Key result
A 1% decrease in apical longitudinal strain was independently associated with heart failure with preserved ejection fraction compared to hypertensive heart disease (OR 1.18; 95% CI 1.02-1.37; P=0.030).
Why the study?
Hypertensive heart disease (HHD) is a key precursor to HFpEF, but whether regional differences in impaired myocardial function underlie greater mechanical dysfunction in HFpEF compared to HHD is not well understood.
Does regional myocardial deformation differ between patients with HFPEF, hypertensive heart disease, and normotensive controls?
Cohort (n=327)
Does regional myocardial deformation differ between patients with HFPEF, hypertensive heart disease, and normotensive controls?
Impaired apical mechanical function differentiates HFPEF from hypertensive heart disease and may contribute to the transition to symptomatic heart failure.
AIMS: Hypertensive heart disease (HHD) is recognized as a key clinical precursor to heart failure with preserved ejection fraction (HFPEF). However, pathophysiological transition from HHD to HFPEF is not well understood. We sought determine whether regional differences in impaired myocardial function may underlie the greater mechanical dysfunction seen in HFPEF compared to HHD. METHODS AND RESULTS: We used standardized echocardiography to assess regional myocardial deformation in a cohort of n = 327 adults with preserved left ventricular (LV) ejection fraction (≥45%), including: n = 129 with HFPEF, n = 158 with HHD and no heart failure, and n = 40 normotensive controls. From detailed measurements of LV systolic strain performed in multiple views, we derived and then compared regional measures of basal, mid-ventricular, and apical longitudinal strains. In models adjusting for clinical covariates, basal and mid-ventricular LV myocardial deformation was more impaired in HHD than in controls (P ≤ 0.003), whereas apical deformation was more impaired in HFPEF than in HHD (P = 0.005). In multivariable-adjusted analyses, only apical strain remained independently associated with HFPEF vs. HHD status [odds ratio 1.18 (1.02-1.37), P = 0.030 per 1% decrease in apical strain]. Compared to other regional strains, apical longitudinal strain optimally differentiated HFPEF from HHD (area under the receiver operating curve: apical longitudinal strain = 0.67; mid-ventricular longitudinal strain = 0.59; basal longitudinal strain = 0.60). CONCLUSION: We found that while apical mechanical function is preserved in HHD, it was impaired in HFPEF and may contribute to the transition from an asymptomatic heart disease to a symptomatic heart disease.
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Biering‐Sørensen et al. (2023) conducted a cohort in Heart failure with preserved ejection fraction (HFPEF) and Hypertensive heart disease (HHD) (n=327). Decrease in apical longitudinal strain was evaluated on HFPEF vs. HHD status (OR 1.18, 95% CI 1.02-1.37, p=0.030). A 1% decrease in apical longitudinal strain was independently associated with heart failure with preserved ejection fraction compared to hypertensive heart disease (OR 1.18; 95% CI 1.02-1.37; P=0.030).
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