing the use of LV GLS and LLM to assess mFR in this clinical setting. The absolute increase of LV GLS in the healthy population suggests that this may be a reliable method and a sensitive marker to assess the mFR. Conversely, patients with HCM and with SystDysf show poor or no response to the LLM, suggesting, as expected, a low myocardial functional reserve. Given the non-invasiveness and cost-effectiveness nature of this technique, we suggest that this maneuver could pose a feasible way to assess mFR. Further studies are needed to validate this technique and to assess the role of mFR by 2D-STE as a prognostic marker.