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Left atrial myocardial function in either physiological or pathological left ventricular hypertrophy: a two-dimensional speckle strain study
  1. A D’Andrea1,
  2. G De Corato2,
  3. R Scarafile1,
  4. S Romano3,
  5. L Reigler1,
  6. C Mita1,
  7. F Allocca1,
  8. G Limongelli1,
  9. G Gigantino1,
  10. B Liccardo1,
  11. S Cuomo1,
  12. G Tagliamonte1,
  13. P Caso1,
  14. R Calbrò1
  1. 1
    Department of Cardiology, Second University of Naples, Naples, Italy
  2. 2
    Department of Anatomy, Federico II° University, Naples, Italy
  3. 3
    Cardiology, Department of Internal Medicine and Public Health, University of L'Aquila, L'Aquila, Italy
  1. A D’Andrea, Department of Cardiology, Second University of Naples, Naples 80121, Italy; adandrea{at}napoli.com

Abstract

Background: Atrial function is an integral part of cardiac function that is often neglected. The presence of left ventricule hypertrophy (LVH) due to arterial hypertension may impair atrial function. However, it has also been suggested that physical training attenuates the age-associated impairment of diastolic filling. This study investigated whether mechanical dysfunction in the left atrium (LA) is present in patients with either physiological or pathological LVH, using two-dimensional strain rate imaging (2D strain echocardiography; 2DSE).

Methods: Standard echocardiography, exercise stress echo and 2DSE of the left atrium were performed in 40 patients with arterial hypertension, 45 age-matched elite athletes (>40 years) and 25 healthy sedentary controls. Atrial longitudinal strain was performed from the apical views for the basal segments of the LA septum, lateral wall and roof.

Results: LV mass index and ejection fraction were comparable between patients with either physiological or pathological LVH. Elite athletes showed increased LV end-diastolic diameter, end-diastolic volume and stroke volume, whereas circumferential end-systolic stress was higher in patients with hypertension. LA diameter and maximum volume were increased but similar between the two groups of patients with LVH. LA active emptying volume and fraction were both higher in patients with hypertension. Conversely, peak systolic myocardial atrial strain was significantly reduced in patients with pathological LVH compared with controls and athletes for all the analysed atrial segments (p<0.0001). Using multivariate analysis, LV end-diastolic volume/body surface area (BSA) (β coefficient 0.52; p<0.0001) and LV mass (β = 0.48; p<0.001) in athletes emerged as the only independent determinants of LA lateral wall peak systolic strain. In contrast, in patients with hypertension, an independent negative association of LA lateral wall peak systolic strain with both LV mass (β = −0.42; p<0.001) and circumferential end-systolic stress (β = −0.43; p<0.001) was found. In addition, in the overall population of patients with LVH, LA lateral wall systolic strain (β = 0.49; p<0.0001) was a powerful independent predictor of maximum workload during exercise testing.

Conclusions: 2DSE represents a promising, non-invasive, simple and reproducible technique to assess LA myocardial function in patients with either physiological or pathological LVH. LA myocardial deformation is impaired in patients with hypertension compared with age-matched sedentary controls and elite athletes, and is closely associated with functional capacity during effort.

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Footnotes

  • Competing interests: None declared.

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