Abstract

BackgroundAtrial fibrillation (AF) is the most common arrhythmia in hypertrophic cardiomyopathy (HCM) and is associated with adverse outcomes in HCM patients. Although the left atrial (LA) diameter has consistently been identified as a strong predictor of AF in HCM patients, the relationship between LA dysfunction and AF still remains unclear. The aim of this study is to evaluate the LA function in patients with non-obstructive HCM (NOHCM) utilizing cardiovascular magnetic resonance feature tracking (CMR-FT).MethodsThirty-three patients with NOHCM and 28 healthy controls were studied. The global and regional LA function and left ventricular (LV) function were compared between the two groups. The following LA global functional parameters were quantitively analyzed: reservoir function (total ejection fraction [LA total EF], total strain [εs], peak positive strain rate [SRs]), conduit function (passive ejection fraction [LA passive EF], passive strain [εe], peak early-negative SR [SRe]), and booster pump function (active ejection fraction [LA active EF], active strain [εa], peak late-negative SR [SRa]). The LA wall was automatically divided into 6 segments: anterior, antero-roof, inferior, septal, septal-roof and lateral. Three LA strain parameters (εs, εe, εa) and their corresponding strain rate parameters (SRs, SRe, SRa) during the reservoir, conduit and booster pump LA phases were segmentally measured and analyzed.ResultsThe LA reservoir (LA total EF: 57.6 ± 8.2% vs. 63.9 ± 6.4%, p < 0.01; εs: 35.0 ± 12.0% vs. 41.5 ± 11.2%, p = 0.03; SRs: 1.3 ± 0.4 s− 1 vs. 1.5 ± 0.4 s− 1, p = 0.02) and conduit function (LA passive EF: 28.7 ± 9.1% vs. 37.1 ± 10.0%, p < 0.01; εe: 18.7 ± 7.9% vs. 25.9 ± 10.0%, p < 0.01; SRe: − 0.8 ± 0.3 s− 1 vs. -1.1 ± 0.4 s− 1, p < 0.01) were all impaired in patients with NOHCM when compared with healthy controls, while LA booster pump function was preserved. The LA segmental strain and strain rate analysis demonstrated that the εs, εe, SRe of inferior, SRs, SRe of septal-roof, and SRa of antero-roof walls (all p < 0.05) were all decreased in the NOHCM cohort. Correlations between LA functional parameters and LV conventional function and LA functional parameters and baseline parameters (age, body surface area and NYHA classification) were weak. The two strongest relations were between εs and LA total EF(r = 0.84, p < 0.01), εa and LA active EF (r = 0.83, p < 0.01).ConclusionsCompared with healthy controls, patients with NOHCM have LA reservoir and conduit dysfunction, and regional LA deformation before LA enlargement. CMR-FT identifies LA dysfunction and deformation at an early stage.

Highlights

  • Atrial fibrillation (AF) is the most common arrhythmia in hypertrophic cardiomyopathy (HCM) and is associated with adverse outcomes in HCM patients

  • The left atrial (LA) reservoir (LA total ejection fraction (EF): 57.6 ± 8.2% vs. 63.9 ± 6.4%, p < 0.01; εs: 35.0 ± 12.0% vs. 41.5 ± 11.2%, p = 0.03; strain rate (SR): 1.3 ± 0.4 s− 1 vs. 1.5 ± 0.4 s− 1, p = 0.02) and conduit function (LA passive EF: 28.7 ± 9.1% vs. 37.1 ± 10.0%, p < 0.01; εe: 18.7 ± 7.9% vs. 25.9 ± 10.0%, p < 0.01; Peak early-negative strain rate (SRe): − 0.8 ± 0.3 s− 1 vs. -1.1 ± 0.4 s− 1, p < 0.01) were all impaired in patients with non-obstructive HCM (NOHCM) when compared with healthy controls, while LA booster pump function was preserved

  • The LA segmental strain and strain rate analysis demonstrated that the εs, εe, SRe of inferior, SRs, SRe of septal-roof, and Peak late-negative strain rate (SRa) of antero-roof walls were all decreased in the NOHCM cohort

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Summary

Introduction

Atrial fibrillation (AF) is the most common arrhythmia in hypertrophic cardiomyopathy (HCM) and is associated with adverse outcomes in HCM patients. The left atrial (LA) diameter has consistently been identified as a strong predictor of AF in HCM patients, the relationship between LA dysfunction and AF still remains unclear. Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disorder and has a prevalence of 1/ 200 people [1]. Increased LA diameter has consistently been identified as a strong predictor of AF in HCM [2, 3]. Some studies have shown that enlargement of the LA results from left ventricular (LV) diastolic dysfunction [4, 5]. Elevated LV filling pressures from LV diastolic dysfunction are transmitted back to the LA, which results in LA enlargement and dysfunction [6]. The normal function of the LA is to fill the LV and can be separated into three portions: (1) reservoir function (collection of pulmonary venous blood during LV systole); (2) conduit function (passage of pulmonary venous blood flow to LV during early LV diastole); (3) booster pump function (augment LV filling during late LV diastole/atrial systole) [7]

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