Aims Atrial fibrillation (AF) is more common in athletes and may be associated with adverse left atrial (LA) remodelling. We compared LA structure and function in athletes and non-athletes with and without AF. Methods and results Individuals (144) were recruited from four groups (each n = 36): (i) endurance athletes with paroxysmal AF, (ii) endurance athletes without AF, (iii) non-athletes with paroxysmal AF, and (iv) non-athletic healthy controls. Detailed echocardiograms were performed. Athletes had 35% larger LA volumes and 51% larger left ventricular (LV) volumes vs. non-athletes. Non-athletes with AF had increased LA size compared with controls. LA/LV volume ratios were similar in both athlete groups and non-athlete controls, but LA volumes were differentially increased in non-athletes with AF. Diastolic function was impaired in non-athletes with AF vs. non-athletes without, while athletes with and without AF had normal diastolic function. Compared with non-AF athletes, athletes with AF had increased LA minimum volumes (22.6 ± 5.6 vs. 19.2 ± 6.7 mL/m2, P = 0.033), with reduced LA emptying fraction (0.49 ± 0.06 vs. 0.55 ± 0.12, P = 0.02), and LA expansion index (1.0 ± 0.3 vs. 1.2 ± 0.5, P = 0.03). LA reservoir and contractile strain were decreased in athletes and similar to non-athletes with AF. Conclusion Functional associations differed between athletes and non-athletes with AF, suggesting different pathophysiological mechanisms. Diastolic dysfunction and reduced strain defined non-athletes with AF. Athletes had low atrial strain and those with AF had enlarged LA volumes and reduced atrial emptying, but preserved LV diastolic parameters. Thus, AF in athletes may be triggered by an atrial myopathy from exercise-induced haemodynamic stretch consequent to increased cardiac output.
Aims Ventricular tachycardia (VT) in ischaemic cardiomyopathy (ICM) originates from scar, identified as low-voltage areas with invasive high-density electroanatomic mapping (EAM). Abnormal myocardial deformation on speckle tracking strain echocardiography can non-invasively identify scar. We examined if regional and global longitudinal strain (GLS) can localize and quantify low-voltage scar identified with high-density EAM. Methods and results We recruited 60 patients, 40 ICM patients undergoing VT ablation and 20 patients undergoing ablation for other arrhythmias as controls. All patients underwent an echocardiogram prior to high-density left ventricular (LV) EAM. Endocardial bipolar and unipolar scar location and percentage were correlated with regional and multilayer GLS. Controls had normal GLS and normal bipolar and unipolar voltages. There was a strong correlation between endocardial and mid-myocardial longitudinal strain and endocardial bipolar scar percentage for all 17 LV segments (r = 0.76–0.87, P < 0.001) in ICM patients. Additionally, indices of myocardial contraction heterogeneity, myocardial dispersion (MD), and delta contraction duration (DCD) correlated with bipolar scar percentage. Endocardial and mid-myocardial GLS correlated with total LV bipolar scar percentage (r = 0.83; 0.82, P < 0.001 respectively), whereas epicardial GLS correlated with epicardial bipolar scar percentage (r = 0.78, P < 0.001). Endocardial GLS −9.3% or worse had 93% sensitivity and 82% specificity for predicting endocardial bipolar scar >46% of LV surface area. Conclusions Multilayer strain analysis demonstrated good linear correlations with low-voltage scar by invasive EAM. Validation studies are needed to establish the utility of strain as a non-invasive tool for quantifying scar location and burden, thereby facilitating mapping and ablation of VT.
Purpose: Left atrial (LA) function by two-dimensional (2D) strain is an emerging tool with increasing clinical utility. Age and gender are key modulators of strain parameters; however, the specific time course for LA structural and functional changes is not clearly defined. Methods: A total of 147 healthy individuals (20-69 years) underwent transthoracic echocardiography; subjects were evaluated by age (decade) and gender. LA and left ventricular (LV) volumetric and strain measurements were performed. Results: Left atrial reservoir (ƐR) and conduit strain (ƐCD) with negatively correlated with age (r =−.36; r = −.56; P < .001, respectively) being significantly lower by the 6th and 5th decades, respectively. Contractile strain (ƐCT) positively correlated with age (r = .36; P < .001), being significantly higher by the 6th decade. ƐR and ƐCD were higher in young females (20-34 years) compared to young males (P = .033 and P < .001, respectively). ƐCT was significantly higher in middle-aged adult males (35-50yrs; P = .010), though seen later in females (≥51 years; P = .005). Standard deviation of time to positive strain (SD-TPS) significantly higher by the 5th decade and correlated with age in both males (r = .44; P <.001) and females (r = .40; P = .001). Conclusion: We demonstrate that ƐR and ƐCD are lower with age, with differing rates between males and females. As a compensatory mechanism for decline in ƐCD, ƐCT is higher, more notably in males; comparatively, females display a more prominent decline in ƐR and ƐCD with age. Alteration in electromechanical properties occurred in both genders with SD-TPS becoming higher with age.
Background Subclinical left ventricular dysfunction detected by 2‐dimensional global longitudinal strain post breast radiotherapy has been described in patients with breast cancer. We hypothesized that left ventricular dysfunction postradiotherapy may be site specific, based on differential segmental radiotherapy dose received. Methods and Results Transthoracic echocardiograms were performed at baseline, 6 weeks, and 12 months postradiotherapy on 61 chemotherapy‐naïve women with left‐sided breast cancer undergoing tangential breast radiotherapy. Radiation received within basal, mid, and apical regions for the 6 left ventricular walls was quantified from the radiotherapy treatment planning system. Anterior, anteroseptal, and anterolateral walls received the highest radiation doses, while inferolateral and inferior walls received the lowest. There was a progressive increase in the radiation dose received from basal to apical regions. At 6 weeks, the most significant percentage deterioration in strain was seen in the apical region, with greatest reductions in the anterior wall followed by the anteroseptal and anterolateral walls, with a similar pattern persisting at 12 months. There was a within‐patient dose–response association between the segment‐specific percentage deterioration in strain at 6 weeks and 12 months and the radiation dose received. Conclusions Radiotherapy for left‐sided breast cancer causes differential segmental dysfunction, with myocardial segments that receive the highest radiation dose demonstrating greatest strain impairment. Percentage deterioration in strain observed 6 weeks postradiotherapy persisted at 12 months and demonstrated a dose–response relationship with radiotherapy dose received. Radiotherapy‐induced subclinical cardiac dysfunction is of importance because it could be additive to chemotherapy‐related cardiotoxicity in patients with breast cancer. Long‐term outcomes in patients with asymptomatic strain reduction require further investigation.
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