International heart journal最新文献

Atrial fibrillation (AF) is a common arrhythmia that can reduce the quality of life of patients. Observational studies have reported that work and sleep are associated with the development of AF, but the causal relationship is unclear.Based on published genome-wide association studies (GWASs), we conducted a two-sample Mendelian Randomization (MR) analysis employing inverse variance weighted (IVW), weighted median, and MR-Egger regression analyses. We chose statistical data of 3 work factors from the MRC-IEU GWAS pipeline and 2 sleep factors from the Sleep Disorders Knowledge Portal as the exposure and the FinnGen study of AF as the outcome.The study revealed that engaging in heavy physical work was associated with an increased risk of AF (IVW OR, 1.787; 95% CI, 1.082-2.853; P = 0.023), and job satisfaction was negatively correlated with AF risk (IVW OR, 0.719; 95% CI, 0.536-0.964; P = 0.028). In addition, jobs that primarily involved walking or standing, short sleep duration (< 7 hours), and long sleep duration (≥ 9 hours) were not associated with AF. The results of the sensitivity analysis are consistent with these trends.The results support a causal relationship between heavy physical labor and increased risk of AF, and that job satisfaction has some protective effect on AF.

A 70-year-old man with esophageal cancer undergoing nivolumab treatment presented to our hospital with suspected myocarditis associated with immune checkpoint inhibitor (ICI) therapy. The initial echocardiographic assessment upon admission demonstrated a preserved left ventricular (LV) ejection fraction but impaired right ventricular (RV) function. An endomyocardial biopsy revealed significant lymphocytic infiltration and myocyte necrosis. High-dose steroid therapy was initiated on the day of admission. However, on the following day, RV function deteriorated further, and LV dysfunction emerged, resulting in hemodynamic collapse and necessitating mechanical circulatory support. Despite additional immunoglobulin therapy, cardiac function failed to improve, and the patient died 9 days after admission. This case underscores the critical need for vigilant monitoring of both LV and RV function in patients undergoing ICI therapy to detect and manage potential cardiovascular complications promptly.

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.

Coronary computed tomography angiography-derived fractional flow reserve (FFR_CT) is useful for noninvasively detecting coronary artery disease. This procedure has been covered by health insurance reimbursement in the United Kingdom, the United States of America, and Japan. This is the first study to investigate the 1-year outcomes of the FFR_CT, with management covered by health insurance from the DiscoverY of Novel Assessment Myocardial IsChemia by FFR_CT (DYNAMIC-FFR_CT) registry.In this multicenter DYNAMIC-FFR_CT registry, 410 participants who underwent FFR_CT analysis under health insurance reimbursement were prospectively enrolled at six Japanese sites between October 2019 and November 2021. In accordance with recent guidelines, all participants received appropriate revascularization and/or optimal medication therapy after FFR_CT. The following clinical outcomes through the 1-year defined major adverse cardiovascular event (MACE) were investigated: all-cause death, cardiovascular events including non-fatal myocardial infarction, and unplanned hospitalization for acute coronary syndrome leading to revascularization.Of the six MACE cases, four (1.6%) occurred in participants with an FFR_CT value ≤ 0.80, whereas two (1.3%) occurred in a participant with an FFR_CT value > 0.80.This analytical study based on the DYNAMIC-FFR_CT registry for cardiovascular conditions found no significant difference in 1-year MACE between FFR_CT≤ 0.80 and > 0.80 following guideline-based therapy. The registry was started shortly after reimbursement and had limited statistical power and selection bias. Further studies with sufficient statistical power are required.

Genetic diagnosis is becoming more prevalent in the routine care of cardiovascular disease (CVD) but is still limited to specialized institutions. Therefore, general cardiologists are also expected to acquire fundamental knowledge for incorporating genomics into the clinical practice of inherited to multifactorial CVDs. To accomplish this, the present study evaluated the utility and limitations of genetic testing in a general hospital setting.We examined 2 clinical issues: 1) the diagnostic potential of genetic tests for known inherited CVDs across 4 disease entities, i.e., familial hypercholesterolemia (FH), hypertrophic cardiomyopathy (HCM), suspected lethal arrhythmia, and aortic aneurysm/dissection (total n = 84) and 2) the genetic components associated with 2 multifactorial pathologies, cardiac hypertrophy and atrial fibrillation (AF), through a case-control study (total n = 594). We first performed targeted gene panel tests or whole-exome sequencing to identify causative gene variants for inherited CVDs; this yielded a positive test rate of 14 to 40%. The diagnosis rate for FH increased to 70% if strict eligibility criteria were adopted. The diagnosis rate for HCM also markedly increased by modifying the interpretation criteria for genetic variant pathogenicity. Furthermore, we performed gene-based burden tests and polygenic risk score (PRS) calculations for cardiac hypertrophy and AF. For example, the PRS-based genetic risk was significantly increased in early-onset (≤ 60 years) AF compared to non-AF controls (per-SD odds ratio in standardized PRS: 1.83, P = 2.6 × 10^-4).Genetic tests for CVDs may complement the diagnosis based on traditional laboratory-based diagnostics, although the currently limited capabilities of variant interpretation necessitate careful attention.

Despite its significant clinical implications, pressure overload-induced cardiac remodeling is poorly understood. This study aimed to investigate the role of Caveolae-Gαq interaction in the pathophysiology of pressure overload-induced cardiac remodeling. We used the abdominal aortic constriction (AAC) rat model and the angiotensin II-treated cell model to simulate pressure overload-induced cardiac remodeling. Histological changes were assessed using hematoxylin-eosin staining, immunofluorescence staining, and transmission electron microscopy. The expression, colocalization, and calcium response of the Caveolae-Gαq-PLCβ3 signaling pathway were evaluated using western blotting, quantitative real-time PCR, immunofluorescence staining, and calcium green labeling. We found AAC decreased Caveolin-3 expression but increased Gαq and PLCβ3 expressions. Similar trends in mRNA expression levels were observed. The caveolae's ultrastructure was deformed at 4 and 12 weeks after AAC surgery. AAC and angiotensin II treatments reduced Caveolin-3 and Gαq colocalization while increasing Gαq and PLCβ3 colocalization, and prolonging intracellular calcium response after Gαq activation. In conclusion, pressure overload-induced cardiac remodeling involves caveolar deformation and decreased Caveolae-Gαq interactions, which result in enhanced expression and functionality of Gαq-PLCβ3 signaling. These findings highlight the mechanistic importance of Caveolae-Gαq interactions in cardiac hypertrophy under pressure overload conditions.

The West Tokyo Heart Failure (WET-HF) registry has recently reported that the post-discharge prognosis for hospitalized patients with heart failure (HF) between 2011 and 2021 has been improving over time and that there has been an upward trend in the use of guideline-directed medical therapy (GDMT). However, there are few post-discharge prognostic data for elderly and frail hospitalized patients with HF. A total of 738 consecutive patients with HF hospitalized at the Konan Medical Center between April 2020 and March 2024 were retrospectively studied. The primary endpoint was cardiovascular death or HF hospitalization. The mean age and clinical frailty scale were 83.4 ± 11.0 years and 4.8 ± 2.3, respectively. The average prescription rates of GDMT at discharge over the 4-year period were 71.0% for beta-blockers, 23.4% for angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB), 42.7% for angiotensin receptor neprilysin inhibitor (ARNI), 56.1% for mineralocorticoid receptor antagonists (MRA), and 23.2% for sodium-glucose cotransporter 2 (SGLT2) inhibitors. Although, there has been an upward trend in the use of GDMT, the Kaplan-Meier curve showed no improvement in prognosis over time. Multivariate analyses showed that none of the beta-blockers, ACE-I, ARB, ARNI, MRA, or SGLT2-inhibitors at discharge reduced the primary endpoint for hospitalized patients with HF. GDMT alone may not be sufficient to improve the prognosis of elderly and frail hospitalized patients with HF. In addition to GDMT, comprehensive management by a multidisciplinary team may be vital, since currently there seems to be no one-size-fits-all approach for these patients.

Myocardial infarction (MI) is one of the leading causes of mortality in the world. Ischemia-reperfusion injury (IR) means that reperfusion therapy after MI aggravates its structural destruction, causes cell death, and leads to further damage to cardiac function. Remimazolam shows significant anti-myocardial I/R injury activity by inhibiting inflammation, alleviating MI, and enhancing cardiac function. However, the molecular mechanism is not clear. RNA N4-acetylcytidine (ac4C) modification, which is mediated by the ac4C writer N-acetyltransferase 10 (Nat10), is involved in MI. In this study, we explored the role of ac4C acetylation in the reduction of myocardial damage by treatment with remimazolam. The effect of remimazolam on myocardial I/R injury (MIRI) was examined using an MIRI mouse model. The H9C2 cells received hypoxia/reoxygenation (H/R) to simulate the condition of I/R in vivo. Pyroptosis in H9C2 cells was assessed by measuring the release of lactic dehydrogenase, and NLRP3-dependent release of inflammatory factors. The underlying mechanism was investigated by quantitative real-time PCR, Western blot, and RNA immunoprecipitation (RIP). The results suggested that remimazolam alleviated myocardial damage and inhibited NLRP3-dependent pyroptosis induced by H/R injury. Nat10-mediated ac4C acetylation levels were inhibited by treatment with remimazolam, which was reversed by Nat10 overexpression in the H/R cell model. We then found that Nat10 facilitated the ac4C acetylation of Nek7 and promoted the pyroptosis of cardiomyocytes through Nek7. In conclusion, we demonstrate that remimazolam ameliorates MI by suppressing cardiomyocyte pyroptosis via inhibiting the ac4C acetylation of Nek7. The results of this study suggest a therapeutic value for remimazolam and may provide a new potential therapeutic target for MI.

Ventricular diverticula can be divided into congenital and acquired ventricular diverticulum. Cardiac rupture is a rare occurrence of cardiac injury, but the mortality rate is very high. Some cardiac ruptures may form an acquired ventricular diverticulum. We report the case of a 57-year-old man who presented with a right ventricular diverticulum caused by traumatic ventricle rupture.A 57-year-old man was admitted with chest pain and dyspnea after falling from a high place. His condition gradually stabilized after emergency surgery and rescue treatment. One week later, the patient suddenly presented with swelling of the right upper limb. Venous thrombosis in the right upper extremity was detected by vascular color ultrasound. Further pulmonary artery computed tomography angiography (CTA) revealed an upper right pulmonary artery embolism and a diverticulum in the right ventricular wall; no obvious diverticulum or pericardial effusion was found by echocardiography. After a thorough discussion with the cardiac surgeon, anticoagulant therapy was administered and his condition was closely monitored. After 10 days, pulmonary CTA showed that the pulmonary thrombus had disappeared, but the right ventricular diverticulum was more prominent than before; therefore, anticoagulant therapy was stopped, although hemostatic drugs were not administered. The right ventricular diverticulum gradually shrank and healed.Asymptomatic cardiac diverticula may resolve spontaneously with conservative treatment. We learned from this case that the diagnostic value of cardiac CTA or pulmonary artery CTA for occult heart injury might be superior to that of cardiac ultrasound.