The aim was to investigate LA strain by feature tracking cardiac MRI in mitral stenosis (MS) patients before and after percutaneous balloon mitral valvuloplasty (PBMV). Patients underwent cardiac MRI before and after successful PBMV (n = 18). Mitral valve area, transmitral velocity and gradients, LA volumes and ejection fraction (LAEF) were measured. LA strain feature tracking analysis was used to calculate LA reservoir, conduit, and booster strain. LA strain, LA volumes, LAEF and mitral valve severity indices were compared before and after PBMV. Correlations between LA strain and other cardiac MRI parameters were assessed. After PBMV, mitral valve area increased from 1.18 ± 0.25 cm2 to 2.26 ± 0.27 cm2, p < 0.001. Transmitral peak velocity decreased from 1.7 ± 0.37 m/s to 1.3 ± 0.27 m/s, p < 0.001. Transmitral peak gradient decreased from 12.4 ± 4.8 mmHg to 6.8 ± 2.9 mmHg, p < 0.001, and mean gradient decreased from 6.9 ± 3.8 mmHg to 2.9 ± 1.4 mmHg, p < 0.001. Maximal LA volume decreased from 73.1 ± 14.2 ml/m2 to 62.7 ± 16.3 ml/m2, p = 0.018; corrected p value = 0.054. LAEF increased from 36.3 ± 8.7% to 44.4 ± 9.5%, p = 0.010. Reservoir strain increased from 11.7 ± 3.1% to 14.9 ± 3.6% after PBMV, p = 0.009, and conduit strain from 3.8 ± 2% to 6 ± 2.3%, p = 0.005. Booster strain insignificantly increased after PBMV. Cardiac MRI feature tracking provides information on the 3 LA functional phases. Significant improvement was observed in reservoir and conduit functions after successful PBMV.

UNASSIGNED: The aim of this study was to evaluate the reservoir, conduit, and contraction function of the left atrium and to evaluate the predictive value of left atrial strain (LAS) on exercise tolerance in hypertrophic cardiomyopathy (HCM) patients with an E/e\' between 8 and 14 by two-dimensional speckle tracking using treadmill stress echocardiography.
UNASSIGNED: This was a retrospective study in which we analyzed a total of 70 patients with HCM between 2016 and 2017. According to the resting state E/e\', patients were either assigned to an HCM-1 group (E/e\' > 14) or an HCM-2 group (E/e\' of 8 to 14). Thirty age-matched healthy controls were included in the normal group. Analysis involved the left atrial reservoir, conduit, contraction strain and reserve function.
UNASSIGNED: The normal group had a higher left atrial reservoir and conduit strain than the HCM-2 group; the lowest values were in the HCM-1 group. The LAS reserve capacity of the HCM-1 and HCM-2 groups was lower than those of the normal group. The left atrial contraction strain reserve ( Δ LASct%) and global longitudinal strain reserve ( Δ GLS%) were lower in the HCM-2 and HCM-1 groups than in the normal group. We also found that the Δ LASct% and Δ GLS% in the HCM-2 group were higher than in the HCM-1 group. Furthermore, the metabolic equivalents (METS) in the HCM-2 group was greater than that in the HCM-1 group. Finally, the Rest-LASr indicated the highest differential diagnostic performance for METS < 6.0 (area under curve [AUC]: 0.759); the AUC of the composite model Rest-LASr+E/e\'-rest was 0.8.
UNASSIGNED: Analysis showed that when the E/e\' was between 8 and 14, the LAS and reserve capacity of HCM patients were significantly reduced. Our findings suggest that the routine assessment of LAS +E/e\' can be a strategy with which to supplement current predictive models and facilitate clinical management strategies.

OBJECTIVE: The aims of this study were to compare global longitudinal strain of the left ventricle (LV-GLS) and reservoir strain of the left atrium (R-LAS) values between patients with acute decompensation of chronic heart failure (HF) and a control group.
METHODS: Sixteen patients admitted to our ward for acute decompensation of HF were enrolled in this study. Transthoracic echocardiography (TTE) with two-dimensional speckle-tracking analysis (2D ST) was performed in each patient. The patients were divided into two subgroups according to the value of left ventricular ejection fraction (EF) using a cut-off value of ≤40% to distinguish heart failure with reduced ejection fraction (HFrEF) from heart failure with preserved ejection fraction (HFpEF). The control group consisted of 16 individuals without a history of cardiovascular disease, each of whom underwent 2D ST analysis as well.
RESULTS: We found that LV-GLS and R-LAS were significantly lower in both the HFrEF and HFpEF subgroups in comparison with the control group (LV-GLS: -13.4 ± 4.7% vs. -19.7 ± 2.5%, p ˂ 0.05; R-LAS: +12.2 ± 6.9% vs. +40.3 ± 7.4%, p ˂ 0.05). Furthermore, there was a significant difference in LV-GLS (-9.6 ± 3.2% vs. -15.2 ± 4.3%, p ˂ 0.05) but not in R-LAS (+13.7 ± 8.6% vs. +11.4 ± 6.2%) between the HFrEF and HFpEF subgroups.
CONCLUSIONS: Our study demonstrated a significant difference in LV-GLS and R-LAS in all enrolled HF patients compared to the control group. There was also a significant difference in LV-GLS between the HFrEF and HFpEF subgroups.

BACKGROUND: Four-dimensional flow magnetic resonance imaging (MRI) enables blood flow visualization. The absence of left atrial vortex flow (LAVF) has been implicated in the development of thrombus formation and arrhythmias. However, the clinical relevance of this phenomenon in patients with congenital heart disease (CHD) remains unclear. This study aimed to unravel the relationship of LAVF with left atrial functions in patients with CHD.
RESULTS: Twenty-five participants who underwent cardiac MRI examinations were included (8 postoperative patients with CHD aged 17-41 years and 17 volunteers aged 21-31 years). All participants were in sinus rhythm. Four-dimensional flow MRI (velocity encoding 100 cm/s) assessed the presence of LAVF, and its relationship with left atrial function determined by transthoracic echocardiography was explored. LAVF was detected in 16 patients. Upon classification of the participants based on the presence or absence of LAVF, 94% of participants in the LAVF group were volunteers, while 78% of those in the without LAVF group were postoperative patients. Participants without LAVF had a significantly lower left atrial ejection fraction (61% vs. 70%, p = 0.019), reservoir (32% vs. 47%, p = 0.006), and conduit (22% vs. 36%, p = 0.002) function than those with LAVF.
CONCLUSIONS: LAVF occurred during the late phase of ventricular systole, and left atrial reservoir function may have contributed to its occurrence. Many postoperative patients with CHD experienced a loss of LAVF. LAVF may indicate early left atrial dysfunction resulting from left atrial remodeling.

(1) Background: Atrial cardiomyopathy constitutes an intrinsically prothrombotic atrial substrate that may promote atrial fibrillation and thromboembolic events, especially stroke, independently of the arrhythmia. Atrial reservoir strain is the echocardiography marker with the most robust evidence supporting its prognostic utility. The main aim of this study is to identify atrial cardiomyopathy by investigating the association between left atrial dysfunction in echocardiography and P-wave abnormalities in the surface electrocardiogram. (2) Methods: This is a community-based, multicenter, prospective cohort study. A randomized sample of 100 patients at a high risk of developing atrial fibrillation were evaluated using diverse echocardiography imaging techniques, and a standard electrocardiogram. (3) Results: Significant left atrial dysfunction, expressed by a left atrial reservoir strain < 26%, showed a relationship with the dilation of the left atrium (p < 0.001), the left atrial ejection fraction < 50% (p < 0.001), the presence of advanced interatrial block (p = 0.032), P-wave voltage in lead I < 0.1 mV (p = 0.008), and MVP ECG score (p = 0.036). (4) Conclusions: A significant relationship was observed between left atrial dysfunction and the presence of left atrial enlargement and other electrocardiography markers; all of them are non-invasive biomarkers of atrial cardiomyopathy.

BACKGROUND: Atrial fibrillation (AF) is associated with higher risks of ischemic stroke (IS) and dementia. Whether alterations in left atrial (LA) function or size-atrial myopathy-confound these associations remains unknown.
OBJECTIVE: The purpose of this study was to examine the association of prevalent and incident AF with ischemic stroke and dementia in the ARIC (Atherosclerosis Risk In Communities) study, adjusting for LA function and size.
METHODS: Participants at visit 5 (2011-2013) with echocardiographic LA function (reservoir, conduit, contractile strain, and emptying fraction) and size (maximal, minimal volume index) data, and without prevalent stroke or dementia were followed through 2019. For analysis, we used time-varying Cox regression.
RESULTS: Among 5,458 participants (1,193 with AF, mean age of 76 years) in the stroke analysis and 5,461 participants (1,205 with AF, mean age of 75 years) in the dementia analysis, 209 participants developed ischemic stroke, and 773 developed dementia over 7.1 years (median). In a demographic and risk factor-adjusted model, AF was significantly associated with ischemic stroke (HR, 1.63; 95% CI: 1.11-2.37) and dementia (HR: 1.38, 95% CI: 1.13-1.70). After additionally adjusting for LA reservoir strain, these associations were attenuated and no longer statistically significant (stroke [HR: 1.33, 95% CI: 0.88-2.00], dementia [HR: 1.15, 95% CI: 0.92-1.43]). Associations with ischemic stroke and dementia were also attenuated and not statistically significant after adjustment for LA contractile strain, emptying fraction, and minimal volume index.
CONCLUSIONS: AF-ischemic stroke and AF-dementia associations were not statistically significant after adjusting for measures of atrial myopathy. This proof-of-concept analysis does not support AF as an independent risk factor for ischemic stroke and dementia.

Background Obesity is associated with left atrial (LA) remodeling (ie, dilatation and dysfunction) which is an independent determinant of future cardiovascular events. We aimed to assess whether LA remodeling is present in obesity even in individuals without established cardiovascular disease and whether it can be improved by intentional weight loss. Methods and Results Forty-five individuals with severe obesity without established cardiovascular disease (age, 45±11 years; body mass index; 39.1±6.7 kg/m2; excess body weight, 51±18 kg) underwent cardiac magnetic resonance for quantification of LA and left ventricular size and function before and at a median of 373 days following either a low glycemic index diet (n=28) or bariatric surgery (n=17). Results were compared with those obtained in 27 normal-weight controls with similar age and sex. At baseline, individuals with obesity displayed reduced LA reservoir function (a marker of atrial distensibility), and a higher mass and LA maximum volume (all P<0.05 controls) but normal LA emptying fraction. On average, weight loss led to a significant reduction of LA maximum volume and left ventricular mass (both P<0.01); however, significant improvement of the LA reservoir function was only observed in those at the upper tertile of weight loss (≥47% excess body weight loss). Following weight loss, we found an average residual increase in left ventricular mass compared with controls but no residual significant differences in LA maximum volume and strain function (all P>0.05). Conclusions Obesity is linked to subtle LA myopathy in the absence of overt cardiovascular disease. Only larger volumes of weight loss can completely reverse the LA myopathic phenotype.

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.
We assessed LA size, function, and deformation on cardiovascular magnetic resonance (CMR) in 238 genotyped HCM patients and compared this with twenty age, sex, blood pressure and body mass index matched control subjects. We further evaluated the determinants of new onset AF in HCM patients.
Compared to control subjects, HCM patients had higher LA antero-posterior diameter, lower LA ejection fraction and lower LA reservoir (19.9 [17.1, 22.2], 21.6 [19.9, 22.9], P = 0.047) and conduit strain (10.6 ± 4.4, 13.7 ± 3.3, P = 0.002). LA booster strain did not differ between healthy controls and HCM patients, but HCM patients who developed new onset AF (n = 33) had lower booster strain (7.6 ± 3.3, 9.5 ± 3.0, P = 0.001) than those that did not (n = 205). In separate multivariate models, age, LA ejection fraction, and LA booster and reservoir strain were each independent determinants of AF. Age ≥ 55 years was the strongest determinant (HR 6.62, 95% CI 2.79-15.70), followed by LA booster strain ≤ 8% (HR 3.69, 95% CI 1.81-7.52) and LA reservoir strain ≤ 18% (HR 2.56, 95% CI 1.24-5.27). Conventional markers of HCM phenotypic severity, age and sudden death risk factors were associated with LA strain components.
LA strain components are impaired in HCM and, together with age, independently predicted the risk of new onset AF. Increasing age and phenotypic severity were associated with LA strain abnormalities. Our findings suggest that the routine assessment of LA strain components and consideration of age could augment LA size in predicting risk of AF, and potentially guide prophylactic anticoagulation use in HCM.