Aims Functional and structural abnormalities of the left atrium have been demonstrated to be clinically and prognostically significant in a range of cardiovascular disorders, increasing the risk of atrial fibrillation. Among the potential contributors to these aberrations, central arterial factors remain insufficiently defined. Accordingly, we sought to investigate the determinants of left atrium abnormalities in hypertension, with special focus on central haemodynamics. Methods In this retrospective, cross-sectional study, 263 patients (age 63.8 ± 8.0 years) with uncomplicated hypertension underwent echocardiography including left atrium strain (LAS) and volume analysis, and central haemodynamics assessment using radial tonometry. Results Patients were grouped depending on LAS and left atrium volume index (LAVI), using externally validated cutpoints (34.1% for LAS and 34 ml/m2 for LAVI). The subset with lower LAS ( n = 124) demonstrated higher central (cPP) and brachial pulse pressure (bPP), ventricular- arterial coupling, left ventricular mass index (LVMI) and LAVI, and lower global left ventricular longitudinal strain and early diastolic tissue velocity (e′). Patients with higher LAVI ( n = 119) presented higher systolic blood pressure, cPP, bPP, central augmentation pressure, LVMI and E/e′ ratio and lower LAS. In multivariable analysis, cPP was independently associated with both LAS ( β = –0.22; p = 0.002) and LAVI ( β = 0.21; p = 0.003). No independent associations with left atrium parameters were shown for bPP. Conclusion Higher cPP is detrimentally associated with left atrium structural and functional characteristics, thus providing a possible pathophysiological link with the development of substrate for atrial fibrillation. Prophylaxis of atrial fibrillation might be another argument for consideration in the treatment strategy in hypertension targeted measures addressing central blood pressure.
Background Recent evidence suggests that iron depletion may be involved in the pathophysiology of acute myocarditis (MCD), however no data on the contribution of this mechanism to the MCD-associated cardiac performance abnormalities are available. The decrease in longitudinal deformation is an early manifestation of left ventricular (LV) dysfunction. Nonetheless, global longitudinal strain (GLS) is afterload-dependent, and the estimation of myocardial work correcting GLS for changes in systolic blood pressure may permit a more adequate assessment of LV contractility. Aim We sought to investigate the association between iron status and LV function in patients with MCD. Methods We prospectively included 30 patients (age 32 ± 8 years; 97% male) hospitalized for acute MCD in a tertiary cardiology center. MCD was diagnosed based on the following criteria: 1) new onset symptoms suggestive of myocarditis (exercise intolerance, dyspnea, palpitations or chest pain), 2) elevated high sensitivity cardiac troponin I (hscTnI), 3) exclusion of obstructive coronary artery disease, 4) confirmation of myocardial oedema based on T2 mapping in cardiac magnetic resonance. On admission, each participant underwent echocardiography with LV strain and myocardial work (global work index [GWI], global constructive work [GCW], global wasted work [GWW], global work efficiency [GWE]) analysis, and laboratory assessment including the iron status markers: ferritin and transferrin saturation (TSAT). Iron deficiency (ID) was defined as transferrin saturation (TSAT) <20%; we did not use serum transferrin to categorize iron status because of the strong association of this marker with acute inflammation, which might affect the interpretation of its values. Results ID was found in 16 (53%) enrollees. Patients with reduced TSAT demonstrated lower GCW and GWI than their peers with normal TSAT (Table). No significant between-group differences were found for GLS, LV ejection fraction, early diastolic tissue velocity (e’) and E/e’ ratio. Both subsets did not significantly differ with respect to hemoglobin, creatinine, NT-proBNP, hscTnI and CRP. Both GWI and GCW significantly correlated with TSAT (r = 0.39, p = 0.03, and r = 0.37, p = 0.04, respectively). In multivariable analysis, after adjustment for patient age, body mass index, creatinine, hscTnI and CRP, TSAT was an independent predictor of GWI (beta = 0.40; p = 0.02) and GCW (beta = 0.38; p = 0.02). Conclusion In patients with MCD, ID defined as low TSAT is associated with a worse LV longitudinal performance as assessed by GCW and GWI, which might suggest a role of this pathophysiological pathway in the development of cardiac dysfunction. Myocardial work parameters seem to outperform GLS in diagnosing LV functional impairment in this clinical setting. Abstract P1392 Figure.
The intracellular iron depletion has been recognized to contribute to the dysregulation of cell energetics. The soluble transferrin receptor (sTfR) is regarded as a marker of cellular iron balance, and its elevated level reflects an insufficient iron delivery to target tissues. Despite the strong pathophysiological link, there is a scarcity of data on the impact of intracellular iron status on myocardial performance. Aim To investigate the association between the intracellular iron status, as assessed by sTfR, and left ventricular (LV) function in a well-characterized population with heart failure and preserved ejection fraction (HFpEF). Methods A complete echocardiogram including evaluation of LV global longitudinal deformation by speckle tracking (GLS) was performed at rest and immediately post-exercise in 83 pts (age 66 ± 8 yrs) with symptomatic HFpEF. Results Pts with the highest sTfR concentrations (from the 3rd sTfR tertile) demonstrated significantly lower exertional GLS than their peers from the other 2 tertiles and lower resting GLS vs. the 2nd tertile (Table). Exercise GLS was inversely correlated with sTfR (r=-0.27, p = 0.01), and this association remained significant after adjustment for age, sex, BMI, LV mass, exercise blood pressure, hemoglobin and serum galectin-3 – a marker of fibrosis (beta=-0.24, p = 0.04). Conclusions In HFpEF, higher sTfR reflecting a decreased global intracellular iron content is independently associated with reduced LV longitudinal contractility response to exertion. This might represent another mechanism of exercise intolerance and should be considered in management strategies in this condition. Abstract P935 Figure.
Impaired left ventricular (LV) functional reserve has been shown to contribute to exercise intolerance in heart failure. Little is known about the role of left atrial (LA) functional response to exertion in this context. LA strain has recently emerged as a valuable diagnostic marker reflecting both LA and LV performance. Aim To investigate the association between LA strain response to exercise and exercise capacity across different stages of heart failure with preserved ejection fraction (HFpEF). Methods Transthoracic echocardiography (including peak atrial longitudinal strain (PALS) and LV global longitudinal strain (GLS) assessment) was performed at rest and immediately post exercise test in 55 patients with stage A, 62 patients with stage B and 54 patients with stage C HFpEF. Results There was a progressive worsening of peak oxygen uptake from stage A through stage B to stage C, which was accompanied by a gradual impairment of changes from rest to exercise in PALS, GLS, tissue early diastolic velocity e', LA ejection fraction and E/e' ratio (Table 1). In multivariable analysis including LV and LA components of cardiac functional reserve, changes from rest to exercise in PALS (beta 0.34, SE 0.07, p<0.001), e' (beta 0.29, SE 0.07, p<0.001) and GLS (beta 0.17, SE 0.07, p=0.014) were among the independent correlates of exercise capacity. However, after adjustment for age, sex and beta-blocker treatment, only the former two remained statistically significant. Conclusions LA strain response to exercise progressively deteriorates from stage A through stage B to stage C HFpEF, and is independently associated with exercise capacity. Accordingly, it might be considered in the risk stratification of the transition from the asymptomatic phase to overt HFpEF. Funding Acknowledgement Type of funding sources: None.
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