myocardial functional reserve
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Author(s):  
Odaro J Huckstep ◽  
Holger Burchert ◽  
Wilby Williamson ◽  
Fernando Telles ◽  
Cheryl M J Tan ◽  
...  

Abstract Aims We tested the hypothesis that the known reduction in myocardial functional reserve in preterm-born young adults is an independent predictor of exercise capacity (peak VO2) and heart rate recovery (HRR). Methods and results We recruited 101 normotensive young adults (n = 47 born preterm; 32.8 ± 3.2 weeks’ gestation and n = 54 term-born controls). Peak VO2 was determined by cardiopulmonary exercise testing (CPET), and lung function assessed using spirometry. Percentage predicted values were then calculated. HRR was defined as the decrease from peak HR to 1 min (HRR1) and 2 min of recovery (HRR2). Four-chamber echocardiography views were acquired at rest and exercise at 40% and 60% of CPET peak power. Change in left ventricular ejection fraction from rest to each work intensity was calculated (EFΔ40% and EFΔ60%) to estimate myocardial functional reserve. Peak VO2 and per cent of predicted peak VO2 were lower in preterm-born young adults compared with controls (33.6 ± 8.6 vs. 40.1 ± 9.0 mL/kg/min, P = 0.003 and 94% ± 20% vs. 108% ± 25%, P = 0.001). HRR1 was similar between groups. HRR2 decreased less in preterm-born young adults compared with controls (−36 ± 13 vs. −43 ± 11 b.p.m., P = 0.039). In young adults born preterm, but not in controls, EFΔ40% and EFΔ60% correlated with per cent of predicted peak VO2 (r2 = 0.430, P = 0.015 and r2 = 0.345, P = 0.021). Similarly, EFΔ60% correlated with HRR1 and HRR2 only in those born preterm (r2 = 0.611, P = 0.002 and r2 = 0.663, P = 0.001). Conclusions Impaired myocardial functional reserve underlies reductions in peak VO2 and HRR in young adults born moderately preterm. Peak VO2 and HRR may aid risk stratification and treatment monitoring in this population.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M J Nobre De Matos Pereira Vieira ◽  
D Campos ◽  
M Carrington ◽  
L Goncalves ◽  
R Teixeira

Abstract Introduction 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. Purpose 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. Methods and results 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) Conclusion 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.


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