Cancer therapy-related cardiac dysfunction (CTRCD) is an emerging disease. As there is no specific treatment for CTRCD, the standard therapy for cardiac failure is typically administered. In patients with heart failure and severe secondary mitral regurgitation, transcatheter edge-to-edge repair (TEER) of the mitral valve reduces hospitalization for heart failure and all-cause mortality. However, the effectiveness of TEER in the treatment of patients with CTRCD remains unclear. A 47-year-old woman with severe heart failure was admitted to our hospital. She had a history of a modified radical mastectomy for breast cancer and anti-human epidermal growth factor receptor-2 agents were administered after anthracycline administration. Echocardiographic assessment revealed severe cardiac dysfunction, with a reduction in the left ventricular ejection fraction (LVEF) from 60% to 20%. Cardiac magnetic resonance imaging revealed high native T1 and extracellular volume values, normal T2 values, and mild late gadolinium enhancement involving the left ventricle. An endomyocardial biopsy revealed moderate interstitial and perivascular fibrosis. Electron microscopy revealed degeneration of myofibrils, proliferation of mitochondria, and the presence of autophagosomes causing vacuolation of cardiomyocytes. Due to hemodynamic disturbances, continuous dobutamine infusion therapy was initiated and cardioprotective medication was commenced and titrated. Because low cardiac function (LVEF, 26%) and severe mitral regurgitation persisted, TEER of the mitral valve was performed, resulting in a dramatic improvement in her hemodynamic status. Twelve months post-TEER, cardiac function (LVEF 61%) recovered. We report a valuable case of CTRCD in which TEER was effective for reverse remodeling by comparing imaging and pathological evaluations.

Pulmonary hypertension due to left heart disease (PH-LHD) in heart transplantation (HTx) candidates is associated with increased post-transplant mortality. Although guidelines recommend acute vasodilator challenge (AVC) with nitroprusside or milrinone, the safety and utility of inhaled nitric oxide (iNO) for AVC in this setting remain unclear.

We retrospectively reviewed 18 patients with PH-LHD referred for HTx who underwent AVC with iNO. While arterial oxygen saturation decreased after AVC (95.4 ± 2.6 to 94.1 ± 2.7%, P = 0.013), there were no significant changes in mean aortic pressure (74.5 ± 9.8 versus 74.0 ± 8.0 mmHg, P = 0.680), and no respiratory or circulatory adverse events occurred. Both mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) significantly decreased (mPAP: 36.1 ± 8.0 to 33.2 ± 7.5 mmHg, P = 0.007; PVR: 5.2 ± 2.9 to 2.9 ± 1.3 Wood Units [WU], P < 0.001). Nine patients subsequently underwent left ventricular assist device (LVAD) implantation. At 1 month after implantation, PVR decreased from pre-AVC levels (4.0 ± 1.6 to 2.9 ± 1.3 WU, P = 0.049). The percent change in PVR from pre-AVC to post-LVAD correlated with the percent change from pre-AVC to post-AVC (r = 0.76, P = 0.029).

Our preliminary findings suggest that AVC with iNO may be a useful method for evaluating the reversibility of elevated PVR and could indicate the hemodynamic response to LVAD implantation in patients with PH-LHD.

Acute myocardial infarction (AMI) impacts the regenerative capacity of hematopoietic stem and progenitor cells (HSPCs) following injury, but it remains unclear if these functional alterations persist beyond the initial ischemic event.

A minimally invasive mouse model of recurrent myocardial infarction was established using echocardiography-guided coronary interventions. Bone marrow HSPCs were quantified and analyzed for proliferation by flow cytometry and BrdU incorporation. Peripheral blood leukocytes and inflammatory cytokines (IL-6, G-CSF) were measured by flow cytometry and ELISA. Bone marrow extracellular TGF-β1 was assessed by ELISA, and its functional role was evaluated through antibody-mediated inhibition.

The minimally invasive infarction model was validated through electrocardiography, cardiac biomarkers, echocardiography, and cardiac pathology staining. Fourteen days post-I/R or sham treatment, bone marrow hematopoiesis returned to a steady state with no significant differences in Lin^-Sca-1⁺c-Kit⁺ (LSK), hematopoietic stem cell (HSC), multipotent progenitor (MPP), and granulocyte/macrophage progenitor (GMP) cell numbers. However, after a secondary ischemic challenge, there was a dampened reactive hematopoiesis indicated by reduced HSPCs, compared to the first ischemic event. BrdU incorporation analysis showed decreased HSPC proliferation activity during the reparative phase after initial ischemic challenge, linking dampened hematopoiesis to decreased HSPCs proliferation. Additionally, early recurrent infarct mice had fewer neutrophils released in peripheral blood and lower serum IL-6 and G-CSF levels. Elevated TGF-β1 levels were detected in bone marrow extracellular fluid during the reparative phase of cardiac-ischemic injury, and inhibiting TGF-β1 reversed the dampened reactive hematopoiesis of HSPCs in an early recurrent MI setting.

Our data suggest that initial myocardial ischemia challenges blunt bone marrow reactive hematopoiesis to subsequent ischemic stress, with decreased HSPC proliferation contributing to diminished regenerative capacity. TGF-β1 in bone marrow extracellular fluid may mediate this decreased HSPC proliferation.

Cell-free eosinophil granules, harmful to the heart, are stained red by haematoxylin-eosin (HE); however, they can be overlooked in cardiac tissues. Direct fast scarlet (DFS) and Congo red (CR), known for staining amyloids, may offer clearer detection of eosinophil granules; however, no firm evidence exists. This study aimed to confirm that DFS and CR stain eosinophil granules and evaluate their advantages over HE.

Paraffin-embedded endomyocardial biopsy samples from 6 patients with eosinophil-infiltrating cardiac disorders and 6 with lymphocytic myocarditis were stained.

The distributions of red granules stained with DFS and CR resembled those stained with HE in serial sections. Eosinophil granules, identified by major basic protein (MBP), were detected in intact eosinophils, identified by galectin-10, using immunofluorescence pre-scanning and were subsequently stained red by HE, DFS, and CR. MBP-positive granules surrounding galectin-10-negative cells with degenerated nuclei, indicative of cytolytic degranulation (ETosis), were also stained by HE, DFS, and CR. Non-granular MBP-positive interstitial areas were not visualised by HE, DFS, or CR, suggesting that they did not detect the deposition of granule proteins released from disrupted granules. Eosinophil granules were identified by extracting the red colour using ImageJ software in DFS-stained images, more specifically than in CR-stained or HE-stained images. Cardiologists counted more eosinophils in DFS-stained sections than in HE-stained serial sections within a certain time without miscounting.

DFS staining effectively identifies eosinophils and their cell-free granules in cardiac tissues, outperforming HE and CR. DFS may advance the diagnosis and management of eosinophil-related heart diseases.

Changes in the left ventricular ejection fraction (LVEF) of patients with cardiac sarcoidosis (CS) have been reported; however, the prognostic implications remain unknown. This study aimed to investigate the predictive factors for LVEF improvement in patients with CS and the association between LVEF improvement and prognosis. This was a post hoc analysis of the ILLUMINATE-CS registry, a multicenter retrospective study on CS. Patients with a baseline LVEF ≥ 50% were excluded. LVEF improvement was defined as the difference between the baseline and follow-up echocardiographic results. Patients were stratified based on tertiles of LVEF improvement: 1st (≤ 0%, least improved), 2nd (0-9%), and 3rd (> 9%, most improved) tertile groups. The primary outcome was all-cause mortality after follow-up echocardiography. Overall, 188 patients with CS (age: 62.1 ± 10.7 years; male proportion: 42.6%) were analyzed. In the multivariate linear regression analysis, narrower QRS duration, lower baseline LVEF, and no prescription of beta-blockers at baseline were independently associated with greater LVEF improvement. During the median follow-up period of 407 days, 26 deaths occurred. The Kaplan-Meier curves showed a significant difference between the 3 groups (log-rank test, P = 0.002). In the adjusted Cox proportional hazard analysis, the 1st and 2nd tertile groups showed progressively higher mortality rates than the 3rd tertile group. Independent of other variables, LVEF improvement as a continuous variable was associated with a lower mortality rate. Among patients with CS, LVEF improvement was significantly associated with favorable outcomes. LVEF should be monitored if baseline LVEF is decreased.

Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA) is a life-threatening condition caused by the deposition of amyloid fibrils from misfolded transthyretin in the myocardium. While protein misfolding underlies its pathogenesis, the triggers and factors driving disease progression remain unclear. This study explores the relationship between lifestyle factors, particularly oxidative stress, and the incidence of ATTRwt-CA. A lifestyle questionnaire survey was conducted among patients with and without ATTRwt-CA at Kochi Medical School Hospital, Japan. Multivariate regression models were used to assess the odds of ATTRwt-CA occurrence in individuals with identified risk factors. The mean ages of patients in the ATTRwt-CA group (n = 65) and the non-ATTRwt-CA group (n = 65) were 77.9 ± 6.5 years and 78.5 ± 7.4 years, respectively. Multiple logistic regression analysis identified male sex (adjusted odds ratio, 4.35; 95% confidence interval, 1.39-14.29; P = 0.01) as an independent risk factor for ATTRwt-CA. Past sunlight exposure of ≥ 1 hour per day (adjusted odds ratio, 3.21; 95% confidence interval, 0.87-11.88; P = 0.08) showed a tendency towards a positive association with ATTRwt-CA occurrence. In contrast, past black tea consumption (adjusted odds ratio, 0.13; 95% confidence interval, 0.01-1.28; P = 0.08) and past smoking (adjusted odds ratio, 0.29; 95% confidence interval, 0.12-0.72; P < 0.01) were tentatively or significantly associated with ATTRwt-CA occurrence. Lifestyle factors may be linked to the occurrence of ATTRwt-CA, potentially through mechanisms involving oxidative stress.

Diagnosing the cause of post-acute sequelae of COVID-19 (PASC, also known as long COVID)-related chest pain is often challenging in patients with a low pre-test probability of coronary artery disease. In a retrospective review of 273 consecutive patients who presented to the cardiovascular outpatient unit for cardiovascular PASC at the Hokkaido Cardiovascular Hospital, Japan, 8 patients were suspected to have vasospastic angina (VSA) and underwent acetylcholine provocation testing, 5 of whom (1.8%, 5/273) were newly diagnosed with VSA. Although the causal relationship between VSA and PASC should be studied further, the present study suggests that VSA can be a potential cause of chest pain in patients with PASC.

Although state-of-the-art therapy for left main disease (LMD) has been demonstrated to improve overall cardiovascular outcomes, it remains unclear whether differences in strategy and outcomes for Japanese and non-Japanese patients can be observed in a contemporary treatment.

In this international multicenter registry, we analyzed 314 patients who received state-of-the-art management for LMD, including physiology-guided revascularization, coronary interventions using the latest drug-eluting stents aided by intracoronary imaging, or surgical procedures employing internal thoracic artery grafts, in conjunction with guideline-directed medical therapy. The patient cohort was divided into Japanese (n = 122) and non-Japanese (n = 192) groups. The primary endpoint was major adverse cardiovascular events (MACE), defined as death, non-fatal myocardial infarction, and ischemia-driven target lesion revascularization. Propensity score matching was utilized to account for baseline clinical variables.

Baseline and lesion characteristics differed among groups, demonstrating higher frequency of diabetes and chronic kidney disease, higher SYNTAX score, and more severe stenosis in the Japanese cohort, resulting in a higher rate of revascularization performed (P < 0.05 for all). Percutaneous coronary intervention was significantly more frequently selected as the revascularization option (P < 0.001). While there were no significant differences in MACE between the 2 groups before adjustment, following adjustment, the Japanese cohort demonstrated significantly lower MACE at 4 years (6.3% versus 16.7%; HR: 0.37; 95%CI: 0.14-0.97; P = 0.042). Multivariate analysis further confirmed an independent association between Japanese patients and a reduced 4-year MACE risk (HR: 0.37; 95%CI: 0.14-0.96; P = 0.040).

In a contemporary study with state-of-the-art therapy for LMD, patients who underwent treatment in Japan demonstrated better cardiovascular outcomes.

Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by progressive obliteration of pulmonary arteries. Dysregulated bone morphogenetic protein (BMP) signaling pathway contributes to the development of PAH, and pulmonary vasodilators including endothelin receptor antagonists, phosphodiesterase 5 inhibitors, prostaglandins and soluble guanylate cyclase stimulators, dramatically improve the long-term prognosis. However, there still exist refractory patients who require continuous catecholamine support or lung transplantation, and the development of new treatment strategies targeting molecular mechanisms of PAH is highly anticipated. Sotatercept, a first-in-class activin signaling inhibitor, has recently been approved for the treatment of PAH, and it targets and restores an imbalance in activin-growth differentiation factor and BMP pathway signaling. In addition, treatment strategies targeting peroxisome proliferator-activated receptor-γ signaling, inflammatory and immune systems, DNA damage response and cellular senescence, and growth factor receptors including vascular endothelial growth factor and platelet-derived growth factor receptors, are being devised. In this review, we briefly summarize the recent advances in basic research paving the way for the development of more effective treatments for PAH and their potential in clinical therapeutic applications.

To date, only a few studies have assessed the dietary preferences, lifestyle habits, and risk factors of patients with acute myocardial infarction. This study aimed to investigate the dietary preferences and lifestyle habits of these patients to reflect on the implementation of an effective comprehensive diet therapy in the future.

In total, 117 patients who were admitted to Fukuoka University Nishijin Hospital due to acute myocardial infarction from April 2014 to January 2020 were enrolled. Test values, dietary preferences, and lifestyle habits as well as specificity were investigated in patients aged < 70 years (n = 62) and ≥ 70 years (n = 55).

Of the patients < 70 years of age, 56.5% preferred high-fat foods and 29.0% preferred high-salt foods, whereas of the patients ≥ 70 years of age, 41.8% preferred high-sugar foods and 32.7% preferred high-salt foods (P < 0.01). The percentages of patients who tended to eat out and drink were 60.7% and 34.2%, respectively. The percentage of patients with a smoking habit was 31.6%.

Since improved lipid levels are an important target in nutritional guidance, we should consider adjusting the diet and guiding patients to stop drinking and smoking among young people and reducing sugar and salt intake in the elderly.

Isolated cardiac sarcoidosis (iCS) is increasingly recognized; however, its prognosis and the efficacy of immunosuppressive therapy remain undetermined. We aimed to compare the prognosis of iCS and systemic sarcoidosis including cardiac involvement (sCS) under immunosuppressive therapy.

We retrospectively reviewed the clinical data of 42 patients with sCS and 30 patients with iCS diagnosed at Kyushu University Hospital from 2004 through 2022. We compared the characteristics and the rate of adverse cardiac events including cardiac death, fatal ventricular tachyarrhythmia, and heart failure hospitalization between the 2 groups. The median follow-up time was 1535 [interquartile range, 630-2555] days, without a significant difference between the groups. There were no significant differences in gender, NYHA class, or left ventricular ejection fraction. Immunosuppressive agents were administered in 86% of sCS and in 73% of iCS patients (P = 0.191). When analyzed only with patients receiving immunosuppressive therapy (sCS, n = 36; iCS, n = 21), the cardiac event-free survival was significantly lower in iCS than sCS (37% versus 79%, P = 0.002). Myocardial LGE content at the initial diagnosis was comparable in both groups. The disease activity was serially evaluated in 26 sCS and 16 iCS patients by quantitative measures of FDG-PET including cardiac metabolic volume and total lesion glycolysis, representing 3-dimensional distribution and intensity of inflammation in the entire heart. Although iCS patients had lower baseline disease activity than sCS patients, immunosuppressive therapy did not attenuate disease activity in iCS in contrast to sCS.

iCS showed a poorer response to immunosuppressive therapy and a worse cardiac prognosis compared to sCS despite lower baseline disease activity.

Congenital heart disease (CHD) accounts for nearly one-third of all major congenital anomalies, with atrial septal defect (ASD) and ventricular septal defect (VSD) being the most common forms of simple CHD, which involve a large number of susceptibility genes. However, despite extensive research, the etiology of ASD and VSD remains unclear. Yunnan Province has advantages in exploring CHD pathogenesis due to its unique genetic background. Therefore, we aimed to evaluate the association between single nucleotide polymorphisms (SNPs) of genes and susceptibility to simple CHD in a specific population by means of a case-control study. A total of 337 healthy controls and 767 patients with simple CHD (501 ASD and 266 VSD) from China were recruited. Candidate SNPs were identified through whole-genome sequencing of pooled CHD patients and controls (pool-seq). Genotyping from 1,104 samples was performed, and stratified analysis was conducted to explore the association between positive SNPs and CHD subtypes. χ² tests and logistic regression were used to analyze the relationship between each SNP and simple CHD. Of 11 SNPs identified, SOD2 rs62437333 (P = 0.005) and POU5F1 rs3130504 (P = 0.017) showed differences between the control and ASD cohorts. In the dominant inheritance model hypothesis, rs62437333 allele C carriers had increased ASD (odds ratio (OR) = 2.04, P = 0.005) and combined simple CHD risk (OR = 2.33, P = 0.012) compared to DD genotype, while rs3130504 allele C carriers had increased ASD risk (OR = 1.121, P = 0.045) compared to DD genotype.

Cholesterol crystal (CC) embolism is a disease in which CCs from atherosclerotic lesions embolize peripheral arteries, causing organ dysfunction. In this case, a patient with spontaneously ruptured aortic plaques (SRAPs) identified by non-obstructive general angioscopy (NOGA) may have developed a CC embolism. This is the first report of a CC embolism in a patient with SRAPs identified using NOGA, which further supports the previously speculated pathogenesis of CC embolism due to SRAPs.

Shoshin beriberi is a fulminant form of wet beriberi, but there are no large-scale studies detailing the clinical features of this disease. We investigated the clinical features and outcomes of Shoshin beriberi using data from a nationwide database in Japan.

Using the Diagnosis Procedure Combination database, we identified patients with Shoshin beriberi between July 2010 and March 2021. We retrospectively investigated the characteristics, comorbidities, treatment, and in-hospital mortality of patients with Shoshin beriberi. The chi-square test or Fisher's exact test was used for categorical variables, and the Mann-Whitney U-test was used for continuous variables.

We identified 62 patients with Shoshin beriberi. The median (interquartile range) age was 63 (48-69) years. Furthermore, 54 patients were male (87%). The most common comorbidity was alcohol-related disorder (34%). The median (interquartile range) length of hospital and intensive care unit stays were 17 (range, 10-35) and 5 (range, 1-9) days, respectively. The proportion of patients who received venoarterial extracorporeal membrane oxygenation, intra-aortic balloon pump, continuous renal replacement therapy, and mechanical ventilation was 11, 5, 29, and 63%, respectively. Among the patients with Shoshin beriberi, 53% received 2 or more catecholamines or inotropes. The in-hospital mortality was 23%. Impaired consciousness at admission was significantly related to in-hospital death (P < 0.001).

The present study is the first and largest to describe the clinical features of patients with Shoshin beriberi using a nationwide database. Impaired consciousness at admission was significantly associated with in-hospital death.

This study present a case of a 49-year-old woman who suffered from resistant hypertension, hypokalemia, hypomenorrhea, and infertility. She was hospitalized 6 years earlier for hypomenorrhea and abdominal pain at the Xiamen Maternity and Child Health Hospital, where she was diagnosed with Asherman syndrome. During hospitalization, a computed tomography examination revealed an adrenal mass. She was referred to Xiamen University Affiliated Zhongshan Hospital for pheochromocytoma and underwent surgical resection of the left adrenal gland. The adrenal cortex adenoma was confirmed by pathological biopsy. Six years later, the patient also presented with hypertension and hypokalemia to our emergency department. A diagnosis of 17α-hydroxylase deficiency was established through the analysis of clinical and laboratory characteristics. The genetic analysis of CYP17A1 revealed compound heterozygous mutations, 1 of which was a mutation of c.1226 C>G, and the other c.297+2T>C.

Sacubitril/valsartan improves outcomes in patients with heart failure (HF) with reduced ejection fraction. However, the relationship between longitudinal changes in natriuretic peptides and echocardiographic parameters in patients with HF treated with sacubitril/valsartan across the left ventricular ejection fraction (LVEF) range is not fully understood.

In patients with HF treated with sacubitril/valsartan, comprehensive data on natriuretic peptides, including atrial natriuretic peptide (ANP), N-terminal pro-brain-type natriuretic peptide (NT-proBNP), BNP, and echocardiography, were measured after 6 months of treatment. We assessed the change in natriuretic peptides and echocardiographic parameters in LVEF classification subgroups.

Among 49 patients, the median ANP concentration increased from 55 pg/mL at baseline to 78 pg/mL (P < 0.001). The NT-proBNP concentration decreased from 250 pg/mL to 146 pg/mL (P < 0.001). No significant change was observed in the BNP concentration (P = 0.640). The trajectories of each natriuretic peptide in patients with LVEF > 40% (n = 22) were similar to those in individuals with LVEF ≤ 40% (n = 27). Regardless of LVEF classification, echocardiography at 6 months showed a significant improvement in LVEF, left ventricular end-diastolic volume, and the ratio of early diastolic mitral inflow velocity to early diastolic mitral annulus velocity (E/e'). The reduction in natriuretic peptide concentration was related to LV reverse remodeling and decreased left and right atrial pressures assessed by E/e' and inferior vena cava diameter.

Sacubitril/valsartan induced an increase in ANP, a reduction in NT-proBNP, and no change in plasma BNP, regardless of LVEF. It caused LV reverse remodeling, and the natriuretic peptide concentration changes were associated with structural and functional echocardiographic parameters.

Whether a nodular calcification (NC), which is the precursor to intracoronary thrombosis, is focally or diffusely distributed in the coronary tree has major implications for ongoing efforts to identify. This study aimed to investigate the frequency and spatial distribution patterns of sheet calcification (SC) and NC in a 3-vessel examination of autopsied human hearts.

A total of 323 coronary artery specimens from 110 cadavers were obtained from autopsy cases. After fixation and decalcification, the coronary artery trees were cut every 5 mm into 4-μm transverse cross-sections for histological assessment. An SC was defined as a plate-like calcification of > 1 quadrant of the vessel or > 3 mm in diameter, and NC as nodular calcium deposits separated by fibrin, and a deposit size > 1 mm in diameter.

Of the 6,306 histological cross-sections, SCs and NCs were identified in 1,627 (26%) and 233 (4%) cross-sections, respectively. SCs and NCs had a similar distribution pattern in all 3 coronary arteries. In the left anterior descending artery (LAD), NCs were predominantly located in the proximal segment: the first 45 mm from the LAD ostium (72%) and the first 60 mm from the LAD ostium (84%), respectively. However, NCs were evenly distributed throughout the length of the coronary artery in the right coronary artery (RCA) and left circumflex artery (LCX).

NCs coexisted with SCs, and tended to cluster in predictable parts within the proximal segments of the LAD, but were evenly distributed throughout the RCA and LCX in coronary arteries from cadavers.

Takayasu arteritis (TA or TAK) is a chronic large vessel vasculitis with predilection to affect the aorta and its branches. The new 2022 ACR/EULAR classification criteria for Takayasu arteritis incorporated imaging characteristics as an absolute requirement. ESR and CRP fails in accuracy as disease activity markers. Pentraxin 3 appears to be a relatively superior biomarker, which correlates with ITAS 2010 as per several studies. PET-CT is also increasingly being studied for assessing disease activity with variable results. The management of TAK involves use of steroids with upfront steroid sparing immunosuppressive agents. MMF is one such conventional DMARD/immunosuppressant with good efficacy and better safety profile, as reported in various cohort studies. Tocilizumab is proved to be a rapid remission inducing agent in refractory Takayasu arteritis in observational studies. TNF inhibitors in many uncontrolled studies showed good responses, and there is a need for good RCTs for confirmation. JAK inhibitors have also been used with success in a few reports.

Arrhythmia-induced cardiomyopathy (AIC) occurring in patients with atrial fibrillation (AF) is a reversible form of cardiomyopathy characterized by LV systolic dysfunction. However, it is difficult to predict the reversibility before rhythm control therapy. We performed this study to develop a parameter for the identification of AIC in routine transthoracic echocardiography (TTE) in patients with presumptive AIC due to AF.

We retrospectively studied 72 patients treated with catheter ablation therapy for persistent AF, and LV ejection fraction (LVEF) ≤ 45%. The patients were divided into 2 groups by follow-up TTE performed within 12 ± 6 months postoperatively. Patients with ≥ 15% improvement in LVEF or ≥ 10% improvement and ≥ 50% in LVEF were classified as the AIC group, and the others were classified as the non-AIC group.

A total of 57 (79%) patients were classified as the AIC group. In the stepwise multivariate logistic regression model, LV end-diastolic dimension (LVDd) and e' (septal) were independent predictors of AIC. The sensitivities of LVDd ≤ 53 mm and e' (septal) ≥ 6.3 cm/second were 60% and 75%, respectively. Their specificities were 80% and 67%, respectively. The presence of either LVDd ≤ 53 mm or e' (septal) ≥ 6.3 cm/second had a higher sensitivity (90%); their co-occurrence had a higher specificity (93%) in predicting AIC.

The functional recovery in patients with AIC can occur in LV systolic dysfunction without remodeling and impairment of relaxation. The combination of LVDd and e' (septal) is useful in predicting AIC due to AF with routine TTE.

In heart failure with preserved ejection fraction (HFpEF), left atrial enlargement is a surrogate marker reflecting chronic left ventricular diastolic dysfunction. As a result, the left atrial volume is often evaluated in daily clinical practice to determine the presence of left ventricular diastolic dysfunction. However, recent studies have shown that left atrial dysfunction is an important factor contributing to the pathogenesis of HFpEF, and it is expected to become one of the therapeutic targets of HFpEF, rather than just a surrogate marker. Echocardiography plays a central role in the identification of left atrial dysfunction and remodeling in HFpEF. In this review, we describe an approach to the evaluation of left atrial function in HFpEF using echocardiography.