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Left atrial (LA) size and function are known predictors of new onset atrial fibrillation (AF) in hypertrophic cardiomyopathy (HCM) patients. Components of LA deformation including reservoir, conduit, and booster function provide additional information on atrial mechanics. Whether or not LA deformation can augment our ability to predict the risk of new onset AF in HCM patients beyond standard measurements is unknown.

The role of LA volume and diameter in predicting AF onset in HCM is well established. However, studies assessing the link between LA function and AF risk are limited. Determinants of LA function in HCM are complex and may include direct, myopathic aspects (where the mutant sarcomeric protein is expressed in atrial muscle) as well as secondary hemodynamic forces relating to increased atrial pressures in outflow obstruction, mitral regurgitation and diastolic dysfunction [9, 10]. LA function can be assessed using LA ejection fraction (LAEF) and/or LA deformation analysis on 2-dimensional (2D) cardiovascular magnetic resonance (CMR) feature tracking such as LA strain. LA strain consists of reservoir, conduit, and booster components. Whilst LA conduit strain is derived from the motion of atrial tissue during passive ventricular filling, LA reservoir strain and booster strain reflect passive and active LA functions, respectively [11, 12]. Comprehensive studies in HCM patients examining the association between AF and LA reservoir, conduit, and booster strain parameters on (CMR are lacking, yet LA strain components are emerging as sensitive markers for detecting impairment in LA function [13,14,15,16,17].

In this work, we set out to test the hypothesis that LA reservoir and booster strain on CMR will improve our ability to predict risk of incident AF. We further examined the determinants of LA strain components in HCM patients.

We then included all the parameters that retained significance in the Cox multiple regression models on all HCM patients in a model (Table 4). In this, only age and LA booster function retained significance, with age being a more powerful predictor than booster strain (HR of 5.22 vs 3.08).

Univariate and multivariable determinants of LA reservoir, conduit, and booster strain are shown in Table 5. On multivariable regression analysis, age at scan associated with all three of reservoir, conduit, and booster strain. In addition, NYHA class, LV maximal wall thickness, LV mass, and LV ejection fraction (LVEF) also remained significantly associated with reservoir strain. Presence of LGE, mitral regurgitation, LV mass, and LV stroke volume also independently associated with conduit strain, whilst a history of smoking also associated with booster strain.

In this study, we used CMR to assess the role of LA deformation when compared to standard LA parameters and baseline characteristics in predicting new onset AF in HCM. In addition to age and LAEF, we have shown that LA reservoir and booster strain have the ability to augment prediction of new onset AF in HCM. Specifically, we show that LA reservoir and booster strain dysfunction are important determinants of AF risk even in those with an LA diameter less than 45 mm, a threshold set by the ESC to escalate arrhythmia surveillance frequency. Of interest, a marginally higher risk of incident AF was specifically seen in those with booster strain dysfunction compared to other parameters. We also determined the factors that associate with markers of atrial deformation and show that age and phenotypic severity adversely influenced LA deformation.

Here, we systematically examined components of LA strain as assessed on CMR, in addition to standard metrics of LA size and function. Consistent with previous studies, we found LA reservoir and conduit strain to be impaired in HCM patients [13, 31], though after correcting for multiple comparisons only conduit strain remained impaired. By contrast, LA booster strain, the active component of LA deformation, was not significantly different between HCM patients and healthy control subjects. Indeed, the evidence in support of booster dysfunction in HCM patients is conflicting. In a study by Yang and colleagues [17], LA booster strain was not different between non-obstructive HCM patients and controls. In contrast, Kowallick et al. reported a significant impairment in LA booster strain in HCM patients relative to controls [32].

A number of studies have postulated that booster function could indicate an increase in fibrotic burden of the atria [33, 34]. In a recent study by Sivalokanathan et al. [35], atrial fibrosis as detected by atrial LGE was found to be greater in those with new onset AF [35]. Likewise, in our study booster strain was reduced in those patients that developed AF compared to those that did not. Thus, the relationship between booster strain and AF may potentially reflect an increased burden of atrial fibrosis or an underlying atrial myopathy in HCM patients.

The absolute values of LA strain reported in this study were lower than those reported elsewhere [36], though comparable with some studies using CMR myocardial feature tracking. Values from healthy, yet elderly controls in studies by Evin et al. [37] and Lamy et al. [38] matched our relatively old and obese control group closely [37, 38]. The values from all HCM patients in this study are within reasonable range of those presented by Sivalokanathan et al. and Kowallick [13, 35]. In the present study, LA diameter [5], volume [6] and LAEF [7] were univariate determinants of AF risk, largely consistent with earlier work. We additionally showed that LA reservoir and booster strain are associated with a threefold and fourfold increase in new onset AF risk, respectively, and, as illustrated by the freedom-from-AF survival curves (see Fig. 2 and Additional file 1: Fig. S2), both measures discriminated risk of new onset AF with reasonable diagnostic accuracies (see Additional file 1: Table S2). Of importance, in patients with LA diameter of less than 45 mm, booster and reservoir strain remained strong independent determinants of new onset AF.

We used CMR in HCM and demonstrate that LA strain components are reduced in patients who develop AF. Specifically, reservoir and booster LA strain augment risk prediction of new onset AF in HCM patients. Our work underscores the importance of age as a guide to arrhythmia surveillance and suggests that the routine assessment of LA strain in HCM patients could augment existing tools for AF and potentially stroke prediction in HCM.

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