Left atrial systolic force in hypertensive patients with left ventricular hypertrophy predicts atrial fibrillation. (3rd October 2022)

• Record Type: Journal Article
• Authors: Bang, C; Gerholt, L; Gerdts, E; Larstorp, A C; Kjeldsen, S; Julius, S; Wachtell, K; Okin, P; Devereux, R B
• Is Part Of: European heart journal. Volume 43(2022)Supplement 2
• Publication Date: 2022-10-03
• Subjects: Cardiology -- Periodicals; Heart -- Diseases -- Periodicals; 616.12005
• DOI: 10.1093/eurheartj/ehac544.2174
• Languages: English
• ISSNs: 0195-668X

Abstract

Abstract: Background: Recently increased left atrial systolic force (LASF), a measure of left atrial function, has been associated with left ventricular hypertrophy (LVH) in hypertensive patients. Impaired left ventricular relaxation is often seen in hypertensive patients and because of the correlated left ventricular filling impairment the atrial contribution to ventricular filling is important. LASF may increase as a compensatory response to preserve a sufficient stroke volume, which partly could explain the association between age-related prolonged left ventricular relaxation and increased LASF. Reduced left atrial function has also been shown to be associated with poor prognosis in patients with atrial fibrillation. It remains unknown whether LASF can be used as a predictor of new-onset atrial fibrillation (NOAF). Furthermore, the influence of treatment with atenolol and losartan on LASF is unclear. Purpose: We aimed to determine whether LASF correlates to incident atrial fibrillation and whether the preservation of LASF reduces the risk of new onset atrial fibrillation (NOAF). Methods: N=758 patients without atrial fibrillation at baseline were enrolled from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography sub study. Participants of the LIFE-study were randomized to either atenolol- or losartan-based treatment. Mean follow-up was 59 month. LASF was calculated using average mitral orifice area and mitral peak A velocity obtained by Doppler echocardiography. Results: At baseline 25% of patients had a LASF≤10.3kdyn. Compared to other quartiles this quartile had a higher proportion of men, lower heart rate, body mass index and age. After controlling for these variables patients in the first quartile had lower stroke volume compared to other quartiles. New-onset AF occurred in 29 (8.1/1, 000 patients-years of follow-up) patients. In multivariable Cox regression analyses with backwards elimination increasing LASF was associated with lower risk of NOAF (HR=0.90 [95% confidence interval 0.85–0.96], p=0.001). Integrated discrimination improvement was 0.054 (p=0.004) and there was a borderline significant net reclassification improvement of 19.2% (p=0.075). Over time LASF decreased more in the atenolol-based than the losartan-based treatment group (p<0.001). Conclusions: Low left atrial systolic force (LASF) was associated with higher risk of NOAF. Losartan-based treatment was associated with better preservation of LASF compared to atenolol-based treatment. Our data thus suggest that hypertensive patients with LVH and low LASF identifies a patient group with progressed left atrial dysfunction and with high risk of NOAF. Because of the preserving effect of losartan on the function and structure of the left atrium, treating hypertensive patients with LVH with losartan might decrease their risk of incident atrial fibrillation. Funding Acknowledgement: Type of funding sources: Private company. Main funding source(s): The LIFE study originally received support from Merck & Co., Inc.