Background The aim of this study was to investigate left atrial (LA) function and synchrony in paroxysmal atrial fibrillation (PAF) patients using two‐dimensional speckle tracking echocardiography (STE). Methods Forty‐five PAF patients and 30 healthy controls were enrolled. LA peak ventricular systolic longitudinal strain (LAS‐S) and strain rate (LASR‐S) and left atrial longitudinal strain (LAS‐A) and strain rate (LASR‐A) during late diastole were determined using STE, and the standard deviation of the time to peak (TPSD) of the regional strains was calculated to quantify LA dyssynchrony. TPSD during ventricular systole and late diastole were named SDs and SDa, respectively. Results Left atrial peak longitudinal strain during ventricular systole (LAS‐S) (29.34±8.57 vs 36.73±6.13), LASR‐S (1.27±0.311 vs 1.57±0.25), LAS‐A (13.11±4.91 vs 17.86±3.57), and LASR‐A (−1.51±0.58 vs −1.90±0.30) were reduced in the PAF group compared with the controls (P<.05 for all). SDs (8.11±3.00% vs 4.67±1.48%) and SDa (5.57±2.26% vs 3.11±1.13%) were greater in PAF patients than in the controls (P<.05 for both). Furthermore, PAF patients with normal LA sizes exhibited lower LAS‐S (P<.05), LASR‐S (P<.05), LAS‐A (P<.05), and LASR‐A (P<.05) values and increased SDs (P<.05) and SDa (P<.05) values compared with the controls. Multivariate regression confirmed that SDs and SDa were powerful parameters for differentiating PAF patients from controls (SDs: sensitivity, 83%; specificity, 72%; SDa: sensitivity, 81%; specificity, 76%). Conclusions Left atrial (LA) dysfunction and dyssynchrony in PAF patients can be detected with STE even in the absence of LA enlargement. STE‐derived SDs and SDa were powerful parameters for identifying PAF patients.

BackgroundAtrial fibrillation (AF) can result in atrial functional mitral regurgitation (MR), but the mechanism remains controversial. Few data about the relationship between the 3-dimensional morphology of the MV and the degree of MR in AF exist.MethodsReal-time 3-dimensional transesophageal echocardiography (3D-TEE) of the MV was acquired in 168 patients with AF (57.7% persistent AF), including 25 (14.9%) patients with moderate to severe MR (the MR+ group) and 25 patients without AF as controls. The 3-dimensional geometry of the MV apparatus was acquired using dedicated quantification software.ResultsCompared with the group of patients with no or mild MR (the MR- group) and the controls, the MR+ group had a larger left atrium (LA), a more dilated mitral annulus (MA), a reduced annular height to commissural width ratio (AHCWR), indicating flattening of the annular saddle shape, and greater leaflet surfaces and tethering. MR severity was correlated with the MA area (r2 = 0.43, P < 0.01) and the annulus circumference (r2 = 0.38, P < 0.01). A logistic regression analysis indicated that the MA area (OR: 1.02, 95% CI: 1.01–1.03, P < 0.01), AHCWR (OR: 0.24, 95% CI: 0.14–0.35, P = 0.04) and MV tenting volume (OR: 3.24, 95% CI: 1.16–9.08, P = 0.03) were independent predictors of MR severity in AF patients.ConclusionsThe mechanisms of “atrial functional MR” are complex and include dilation of the MA, flattening of the annular saddle shape and greater leaflet tethering.

Background Left atrial (LA) function and mechanical dispersion changes in breast cancer patients treated with chemotherapy remain unclear. Hypothesis LA function and LA mechanical dispersion in breast cancer patients would be impaired after chemotherapy. Methods This single‐center retrospective study included 91 consecutive breast cancer patients treated with chemotherapy and 30 controls. Patients were examined by echocardiography three times at intervals. Conventional parameters, left ventricular strain, LA strain, and LA mechanical dispersion were evaluated and compared. Results LA strain during reservoir phase (LASr), conduit phase (LAScd), and contraction phase (LASct) all decreased markedly after chemotherapy and were lower than those of the controls (all p < .01). The standard deviation of time to peak positive strain during LA reservoir phase corrected by R‐R interval (LA SD‐TPSr) was significantly increased after chemotherapy and was higher than that of the controls ( p < .001). The change of LA function was expressed as Δ. Multivariate linear regression analyses showed that LAVIp (0.399, 95% confidence interval [CI]: 0.610, 1.756, p = .000) was independently associated with ΔLASr, LAPEF (−0.325, 95% CI: −45.123, −10.676, p = .002) and age (0.227, 95% CI: 0.021, 0.350, p = .027) were independently associated with ΔLAScd, and LAVImax (0.341, 95% CI: 0.192, 0.723, p = .001) was independently associated with ΔLASct. LAVImax (0.505, 95% CI: 0.000, 0.001, p = .039) and mitral E (−0.256, 95% CI: 0.000, 0.000, p = .024）were independently associated with ΔLA SD‐TPSr. Conclusions Mechanical function of LA declined after chemotherapy in breast cancer patients. With the decrease of LA mechanical function, LA mechanical dispersion assessed by two‐dimensional speckle‐tracking echocardiography increased significantly, and its clinical value needs to be further studied.

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Coronary artery occlusion (CAO) is a rare but life‐threatening complication of transcatheter aortic valve implantation (TAVI). The mechanism of CAO is the displacement of the native calcified valve leaflet over the coronary ostium. Here, we report on a woman who experienced sudden cardiac arrest and abrupt CAO during TAVI, which was caused by two different original obstructions, a rupture of aortic plaque or a partial tear of the aortic intima blocking the upper 2/3 of the left main trunk (LMT) ostium, and the transcatheter heart valve (THV) blocking the lower 1/3 of the LMT ostium. She was eventually successfully treated with the chimney stenting technique. Aortography other than coronary angiography was used to ascertain CAO. In patients presenting with abrupt cardiac arrest or cardiogenic shock with LMT occlusion, there must be prompt identification, and the causes of CAO may be various and rare. The identification of CAO relies not only on CAG but also on aortography, especially if the locations and origins of obstructions are special. Supportive therapy with an attempt at percutaneous revascularization is necessary. Pre‐procedural assessment is crucial prior to TAVI interventions. In cases with high risk of CAO, upfront coronary artery protection can be provided.