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Mitral annular calcification (MAC) is a chronic degenerative process involving the fibrous support structure of the mitral valve. The prevalence of this condition significantly increases with age, and is higher in patients with cardiovascular risk factors or end-stage renal disease. However, patients with systemic lupus erythematosus (SLE) may develop atherosclerosis and MAC at a relatively young age. Caseous calcification of the mitral annulus (CCMA) is a rare subtype of MAC that occurs because of caseous transformation of the inner material. Rarely, CCMA merges with infective endocarditis (IE). This case presented an unusual example of a recurrent mass caused by CCMA after surgery for IE. A 62-year-old Japanese woman was admitted to our hospital with fever of unknown origin. She had a documented history of SLE. Blood cultures were positive, and a transesophageal echocardiography, performed to investigate IE, revealed a mass attached to the CCMA. The patient was diagnosed with IE and underwent lumpectomy. Postoperatively, the patient remained free of fever and embolism; however, the mass recurred. She was considered to have a mass due to CCMA recurrence; although revision surgery was scheduled, the mass resolved spontaneously. Therefore, owing to the risk of recurrence, CCMA requires careful preoperative and postoperative observation. Caseous calcification of the mitral annulus may rarely occur, even in middle-aged patients. This condition carries the risk of infective endocarditis complications and postoperative recurrence, and careful follow-up is required. [ABSTRACT FROM AUTHOR]

Aims Higher left ventricular (LV) ejection fraction (EF) is related to unfavourable prognosis in patients with heart failure (HF) with preserved ejection fraction (HFpEF). The cause of this finding needs to be haemodynamically explained. Thus, we investigated this crucial issue from the perspective of LV–arterial (A) and right ventricular (RV)–pulmonary arterial (PA) coupling. Methods and results Study patients were derived from our prospective cohort study of patients hospitalized due to acute decompensated HF and LVEF > 40%. We divided the 255 patients into three groups: HF with mildly reduced EF (HFmrEF), HFpEF with 50% ≤ LVEF < 60%, and HFpEF with LVEF ≥ 60%. We compared LV end-systolic elastance (Ees), effective arterial elastance (Ea), and Ees/Ea as a representative of LV–A coupling among groups and compared the ratio of tricuspid annular plane excursion to peak pulmonary arterial systolic pressure (TAPSE/PASP) as a representative of RV–PA coupling. All-cause death and readmission due to HF-free survival was worse in the group with a higher LVEF range. Ees/Ea was greater in HFpEF patients with LVEF ≥ 60% (2.12 ± 0.57) than in those with 50% ≤ LVEF < 60% (1.20 ± 0.14) and those with HFmrEF (0.82 ± 0.09) (P < 0.001). PASP was increased in the groups with higher LVEF; however, TAPSE/PASP did not differ among groups (n = 168, P = 0.17). In a multivariate Cox proportional hazard model, TAPSE/PASP but not PASP was significantly related to event-free survival independent of LVEF. Conclusion HFpEF patients with higher LVEF have unfavourable prognosis and distinctive LV–A coupling: Ees/Ea is elevated up to 2.0 or more. Impaired RV–PA coupling also worsens prognosis in such patients. Clinical trial registration URL: https://www.umin.ac.jp/ctr/index.htm Unique identifier: UMIN000017725. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to identify phenotypes with potential prognostic significance in aortic stenosis (AS) patients after transcatheter aortic valve replacement (TAVR) through a clustering approach. Methods and results: This multi-centre retrospective study included 1365 patients with severe AS who underwent TAVR between January 2015 and March 2019. Among demographics, laboratory, and echocardiography parameters, 20 variables were selected through dimension reduction and used for unsupervised clustering. Phenotypes and outcomes were compared between clusters. Patients were randomly divided into a derivation cohort (n = 1092: 80%) and a validation cohort (n = 273: 20%). Three clusters with markedly different features were identified. Cluster 1 was associated predominantly with elderly age, a high aortic valve gradient, and left ventricular (LV) hypertrophy; Cluster 2 consisted of preserved LV ejection fraction, larger aortic valve area, and high blood pressure; and Cluster 3 demonstrated tachycardia and low flow/low gradient AS. Adverse outcomes differed significantly among clusters during a median of 2.2 years of follow-up (P < 0.001). After adjustment for clinical and echocardiographic data in a Cox proportional hazards model, Cluster 3 (hazard ratio, 4.18; 95% confidence interval, 1.76–9.94; P = 0.001) was associated with increased risk of adverse outcomes. In sequential Cox models, a model based on clinical data and echocardiographic variables (χ2 = 18.4) was improved by Cluster 3 (χ2 = 31.5; P = 0.001) in the validation cohort. Conclusion: Unsupervised cluster analysis of patients after TAVR revealed three different groups for assessment of prognosis. This provides a new perspective in the categorization of patients after TAVR that considers comorbidities and extravalvular cardiac dysfunction. Graphical Abstract [ABSTRACT FROM AUTHOR]

Atrial echo beats due to a dual‐atrioventricular nodal pathway are a possible cause of fluctuating tachycardia in cycle length (CL) but have not been reported so far. Here, we present a case of an 82‐year‐old man with symptomatic atrial tachycardia (AT), which was accompanied by periodic fluctuations in atrial sequence at the coronary sinus. Electrophysiological study (EPS) for atrioventricular conduction and three‐dimensional (3D) electro‐anatomical mapping system explained that the mechanism of periodic fluctuations was due to atrial echo beats through a dual‐atrioventricular nodal pathway. [ABSTRACT FROM AUTHOR]

To investigate the effect of left ventricular ejection fraction (LVEF) on the behavior of N-terminal pro-brain natriuretic peptide (NT-proBNP) levels in patients with heart failure and type 2 diabetes mellitus with the use of canagliflozin compared to glimepiride. Patients (n = 233) from the CANDLE trial were randomly assigned to either the add-on canagliflozin (n = 113) or glimepiride treatment groups (n = 120). The patients were followed-up for 24 weeks. The NT-proBNP levels were measured at baseline and after 24 weeks. The LVEF was determined at baseline. There was a significant relationship between the baseline NT-proBNP level (X1) and the change in NT-proBNP levels from baseline to 24 weeks (Y) in the canagliflozin group (Y = −0.533 × X1 + 178; r = −0.860, p < 0.001). However, this relationship was not observed in the glimepiride group (p = 0.428). The baseline LVEF (X2) correlated with Y with a marginal significance in the canagliflozin group (Y = 7.72 × X2–549; r = 0.192, p = 0.054), but no relationship was observed in the glimepiride group. In the canagliflozin group, bivariate regression analysis showed a significant correlation between Y, X1, and X2; Y = −0.567 × X1–6.04 × X2 + 542 (R = 0.871, p < 0.001). The partial regression coefficients of X1 (p < 0.001) and X2 (p = 0.006) significantly explained the variance in Y. The correlation coefficient for X2 was negative. There was a significant relationship between the logarithmically transformed NT-proBNP [ln(NT-proBNP)] at baseline (X1′) and the change in ln(NT-proBNP) values from baseline to 24 weeks (Y′), a surrogate of the rate of change in NT-proBNP levels, in the canagliflozin group (Y′ = −0.18 × X1′ + 0.93; r = 0.450, p = 0.001). The baseline NT-proBNP level significantly affected the extent and the rate of its decrease by canagliflozin. The reduction in NT-proBNP levels by canagliflozin was prominent in patients with a higher LVEF at baseline. However, its confounding effect of LVEF on canagliflozin treatment was not recognized without adjusting for the NT-proBNP level at baseline. [Display omitted] • Baseline N-terminal pro-brain natriuretic peptide (NT-proBNP) levels affected the extent of its decrease by canagliflozin. • Decrease in NT-proBNP levels was prominent in patients with a higher left ventricular ejection fraction (LVEF). • Baseline LVEF confounded those changes after adjusting for baseline NT-proBNP levels. [ABSTRACT FROM AUTHOR]

Aims Newly introduced drugs for heart failure (HF) have been reported to improve the prognosis of HF with preserved ejection fraction (HFpEF) in the lower range of left ventricular ejection fraction (LVEF). We hypothesized that a higher LVEF is related to an unfavourable prognosis in patients with HFpEF. Methods and results We tested this hypothesis by analysing the data from a prospective multicentre cohort study in 255 patients admitted to the hospital due to decompensated HF (LVEF > 40% at discharge). The primary endpoint of this study was a composite outcome of all-cause death and readmission due to HF, and the secondary endpoint was readmission due to HF. LVEF and the mitral E / e ′ ratio were measured using echocardiography. In multicovariate parametric survival time analysis, LVEF [hazard ratio (HR) = 1.046 per 1% increase, P = 0.001], concurrent atrial fibrillation (AF) (HR = 3.203, P < 0.001), and E / e ′ (HR = 1.083 per 1.0 increase, P < 0.001) were significantly correlated with the primary endpoint. In addition to these covariates, angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) use was significantly correlated with the secondary endpoint (HR = 0.451, P = 0.008). Diagnostic performance plot analysis demonstrated that the discrimination threshold value for LVEF that could identify patients prone to reaching the primary endpoint was ≥57.2%. The prevalence of AF or E / e ′ ratio did not differ significantly between patients with LVEF ≥ 58% and with 40% < LVEF < 58%. Conclusion A higher LVEF is independently related to poor prognosis in patients with HFpEF, in addition to concurrent AF and an elevated E / e ′ ratio. ACEI/ARB use, in contrast, was associated with improved prognosis, especially with regard to readmission due to HF. Clinical Trial Registration https://www.umin.ac.jp/ctr/index.htm Unique identifier UMIN000017725 [ABSTRACT FROM AUTHOR]